Charles Barker : Copper I vs Lyme's Disease -- video, patents **[![](0logo.gif)](http://www.rexersearch.com)** [**rexresearch.com**](http://www.rexersearch.com) --- **Charles BARKER*, et al.* Copper-1 vs Lyme's Disease** --- [**https://mitocopper.com**](https://mitocopper.com)[**https://mitocopper.com/?afmc=5c&utm\_campaign=5c&utm\_source=leaddyno&utm\_medium=affiliate**](https://mitocopper.com/?afmc=5c&utm_campaign=5c&utm_source=leaddyno&utm_medium=affiliate) **Mitocopper battles Lyme and Syphilis Bacteria ! Check out Mitocopper !** --- [**https://vimeo.com/348475547**](https://vimeo.com/348475547) **Lyme Disease Natural Cure, Treatment** --- **US9040514** **CHLOROBIS COPPER (I) COMPLEX COMPOSITIONS AND METHODS OF MANUFACTURE AND USE** Inventor(s): KERRIGAN SEANa[US]; MENTE NOLANa[US]; BARKER CHARLES LOUIS ALBARTUSa[US] + Applicant(s): LAB PHARMA INTERNATIONAL A method of manufacturing an anhydrous copper complex of formula C12H10ClCuN2O4 and methods of treating neuromuscular and other diseases, including but not limited to fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, Alzheimer's, dementia, amyotrophic lateral sclerosis, depression, lyme disease, lyme disease co-infection, gastroparesis (GP), myopathy, chronic inflammation and/or incontinence. The anhydrous copper complex preferably is administered in a pharmaceutical and/or dietary supplement composition of the invention. **RELATED APPLICATION DATA** [0001] This application is a continuation of U.S. patent application Ser. No. 14/237,876 filed Feb. 8, 2014 (published as U.S. Publication No. 20140243301), which is the U.S. National Stage of International Application No. PCT/US2012/050212, filed Aug. 9, 2012, which claims the benefit of U.S. Provisional Application No. 61/521,698 filed Aug. 9, 2011, the contents of each of which are hereby incorporated by reference in their entireties. **BACKGROUND OF THE INVENTION****[0002] 1. Field of the Invention** [0003] The present invention is directed to pharmaceutical and/or dietary supplement compositions and methods of treating neuromuscular and other diseases, including but not limited to fibromyalgia, multiple sclerosis, muscular dystrophy, Alzheimer's, dementia, amyotrophic lateral sclerosis, depression, and/or rheumatoid arthritis. The present invention also encompasses pharmaceutical and/or dietary supplement compositions and methods of treating other physical ailments and disorders, including but not limited to pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, lyme disease, lyme disease co-infection, gastroparesis (GP), myopathy, chronic inflammation and/or incontinence. The method typically comprises administration to a subject in need thereof an anhydrous copper complex of formula C12H10ClCuN2O4. The invention also generally relates to pharmaceutical treatment regimes and methods of making the anhydrous copper complex of the present invention. **[0004] 2. Discussion of the Background** [0005] A litany of human diseases and other ailments are characterized by neuromuscular degeneration and muscle weakness. The term aneuromuscular diseasea refers to disorders that adversely affect muscle function and/or the control thereof by the central nervous system (CNS). In general, neuromuscular diseases encompass a wide range of physical ailments characterized by impaired muscle function. The following (non-limiting) list of conditions is generally recognized as neuromuscular diseases or conditions: multiple sclerosis, muscular dystrophy, rheumatoid arthritis, fibromyalgia, myopathy, inflammatory bowel disease (IBD), incontinence, inflexibility, impaired fine motor skills, and amyotrophic lateral sclerosis (aALSa or Lou Gehrig's disease). [0006] A stroke, formerly known as a cerebrovascular accident (CVA), often results in severe neurological impairment. Post-stroke, many individuals suffer one or more neurological impairments including, but not limited to: loss of fine motor control, paralysis, speech impairment/loss (aphasia and/or dysarthria), altered smell, taste, hearing, or vision, ptosis, ocular and facial muscle weakness, diminished reflexes, loss of balance, altered heart rate, apraxia, loss of memory, and/or confusion. [0007] Numerous therapeutic methodologies are presently available for the treatment of neurological conditions such as the ones listed above. Efficacious treatments have proven elusive, however, and existing drugs with the most promise often exhibit the most undesirable side effects. [0008] Two of the most prominent diseases associated with impaired neurological function are MD, MS and RA. These diseases and currently available treatments therefore, are discussed in greater detail herein below. **Muscular Dystrophy** [0009] The term Muscular Dystrophy (MD) actually refers to a group of diseases characterized by muscle weakness and/or impaired muscle function. The specific diseases include, but are not limited to Becker, Duchenne, and Emery-Dreifuss. Over 100 diseases, however, display symptoms similar to MD. All are characterized by reduced muscle function and muscle weakness. [0010] No cure exists for MD and many of the related pathologies. Physical and occupational therapy may help those afflicted with MD manage life with the disease, but neither therapy ameliorates or reverses the disease's underlying causes or symptoms. Antisense oligonucleotides have shown promise as a treatment, but are costly and difficult to obtain for many MD patients. As a result, a significant need exists for a cost-effective, widely available treatment for MD (and related pathologies). **Multiple Sclerosis** [0011] Multiple Sclerosis (MS) is an autoimmune disease diagnosed in 350,000-500,000 people in the United States. The disease is characterized by multiple areas of inflammation and scarring of the myelin in the brain and spinal cord. Patients inflicted with the disease exhibit varying degrees of neurological impairment depending on the location and extent of the myelin scarring. Typical MS symptoms include fatigue, weakness, spasticity, balance problems, bladder and bowel problems, numbness, loss of vision, tremors, and depression. Available treatments of MS generally only alleviate symptoms or delay the progression of the disability. Recently developed treatments for MS (including stem cell implantation and gene therapy) appear to be only conservatory. Consequently, improved approaches for the treatment of MS are needed. **Rheumatoid Arthritis** [0012] Rheumatoid Arthritis (RA) is another troublesome disorder associated with inflammation. It is signified by chronic inflammation in the membrane lining (the synovium) of the joints and/or other internal organs. These inflammatory cells can also damage bone and cartilage. For example, a joint inflicted with RA may lose its shape and alignment, which can result in the loss of range of motion. RA is characterized by pain, stiffness, warmth, redness and swelling in the joint, and other systemic symptoms like fever, fatigue, and anemia. RA currently affects roughly 1% of the entire U.S. population (approximately 2.2 million people). The pathology of RA is not fully understood, although it has been hypothesized to result from a cascade of aberrant immunological reactions. [0013] In many cases, conventional treatments for RA have proven inefficient. For example, RA responds only partially to symptomatic medications such as corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). These medications have been around since the 1950's, and possess a significant risk of contraindications. Moreover, the therapeutic effects of anti-rheumatic drugs (DMARDs) such as Methotrexate (MTX) are frequently inconsistent and only temporary. The latest class of abiologica DMARDs (including ENBRELA(r), REMICADEA(r), HUMIRAA(r), and KINERETA(r)) have shown promising treatment results, but significant concerns exist regarding their long term safety profile. For example, studies have shown an association between the use of both ENBRELA(r) or REMICADEA(r) and the development of lymphoma. Other reports have demonstrated that patients treated with either drug exacerbate their congestive heart failure and develop serious infection and sepsis, and aggravate symptoms of MS and other central nervous system problems. As with MS, a need exists for more effective treatments of RA. **Lyme Disease** [0014] Lyme disease is a bacterial infection (borrelia burgdorferi) spread by ticks. The number of reported cases of Lyme disease, and the number of geographical areas in which it is found, has been increasing. In addition to causing arthritis, lyme disease can also cause heart, brain, and nerve problems. Early symptoms include skin-rash, flu-like symptoms (.e.g. chills, fever, swollen lymph nodes, headaches, fatigue, muscle aches/pains, and joint pain). More advanced symptoms include nerve problems and arthritis. Currently, there is no available vaccine on the market in the US for lyme disease. **Lyme Disease Co-Infection** [0015] Often, ticks can become infected with multiple disease-causing microbes, resulting in co-infection. This may be a potential problem for humans, due to Borrelia burgdorferi, and other harmful pathogens carried and transmitted by some ticks. Possible co-infections with viruses such as lyme borreliosis, anaplasmosis, babesiosis, or encephalitis may occur. It is not known how co-infection may affect disease transmission and progression, but may help in diagnosing and treating lyme and other such diseases. Currently, there is no reliable and regular treatment for lyme disease co-infection. **Gastroparesis** [0016] Gastroparesis is a condition characterizes by the inability of the stomach to empty its contents, when there is no blockage (obstruction). The cause of gastroparesis is not known. There is some evidence that it may be caused by a disruption of nerve signals to the stomach. The condition is a complication of diabetes and of some surgeries. Risk factors associated with gastroparesis may include diabetes, gastrectomy (surgery to remove part of the stomach), systemic sclerosis, use of medication that blocks certain nerve signals (anticholinergic medication). Symptoms may include abdominal distention, hypoglycemia (in people with diabetes), nausea, premature abdominal fullness after meals, weight loss, and vomiting. If gastroparesis is caused by a condition that is reversible (e.g. pancreatitis), when the condition is resolved, the symptoms will subside. For some diabetics, better control of their blood sugar can also improve the symptoms. If there is no reversible cause, gastroparesis rarely resolves itself and the symptoms often grow more sever with time. When accompanied by motility disorders of the muscles of the small intestine, gastroparesis is particularly difficult to treat. **SUMMARY OF THE INVENTION** [0017] The objective of the present invention is to provide pharmaceutical and/or dietary supplement compositions and methods of making and using the same to treat and reduce many of the symptoms of several diseases. The compositions contain an active pharmacological ingredient comprised of a novel anhydrous copper complex of formula C12H10ClCuN2O4. The pharmacologically active ingredient may be administered alone or in combination with additional active or inert agents or therapies (e.g. other anti-inflammatory agents, diluents, and/or excipients). [0018] The pharmacologically active ingredient of the present invention possesses the following chemical structure, referred to herein as Formula I: [0019] The present invention is also directed to a method of treating diseases and other physical ailments or disorders. In a preferred embodiment the method comprises the step of administering to a subject in need thereof an anhydrous copper complex of formula [0020] C12H10ClCuN2O4 to reduce and/or treat a disease or physical ailment or disorder. Preferably the disease or physical ailment being treated is a neuromuscular disease. The treated diseases or disorders (or other physical ailments) include, but are not limited to: fibromyalgia, spinal cord injury, multiple sclerosis, muscular dystrophy, stroke, rheumatoid arthritis, pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, lyme disease, lyme disease co-infection, gastroparesis (GP), chronic inflammation, myopathy, chronic inflammation, and/or incontinence. It is also preferable that the subject be diagnosed with one of the diseases and/or disorders prior to treatment. Preferred embodiments of the compositions of the present invention, including recommended dosages and methods of use, are more fully described below in the Detailed Description. **BRIEF DESCRIPTION OF THE DRAWINGS** [0021] Illustrative and exemplary embodiments of the invention are shown in the drawings in which: [0022] FIG. 1 depicts imagery obtained from Scanning Electron Microscope (SEM) analysis of a preferred embodiment of the present invention. [0023] FIG. 2 depicts imagery obtained from Scanning Electron Microscope (SEM) analysis of a preferred embodiment of the present invention. [0024] FIG. 3 shows the quantitative results obtained by mass spectrometry analysis of a preferred embodiment of the composition of the invention. [0025] FIG. 4 shows the O K results obtained by mass spectrometry analysis of a preferred embodiment of the composition of the invention. [0026] FIG. 5 shows the Cl K results obtained by mass spectrometry analysis of a preferred embodiment of the composition of the invention. [0027] FIG. 6 shows the Cu K results obtained by mass spectrometry analysis of a preferred embodiment of the composition of the invention. [0028] FIG. 7 shows the N K results obtained by mass spectrometry analysis of a preferred embodiment of the composition of the invention. [0029] FIG. 8 depicts imagery obtained from Scanning Electron Microscope (SEM) analysis of a preferred embodiment of the present invention. [0030] FIG. 9 depicts imagery obtained from Scanning Electron Microscope (SEM) analysis of a preferred embodiment of the present invention. [0031] Elements and facts in the figures are illustrated for simplicity and have not necessarily been rendered according to any particular sequence or embodiment. **DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS** Chemical Structure and Properties: [0032] The present invention is directed to pharmaceutical and/or dietary supplement compositions for treating a neuromuscular disease or other disorder. The diseases capable of treatment by the compositions of the present invention include, but are not limited to: fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, Alzheimer's, dementia, amyotrophic lateral sclerosis (aALSa or Lou Gehrig's disease), amyotrophic lateral sclerosis, depression, pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, lyme disease, lyme disease co-infection, gastroparesis (GP), myopathy, chronic inflammation, incontinence and/or depression. The treatment of the present invention comprises administering to a subject in need thereof a compound of formula C12H10ClCuN2O4, preferably the chemical structure is of Formula I: [0033] The present invention is further directed to pharmaceutical and/or dietary supplement compositions for treating a physical ailment or disorder including, but not limited to: stroke, pain, fatigue, sleeplessness, inflexibility, myopathy, incontinence, impaired fine motor skills, high cholesterol, low sperm count, obesity, alopecia, burns, stretch marks, scars, Attention Deficit Disorder (ADD), Attention Deficit Hyperactivity Disorder (ADHD), and erectile dysfunction. The treatment of the present invention comprises administering to a subject in need thereof a compound of formula C12H10ClCuN2O4 (e.g., aFormula Ia): Preferably the subject is first diagnosed with one of the disease listed above before treatment. [0034] In an alternate embodiment, the present invention is further directed to pharmaceutical and/or dietary supplement compositions for treating post-stroke symptoms, including, but not limited to: loss of fine motor control, paralysis, speech impairment/loss (aphasia and/or dysarthria), altered smell, taste, hearing, or vision, ptosis, ocular and facial muscle weakness, diminished reflexes, loss of balance, altered heart rate, apraxia, loss of memory, and/or confusion. The treatment of the present invention comprises administering to a subject in need thereof a compound of formula C12H10ClCuN2O4 (e.g., aFormula Ia): [0035] Advantageously, the present invention is further directed to pharmaceutical and/or dietary supplement compositions for promoting one or more desired health benefits. In a preferred embodiment, the compositions of the present invention promote hair growth, skin healing, scar removal, nerve growth, muscle growth, enhanced athletic performance, reduced post-traumatic healing time, post-surgery healing, and/or enhanced libido. [0036] Optionally, the compositions of the present invention are used in combination with additional active or inert agents or alternative therapies (e.g. other anti-inflammatory agents, diluents, and/or excipients). In a preferred embodiment, the alternative therapy is ozone therapy. Preferably, use of the compositions of the present invention enhances the effectiveness of the alternative therapy. Preparations and Administrations: [0037] The invention may be used to treat an animal with a disease or physical ailment or disorder including, but not limited to, one or more of the following: fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, Alzheimer's, dementia, ALS, depression, pain, fatigue, sleeplessness, inflexibility, myopathy, lyme disease, lyme disease co-infection, gastroparesis (GP), chronic inflammation, incontinence, impaired fine motor skills, high cholesterol, low