Thioglycolic acid (TGA, also known as MERCAPTOACETIC ACID) is widely used in the hairdressing industry, which mostly caters to women. TGA has been reported to impair several organs, especially reproductive ones such as testes and ovaries. Thioglycolates (the salt forms of TGA) was shown to penetrate the skin and distribute to the kidneys, lungs, small intestine, and spleen; excretion is primarily in the urine. In addition, thioglycolates can be skin irritants of an animal and can be sensitizers.

Fosfructose is a cytoprotective natural sugar phosphate under development by Questcor (formerly Cypros) for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. Fosfructose acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions and improve the cellular energy metabolism in ischemic and hypoperfused tissues. Hypoxia forces ischemic tissue to anaerobic glycolysis for energy, which yields two molecules of ATP per glucose in contrast to 36 molecules of ATP generated during oxidative phosphorylation . Addition of exogenous Fosfructose can produce two more molecules of ATP in an uncompensated anaerobic environment and hence facilitate the recovery of ischemia tissue. Fosfructose breaks down into glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which will further break down into two molecules of pyruvate and finally produce two molecules of ATP. Other mechanisms include inhibition of the generation of oxygen free radicals by neutrophils, stabilization of cell membranes, and maintainance of the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds in ischemic tissues. In myocardial infarction patients, FDP can improve the hemodynamic parameters, attenuate ECG proven ischemic injury and arrhythmia, prevent ATP and creatine phosphate depletion from ischemic myocardium, reduce infarct size, and increase survival rate. Exogenously administered Fosfructose has also been proven beneficial for a variety of other ischemic organs, such as liver, kidney, bowel and even brain as a consequence of its ability to penetrate to the blood brain barrier. Fosfructose trisodium had been in phase I clinical trials for the treatment of heart transplant rejection. Fosfructose trisodium had been in phase II clinical trials for the treatment of heart failure, perioperativ eischaemia and reperfusion injury. Fosfructose trisodium had been in phase III clinical trials for the treatment of sickle cell anaemia. However, all these research has been discontinued. In China, FDP has been approved and marketed as a commercial drug.

Aminomethylbenzoic acid (or p-aminomethylbenzoic acid, or PAMBA) an antifibrinolytic agent. This drug has been used for the treatment of internal hemorrhage during chronic disseminated intravascular coagulation.

Orotic acid is a minor dietary constituent. Historically it was believed to be part of the vitamin B complex and was called vitamin B13, but it is now known that it is not a vitamin and is synthesized in the body, where it arises as an intermediate in the pathway for the synthesis of pyrimidine nucleotides. Orotic acid is converted to UMP by UMP synthase, a multifunctional protein with both orotate phosphoribosyl transferase and orotidylate decarboxylase activity. The most frequently observed inborn error of pyrimidine nucleotide synthesis is a mutation of the multifunctional protein UMP synthase. As a result, plasma orotic acid accumulates to high concentrations, and increased quantities appear in the urine. Orotic acid levels are elevated in the urea cycle defects ornithine transcarbamylase (OTC) deficiency, citrullinemia and argininosuccinic acidemia, as well as the mitochondrial transport disorder hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome. Orotic acid is also elevated in hereditary orotic aciduria, or uridine monophosphate synthase deficiency, an autosomal recessive disorder characterized by megaloblastic anemia and crystalluria. In addition, orotic acid in combination with leflunomide is in the phase II of clinical trial to evaluate the clinical efficacy and safety of a combination in kidney transplant patients with high levels of Polyoma BK viruria for the purpose of preventing polyoma BK viremia and nephropathy, that could lead to kidney transplant loss from viral damage, acute rejection or both.