sperm count, obesity, alopecia, burns, stretch marks, scars, ADD, ADHD, and/or erectile dysfunction, wherein it is preferable that the animal is a mammal and more preferable that the mammal is a human. [0038] Formula I is comprised of an anhydrous chlorobis copper I complex (nicotinic acid). Preferably, the pharmaceutical composition containing an effective amount of Formula I further comprises copper ascorbate (esterified Vitamin C), ascorbic acid (Vitamin C), and/or a pharmaceutically acceptable excipient (carrier). More preferably, the pharmaceutically acceptable carrier is an inert diluent. [0039] Frequency of dosage may vary depending on the purity of the compound and the particular disease or physical ailment treated. However, for treatment of most diseases and physical ailments, a dosage regimen of (4) 2.5 mg capsules (for a total of 10 mg/day) containing Formula I is preferred. As will be understood by one skilled in the art, however, the optimal dosage level for a particular subject will vary depending on a plurality of factors including the potency and activity of the pharmacologically active ingredient (e.g., Formula I), as well as the age, body weight, general health, sex, diet, time of administration, route of administration and rate of excretion, drug combination (if any) and the severity of the particular disease or physical ailment undergoing therapy. Subject to the above factors, a generally effective amount of Formula I is between 1 mg and 20 mg per day. More preferably, the effective amount of Formula I is between 5 mg and 10 mg per day. Advantageously, the effective amount of Formula I is between 7.5 mg to 10 mg per day. Most preferably (subject to the factors listed above), the effective amount of Formula I is 10 mg/per day. [0040] Formula I may also comprise a component of an overall pharmaceutical treatment regime for reducing and/or treating a disease or physical ailment or other disorder including, but not limited to: fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, Alzheimer's, dementia, ALS, depression, pain, fatigue, sleeplessness, inflexibility, myopathy, incontinence, impaired fine motor skills, high cholesterol, low sperm count, obesity, alopecia, burns, stretch marks, scars, ADD, ADHD, and/or erectile dysfunction, the treatment regime comprising: administering to a subject at the least the following pharmacologically active ingredient(s) within a 24-hour period: a compound of Formula I, and optionally a pharmaceutically acceptable carrier, wherein the pharmacologically active ingredient(s) is in an amount sufficient to reduce the symptoms of the ailment. [0041] Optionally, the pharmaceutical treatment regime including Formula I may include (or be combined with) additional pharmacologically active ingredients or other complementary treatments in order to provide synergistic therapeutic effects. For example, Formula I may be administered in combination with additional pharmacologically active agents including, but not limited to, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, disease modifying anti-rheumatic drugs (DMARDs), biologic DMARDs, and/or cyclooxygenase-2 (COX-2) inhibitors. In a preferred embodiment, Formula I is administered in combination with ozone therapy. [0042] The pharmaceutical and/or dietary supplement compositions (containing Formula I) of the present invention may take a variety of forms specially adapted to the chosen route of administration. The compositions may be administered orally, topically, parenterally, by inhalation or spray, or by any other conventional means. Preferably, the compositions are prepared and administered in dosage unit formulations containing conventional non-toxic pharmaceutically acceptable carriers, adjuvants and vehicles. In one preferred embodiment, the composition is administered sublingually. It is further understood that the preferred method of administration may be a combination of methods. Oral administration in the form of a capsule, pill, elixir, syrup, lozenge, troche, or the like is particularly preferred. The pharmaceutical compositions of the present invention (containing Formula I) are preferably in a form suitable for oral use, for example, as tablets, troches, lozenges, aqueous or oily suspensions, dispersible powders or granules, emulsion, hard or softgel capsules, or syrups or elixirs. [0043] Compositions intended for oral use may be prepared according to any method known in the art for manufacture of pharmaceutical compositions, and such compositions may contain one or more agents selected from the group consisting of sweetening agents, flavoring agents, coloring agents and preserving agents in order to provide pharmaceutically elegant and palatable preparations. Tablets may contain the active ingredient in admixture with non-toxic pharmaceutically acceptable excipients suitable for the manufacture of tablets. Such excipients may include, for example, inert diluents, such as calcium carbonate, sodium carbonate, lactose, calcium phosphate or sodium phosphate; granulating and disintegrating agents, for example, corn starch, or alginic acid; binding agents, for example starch, gelatin or acacia; and lubricating agents, for example magnesium stearate, stearic acid or talc. The tablets may be uncoated or they may be coated by techniques to delay disintegration and absorption in the gastrointestinal tract and thereby provide a sustained action over a longer period. For example, a time delay material such as glyceryl monostearate or glyceryl distearate may be utilized. [0044] Formulations for oral use may also be presented as hard gelatin capsules wherein the active ingredient is mixed with an inert solid diluent, for example, calcium carbonate, calcium phosphate or kaolin, or as soft gelatin capsules wherein the active ingredient is mixed with water or an oil medium, for example peanut oil, liquid paraffin or olive oil. [0045] Aqueous suspensions contain the active materials in admixture with excipients suitable for the manufacture of aqueous suspensions. Such excipients are suspending agents, for example sodium carboxymethylcellulose, methylcellulose, hydroxypropylmethylcellulose, sodium alginate, polyvinylpyrrolidone, gum tragacanth and gum acacia; and dispersing or wetting agents, which may be a naturally-occurring phosphatide, for example, lecithin, or condensation products of ethylene oxide with long chain aliphatic alcoholsafor example, heptadecaethyleneoxycetanol, or condensation products of ethylene oxide with partial esters derived from fatty acids and hexitol anhydrides, for example polyethylene sorbitan monooleate. The aqueous suspensions may also contain one or more preservatives, for example ethyl, or n-propyl-p-hydroxybenzoate, one or more coloring agents, one or more flavoring agents, and one or more sweetening agents, such as sucrose or saccharin. [0046] Oily suspensions may be formulated by suspending the active ingredients in a vegetable oil, for example arachis oil, olive oil, sesame oil or coconut oil, or in a mineral oil such as liquid paraffin. The oily suspensions may contain a thickening agent, for example beeswax, hard paraffin or cetyl alcohol. Sweetening agents such as those set forth above, and flavoring agents may be added to provide palatable oral preparations. These compositions may be preserved by the addition of an anti-oxidant such as ascorbic acid and/or copper ascorbate. [0047] Dispersible powders and granules suitable for preparation of an aqueous suspension by the addition of water provide the active ingredient (Formula I) in admixture with a dispersing or wetting agent, suspending agent and one or more preservatives. Suitable dispersing or wetting agents and suspending agents are exemplified by those already mentioned above. Additional excipients, for example sweetening, flavoring and coloring agents, may also be present. [0048] Pharmaceutical compositions of the invention may also be in the form of oil-in-water emulsions. The oily phase may be a vegetable oil, for example olive oil or arachis oil, or a mineral oil, for example liquid paraffin or mixtures of these. Suitable emulsifying agents may be naturally occurring gums, for example gum acacia or gum tragacanth; naturally-occurring phosphatide, for example soy bean, lecithin, and esters or partial esters derived from fatty acids and hexitol; anhydrides, for example sorbitan monooleate; and condensation products of the said partial esters with ethylene oxide, for example polyoxyethylene sorbitan monooleate. The emulsions may also contain sweetening and flavoring agents. [0049] Syrups and elixirs may be formulated with sweetening agents, for example glycerol, propylene glycol, sorbitol or sucrose. Such formulations may also contain a demulcent, a preservative, and flavoring or coloring agents. The pharmaceutical compositions may be in the form of a sterile injectable aqueous or oleaginous suspension. This suspension may be formulated according to the known art using those suitable dispersing or wetting agents and suspending agents, which have been mentioned above. The sterile injectable preparation may also be a sterile injectable solution or suspension in a non-toxic parenterally acceptable diluent or solvent, for example as a solution in 1,3-butanediol. Among the acceptable vehicles and solvents that may be employed are water, Ringer's solution and isotonic sodium chloride solution. In addition, sterile, fixed oils are conventionally employed as a solvent or suspending medium. For this purpose any bland fixed oil may be employed including synthetic mono- and diglycerides. In addition, fatty acids such as oleic acid find use in the preparation of injectables. [0050] Alternatively, the compositions can be administered parenterally in a sterile medium. Formula I, depending on the vehicle and concentration used, can either be suspended or dissolved in the vehicle. Advantageously, adjuvants such as local anesthetics, preservatives and buffering agents can be dissolved in the vehicle. [0051] For administration to non-human animals, the composition containing Formula I may be added to the animal's feed or drinking water. Optionally, one skilled in the art will recognize that animal feed and drinking products may be formulated such that the animal takes in an effective amount of Formula I via their diet. For example, Formula I may constitute a component of a premix formulated for addition to the feed or drinking water of an animal. Compositions containing Formula I may also be formulated as food or drink supplements for humans. [0052] Preferred embodiments of compositions containing Formula I will have desirable pharmacological properties that include, but are not limited to, oral bioavailability, low toxicity, and desirable in vitro and in vivo half-lives. The half-life of Formula I is inversely proportional to the frequency of dosage of Formula I. [0053] It is to be understood that the foregoing describes preferred embodiments of the present invention and that modifications may be made thereto without departing from the scope or spirit of the present invention as set forth in the claims. Such scope is limited only by the claims below as read in connection with the above specification. Many additional advantages of applicant's invention will be apparent to those skilled in the art from the descriptions, drawings, and the claims set forth herein. Representative Elemental and SEM Analysis [0054] The following Tables (1-2) illustrate the results of an elemental analysis of a composition comprising Formula I. The elemental analysis depicts only one preferred embodiment of the invention and is no way intended to limit the scope of the invention. TABLE 1 Run 1 Element Theoretical Found Diff Cu 18.41% 15.73% a2.68 TABLE 2 Run 29129 Run 29130 Element Theoretical Found Diff Found Diff C 41.75%a 45.45%a 3.7 45.3% 3.55 H 2.92% a2.8% a0.12 2.93% 0.01 N 8.11% 8.51% 0.4 8.47% 0.36 [0055] As indicated in Tables 1-2, a representative sample of Formula I comprises 15.73% copper. Given this data, one can calculate the amount of copper in a particular dose of Formula I. For example, a 2.5 mg dose (i.e. one capsule) yields 0.39 mg of copper. Similarly, a 10 mg dose (the preferred dose) yields 1.57 mg of copper. As will be readily apparent to one skilled in the art, however, the actual percentage of copper present in any given sample of Formula I will vary depending on a number of factors including, but not limited to, the purity, consistency and source of the sample, as well as the synthetic methodology employed to obtain the sample. [0056] FIGS. 1-9 depict data and imagery obtained from Scanning Electron Microscope (SEM) and spectrometer analysis of a preferred embodiment of the present invention. As shown in FIG. 9, the copper particles are approximately 1.4 micrometers (I1/4m) in size. **EXAMPLE****Preparation of Formula I****[0057] Those skilled in the art will recognize various synthetic methodologies that may be employed to prepare non-toxic pharmaceutically acceptable compositions of Formula I. One such (representative) example is set forth below:****[0058] A 3 L 3-neck round bottomed flask equipped with a mechanical stirrer, reflux condenser and a solid addition funnel was charged with nicotinic acid (131.61 g, 1.07 mol), ascorbic acid (21.4 g, 0.12 mol) and 90% aqueous ethanol (2 L) then placed in an appropriately sized heating mantle. The resultant white suspension was stirred and heated gently to 45A deg C. and cuprous chloride (35.2 g 0.36 mol) was introduced via the addition funnel over 15 minutes while maintaining an inert atmosphere of Nitrogen throughout the system. During previous experiment attempts, an ethanolic suspension of cuprous chloride was introduced to the reaction mixture as described in Patent Application WO/2010/009739, however, partial oxidation to Copper (II) chloride was observed during addition. To avoid such oxidation, the cuprous chloride was added via the aforementioned ascrew-mechanisma solid addition funnel and no oxidation to Copper (II) chloride was observed. The mixture was then placed under reflux and stirring was continued for a further 4.5 hours. Heating under reflux conditions was maintained for 4.5 hours rather than the recommended 5 minutes to ensure complete complexation. Previous experiment attempts had shown incomplete reaction following just 5 minutes of stirring. Upon cooling to 50A deg C., the mixture was filtered under suction and the red filter cake was washed with aqueous ascorbic acid 5% w/v solution (400 mL), ethanol 90% (400 mL) and then acetone (100 mL). The red filter cake was then collected and dried en vacuo to afford a red solid (123 g).** [0059] It is to be understood that the method set forth hereinabove describes a preferred synthetic methodology and that modifications thereto may be made without departing from the scope or spirit of the invention. Such scope is limited only by the claims below as read in connection with the above specification. May additional synthetic methodologies and additional advantages of applicant's invention will be apparent to those skilled in the art from the above descriptions and the claims below. --- **COPPER (I) COMPLEXES WITH GLYCINE, PYRUVATE, AND SUCCINATE** **US2018071336** Inventor: BARKER CHARLES LOUIS ALBARTUSa/ BOULANGER WILLIAM Aa[US] Applicant: C LAB PHARMA INTERNATIONAL The present invention is directed to a pharmaceutical and/or dietary supplement composition comprising an effective amount of a copper (I) complex with glycine, pyruvate, or succinic acid and methods of treating mitochondrial, neuromuscular, and other diseases. Also provided are pharmaceutical treatment regimes and kits comprising a copper (I) complex with glycine, pyruvate, or succinate. **RELATED APPLICATION DATA** [0001] This application is a continuation in-part of U.S. patent application Ser. No. 14/773,289, filed on Sep. 4, 2015, which is the U.S. national-stage application of International Application No. PCT/US2014/021772, filed on Mar. 7, 2014, which claims the benefit of U.S. Provisional Application No. 61/774,543, filed on Mar. 7, 2013, the contents of each of which are hereby incorporated by reference in its entirety. **TECHNICAL FIELD** [0002] This application relates to pharmaceutical and/or dietary supplement compositions comprising copper (I) complexes and the methods of preparing such copper (I) complexes. The application also encompasses methods of treating mitochondria, neuromuscular, and other diseases, and pharmaceutical and/or dietary supplement compositions and methods of treating other physical ailments and disorders, including but not limited to pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, Lyme disease, Lyme disease co-infection, gastroparesis (GP), myopathy, chronic inflammation and/or incontinence. **BACKGROUND OF THE INVENTION** [0003] Copper (as copper amino acid chelate) plays a role in transporting oxygen throughout the body. The production of collagen, which determines the integrity of bones, skin, cartilage, and tendons, is copper dependent. Copper is also crucial for making melanin, which provides color to skin and hair. Copper helps keep blood vessels elastic, is needed for the formation of elastin, functions as an iron oxidizer, and is needed for the proper functioning of vitamin C. [0004] Copper is also an important cofactor for metalloenzymes, and is a necessary cofactor for superoxide dismutase (Beem J BIOL CHEM 249:7298 (1974)). Copper has been shown to decrease in individuals over 70 years of age and to be basically zero in cataractous lenses (Swanson BIOCHEM BIPHY RES COMM 45:1488-96 (1971)). If copper is significantly decreased, superoxide dismutase has been shown to have decreased function, thereby hampering an important protective lens mechanism (Williams PEDIAT RES 1:823 (1977)). For these and many other reasons, copper is required for optimal human health. [0005] The two principal oxidation states of copper are +1 and +2 although some +3 complexes are known. Copper (I) compounds are expected to be diamagnetic in nature and are usually colorless, except where color results from charge transfer or from the anion. The +1 ion has tetrahedral or square planar geometry. In solid compounds, copper (I) is often the more stable state at moderate temperatures. [0006] The copper (II) ion is usually the more stable state in aqueous solutions. Compounds of this ion, often called cupric compounds, are usually colored. They are affected by Jahn Teller distortions and exhibit a wide range of stereochemistries with four, five, and six coordination compounds predominating. The +2 ion often shows distorted tetrahedral geometry. [0007] Complexes of copper (I) are thought to have a unique mechanism of action in promoting aerobic respiration via the electron transport chain. By causing the mitochondria in the cells to produce adenosine triphosphate (ATP) more efficiently and avoiding the production of lactic acid and ethanol that accompanies anaerobic respiration, pharmaceutical preparations and dietary supplements with copper (I) may alleviate and treat many illness and diseases. Among these diseases are those involving neuromuscular degeneration and muscle weakness. Accordingly, there is a need to develop novel copper (I) compounds that may stimulate ATP production in the mitochondria. **SUMMARY OF THE INVENTION** [0008] The objective of the present invention is to provide pharmaceutical and/or dietary supplement compositions and methods of making and using the same to treat and reduce many of the symptoms of several diseases. The compositions contain an active pharmacological ingredient comprised of a copper (I) complex. The pharmacologically active ingredient may be administered alone or in combination with additional active or inert agents or therapies (e.g. other anti-inflammatory agents, diluents, and/or excipients). [0009] The pharmacologically active ingredient of the present invention possesses a chemical structure selected from: [0010] The present invention is also directed to a method of treating diseases and other physical ailments or disorders. In a preferred embodiment the method comprises the step of administering to a subject in need thereof a copper (I) complex having a formula of Formula (I), Formula (II), Formula (III) or Formula (IV) to reduce and/or treat a disease or physical ailment or disorder. Preferably the disease or physical ailment being treated is a mitochondrial or neuromuscular disease. The treated diseases or disorders (or other physical ailments) include, but are not limited to fibromyalgia, spinal cord injury, multiple sclerosis, muscular dystrophy, stroke, rheumatoid arthritis, pain, fatigue, sleeplessness, loss of fine motor control, speech loss, inflexibility, Lyme disease, Lyme disease co-infection, gastroparesis (GP), chronic inflammation, myopathy, chronic inflammation, and/or incontinence. It is also preferable that the subject be diagnosed with one of the diseases and/or disorders prior to treatment. [0011] The present invention encompasses a method of treating a mitochondrial disease selected from the group consisting of Myoclonic Epilepsy with Ragged Red Fibers (MERRF); Mitochondrial Myopathy, Encephalopathy, Lactacidosis, and Stroke (MELAS); Diabetes mellitus and deafness (DAD); Maternally Inherited Diabetes and Deafness (MIDD), Leber's Hereditary Optic Neuropathy (LHON); chronic progressive external ophthalmoplegia (CPEO); Leigh Disease; Kearns-Sayre Syndrome (KSS); Friedreich's Ataxia (FRDA); Co-Enzyme Q10 (Co-Q10) Deficiency; Neuropathy, ataxia, retinitis pigmentosa, and ptosis (NARP); Myoneurogenic gastrointestinal encephalopathy (MNGIE); Complex I Deficiency; Complex II Deficiency; Complex III Deficiency; Complex IV Deficiency; Complex V Deficiency; and other myopathies that effect mitochondrial function. [0012] Preferred embodiments of the compositions of the present invention, including recommended dosages and methods of use, are more fully described below in the Detailed Description. **BRIEF DESCRIPTION OF THE DRAWINGS** [0013] Illustrative and exemplary embodiments of the invention are shown in the drawings in which: [0014] FIG. 1 depicts a proton NMR of an embodiment of a copper (I) glycinate complex dissolved in deuterium oxide (D2O). [0015] FIG. 2 depicts a proton NMR of sodium glycinate dissolved in D2O. [0016] FIG. 3 depicts a proton NMR of sodium ascorbate dissolved in D2O. [0017] FIG. 4 depicts an image of a copper (I) glycinate complex captured with a scanning electron microscope (SEM). The scale bar represents 200 I1/4m. [0018] FIG. 5 depicts the results of an Energy Dispersive Spectroscopy analysis on an SEM (EDS-SEM) with a copper (I) glycinate complex. The elements identified in the analysis are carbon (C), oxygen (O), sodium (Na), aluminum (Al), chlorine (CO, and copper (Cu). [0019] FIGS. 6A and 6B depict two versions of the SEM image of a copper (I) glycinate complex that was analyzed by EDS-SEM. The scale bar represents 50 I1/4m. [0020] FIG. 7 depicts the distribution and relative proportion (intensity) of the specified elements over the area scanned by the EDS-SEM of a copper (I) glycinate complex. [0021] FIG. 8 depicts an image of a copper (I) pyruvate complex captured with an SEM. The scale bar represents 200 I1/4m. [0022] FIG. 9 depicts the results of an EDS-SEM analysis with a copper (I) pyruvate complex. The elements identified in the analysis are carbon (C), oxygen (O), sodium (Na), chlorine (Cl), calcium (Ca), and copper (Cu). [0023] FIGS. 10A and 10B depict two versions of an SEM image of a copper (I) pyruvate complex that was analyzed by EDS-SEM. The scale bar represents 500 I1/4m. [0024] FIG. 11 depicts the distribution and relative proportion (intensity) of the specified elements over the area scanned by the EDS-SEM of a copper (I) pyruvate complex. [0025] FIG. 12 depicts an image of a copper (I) succinate complex captured with an SEM. The scale bar represents 200 I1/4m. [0026] FIG. 13 depicts the results of an EDS-SEM analysis with a copper (I) succinate complex. The elements identified in the analysis are carbon (C), oxygen (O), sodium (Na), chlorine (Cl), and copper (Cu). [0027] FIGS. 14A and 14B depict two versions of an SEM image of a copper (I) succinate complex that was analyzed by EDS-SEM. The scale bar represents 500 I1/4m. [0028] FIG. 15 depicts the distribution and relative proportion (intensity) of the specified elements over the area scanned by the EDS-SEM of a copper (I) succinate complex. [0029] FIG. 16 depicts the time course of the XF Cell Mito Stress Test. [0030] FIG. 17 depicts the compares results of the XF cell Mito Stress Test in lymphoblasts from control individuals (C) and autistic subjects with (A) or without mitochondrial dysfunction (N). The figure also compares the effect of administering 100 I1/4M or 500 I1/4M copper (I) glycinate complex on the oxygen consumption rate of these cells. [0031] Elements and facts in the figures are illustrated for simplicity and have not necessarily been rendered according to any particular sequence or embodiment. **DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS** [0032] The verb acomprisea as is used in this description and in the claims and its conjugations are used in its non-limiting sense to mean that items following the word are included, but items not specifically mentioned are not excluded. In addition, reference to an element by the indefinite article aaa or aana does not exclude the possibility that more than one of the elements are present, unless the context clearly requires that there is one and only one of the elements. The indefinite article aaa or aana thus usually means aat least one.a [0033] The terms acopper (I) complexa and acopper (I) compounda as used herein are interchangeable and refer to a chemical compound in which copper is present in its +1 oxidation state and interacts with at least one other element through ionic or covalent bonding. [0034] The term aextended releasea herein refers to any formulation or dosage form that comprises an active drug and which is formulated to provide a longer duration of pharmacological response after administration of the dosage form than is ordinarily experienced after administration of a corresponding immediate release formulation comprising the same drug in the same amount. Controlled release formulations include, inter alia, those formulations described elsewhere as acontrolled releasea, adelayed releasea, asustained releasea, aprolonged releasea, aprogrammed releasea, atime releasea and/or arate controlleda formulations or dosage forms. Further for the purposes of this invention refers to release of an active pharmaceutical agent over a prolonged period of time, such as for example over a period of 8, 12, 16 or 24 hours. [0035] As used herein, the term asubjecta or apatienta refers to any vertebrate including, without limitation, humans and other primates (e.g., chimpanzees and other apes and monkey species), farm animals (e.g., cattle, sheep, pigs, goats and horses), domestic mammals (e.g., dogs and cats), laboratory animals (e.g., rodents such as mice, rats, and guinea pigs), and birds (e.g., domestic, wild and game birds such as chickens, turkeys and other gallinaceous birds, ducks, geese, and the like). In some embodiments, the subject is a mammal. In other embodiments, the subject is a human. **Compositions** [0036] The compositions of the present invention may comprise an effective amount of a copper (I) complex having a formula selected from: Preferably, the pharmaceutical composition further comprises copper ascorbate (esterified Vitamin C), ascorbic acid (Vitamin C), and/or a pharmaceutically acceptable excipient (carrier). More preferably, the pharmaceutically acceptable carrier is an inert diluent. [0037] The compositions of the present invention may comprise a delivery vehicle. Suitable delivery vehicles include a liposome, a microsome, a nanosome, a picosome, a pellet, a granular matrix, a bead, a microsphere, a nanoparticle formulation, or an aqueous solution. [0038] Liposomes can aid in the delivery of the copper (I) compounds to a particular tissue and can also increase the blood half-life of the compounds. Liposomes suitable for use in the invention are formed from standard vesicle-forming lipids, which generally include neutral, positively or negatively charged phospholipids and, optionally, a sterol, such as cholesterol. The selection of lipids is generally guided by consideration of factors such as the desired liposome size and half-life of the liposomes in the blood stream. A variety of methods are known for preparing liposomes, for example as described in Szoka et al. (1980), Ann. Rev. Biophys. Bioeng. 9: 467; and U.S. Pat. Nos. 4,235,871, 4,501,728, 4,837,028, and 5,019,369, the entire disclosures of which are herein incorporated by reference. [0039] Polyacrylates represent a further example of a suitable delivery vehicle for use in the present invention. By way of example, a terpolymer of styrene and hydroxyethyl methacrylate cross-linked with a difunctional azo-compound may be employed. The system depends on cleavage of the azo bond by intestinal microflora resulting in degradation of polymer. Similarly, a pH responsive poly (methacrylic-g-ethylene glycol) hydrogel may be employed as an oral delivery vehicle. Once inside the basic and neutral environment of the small intestine, the gels rapidly swell and dissociate. [0040] In another embodiment, a microcapsule formulation may be employed for peroral delivery. In more detail, aqueous colloidal terpolymers of ethylacrylate/methyl methacrylate/2-hydroxylethyl methacrylate (poly (EA/MME/HEMA), for example as synthesized by emulsion polymerization technique(s) may be employed. These polymers exhibit delayed release profiles, which were characterized by a long lag time and subsequent rapid release of the entrapped moiety. [0041] In another embodiment, orally administered nanoparticles may serve as suitable delivery vehicles. By way of example, loaded nanoparticles may be entrapped into pH sensitive microspheres, which serve to deliver the incorporated nanoparticle to the desired site of action. Nanoparticles have a large specific surface, which is indicative of high interactive potential with biological surfaces. Thus, bioadhesion can be induced by binding nanoparticles with different molecules. By way of example, nanoparticles may be prepared from gliadin protein isolate from wheat gluten and then conjugated with lectins (glycoproteins of non-immune origin which provide specific bioadhesion). Accordingly, nanoparticles are provided, which have a high capacity for non-specific interaction with intestine. [0042] The compositions of the present invention may take the form of differently sized particles. In some embodiments, particles are microparticles (aka microspheres or microsomes). In general, a amicroparticlea refers to any particle having a diameter of less than 1000 I1/4m. In some embodiments, particles are nanoparticles (aka nanospheres or nanosomes). In general, a ananoparticlea refers to any particle having a diameter of less than 1000 nm. In some embodiments, particles are picoparticles (aka picospheres or picosomes). In general, a apicoparticlea refers to any particle having a diameter of less than 1 nm. In some embodiments, particles are micelles. [0043] In one embodiment, a delivery vehicle based on an albumin-chitosan mixed matrix microsphere-filled coated capsule formulation may be employed. In this regard, a preparation of a copper (I) compound of the invention is filled into hard gelatin capsules and enteric coated. [0044] In one embodiment, albumin microspheres may be employed as the oral delivery system. [0045] In one embodiment, squalane oil-containing multiple emulsions may be employed. [0046] In one embodiment, poly(lactide-co-glycolide) microspheres may be employed as the oral delivery vehicle. [0047] In one embodiment, a delivery coating comprising a mixture of pH-responsive enteric polymer (Eudragit S) and biodegradable polysaccharide (resistant starch) in a single layer matrix film may be employed. [0048] In one embodiment, delivery capsules such as liposomes, micro- or nanocapsules (e.g. chitosan nanocapsules) may be chemically modified with poly(ethylene glycol) (PEG). The typical degree of PEGylation is in the range of 0.1% to 5%, such as 0.5% to 2%, for example 0.5% or 1%. The presence of PEG, whether alone or grafted to chitosan, improves the stability of the delivery capsules in the gastrointestinal fluids. [0049] PEGylated delivery vehicles such as liposomes, micro- or nanocapsules have an intrinsic ability to accumulate at disease sites and facilitate transfection of target cells. Unlike many viral vectors, PEGylated liposomes are generally considered to be non-immunogenic. [0050] In one embodiment, a branched PEGylating reagent is employed as branched PEG protecting groups are more effective than linear PEG molecules. [0051] In one embodiment, the copper (I) compounds of the invention are prepared with carriers that will protect the compound against rapid elimination from the body, such as an extended release formulation, including implants and microencapsulated delivery systems. Biodegradable, biocompatible polymers can be used, such as ethylene vinyl acetate, polyanhydrides, polyglycolic acid, collagen, polyorthoesters, and polylactic acid. Methods for preparation of such formulations will be apparent to those skilled in the art. The materials can also be obtained commercially from Alza Corporation and Nova Pharmaceuticals, Inc. [0052] Other embodiments of the invention are directed to a single crystalline form of the copper (I) complexes characterized by a combination of the characteristics of any of the single crystalline forms discussed herein. The characterization can be any combination of one or more of the XRPD, TGA, DSC, moisture sorption/desorption measurements and single crystal structure determination described for a particular crystalline form. For example, the single crystalline form of a copper (I) complex can be characterized by any combination of the XRPD results regarding the 2I, position of the major peaks in an XRPD scan; and/or any combination of one or more of the unit cell parameters derived from data obtained from the single crystal structure analysis. DSC determinations of the temperature associated with the maximum heat flow during a heat flow transition and/or the temperature at which a sample begins to undergo a heat flow transition may also characterize the crystalline form. Weight change in a sample and/or change in sorption/desorption of water per molecule of a copper (I) complex of the present invention as determined by moisture sorption/desorption measurements over a range of relative humidity can also characterize a single crystalline form of a copper (I) complex. [0053] Examples of combinations of single crystalline form characterizations using multiple analytical techniques include the 2I, positions of at least one of the major peaks of an XRPD scan and the temperature associated with the maximum heat flow during one or more heat flow transitions observed by a corresponding DSC measurements; the 2I, positions of at least one of the major peaks of an XRPD scan and one or more weight losses associated with a sample over a designated temperature range in a corresponding TGA measurement; the 2I, positions of at least one of the major peaks of an