Fosfructose is a cytoprotective natural sugar phosphate under development by Questcor (formerly Cypros) for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. Fosfructose acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions and improve the cellular energy metabolism in ischemic and hypoperfused tissues. Hypoxia forces ischemic tissue to anaerobic glycolysis for energy, which yields two molecules of ATP per glucose in contrast to 36 molecules of ATP generated during oxidative phosphorylation . Addition of exogenous Fosfructose can produce two more molecules of ATP in an uncompensated anaerobic environment and hence facilitate the recovery of ischemia tissue. Fosfructose breaks down into glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which will further break down into two molecules of pyruvate and finally produce two molecules of ATP. Other mechanisms include inhibition of the generation of oxygen free radicals by neutrophils, stabilization of cell membranes, and maintainance of the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds in ischemic tissues. In myocardial infarction patients, FDP can improve the hemodynamic parameters, attenuate ECG proven ischemic injury and arrhythmia, prevent ATP and creatine phosphate depletion from ischemic myocardium, reduce infarct size, and increase survival rate. Exogenously administered Fosfructose has also been proven beneficial for a variety of other ischemic organs, such as liver, kidney, bowel and even brain as a consequence of its ability to penetrate to the blood brain barrier. Fosfructose trisodium had been in phase I clinical trials for the treatment of heart transplant rejection. Fosfructose trisodium had been in phase II clinical trials for the treatment of heart failure, perioperativ eischaemia and reperfusion injury. Fosfructose trisodium had been in phase III clinical trials for the treatment of sickle cell anaemia. However, all these research has been discontinued. In China, FDP has been approved and marketed as a commercial drug.

Fosfructose is a cytoprotective natural sugar phosphate under development by Questcor (formerly Cypros) for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. Fosfructose acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions and improve the cellular energy metabolism in ischemic and hypoperfused tissues. Hypoxia forces ischemic tissue to anaerobic glycolysis for energy, which yields two molecules of ATP per glucose in contrast to 36 molecules of ATP generated during oxidative phosphorylation . Addition of exogenous Fosfructose can produce two more molecules of ATP in an uncompensated anaerobic environment and hence facilitate the recovery of ischemia tissue. Fosfructose breaks down into glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which will further break down into two molecules of pyruvate and finally produce two molecules of ATP. Other mechanisms include inhibition of the generation of oxygen free radicals by neutrophils, stabilization of cell membranes, and maintainance of the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds in ischemic tissues. In myocardial infarction patients, FDP can improve the hemodynamic parameters, attenuate ECG proven ischemic injury and arrhythmia, prevent ATP and creatine phosphate depletion from ischemic myocardium, reduce infarct size, and increase survival rate. Exogenously administered Fosfructose has also been proven beneficial for a variety of other ischemic organs, such as liver, kidney, bowel and even brain as a consequence of its ability to penetrate to the blood brain barrier. Fosfructose trisodium had been in phase I clinical trials for the treatment of heart transplant rejection. Fosfructose trisodium had been in phase II clinical trials for the treatment of heart failure, perioperativ eischaemia and reperfusion injury. Fosfructose trisodium had been in phase III clinical trials for the treatment of sickle cell anaemia. However, all these research has been discontinued. In China, FDP has been approved and marketed as a commercial drug.

Orotic acid is a minor dietary constituent. Historically it was believed to be part of the vitamin B complex and was called vitamin B13, but it is now known that it is not a vitamin and is synthesized in the body, where it arises as an intermediate in the pathway for the synthesis of pyrimidine nucleotides. Orotic acid is converted to UMP by UMP synthase, a multifunctional protein with both orotate phosphoribosyl transferase and orotidylate decarboxylase activity. The most frequently observed inborn error of pyrimidine nucleotide synthesis is a mutation of the multifunctional protein UMP synthase. As a result, plasma orotic acid accumulates to high concentrations, and increased quantities appear in the urine. Orotic acid levels are elevated in the urea cycle defects ornithine transcarbamylase (OTC) deficiency, citrullinemia and argininosuccinic acidemia, as well as the mitochondrial transport disorder hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome. Orotic acid is also elevated in hereditary orotic aciduria, or uridine monophosphate synthase deficiency, an autosomal recessive disorder characterized by megaloblastic anemia and crystalluria. In addition, orotic acid in combination with leflunomide is in the phase II of clinical trial to evaluate the clinical efficacy and safety of a combination in kidney transplant patients with high levels of Polyoma BK viruria for the purpose of preventing polyoma BK viremia and nephropathy, that could lead to kidney transplant loss from viral damage, acute rejection or both.