XRPD scan, and the temperature associated with the maximum heat flow during one or more heat flow transitions observed by a corresponding DSC measurements, and one or more weight losses associated with a sample over a designated temperature range in a corresponding TGA measurement; the 2I, positions of at least one of the major peaks of an XRPD scan, and the temperature associated with the maximum heat flow during one or more heat flow transitions observed by a corresponding DSC measurements, one or more weight losses associated with a sample over a designated temperature range in a corresponding TGA measurement, and the change in sorption/desorption measurements over a range of relative humidity. As well, each of the aforementioned examples can replace the use of 2I, positions of at least one of the major peaks of an XRPD scan with one or more unit cell parameters of the single crystalline form. [0054] The combinations of characterization that are discussed above can be used to describe any of the single crystalline forms of a copper (I) complex of the present invention. [0055] The D90 particle size diameter of the copper (I) complexes of the present invention may be 1 to 500 microns; e.g., any range within 1 and 500 microns, such as 1 to 100 microns, 50 to 250 microns, 100 to 300 microns, 250 to 500 microns, etc. **Indications** [0056] The compositions of the present invention may be used to effectively treat numerous human diseases and other ailments characterized by neuromuscular degeneration and muscle weakness. These diseases are described in detail below. [0057] The copper (I) complexes of the present invention are particularly effective in treating mitochondrial diseases. Mitochondrial diseases are often the result a deficiency in ATP production, via the oxidative phosphorylation, which makes high energy-demanding tissues or organs such as heart, brain, and muscles, the main targets for these disorders. By restoring ATP production to normal, the copper (I) complexes may prevent, treat, or reverse mitochondrial disease. [0058] Impairments in oxidative phoshporylation are often referred to as mitochondrial dysfunction (and are associated with mitochondrial disease). They can result from hereditary and somatic mutations in nuclear genes or mtDNA, or functional impairments by drugs or toxins. Mutations in over 100 genes constituting the oxidative phosphorylation machinery are linked with mitochondrial encephalopathies in humans, which are the most common metabolic diseases with an incidence of over 1/5000 in live births. [0059] Respiratory chain Complex I deficiency is a cause of mitochondrial diseases in many cases. Twenty-five of at least fifty known genes implicated in Complex I biogenesis are found associated with mitochondrial diseases. Pathogenic mutations in structural subunits (e.g., NDUFA 1, 2, 11; NDUFS 1-4, 6-8; NDUFV 1, 2) and assembly factors (e.g., NDUFAF1-6) have been identified. Neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Huntington's disease are also associated with mitochondrial dysfunction. Further, mtDNA mutations are found associated with almost all types of cancers. Type 2 diabetes is also linked with declining mitochondrial function in relevant tissues such as I2-cells and muscles. Type 2 diabetes represents a major clinical challenge due to the sharp rise in obesity-induced disease. Thus, in some embodiments, methods are provided for treating a mitochondrial disease or a mitochondrial dysfunction. [0060] Symptoms of mitochondrial diseases usually include slow growth, loss of muscle coordination, muscle weakness, visual defect, hearing defects, learning disabilities, mental retardation, heart disease, liver disease, kidney disease, gastrointestinal disorders, respiratory disorders, neurological problems, and dementia. [0061] The copper (I) complexes of the present invention may be used to treat mitochondrial diseases such as Myoclonic Epilepsy with Ragged Red Fibers (MERRF); Mitochondrial Myopathy, Encephalopathy, Lactacidosis, and Stroke (MELAS); Diabetes mellitus and deafness (DAD); Maternally Inherited Diabetes and Deafness (MIDD), Leber's Hereditary Optic Neuropathy (LHON); chronic progressive external ophthalmoplegia (CPEO); Leigh Disease; Kearns-Sayre Syndrome (KSS); Friedreich's Ataxia (FRDA); Co-Enzyme Q10 (Co-Q10) Deficiency; Neuropathy, ataxia, retinitis pigmentosa, and ptosis (NARP); Myoneurogenic gastrointestinal encephalopathy (MNGIE); Complex I Deficiency; Complex II Deficiency; Complex III Deficiency; Complex IV Deficiency; Complex V Deficiency; and other myopathies that effect mitochondrial function. [0062] The copper (I) complexes of the present invention may also be used to treat a neuromuscular disease. The term aneuromuscular diseasea refers to disorders that adversely affect muscle function and/or the control thereof by the central nervous system (CNS). In general, neuromuscular diseases encompass a wide range of physical ailments characterized by impaired muscle function. The following (non-limiting) list of conditions is generally recognized as neuromuscular diseases or conditions: multiple sclerosis, muscular dystrophy, rheumatoid arthritis, fibromyalgia, myopathy, inflammatory bowel disease (IBD), incontinence, inflexibility, impaired fine motor skills, and amyotrophic lateral sclerosis (aALSa or Lou Gehrig's disease). [0063] A stroke, formerly known as a cerebrovascular accident (CVA), often results in severe neurological impairment. Post-stroke, many individuals suffer one or more neurological impairments including, but not limited to: loss of fine motor control, paralysis, speech impairment/loss (aphasia and/or dysarthria), altered smell, taste, hearing, or vision, ptosis, ocular and facial muscle weakness, diminished reflexes, loss of balance, altered heart rate, apraxia, loss of memory, and/or confusion. [0064] Three of the most prominent diseases associated with impaired neurological function are muscular dystrophy (MD), multiple sclerosis (MS), and rheumatoid arthritis (RA). [0065] The term Muscular Dystrophy (MD) actually refers to a group of diseases characterized by muscle weakness and/or impaired muscle function. The specific diseases include, but are not limited to Becker, Duchenne, and Emery-Dreifuss. Over 100 diseases, however, display symptoms similar to MD. All are characterized by reduced muscle function and muscle weakness. [0066] Multiple Sclerosis (MS) is an autoimmune disease diagnosed in 350,000-500,000 people in the United States. The disease is characterized by multiple areas of inflammation and scarring of the myelin in the brain and spinal cord. Patients inflicted with the disease exhibit varying degrees of neurological impairment depending on the location and extent of the myelin scarring. Typical MS symptoms include fatigue, weakness, spasticity, balance problems, bladder and bowel problems, numbness, loss of vision, tremors, and depression. Available treatments of MS generally only alleviate symptoms or delay the progression of the disability [0067] Rheumatoid Arthritis (RA) is another troublesome disorder associated with inflammation. It is signified by chronic inflammation in the membrane lining (the synovium) of the joints and/or other internal organs. These inflammatory cells can also damage bone and cartilage. For example, a joint inflicted with RA may lose its shape and alignment, which can result in the loss of range of motion. RA is characterized by pain, stiffness, warmth, redness and swelling in the joint, and other systemic symptoms like fever, fatigue, and anemia. RA currently affects roughly 1% of the entire U.S. population (approximately 2.2 million people). The pathology of RA is not fully understood, although it has been hypothesized to result from a cascade of aberrant immunological reactions. [0068] The compositions of the present invention are particularly effective in treating Lyme disease and Lyme disease co-infections. Lyme disease is a bacterial infection (Borrelia burgdorferi) spread by ticks. The number of reported cases of Lyme disease, and the number of geographical areas in which it is found, has been increasing. In addition to causing arthritis, Lyme disease can also cause heart, brain, and nerve problems. Early symptoms include skin-rash, flu-like symptoms (e.g. chills, fever, swollen lymph nodes, headaches, fatigue, muscle aches/pains, and joint pain). More advanced symptoms include nerve problems and arthritis. [0069] Lyme disease is often associated with muscle degeneration and/or muscle weakness. In one aspect of the present invention, treatment of Lyme disease in a subject with a copper (I) complex results in improved muscle health and/or muscle tone. In some embodiments, the Lyme disease is chronic Lyme disease that persists in spite of treatment with standard antibiotic treatments. [0070] Often, ticks can become infected with multiple disease-causing microbes, resulting in co-infection. This may be a potential problem for humans, due to Borrelia burgdorferi, and other harmful pathogens carried and transmitted by some ticks. Possible co-infections with viruses such as Lyme borreliosis, anaplasmosis, babesiosis, or encephalitis may occur. It is not known how co-infection may affect disease transmission and progression, but may help in diagnosing and treating Lyme and other such diseases. [0071] In one embodiment, the present invention is directed to a method of treating a tickborne disease with a copper (I) complex. Tickborne diseases include Babesiosis, Ehrlichiosis and Anaplasmosis, Lyme Disease, Relapsing Fever, Rocky Mountain Spotted Fever, and Tularemia. [0072] Tickborne diseases can be found throughout the United States. For example, Lyme disease, first discovered in Connecticut in the early 1970s, has since spread to every state except Hawaii. Rocky Mountain spotted fever, a bacterial disease transmitted by the dog tick, was first identified in 1896. [0073] One of the newest tickborne diseases to be identified in the United States is called Southern tick-associated rash illness (STARI). This disease has a bull's-eye rash similar to that found in Lyme disease, which is caused by bacteria transmitted by the deer tick. Although researchers know that the lone star tick transmits the infectious agent that causes STARI, they do not yet know what microbe causes it. [0074] Ticks transmit ehrlichiosis and anaplasmosis, both bacterial diseases. Babesiosis is caused by parasites carried by deer ticks. These diseases are found in several states. [0075] Tularemia, a less common tickborne bacterial disease, can be transmitted by ticks as well as other vectors (carriers) such as the deerfly. Public health experts are concerned that the bacterium that causes tularemia (Francisella tularensis) could be used as a weapon of bioterrorism. [0076] Transmission of tickborne diseases is not limited to ticks. In addition, tickborne diseases may be spread via other vectors (e.g., mosquitoes, flies, or other insects), via contaminated body fluids (e.g., blood transfusions), via sexual transmission or any other number of ways. [0077] The copper (I) complexes may be used to treat gastroparesis. Gastroparesis is a condition characterizes by the inability of the stomach to empty its contents, when there is no blockage (obstruction). The cause of gastroparesis is not known. There is some evidence that it may be caused by a disruption of nerve signals to the stomach. The condition is a complication of diabetes and of some surgeries. Risk factors associated with gastroparesis may include diabetes, gastrectomy (surgery to remove part of the stomach), systemic sclerosis, use of medication that blocks certain nerve signals (anticholinergic medication). Symptoms may include abdominal distention, hypoglycemia (in people with diabetes), nausea, premature abdominal fullness after meals, weight loss, and vomiting. If gastroparesis is caused by a condition that is reversible (e.g. pancreatitis), when the condition is resolved, the symptoms will subside. For some diabetics, better control of their blood sugar can also improve the symptoms. If there is no reversible cause, gastroparesis rarely resolves itself and the symptoms often grow more sever with time. When accompanied by motility disorders of the muscles of the small intestine, gastroparesis is particularly difficult to treat. [0078] The invention may be used to treat an animal with a disease or physical ailment or disorder including, but not limited to, one or more of the following: fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, Alzheimer's, dementia, ALS, depression, pain, fatigue, sleeplessness, inflexibility, myopathy, Lyme disease, Lyme disease co-infection, gastroparesis (GP), chronic inflammation, incontinence, impaired fine motor skills, high cholesterol, low sperm count, obesity, alopecia, burns, stretch marks, scars, ADD, ADHD, and/or erectile dysfunction, wherein it is preferable that the animal is a mammal and more preferable that the mammal is a human. [0079] In an alternate embodiment, the present invention is further directed to pharmaceutical and/or dietary supplement compositions for treating post-stroke symptoms, including, but not limited to: loss of fine motor control, paralysis, speech impairment/loss (aphasia and/or dysarthria), altered smell, taste, hearing, or vision, ptosis, ocular and facial muscle weakness, diminished reflexes, loss of balance, altered heart rate, apraxia, loss of memory, and/or confusion. [0080] Advantageously, the present invention is further directed to pharmaceutical and/or dietary supplement compositions for promoting one or more desired health benefits. In a preferred embodiment, the compositions of the present invention promote hair growth, skin healing, scar removal, nerve growth, muscle growth, enhanced athletic performance, reduced post-traumatic healing time, post-surgery healing, and/or enhanced libido. [0081] In one embodiment, the subject is first diagnosed with one of the diseases listed above before treatment. **Modes of Administration** [0082] Frequency of dosage may vary depending on the purity of the compound and the particular disease or physical ailment treated. However, for treatment of most diseases and physical ailments, a dosage regimen of (4) 2.5 mg capsules (for a total of 10 mg/day) containing copper (I) complexes of the present invention is preferred. As will be understood by one skilled in the art, however, the optimal dosage level for a particular subject will vary depending on a plurality of factors including the potency and activity of the pharmacologically active ingredient, as well as the age, body weight, general health, sex, diet, time of administration, route of administration and rate of excretion, drug combination (if any) and the severity of the particular disease or physical ailment undergoing therapy. Subject to the above factors, a generally effective amount of the copper (I) complexes of the present invention is between 1 mg and 20 mg per day. More preferably, the effective amount of is between 5 mg and 10 mg per day. Advantageously, the effective amount of is between 7.5 mg to 10 mg per day. Most preferably (subject to the factors listed above), the effective amount is about 10 mg/per day. [0083] Copper (I) complexes of the present invention may also comprise a component of an overall pharmaceutical treatment regime for reducing and/or treating a disease or physical ailment or other disorder including, but not limited to: fibromyalgia, multiple sclerosis, muscular dystrophy, rheumatoid arthritis, Alzheimer's, dementia, ALS, depression, pain, fatigue, sleeplessness, inflexibility, myopathy, incontinence, impaired fine motor skills, high cholesterol, low sperm count, obesity, alopecia, burns, stretch marks, scars, ADD, ADHD, and/or erectile dysfunction, the treatment regime comprising: administering to a subject at the least the following pharmacologically active ingredient(s) within a 24-hour period: copper (I) complexes of the present invention, and optionally a pharmaceutically acceptable carrier, wherein the pharmacologically active ingredient(s) is in an amount sufficient to reduce the symptoms of the ailment. [0084] Optionally, the pharmaceutical treatment regime including copper (I) complexes of the present invention may include (or be combined with) additional pharmacologically active ingredients or other complementary treatments in order to provide synergistic therapeutic effects. For example, copper (I) complexes of the present invention may be administered in combination with additional pharmacologically active agents including, but not limited to, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, disease modifying anti-rheumatic drugs (DMARDs), biologic DMARDs, and/or cyclooxygenase-2 (COX-2) inhibitors. In a preferred embodiment, copper (I) complexes of the present invention is administered in combination with ozone therapy. [0085] The pharmaceutical and/or dietary supplement compositions of the present invention may take a variety of forms specially adapted to the chosen route of administration. The compositions may be administered orally, topically, parenterally, by inhalation or spray, or by any other conventional means. Preferably, the compositions are prepared and administered in dosage unit formulations containing conventional non-toxic pharmaceutically acceptable carriers, adjuvants and vehicles. In one preferred embodiment, the composition is administered sublingually. It is further understood that the preferred method of administration may be a combination of methods. Oral administration in the form of a capsule, pill, elixir, syrup, lozenge, troche, or the like is particularly preferred. The pharmaceutical compositions of the present invention are preferably in a form suitable for oral use, for example, as tablets, troches, lozenges, aqueous or oily suspensions, dispersible powders or granules, emulsion, hard or softgel capsules, or syrups or elixirs. [0086] Compositions intended for oral use may be prepared according to any method known in the art for manufacture of pharmaceutical compositions, and such compositions may contain one or more agents selected from the group consisting of sweetening agents, flavoring agents, coloring agents and preserving agents in order to provide pharmaceutically elegant and palatable preparations. Tablets may contain the active ingredient in admixture with non-toxic pharmaceutically acceptable excipients suitable for the manufacture of tablets. Such excipients may include, for example, inert diluents, such as calcium carbonate, sodium carbonate, lactose, calcium phosphate or sodium phosphate; granulating and disintegrating agents, for example, corn starch, or alginic acid; binding agents, for example starch, gelatin or acacia; and lubricating agents, for example magnesium stearate, stearic acid or talc. The tablets may be uncoated or they may be coated by techniques to delay disintegration and absorption in the gastrointestinal tract and thereby provide a sustained action over a longer period. For example, a time delay material such as glyceryl monostearate or glyceryl distearate may be utilized. [0087] Formulations for oral use may also be presented as hard gelatin capsules wherein the active ingredient is mixed with an inert solid diluent, for example, calcium carbonate, calcium phosphate or kaolin, or as soft gelatin capsules wherein the active ingredient is mixed with water or an oil medium, for example peanut oil, liquid paraffin or olive oil. [0088] Aqueous suspensions contain the active materials in admixture with excipients suitable for the manufacture of aqueous suspensions. Such excipients are suspending agents, for example sodium carboxymethylcellulose, methylcellulose, hydroxypropylmethylcellulose, sodium alginate, polyvinylpyrrolidone, gum tragacanth and gum acacia; and dispersing or wetting agents, which may be a naturally-occurring phosphatide, for example, lecithin, or condensation products of ethylene oxide with long chain aliphatic alcoholsafor example, heptadecaethyleneoxycetanol, or condensation products of ethylene oxide with partial esters derived from fatty acids and hexitol anhydrides, for example polyethylene sorbitan monooleate. The aqueous suspensions may also contain one or more preservatives, for example ethyl, or n-propyl-p-hydroxybenzoate, one or more coloring agents, one or more flavoring agents, and one or more sweetening agents, such as sucrose or saccharin. [0089] Oily suspensions may be formulated by suspending the active ingredients in a vegetable oil, for example arachis oil, olive oil, sesame oil or coconut oil, or in a mineral oil such as liquid paraffin. The oily suspensions may contain a thickening agent, for example beeswax, hard paraffin or cetyl alcohol. Sweetening agents such as those set forth above, and flavoring agents may be added to provide palatable oral preparations. These compositions may be preserved by the addition of an anti-oxidant such as ascorbic acid and/or copper ascorbate. [0090] Dispersible powders and granules suitable for preparation of an aqueous suspension by the addition of water provide the active ingredient (i.e., copper (I) complex) in admixture with a dispersing or wetting agent, suspending agent and one or more preservatives. Suitable dispersing or wetting agents and suspending agents are exemplified by those already mentioned above. Additional excipients, for example sweetening, flavoring and coloring agents, may also be present. [0091] Pharmaceutical compositions of the invention may also be in the form of oil-in-water emulsions. The oily phase may be a vegetable oil, for example olive oil or arachis oil, or a mineral oil, for example liquid paraffin or mixtures of these. Suitable emulsifying agents may be naturally occurring gums, for example gum acacia or gum tragacanth; naturally-occurring phosphatide, for example soy bean, lecithin, and esters or partial esters derived from fatty acids and hexitol; anhydrides, for example sorbitan monooleate; and condensation products of the said partial esters with ethylene oxide, for example polyoxyethylene sorbitan monooleate. The emulsions may also contain sweetening and flavoring agents. [0092] Syrups and elixirs may be formulated with sweetening agents, for example glycerol, propylene glycol, sorbitol or sucrose. Such formulations may also contain a demulcent, a preservative, and flavoring or coloring agents. The pharmaceutical compositions may be in the form of a sterile injectable aqueous or oleaginous suspension. This suspension may be formulated according to the known art using those suitable dispersing or wetting agents and suspending agents, which have been mentioned above. The sterile injectable preparation may also be a sterile injectable solution or suspension in a non-toxic parenterally acceptable diluent or solvent, for example as a solution in 1,3-butanediol. Among the acceptable vehicles and solvents that may be employed are water, Ringer's solution and isotonic sodium chloride solution. In addition, sterile, fixed oils are conventionally employed as a solvent or suspending medium. For this purpose, any bland fixed oil may be employed including synthetic mono- and diglycerides. In addition, fatty acids such as oleic acid find use in the preparation of injectables. [0093] Alternatively, the compositions can be administered parenterally in a sterile medium. The copper (I) complexes of the present invention, depending on the vehicle and concentration used, can either be suspended or dissolved in the vehicle. Advantageously, adjuvants such as local anesthetics, preservatives and buffering agents can be dissolved in the vehicle. [0094] For administration to non-human animals, the composition containing copper (I) complexes of the present invention may be added to the animal's feed or drinking water. Optionally, one skilled in the art will recognize that animal feed and drinking products may be formulated such that the animal takes in an effective amount of copper (I) complexes of the present invention via their diet. For example, copper (I) complexes of the present invention may constitute a component of a premix formulated for addition to the feed or drinking water of an animal. Compositions containing copper (I) complexes of the present invention may also be formulated as food or drink supplements for humans. [0095] Preferred embodiments of compositions containing copper (I) complexes of the present invention will have desirable pharmacological properties that include, but are not limited to, oral bioavailability, low toxicity, and desirable in vitro and in vivo half-lives. The half-life of copper (I) complexes of the present invention is inversely proportional to the frequency of dosage of the compounds. **Synthesis of the Copper (I) Complexes** [0096] In one embodiment, the present invention provides a method of synthesizing a copper (I) glycinate complex. The method comprises: a) charging a glycinate salt under a stream of inert gas in an alcohol or water; b) heating the glycinate salt in the alcohol or water at between 40A deg C. to 45A deg C.; c) adding a copper (I) salt to the alcohol and allowing to reflux for at least 12 hours; and d) evaporating the alcohol or water and washing the copper (I) glycinate complex with alcohol and/or water to remove impurities. In a preferred embodiment, the inert gas is nitrogen. In some implementations, the glycinate salt is charged under a stream of inert gas with an ascorbate salt in an alcohol. In one aspect, the glycinate salt in alcohol is heated for 30 minutes. In a preferred embodiment, the mixture of copper (I) salt and glycinate salt in water is refluxed for between 12 to 16 hours. In some implementations, the mixture of the glycinate salt and copper (I) salt in water is cooled to about 37A deg C., in a preferred embodiment, the mixture is further cooled by stirring. In a preferred implementation, evaporating the alcohol or water and washing the copper (I) glycinate complex with alcohol and/or water takes place under nitrogen-purge. For example, the water is dried by flushing a pressure filter with nitrogen. Once the collected products on the filter is semi-dry, the drying process continues in a drying plate, under vacuum conditions, at a temperature of 41A deg C. The isolated crystals of copper (I) glycinate complex prepared in the absence of the ascorbate salt have a lavender purple color, whereas isolated crystals of copper (II) glycinate complex have a blue color. [0097] In an alternate embodiment, the present invention provides a method of synthesizing a copper (I) pyruvate complex. The method comprises: a) charging a pyruvate salt under a stream of inert gas in an alcohol; b) heating the pyruvate salt in the alcohol at about 45A deg C.; c) adding a copper (I) salt to the alcohol and allowing to reflux for at least 12 hours; and d) evaporating the alcohol and washing the copper (I) pyruvate complex with water to remove impurities. In some implementations, the pyruvate salt is charged under a stream of inert gas with an ascorbate salt in an alcohol. In one aspect, the pyruvate salt in alcohol is heated for 30 minutes. In a preferred embodiment, the mixture of copper (I) salt and pyruvate salt in water is refluxed for between 12 to 16 hours. The isolated crystals of copper (I) pyruvate complex prepared in the absence of the ascorbate salt have an orange-yellow color. [0098] In another embodiment, the present invention provides a method of synthesizing a copper (I) succinate complex. The method comprises: a) charging a succinate salt under a stream of inert gas in an alcohol; b) heating the succinate salt and the ascorbate salt in the alcohol at about 45A deg C.; c) adding a copper (I) salt to the alcohol and allowing to reflux for at least 12 hours; and d) evaporating the alcohol and washing the copper (I) succinate complex with water to remove impurities. In some implementations, the pyruvate salt is charged under a stream of inert gas with an ascorbate salt in an alcohol. In one aspect, the succinate salt in alcohol is heated for 30 minutes. In a preferred embodiment, the mixture of copper (I) salt and succinate salt in water is refluxed for between 12 to 16 hours. The isolated crystals of copper (I) succinate complex prepared in the absence of the ascorbate salt have a pink color. [0099] In preferred embodiments of the methods of synthesizing a copper (I) glycinate complex, a copper (I) pyruvate complex, or a copper (I) succinate complex, the copper (I) salt is copper (I) chloride. The molar ratios of glycinate salt, pyruvate salt, or succinate salt to the copper (I) salt may be about 3:1, about 3:1.1, about 3:1.2, about 3:1.3, about 3:1.4, about 3:1.5, about 3:1.6, about 3:1.7, or about 3:1.8. The ascorbate salt used may be sodium ascorbate, and the alcohol may be ethanol. The molar ratios of glycinate salt/pyruvate salt/succinate salt to ascorbate salt to copper (I) salt may be about 3:1:1, about 3:1.1:1.1, about 3:1.2:1.2, about 3:1.3:1.3, about 3:1.4:1.4, about 3:1.5:1.5, about 3:1.6:1.6, about 3:1.7:1.7, or about 3:1.8:1.8. In one embodiment, the alcohol is 90% ethanol. [0100] The methods of synthesizing copper (I) complexes may further comprise trituration with organic solvents and/or recrystallization to further purify the copper (I) complexes. [0101] It is to be understood that the foregoing describes preferred embodiments of the present invention and that modifications may be made thereto without departing from the scope or spirit of the present invention as set forth in the claims. Such scope is limited only by the claims below as read in connection with the above specification. Many additional advantages of applicant's invention will be apparent to those skilled in the art from the descriptions, drawings, and the claims set forth herein. **EXAMPLES** **Example 1a. Preparation of a Copper (I) Glycinate Complex** [0102] Those skilled in the art will recognize various synthetic methodologies that may be employed to prepare non-toxic pharmaceutically acceptable compositions of copper (I) glycinate. One such (representative) example is set forth below. **[0103] A 100 mL, 3-necked flask was charged with 90% ethanol (EtOH), sodium glycinate and sodium ascorbate under a stream of N2 while charging. The mixture was heated to 45A deg C. for 30 minutes. Cuprous chloride (aka copper (I) chloride, CuCl or Cu2Cl2) was then added to the mixture and placed under reflux overnight with N2. The amounts and volumes of each component in the mixture are shown in Table 1. The molar ratio of sodium glycinate:sodium L-ascorbate:cuprous chloride was 3:1:1.****TABLE 1****Reaction mixture for production of copper (I) glycinate****Mass Volume Molecular Molar****Compound (g) (mL) Weight mmol Equivalent Source****Sodium 2 97.05 20.6079 1 Sigma****glycinate Aldrich****Sodium L- 1.34727 198.11 6.80061 0.33 Sigma****ascorbate Aldrich****CuCl 0.67326 99 6.80061 0.33 Strem****Chemicals****90% EtOH 60****[0104] A red suspension was filtrated to furnish a small amount of red powder ( I100 mg), which was washed with water. The mother liquor was concentrated by evaporation of the ethanol and contained most of the mass as a brown powder.** [0105] Proton NMR was performed to identify the copper (I) glycinate product. Proton NMR (dissolved in D2O) of the red powder ( I100 mg) indicated no presence of starting material or product. [0106] Proton NMR (dissolved in D2O) of the concentrated mother liquor indicated a single peak at 3.677 ppm and other small peaks between 3.7-4.7 ppm (see FIG. 1). The D2O solvent peak is at 4.8 ppm. [0107] Proton NMR (dissolved in D2O) of sodium glycinate indicated a single peak at 3.157 ppm, which corresponds to the methylene (CH2) (see FIG. 2). Proton NMR (dissolved in D2O) of sodium ascorbate indicated the following peaks: 3.70-3.73 (CH2), 3.99 (CHOH), and 4.49 (CH) ppm that correspond to the expected sodium L-ascorbate peaks (see FIG. 3). [0108] In the proton NMR spectrum of the mother liquor there is no presence of sodium glycinate (3.157 ppm) (see FIG. 1). There is a singlet peak at 3.67 ppm believed to correspond to the desired Cu (I) chelated methylene (CH2) product, copper (I) glycinate. **Example 1b. Preparation of a Copper (I) Glycinate Complex** **[0109] Component Qty F.W. Moles Equiv.** **1) Glycine 6.7 g 75.07 0.0893 3** **2) Water 70 ml a a 1** **3) Ethanol 350 ml a a 5** **4) Cu(I)Cl 2.95 g 99 0.0298 1** **[0110] The preparation process requires assembly of a nitrogen-purged 500 ml reaction flask equipped with a mechanical stirrer, temperature probe/controller, reflux condenser, solid addition funnel and heating mantle and nitrogen purge. Under nitrogen purge, the reaction flask is charged with glycine (6.7 g or 0.0893 mol) and deionized water (70 ml). The resulting mixture is stirred to complete dissolution. The dissolved mixture is heated to 40-45A deg C. while remaining under nitrogen. The reaction flask is then charge with ethanol (350 ml) under nitrogen and then heated back to 40-45A deg C. Via solid addition funnel, charge the cuprous chloride slowly while maintaining a temperature of 40-5A deg C. during the addition. Turn off the heat and allow the mixture to exothermal (about 5-10A deg C. exothermal is typical). The mixture is cooled to about 37A deg C. and stirred for approximately one hour. Afterwards, the reaction is removed from heat and sparged with nitrogen for approximately one hour. The final product is filtered using a pressure filter under nitrogen purge. The collected product was rinsed with ethanol (200 ml) two times with 15 minutes between each rinse. The collected product on the filter is then flushed with nitrogen for at least 45 minutes until semi-dry. The collected product on the filter is transferred to a drying dish and dried under vacuum at 41A deg C. The drying dish is placed at an angle of 30A deg to 45A deg to facilitate drying and formation of clean crystals. Yield: I95% of copper (I) glycinate, a lavender purple microcrystalline solid.** Example 2. SEM Analysis of Copper (I) Glycinate Complex [0111] The copper (I) glycinate complex synthesized in Example 1 was analyzed with an SEM, and various images of the copper (I) glycinate complex were captured (see FIG. 4 for a representative image). An Energy Dispersive Spectroscopy analysis on the SEM (EDS-SEM) was run with the energy-dispersive spectrometer set at an acceleration voltage of 15.0 kV. The EDS-SEM analysis revealed the presence of carbon I, oxygen (O), and copper (Cu) in the copper (I) glycinate complex. Sodium (Na), aluminum (Al), and chlorine (Cl) were also identified as impurities present in the copper (I) glycinate complex. See FIGS. 5-7. **Example 3. Preparation of a Copper (I) Pyruvate Complex** [0112] Those skilled in the art will recognize various synthetic methodologies that may be employed to prepare non-toxic pharmaceutically acceptable compositions of copper (I) pyruvate. One such (representative) example is set forth below. **[0113] A 100 mL, 3-necked flask was charged with 90% ethanol (EtOH), sodium pyruvate and sodium ascorbate under a stream of N2 while charging. The mixture was heated to 45A deg C. for 30 minutes. Cuprous chloride was then added to the mixture and placed under reflux overnight with N2. The molar ratio of sodium pyruvate:sodium L-ascorbate:cuprous chloride was 3:1:1. The resulting product was concentrated by evaporation of the ethanol and washed with water to remove residual sodium chloride.** Example 4. SEM Analysis of Copper (I) Pyruvate Complex [0114] The copper (I) pyruvate complex synthesized in Example 3 was analyzed with an SEM, and various images of the copper (I) pyruvate complex were captured (see FIG. 8 for a representative image). An EDS-SEM analysis was run with the energy-dispersive spectrometer set at an acceleration voltage of 20.0 kV. The EDS-SEM analysis revealed the presence of carbon (C), oxygen (O), and copper (Cu) in the copper (I) pyruvate complex. Sodium (Na), chlorine (CO, and calcium (Ca) were also identified as impurities present in the copper (I) pyruvate complex. See FIGS. 9-11. **Example 5. Preparation of a Copper (I) Succinate Complex** [0115] Those skilled in the art will recognize various synthetic methodologies that may be employed to prepare non-toxic pharmaceutically acceptable compositions of copper (I) succinate. One such (representative) example is set forth below. **[0116] A 100 mL, 3-necked flask was charged with 90% ethanol (EtOH), sodium succinate and sodium ascorbate under a stream of N2 while charging. The mixture was heated to 45A deg C. for 30 minutes. Cuprous chloride was then added and the mixture placed under reflux overnight with N2. The molar ratio of sodium succinate:sodium L-ascorbate:cuprous chloride was 3:1:1. The resulting product was concentrated by evaporation of the ethanol and washed with water to remove residual sodium chloride.** [0117] Because succinic acid possesses two acidic groups, there are at least two different species of salt possible. The first is the hemi form, in which only one of the carboxylic acids is in the copper salt form, while the other is the full salt form in which there are two coppers to one succinate, one at each carboxylate. Therefore, the product of this synthesis reaction may contain a mixture of the hemi salt and the full salt as shown below. Example 6. SEM Analysis of Copper (I) Succinate Complex [0118] The copper (I) succinate complex synthesized in Example 5 was analyzed with an SEM, and various images of the copper (I) pyruvate complex were captured (see FIG. 12 for a representative image). An EDS-SEM analysis was run with the energy-dispersive spectrometer set at an acceleration voltage of 20.0 kV. The EDS-SEM analysis revealed the presence of carbon (C), oxygen (O), and copper (Cu) in the copper (I) succinate complex. Sodium (Na) and chlorine (Cl) were also identified as impurities present in the copper (I) pyruvate complex. See FIGS. 13-15. Example 7. In Vitro Effects of Copper (I) Glycinate Complex [0119] The copper (I) glycinate complex synthesized in Example 1b was used in a mitochondrial stress test using the XF Cell Mito Stress Test kit (Agilent, Wilmington, Del.). The cells studies were lymphoblasts from normal subjects (C), lymphoblasts from autistic donors without mitochondrial dysfunction (N), and lymphoblasts from autistic donors with mitochondrial dysfunction (A). ATP-linked respiration, proton leak, maximal respiratory capacity, and reserve capacity were determined as measured by the cells' oxygen consumption rate. FIG. 16 depicts the time points during the course of mitochondrial stress tests that are relevant for determining ATP-linked respiration, proton leak, maximal respiratory capacity, and reserve capacity. FIG. 17 depicts the results of the stress test with that compares the administration of 100 I1/4M or 500 I1/4M of the copper (I) glycinate to the respiration of these cells without administration of the copper (I) complex. Panel B of FIG. 17 shows that 500 I1/4M of the copper (I) glycinate significantly reduced proton leak lymphoblasts with mitochondrial dysfunction. Mitochondrial dynfunction in cells was determined using the methods of the Frye lab, which was described in Rose et al., aOxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines,a Transl Psychiatry, 2014 4:e377. [0120] Unless defined otherwise, all technical and scientific terms herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs. Although any methods and materials, similar or equivalent to those described herein, can be used in the practice or testing of the present invention, the preferred methods and materials are described herein. All publications, patents, and patent publications cited are incorporated by reference herein in their entirety for all purposes. [0121] The publications discussed herein are provided solely for their disclosure prior to the filing date of the present application. Nothing herein is to be construed as an admission that the present invention is not entitled to antedate such publication by virtue of prior invention. [0122] It is to be understood that the methods set forth hereinabove describe preferred synthetic methodologies and that modifications thereto may be made without departing from the scope or spirit of the invention. Such scope is limited only by the claims below as read in connection with the above specification. Many additional synthetic methodologies and additional advantages of applicant's invention will be apparent to those skilled in the art from the above descriptions and the claims below. --- **US2016024118** **COPPER (I) COMPLEXES WITH GLYCINE, PYRUVATE, AND SUCCINATE** **Inventor: BARKER CHARLES LOUIS ALBARTUSa/ BOULANGER WILLIAM** **Applicant: C LAB PHARMA INTERNATIONAL** --- **New stable, crystalline organometallic complexes of glycine with metals, e.g. cobalt, magnesium, iron, zinc, manganese or copper, useful as bioavailable metal sources for humans or animals** **FR2833187 (A1)** **FR2843752 (A1)** --- Copper Medicine Copper Development Association COPPER.org Medical Uses of Copper in Antiquity Copper Applications in Health & Environment June 2000 The first recorded medical use of copper is found in the Smith Papyrus, one of the oldest books known. The Papyrus is an Egyptian medical text, written between 2600 and 2200 B.C., which records the use of copper to sterilize chest wounds and to sterilize drinking water. Other early reports of copper's medicinal uses are found in the Ebers Papyrus, written around 1500 B.C. The Ebers Papyrus documents medicine practiced in ancient Egypt and in other cultures that flourished many centuries earlier. Copper compounds were recommended for headaches, "trembling of the limbs" (perhaps referring to epilepsy or St. Vitus' Dance), burn wounds, itching and certain growths in the neck, some of which were probably boils. Forms of copper used for the treatment of disease ranged from metallic copper splinters and shavings to various naturally occurring copper salts and oxides. A "green pigment" is spoken of which was probably the mineral, malachite, a form of copper carbonate. It could also have been chrysocolla, a copper silicate, or even copper chloride, which forms on copper exposed to seawater. In the first century A.D., Dioscorides, in his book De Materia Medica, described a method of making another green pigment known as verdigris by exposing metallic copper to the vapors of boiling vinegar. In this process, blue-green copper acetate forms on the copper surface. Verdigris and blue vitriol (copper sulfate) were used, among other things, in remedies for eye ailments such as bloodshot eyes, inflamed or "bleary" eyes, "fat in the eyes" (trachoma?), and cataracts. In the Hippocratic Collection (named for, although not entirely written by, the Greek physician Hippocrates, 460 to 380 B.C.), copper is recommended for the treatment of leg ulcers associated with varicose veins. To prevent infection of fresh wounds, the Greeks sprinkled a dry powder composed of copper oxide and copper sulfate on the wound. Another antiseptic wound treatment at the time was a boiled mixture of honey and red copper oxide. The Greeks had easy access to copper since the metal was readily available on the island of Kypros (Cyprus) from which the Latin name for copper, cuprum, is derived. By the time the Roman physician Aulus Cornelius Celsus began practicing medicine, during the reign of Tiberius (14 to 37 A.D.), copper and its derivatives had been firmly established as an important drug in the medical practitioner's pharmacopoeia. In Celsus' series, De Medicina, books one through six list many purposes for which copper was used together with the preparation and the form of copper most effective for each ailment. For the treatment of venereal disease, for example, Celsus prescribed a remedy consisting of pepper, myrrh, saffron, cooked antimony sulfide, and copper oxide. These were first pounded together in dry wine and when dry, once again pounded together in raisin wine and heated until dry. For a non-healing chronic ulcer, treatment consisted of copper oxide and other ingredients including enough rose oil to give a soft consistency. Pliny (23 to 79 A.D.) described a number of remedies involving copper. Black copper oxide was given with honey to remove intestinal worms. Diluted and injected as drops into nostrils, it cleared the head and, when taken with honey or honey water, it purged the stomach. It was given for "eye roughness," "eye pain and mistiness," and ulceration of the mouth. It was blown into the ears to relieve ear problems. In the New World the Aztecs also used copper for medical purposes. Don Francisco de Mendoza commissioned two learned Aztec Indian physicians to record the pharmacological treatments known by the Aztecs at the time of the Conquest. For the treatment of "Faucium Calor" (literally, heat of the throat, or, sore throat) they prescribed gargling with a mixture of ingredients containing copper. Copper was also employed in ancient India and Persia to treat lung diseases. The tenth century book, Liber Fundamentorum Pharmacologiae describes the use of copper compounds for medicinal purposes in ancient Persia. Powdered malachite was sprinkled on boils, copper acetate as well as and copper oxide were used for diseases of the eye and for the elimination of "yellow bile." Nomadic Mongolian tribes treated and healed ulcers of venereal origin with orally administered copper sulfate. Turning to more modern times, the first observation of copper's role in the immune system was published in 1867 when it was reported that, during the cholera epidemics in Paris of 1832, 1849 and 1852, copper workers were immune to the disease. More recently copper's role in the immune system has been supported by observations that individuals suffering from Menke's disease (an inherited disease in which there is defective copper absorption and metabolism) generally die of immune system-related phenomena and other infections. Further, animals deficient in copper have been shown to have increased susceptibility to bacterial pathogens such as Salmonella and Listeria. Evidence such as this has led researchers to suggest strongly that copper compounds not only cure disease but also aid in the prevention of disease. In 1885, the French physician, Luton, reported on using copper acetate in his practice to treat arthritic patients. For external application he made a salve of hog's lard and 30% neutral copper acetate. For internal treatment, he used pills containing 10 mg. of copper acetate. In 1895, Kobert published his review of the pharmacological actions of copper compounds. Copper arsenate had been used to treat acute and chronic diarrhea as well as dysentery and cholera. A variety of inorganic copper preparations were found to be effective in treating chronic adenitis, eczema, impetigo, scorphulosis, tubercular infections, lupus, syphilis, anemias, chorea and facial neuralgia. An organic complex of copper developed by Bayer was shown to have curative powers in the treatment of tuberculosis. Copper treatment for tuberculosis continued until the 1940s, and various physicians reported on their success in using copper preparations in intravenous injections. In 1939, the German physician, Werner Hangarter, noticed that Finnish copper miners were unaffected by arthritis as long as they worked in the mining industry. This was particularly striking since rheumatism was a widespread disease in Finland, and workers in other industries and other towns had more rheumatic diseases than did the copper miners. This observation led Finnish medical researchers plus the Germans, Hangarter and LA1/4bke, to begin their now classic clinical trials using an aqueous mixture of copper chloride and sodium salicylate. They successfully treated patients suffering from rheumatic fever, rheumatoid arthritis, neck and back problems, as well as sciatica. Until recently, just as in Pliny's time, the medical profession used copper sulfate as a means to clinically induce vomiting. This is based on the fact that one of the body's natural physiological responses to prevent copper intoxication is vomiting. A Manual of Pharmacology and its Applications to Therapeutics and Toxicology, published by W. B. Saunders Company in 1957 recommends the use of 0.5 gram of copper sulfate, dissolved in a glass of water, in a single dose, or three doses of 0.25 gram fifteen minutes apart, for this purpose. Since 1934, it has been known that individuals suffering from such diseases as scarlet fever, diphtheria, tuberculosis, arthritis, malignant tumors and lymphogranulomas exhibit an elevation of copper in their blood plasma. Since then, the list of maladies bringing about such elevation has been extended to fever, wounds, ulcers, pain, seizures, cancers, carcinogenesis, diabetes, cerebrovascular and cardiovascular diseases, and irradiation and tissue stresses, including restricted blood flow. This suggests that this redistribution of copper in the body has a general role in responding to physiological, disease, or injury stress. On the other hand, the elevation of copper in the affected organ has led some to postulate that it was this excess of copper that caused the disease. Nonetheless, this elevation of copper in diseased states is suggested to account for the natural synthesis of copper-dependent regulatory proteins and enzymes in the body required for biochemical responses to stress. It may be that these natural copper complexes expedite the relief of stress and the repair of tissues. Thus, it appears that in addition to the anti-bacterial and anti-fungal activity of inorganic copper compounds as recognized by the ancients, metallo-organic complexes of copper have medicinal capabilities that are fundamental to the healing process itself. Copper is known to be an essential element in human metabolism. However, copper does not exist in the body in measurable amounts in ionic form. All measurable amounts of copper in the body exist in tissues as complexes with the organic compounds of proteins and enzymes. Therefore, it has been concluded that copper becomes and remains intimately involved in body processes. Some copper complexes serve to store copper, others to transport it, and yet others play important roles in key cellular and metabolic processes. Studies into the roles that these copper complexes play and the mechanisms of these roles have further confirmed that copper enters into the prevention and control of a number of disease states in the body. As will be discussed below, the key to the effective use of copper-based pharmaceuticals is not the use of inorganic compounds of copper, as used by the ancients, but rather the use of metallo-organic complexes or chelates of copper. The process of chelating metals allows them to be smuggled in the transport process across the intestinal wall and thereby enter into the mainstream of nutrient flow and usage in the body. The first modern research on the subject of copper medicinal substances was by Professor John R. J. Sorenson, of the University of Arkansas for Medical Sciences, College of Pharmacy, who, in 1966, demonstrated that copper complexes have therapeutic efficacy in the treatment of inflammatory diseases using doses that are nontoxic. Since then, copper metallo-organic complexes have been used to successfully treat patients with arthritic and other chronic degenerative diseases. More than 140 copper complexes of non-steroidal anti-inflammatory agents (aspirin and ibuprofen, for example) have been shown to be more active than their parent compounds. Copper aspirinate has been shown not only to be more effective in the treatment of rheumatoid arthritis than aspirin alone, but it has been shown to prevent or even cure the ulceration of the stomach often associated with aspirin therapy. Based on these experiences, the work of Professor Sorenson and other researchers around the world has progressed into the medicinal benefits of organic complexes of copper in a number of disease states. This work, thus far mainly based on animal research, has opened a whole new vista both into the understanding of copper's many-fold role in the body and in the practicality of using supplementary copper in the treatment of wound healing and inflammation-related disease states. Some of these potential indications are: Ulcer and Wound-Healing Activities of Copper Complexes It has been demonstrated that copper complexes such as copper aspirinate and copper tryptophanate, markedly increase healing rate of ulcers and wounds. For example, copper complexes heal gastric ulcers five days sooner than other reagents. Further, it has been shown that, whereas non-steroidal anti-inflammatory drugs, such as ibuprofen and enefenamic acid suppress wound healing, copper complexes of these drugs promote normal wound healing while at the same time retaining anti-inflammatory activity. Anticonvulsant Activities of Copper Complexes The brain contains more copper than any other organ of the body except the liver, where copper is stored for use elsewhere. This fact suggests that copper plays a role in brain functions. With reports of seizures in animals and humans following the protracted consumption of copper-deficient diets, it was reasoned that copper has a role to play in the prevention of seizures. It was subsequently discovered that organic compounds that are not themselves anti-convulsants exhibit anticonvulsant activity when complexed with copper. Further, it was found that copper complexes of all anti-epileptic drugs are more effective and less toxic than their parent drugs. Anticancer Activities of Copper Complexes As early as 1912, patients in Germany were treated for facial epithelioma with a mixture of copper chloride and lecithin. Success of such treatment suggested that copper compounds have anticancer activity. Work at the University of Liverpool in 1913 demonstrated that subcutaneous and intravenous injections of a copper salt or colloidal copper softened and degenerated carcinomas transplanted into mice. In 1930, work in France indicated that injections of colloidal copper mobilized and expelled tumor tissue. Recent work with mice in the USA has shown that, indeed, treatment of solid tumors with non-toxic doses of various organic complexes of copper markedly decreased tumor growth and metastasis and thus increased survival rate. These copper complexes did not kill cancer cells but caused them to revert to normal cells. Anticarcinogenic Activity of Copper Complexes Based on work in the treatment of cancers using copper complexes, researchers have found that these same complexes may prevent or retard the development of cancers in mice under conditions where cancers are expected to be induced. Radiation Protection and Radiation Recovery of Copper Complexes Ionizing radiation, such as that used in the treatment of cancer, has been shown to induce massive systemic inflammation. Ideally, such radiation-induced injury might be prevented or ameliorated by chemical repair mechanisms in the body. Thus, pharmacological approaches to the repair of radiation-damaged tissue are needed. As early as 1984, copper metallo-organic complexes have been shown to have radiation protection and radiation recovery activities. They are capable of causing rapid recovery of immunocompetence and recovery from radiation induced tissue changes. The mechanism of this activity appears to be tied to the ability of certain copper complexes to deactivate the superoxide, or "free," radicals liberated by ionizing radiation. In addition, since radiation has the capability of breaking the bonds of natural copper enzymes in the body, supplementing these with non-toxic doses of pharmaceutical copper complexes restores the lost tissue-repair capability. Since these complexes may also have anticarcinogenic activity, it is suggested that there would be merit in using copper complexes in the treatment of cancer and in particular, treating patients undergoing ionizing radiation therapy for their cancer, accidental exposure to radiation, and astronauts undertaking space travel. Heart Disease and Copper Complexes Numerous studies have drawn attention to the relationship between copper deficiency and heart disease. First observed in rats in 1936, this effect has now been traced to both a deficiency in copper and an imbalance in the copper-to-zinc ratio in the body. Work by Dr. L.M. Klevay at the U.S. Department of Agriculture, Human Nutrition Research Center in 1973 has led to the postulation that copper has a direct effect on the control of cholesterol. In continuing work published in 1975, he theorized that a metabolic imbalance between zinc and copper - with more emphasis on copper deficiency than zinc excess - is a major contributing factor to the etiology of coronary heart disease. Subsequent work by other investigators has shown that copper complexes also can have a valuable role in the minimization of damage to the aorta and heart muscle as oxygenated blood reperfuses into tissues following myocardial infarction. This action is based on the anti-inflammatory action of copper complexes. These and other studies suggest the use of copper dietary supplements as a means of preventing and controlling such diseases as atherosclerosis (a form of arteriosclerosis), coronary heart disease, aortic aneurysms and myocardial infarction. It has been speculated that the reason that the heart attack rate in France is lower than in the rest of Europe is because of the French practice of drinking red wine. Red wine has a higher copper content than white wine because it is prepared with the skin of the grape intact. The copper originates in the wine from the copper fungicides used on the grapes in the field. Based on an abundance of historical data such as the foregoing, many researchers anticipate that copper will become an increasingly important component of tomorrow's medical treatments. References The historical part of this paper is based on H.H.A. Dollwet and J.R.J. Sorenson, Historic uses of copper compounds in medicine, Trace Elements in Medicine, Vol. 2, No. 2, 1985, pp 80 - 87. --- Copper Aspirinate IUPAC name -- dicopper 2-acetyloxybenzoate Other names -- tetrakis-Au-acetylsalicylato-dicopper(II), copper(II) aspirinate, cupric acetylsalicylate, cupric aspirinate, cupric aspirin complex Identifiers CAS number -- 23642-01-5 YesY PubChem -- 92244 Properties Copper(II) aspirinate is an aspirin chelate of copper(II) cations (Cu2+). It is used to treat rheumatoid arthritis. Molecular formula C36H28Cu2O16 Molar mass 843.69g/mol Appearance Bright blue crystalline solid. Melting point 248-255 A degC (decomp.) Related compounds -- Aspirin ; Other cations -- Zinc aspirinate, Aluminium aspirinate Except where noted otherwise, data are given for materials in their standard state (at 25 A degC, 100 kPa) Preparation Copper aspirinate can be prepared by several methods. In one route of preparation, an excess of acetylsalicylic acid is dissolved in aqueous sodium carbonate. Sodium hydroxide is not suitable for this purpose, because it will hydrolyse acetylsalicylic acid (ASA) into salicylic acid and sodium acetate. 2 HC9H7O4 + Na2CO3 ? 2 NaC9H7O4 + CO2? + H2O The resulting solution is then filtered to remove any undissolved acetylsalicylic acid and is mixed with a solution containing Cu2+ cations (copper(II) sulfate is suitable), precipitating bright blue crystals of copper aspirinate immediately. The crystals can then be filtered from solution, washed, and dried. An excess of acetylsalicylic acid is used in the first step, because it eliminates the possibility of unreacted carbonate anions precipitating the copper in this step. 4 NaC9H7O4 + 2 CuSO4 ? C36H28Cu2O16? + 2 Na2SO4 Medicinal Use Copper aspirinate has been proven effective as a treatment for rheumatoid arthritis.[1] The studies on animal models suggest that copper aspirinate is very promising in treating against thrombotic diseases and it has all the prospects of success in becoming an antithrombotic drug that prevents and treats thrombotic diseases in humans.[2] Other uses The use of copper aspirinate as a pigment in PVC and Polystyrene has also been investigated.[3] Footnotes 1. ^ "Rheumatoid Arthritis (RA)". Copper Development Association. June 2000. http://www.copper.org/innovations/2000/06/medicine-chest.html. 2. ^ Weiping Liu,corresponding author1 Huizhou Xiong, Yikun Yang Ling Li, Zhiqiang Shen, and Zhihe Chen (1998). "Potential Application of Copper Aspirinate in Preventing and Treating Thromboembolic Diseases". Met Based Drugs. (Hindawi Publishing Corporation) 5 (3): 123a126. doi:10.1155/MBD.1998.123. PMC 2365110. PMID 18475833. http://www.copper.org/innovations/2000/06/medicine-chest.html. 3. ^ Allan, J R; A Renton, W E Smith, D L Gerrard, J Birnie (1991). "A Study of the Performance of Bis(acetylsalicylate) Copper(II) and the Cobalt(II), Nickel(II) and Copper(II) Complexes of Pyridine-3,4-dicarboxylic Acid as Colouring Materials for Poly(vinyl chloride) and Polystyrene". Eur. Polym. J. 27 (7): 669a672. doi:10.1016/0014-3057(91)90155-H. Salicylates Salicylic acid Aspirin Aloxiprin Methyl salicylate Magnesium salicylate Ethyl salicylate Bismuth subsalicylate Sodium salicylate Salicylamide Salicin Benorilate Salsalate Ethenzamide Diflunisal Trolamine salicylate Homosalate Salicylmethylecgonine Octyl salicylate Aluminon Benzyl salicylate Copper aspirinate Potassium salicylate --- Copper Aspirinate Synthesis by Brian Fraser Disclaimer: The following is a summary of the procedure I used to make copper aspirinate. I offer it here for informational purposes to show that copper aspirinate can be made with commonly available materials and equipment. A similar procedure is typically done by second-year college chemistry students as a laboratory exercise in a setting supervised by a professional instructor. I do NOT recommend that people do this at home. Some aspects of these procedures are hazardous, and the typical home kitchen simply has too many distractions and interruptions for a student to carry out these procedures safely. Your wife ( or mom) will also be furious if you get copper sulfate stains on her kitchen counter! Copper Aspirinate synthesis (kitchen method) Equipment and Materials required 1. Saturated copper acetate solution. See procedure below. 2. Pure aspirin crystals. See procedure below. 3. Ethanol (95%; liquor store ethanol like Everclear (190 proof, UPC 088352100036) is what was used here. 4. Vacuum filtration facilities (BA1/4chner funnel, coarse and medium porosity filter paper, aspirator, filter flask, seals, tubing, clamps, stand, etc. These common lab tools are not absolutely necessary, but can speed things up considerably.) 5. Containers for liquid such as Rubbermaid 24 fl. oz. servin' saver tm (used here as a "beaker"). Procedure 1. Add 1 fl. oz. of saturated copper acetate solution to a beaker. 2. Dissolve 1 tsp (teaspoon) pure aspirin crystals in about 1 fl. oz. of ethanol (95%) in another beaker 3. Pour the aspirin solution into the copper acetate solution. Stir occasionally. 4. Dark blue crystals will gradually form on the sides and bottom of the beaker. The initial layer will form immediately if the beaker has been freshly cleaned and scoured. The layer will gradually thicken and become bluer and darker. This process may take several hours. The endpoint is reached when the liquid has turned a light blue and no more blue crystals are forming on the walls of the beaker. (You can verify the endpoint by siphoning the clear liquid, evaporating it in a separate container, and checking the residue. The residue should be mostly aspirin crystals.) This procedure requires no heating. If you heat the liquid to increase the reaction rate, be aware that aspirin can hydrolyze into acetic and salicylic acids in a moist or liquid environment. If that happens, the liquid will turn dark green, and the yield of copper aspirinate will be greatly reduced. 5. Cool the mixture in a refrigerator. 6. Scrape the crystals off the sides and bottom of the beaker. Then vacuum filter the whole mixture. (Save the first filtrate in a separate container if you do ethanol solvent recycling.) 7. Wash the blue powder on the filter with cold distilled water. 8. Dry the powder and filter paper in an oven at about 120F. Store the dry powder in a small dark bottle with a label identifying the contents and the date of creation. Alternative Procedure Substitute isopropanol (99%) for the ethanol in step #2 and use 1/2 teaspoon, instead of 1 teaspoon, of aspirin crystals and 1/2 fl. oz. isopropanol instead of 1 fl. oz of ethanol. After several hours of initial crystallization, add 1/2 fl. oz. of distilled water and place the beaker in the refrigerator and wait a few more hours for more crystals. This variation gives about the same results as the ethanol procedure. Its advantages are that it uses less excess aspirin and a less expensive alcohol. Aspirin purification (kitchen method) Equipment and Materials required 1. One bottle of 1000 commercial aspirin tablets (preferably the uncoated kind). 2. A pint or two of isopropyl alcohol (99%). This is usually available from a hardware store. Sometimes it can be found in a drugstore (UPC: 341226909730 ) Isopropanol is extremely flammable, so be very careful not to expose vapors to hidden or unexpected ignition sources. 3. A couple of gallons of deionized or distilled water. 4. Three, 24 fl. oz. wide-mouthed polypropylene containers with covers, such as Rubbermaid servin' saver tm. 5. Oven thermometer (easily read dial type is best) 6. Modified turkey baster (see construction procedure below) 7. One kitchen (with sink, refrigerator, oven, etc) Procedure: 1. Dump a few hundred aspirin tablets into a wide-mouthed container. 2. Add distilled water to the container and stir. This will break up the aspirin tablets and dissolve the hydroxypropyl methycelluose coating that is usually used to coat aspirin tablets. Let the mixture settle for an hour or so in the refrigerator. 3. Siphon most of the water out with a modified turkey baster. 4. Repeat steps #2 and #3 a total of three to five times. This will largely get rid of the methycellulose coating, which tends to clog filters. You might not need to repeat these steps if you use uncoated aspirin. 5. Vacuum filter the mixture from #4 and dry the powder in air. (Caution: aspirin tends to decompose when heated in a moist environment). 6. Add the powder to a quart container. Add about a half-cup of isopropyl alcohol (99%). Stir. This will dissolve part, but not all, of the aspirin. Let the mixture settle. 7. Vacuum filter the above mixture using medium porosity filter paper. Pour the filtrate into a clear glass container for inspection. If the filtrate is not clear, re-establish vacuum on the filter, and filter it again. (Sometimes simply letting the mixture settle and then siphoning the clear liquid with a turkey baster is more effective than filtration; the latter, however, may be faster.) 8. Pour the clear filtrate containing the dissolved aspirin into the second container, cover it, and place it in the freezer (about 5 F or so). After an hour or so the aspirin will crystallize out of solution. Return the powder on the filter to its original quart container. 9. After the aspirin crystals have formed, remove the container from the freezer. Carefully decant the liquid back into the first container that contains the impure aspirin powder. Then scrape out the pure aspirin crystals into a third container. 10. Cover this first container (impure aspirin powder and recovered isopropanol) and let it warm to room temperature. Agitate it occasionally so that more aspirin will again dissolve. 11. Repeat steps 7 through 10 until you have recovered all the aspirin, and the filter paper has only a thin layer of the excipients (typically calcium phosphate, starch, talc, etc. These impurities are added to the tablets to help them break up in water). Discard the filter paper. Dump the isopropanol down the drain, and wash it down with some tap water. 12. Using new filter paper (medium porosity), filter any remaining isopropanol from the recovered aspirin crystals (third container). Rinse the third container with distilled water and wipe it dry. Dump the filtered crystals back into the third container and cover them with cold distilled water. Re-establish vacuum on the filter and filter the crystals again. This will rinse off any remaining isopropanol. Discard the liquid. (Repeat the procedure if you can still smell isopropanol on the crystals). 13. Finally, gently dry the aspirin crystals. (I dried mine in an oven at 120 F. If you do this, BE SURE you have rinsed the crystals well enough so that there are no isopropanol vapors present. Isopropanol forms explosive vapors with air, and allowing these to accumulate in a confined space is a recipe for serious trouble. Also, aspirin tends to decompose when heated, especially in hot water, so I use only a warm temperature setting. ) Copper acetate synthesis (kitchen method) Equipment and Materials required 1. Copper sulfate pentahydrate 99%. This is usually available from a hardware store in the form of a product used to kill tree roots in sewers and septic tanks, such as Roebic K-77. 2. Arm and Hammer Baking soda (sodium bicarbonate). 3. A couple of quarts of distilled vinegar (5% acetic acid). 4. A Pyrex casserole dish (22 x 11 x 6 cm or similar) 5. Vacuum filtration facilities. 6. Various clean, quart containers. Procedure Preparation of filtered copper sulfate solution 1. Dissolve 3/4 cupful of copper sulfate crystals in about a quart of warm distilled water. 2. Vacuum filter the solution through coarse porosity filter paper. This will filter out suspended solids (metal flecks, "dirt", etc.). Pour the filtrate off into a clear inspection container. Vacuum filter the solution again with medium porosity paper until it is clear blue. Note that the filtrate may still contain significant impurities (lead, arsenic, cadmium, etc.) at this point. Remember that this product is normally used in sewers. 3. Save the clear blue solution for later use. (4. If you want higher purity copper sulfate, you can re-crystallize it at this point.) Preparation of sodium carbonate solution 1. Pour a cup full of sodium bicarbonate into a Pyrex casserole dish. Add distilled water sufficient to dissolve it. 2. Heat the solution in an oven to about 200F. This will cause the bicarbonate to decompose into the carbonate with the evolution of carbon dioxide. The end result will be a solution of sodium carbonate. 3. Let the solution cool to room temperature. Carbonates are somewhat less soluble than bicarbonates; add more distilled water if necessary to keep the material in solution. Preparation of copper carbonate 1. In a large container, gradually combine the copper sulfate solution with the sodium carbonate solution. A blue-green precipitate will immediately form along with the vigorous release of carbon dioxide. Let the precipitate settle out. 2. At this point the liquid portion will have either an excess of sodium carbonate or of copper sulfate. If you add a drop of sodium carbonate and see some precipitate form, then the bulk mixture needs more sodium carbonate solution added. Likewise, if you add a drop of copper sulfate and see a precipitate, then the bulk mixture needs more copper sulfate solution added. Make these adjustments as necessary until there is no longer an unambiguous formation of the blue-green precipitate. 3. Vacuum filter the mixture with a coarse porosity paper filter. Discard the liquid. Wash with cold distilled water and then refilter. This will wash out any excess sodium carbonate or copper sulfate. Preparation of copper acetate solution 4. To a quart container, add the still moist copper carbonate powder from the previous step. Then slowly pour vinegar into the container. Carbon dioxide will evolve and copper acetate will form. The solution will gradually become a deep blue color. A blue-green precipitate may also settle to the bottom of the container. 5. Let the solution settle out. If there is a substantial amount of blue-green precipitate at the bottom of the container, add more vinegar. Try to dissolve most, but not all, of this precipitate. An excess of vinegar is harder to remove than a little of the precipitate. 6. Using coarse paper, vacuum filter the resulting copper acetate solution. Repeat until clear. Discard the paper. Save the blue filtrate. 7. Slowly evaporate the blue filtrate in a Pyrex casserole dish in an oven (150F) for several hours. Periodically scrape down the sides of the dish to prevent a build up of crystals. Continue the evaporation until some blue-black crystals of copper acetate begin to form (and do not redissolve). The mixture may also have some blue-green "pond scum" in it too. 8. Cool and filter the dark blue solution. Store it in a clear glass container for observation (a one quart vinegar bottle works fine). This is the saturated copper acetate solution that will be used to make copper aspirinate. 9. If you want to make copper acetate crystals, continue the evaporation process until blue-black crystals form. This will require evaporating most, but not all, of the solution. Impurities (and excess vinegar) tend to remain in solution instead of crystallizing out. Hence, it is necessary to discard a small portion of the original solution. Collect the crystals on the vacuum filter and discard the leftover liquid. Wash the blue-black crystals with a little bit of cold distilled water. Then dry and store them in a labeled container. Conversion of Aspirin to Salicylic acid (kitchen method) 1. Put about 4 tsp of pure aspirin crystals (see above) and 1/2 cup distilled water into a small, clean jar (such as one used for canning pickles or olives). 2. Place jar on a hot pad in a shallow pan in an oven set to about 225F. Let the aspirin hydrolyze into acetic and salicylic acids for an hour or two. (Add a little more water if all the crystals have not dissolved in the hot liquid.) 3. Cool the liquid in the refrigerator. You should see needle-like crystals. 4. Vacuum filter and wash the crystals with cold distilled water. This will remove acetic acid residue. 5. Dump the crystals out of the filter and air dry them. (they usually come out as a mat of fine needles). Store in a properly labeled bottle. Conversion of Salicylic acid to Phenol Phenol (carbolic acid) is an important disinfectant and germicide, as well as an important organic reagent. According to the Merck Index (10th ed.), salicylic acid sublimes at 76 C, melts at 159 C, and will decompose into phenol and carbon dioxide when rapidly heated at atmospheric pressure. Copper Salicylate Synthesis (kitchen method) 1. In a small custard dish, dissolve 1/4 tsp of sodium bicarbonate (baking soda) in a few of teaspoons of distilled water. 2. Add about 1/2 tsp of the salicylic acid crystals recovered from the conversion described above. Mixture will fizz a little. Stir until all the crystals dissolve. 3. Test the pH. Add more salicylic acid or bicarbonate to get pH of about 6 (slightly acid). This is now a solution of sodium salicylate. 4. Add copper sulfate solution drop by drop. An ugly green precipitate (copper salicylate) will form. --- **NanoCopper Preparation** **Three-step reduction method preparation process for nanocopper** **CN103817345** The invention relates to a three-step reduction method preparation process for nanocopper. The preparation process comprises the following steps: 1, preparing copper sulfate solution, potassium hydroxide solution, ascorbic acid, formaldehyde solution and potassium borohydride solution; 2, single-step reduction: ascorbic acid solution is dropwise added into the copper sulfate solution while stirring is carried out; 3, two-step reduction: the formaldehyde solution is added; 4, three-step reduction: the potassium hydroxide solution is added, the pH value of the solution is adjusted to 9-13, the potassium borohydride solution is dropwise added and is stirred until sediment is completely generated, and copper powder is obtained by filtration; 5; cleaning and drying the copper powder to obtain 300-800 nm nanocopper. By means of three reduction reagents, and according to the reducibility difference of the reduction reagents, the reduction reagents are added into the dissolvable copper sulfate solution in sequence to prepare the nanocopper, and the nanocopper is thinner in grain size, smaller in distribution range and more uniform. **Technical field** The invention relates to the technical field of metal copper powder preparation, in particular to a three-step reduction preparation process of nano copper powder. **Background technique**There are many kinds of preparation methods for copper powder, and there are high energy ball milling method and vapor phase deposition method in physical methods. The ball milling method selects a suitable ball mill and ball milling material, and uses the rotation or vibration of the ball mill to make the hard ball strongly impact, crush and grind the material, and break the copper block into ultrafine particles. The advantages of the ball milling method are simple. The yield is high, and the disadvantage is that the obtained copper powder has a wide particle size distribution, many impurities, and low purity. Vapor deposition is a method of preparing copper powder by rapidly cooling metal copper after heating and melting in an inert gas such as argon gas or helium gas. Electrolytic preparation of copper powder is a relatively common and industrial method for the production of copper powder. Generally, in a copper electrolysis cell, the copper powder deposited on the cathode is scraped off at intervals of 20 minutes to avoid particle growth. The scraped copper powder is subjected to ball milling, sieving and the like to obtain the finally obtained copper powder. Ultrasonic electrolysis is an improved electrolysis process that uses ultrasonic vibration and cavitation to generate high pressure or jets to cause deposited copper particles to detach from the surface of the cathode and to suspend the particles in the electrolyte. In addition, there are high temperature, high pressure hydrothermal method, ?-ray irradiation method, polyol method and microwave polyol method. Among the numerous preparation methods of copper powder, the method of preparing copper powder by reducing soluble copper salt is one of the common methods for preparing copper powder in laboratory and industry. The commonly used reducing agents include reducing agents such as glucose, ascorbic acid, hydrogen peroxide, formaldehyde, sodium hypophosphite, hydrazine hydrate, and potassium borohydride. In many laboratory experiments, copper powder is mostly prepared by the application of a reducing reagent. For example, Liao Wei prepared 40-200 nm copper powder with formaldehyde as a reducing agent; Zhao Bin prepared hydrazine hydrate as a reducing reagent. With ~500nm copper powder, the prepared copper powder has a very wide particle size. **Summary of the invention**The object of the present invention is to provide a three-step reduction preparation process of nano copper powder in order to solve the above-mentioned technical problems, and the obtained copper powder has a particle size ranging from 300 to 800 nm, and the particle size distribution range is small and more uniform. The invention solves the above-mentioned technical problems, and the technical solution adopted is: a three-step reduction preparation process of nano copper powder, comprising the following steps: (1) Preparing a copper sulfate solution having a concentration of 0.1 to 1.0 mol/L, a potassium hydroxide solution of 5 to 10 mol/L, an ascorbic acid of 0.1 to 0.5 mol/L, a formaldehyde solution of 0.1 to 0.5 mol/L, and 0.1 to 2 mol/ L potassium borohydride solution, and the prepared solution is placed in a constant temperature water bath, the temperature of the solution is maintained at 30 ~ 90 A deg C, standby; (2) One-step reduction: in a constant temperature water bath, add ascorbic acid solution to the copper sulfate solution while stirring, and continue stirring for 1 to 10 minutes after the completion of the dropwise addition; (3) two-step reduction: in the constant temperature water bath, continue to add formaldehyde solution, after the completion of the addition, continue to stir for 1 ~ 10min; (4) three-step reduction: in a constant temperature water bath, continue to add potassium hydroxide solution, adjust the pH of the solution 9 ~ 13, then add potassium borohydride solution, stir until the precipitate is completely formed, filtered to obtain copper powder; (5) The copper powder obtained by the step (4) was washed three times with deionized water and absolute ethanol, and then dried in a drier filled with an inert gas to obtain a nano copper powder of 300 to 800 nm. 10 to 50 ml of ascorbic acid is added per 50 to 150 ml of copper sulfate solution. Add 10 to 60 ml of formaldehyde solution per 50 to 150 ml of copper sulfate solution. 10 to 60 ml of potassium hydroxide solution was added per 50 to 150 ml of copper sulfate solution. 100 to 400 ml of potassium borohydride solution is added per 50 to 150 ml of copper sulfate solution. **Beneficial effect**The invention adopts three kinds of reducing reagents, and sequentially adds soluble copper sulfate solution according to different reducing properties of the reducing reagents to prepare nano copper powder, which can make the copper powder have finer particle size, smaller distribution range and more uniformity. . **Detailed ways**A three-step reduction preparation process of nano copper powder, comprising the following steps: (1)Preparing a copper sulfate solution having a concentration of 0.1 to 1.0 mol/L, a potassium hydroxide solution of 5 to 10 mol/L, an ascorbic acid of 0.1 to 0.5 mol/L, a formaldehyde solution of 0.1 to 0.5 mol/L, and 0.1 to 2 mol/ L potassium borohydride solution, and the prepared solution is placed in a constant temperature water bath, the temperature of the solution is maintained at 30 ~ 90 A deg C, standby; 10 to 50 ml of ascorbic acid, 10 to 60 ml of formaldehyde solution, 10 to 60 ml of potassium hydroxide solution, and 100 to 400 ml of potassium borohydride solution are prepared per 50 to 150 ml of copper sulfate solution. (2)One-step reduction: in a constant temperature water bath, add ascorbic acid solution to the copper sulfate solution while stirring, and continue stirring for 1 to 10 minutes after the completion of the dropwise addition; (3), two-step reduction: in the constant temperature water bath, continue to add formaldehyde solution, after the completion of the addition, continue to stir for 1 ~ 10min; (4), three-step reduction: in a constant temperature water bath, continue to add potassium hydroxide solution, adjust the pH of the solution 9 ~ 13, then add potassium borohydride solution, stir until the precipitate is completely formed, filtered to obtain copper powder; (5)The copper powder obtained by the step (4) was washed three times with deionized water and absolute ethanol, and then dried in a drier filled with an inert gas to obtain a nano copper powder of 300 to 800 nm. The following are specific embodiments of the invention: **Example 1** A three-step reduction preparation process of nano copper powder, comprising the following steps: (1)Prepare 100ml of copper sulfate solution with a concentration of 0.5mol/L, potassium hydroxide solution of 7mol/L, 15ml of 0.2mol/L ascorbic acid, 20ml of 0.15mol/L formaldehyde solution and 200ml of 1.0mol/L potassium borohydride solution. And the prepared solution is separately placed in a constant temperature water bath, the temperature of the solution is maintained at 70 A deg C, and used; (2)One-step reduction: in a constant temperature water bath, add ascorbic acid solution to the copper sulfate solution while stirring, and continue stirring for 3 minutes after the completion of the dropwise addition; (3), two-step reduction: in the constant temperature water bath, continue to add formaldehyde solution, after the completion of the addition, continue to stir for 5min; (4)Three-step reduction: in a constant temperature water bath, continue to add potassium hydroxide solution, adjust the pH of the solution to 11, then add potassium borohydride solution, stir until the precipitate is completely formed, and filter to obtain copper powder; (5)The copper powder obtained by the step (4) was washed three times with deionized water and absolute ethanol, and then dried in a drier filled with an inert gas to obtain a nano copper powder of 300 to 800 nm. **Example 2** A three-step reduction preparation process of nano copper powder, comprising the following steps: (1)Prepare 150ml of copper sulfate solution with a concentration of 0.1mol/L, potassium hydroxide solution of 5mol/L, 10ml of 0.5mol/L ascorbic acid, 30ml of 0.4mol/L formaldehyde solution and 300ml of 0.5mol/L potassium borohydride solution. And the prepared solution is separately placed in a constant temperature water bath to keep the temperature of the solution at 60 A deg C, and set aside; (2) One-step reduction: in a constant temperature water bath, add ascorbic acid solution to the copper sulfate solution while stirring, and continue stirring for 3 minutes after the completion of the dropwise addition; (3) two-step reduction: in the constant temperature water bath, continue to add formaldehyde solution, after the completion of the addition, continue to stir for 5min; (4) Three-step reduction: in a constant temperature water bath, continue to add potassium hydroxide solution, adjust the pH of the solution to 10, then add potassium borohydride solution, stir until the precipitate is completely formed, and filter to obtain copper powder; (5)The copper powder obtained by the step (4) was washed three times with deionized water and absolute ethanol, and then dried in a drier filled with an inert gas to obtain a nano copper powder of 300 to 800 nm. **Example 3** A three-step reduction preparation process of nano copper powder, comprising the following steps: (1)60 ml of copper sulfate solution with a concentration of 0.9 mol/L, potassium hydroxide solution of 10 mol/L, 30 ml of 0.4 mol/L ascorbic acid, 50 ml of a 0.3 mol/L formaldehyde solution, and 150 ml of a 1.5 mol/L potassium borohydride solution. And the prepared solution is separately placed in a constant temperature water bath to keep the temperature of the solution at 90 A deg C, and set aside; (2) One-step reduction: in a constant temperature water bath, add ascorbic acid solution to the copper sulfate solution while stirring, and continue stirring for 6 min after the completion of the dropwise addition; (3) two-step reduction: in the constant temperature water bath, continue to add formaldehyde solution, after the completion of the addition, continue to stir for 8min; (4)Three-step reduction: in a constant temperature water bath, continue to add potassium hydroxide solution, adjust the pH of the solution to 13, then add potassium borohydride solution, stir until the precipitate is completely formed, and filter to obtain copper powder; (5)The copper powder obtained by the step (4) was washed three times with deionized water and absolute ethanol, and then dried in a drier filled with an inert gas to obtain a nano copper powder of 300 to 800 nm. --- **Method for preparing hexagonal nanocopper particles by utilizing ionothermal synthesis** **CN104399999** **Summary of the invention**It is an object of the present invention to provide a method for preparing hexagonal nano-copper particles by ion thermal method, which involves simple equipment and processes, and does not require control during the reaction... Embodiment 1 (1)4 g of ammonium bromide, 4 g of succinic acid and 3 g of copper nitrate are weighed together and thoroughly ground to a dark green transparent state; (2)The above mixture was placed in a cleaned lining of tetrafluoroethylene, and 15 ml of hydrazine hydrate was added at a density of 1.03 g/cm < 3 >; (3)The PTFE inner liner is placed in a stainless steel reaction vessel and tightened, and the reaction kettle is placed in a resistance furnace set at a temperature of 120 A deg C for 8 hours; (4)After the above reaction is completed, it is cooled to room temperature, the reaction kettle is taken out, and the reaction product is washed three times with each of alcohol and deionized water; (5)The obtained product was dried under vacuum at 60 A deg C to give dark red copper particles. 5)The obtained product was dried under vacuum at 60 A deg C to give dark red copper particles.. ---