There has been little to no interest in the biological and/or pharmacological application of lauryl phosphate.

Benfotiamine is a derivative of vitamin B1. It was developed in Japan specifically to treat Korsakoff's syndrome and patented in the United States in 1962, but never became popular. It has been in use as a widely used prescription drug in Europe since 1978 to treat diabetes and is available at many vitamin shops in the United States. It has been licensed for use in Germany since 1993 under the trade name Milgamma. (Combinations with pyridoxine or cyanocobalamin are also sold under this name). It is prescribed there for treating sciatica and other painful nerve conditions. It is marketed as a medicine and/or dietary supplement, depending on the respective Regulatory Authority. Unfortunately apparent evidences from human studies are scarce and especially endpoint studies are missing. Benfotiamine has proven to affect glucose metabolic process through various mode of actions, and plays a part in obstructing age-associated glycation end products (AGEs). Benfotiamine reduces the extra biosynthesis and accumulation of a number of glucose metabolites, including glyceraldeyde-3-phosphate and dihydroxyacetone phosphate. Elevated levels of those glucose intermediates function as a trigger to most of the mechanisms accountable for hyperglycemia-caused cell damage. Benfotiamine increases tissue amounts of thiamine diphosphate, consequently growing transketolase activity and producing a significant decrease in glucose metabolites and precursors to AGEs. Up to now, two of the most effective AGE inhibitors in living microorganisms would be the Vitamin B1 derivative, benfotiamine and also the Vitamin B6 derivative, pyridoxamine. Additionally, benfotiamine has long been proven to lessen NF-kB activity, therefore restricting the over-production from the harmful superoxide toxin. Excess superoxide production may partly hinder a vital enzyme in glucose metabolic process, glyceraldehyde-3-phosphate dehydrogenase, directing glucose metabolites from glycolysis in to the major glucose-driven signaling paths that cause hyperglycemic damage. Theoretically, overdose with benfotiamine should cause menopausal flashes, bluish skin (because of rapid utilization of oxygen), tingling, and difficulty breathing, but used, this merely has not happened.

Glycerophosphoinositol choline is a salt of glycerophosphoinositol and choline. It is used in cream or emollient formulation in the treatment of irritative and allergic dermatitis and xerosis of the skin. Glycerophosphoinositol is a natural metabolite, produced in the organism through deacylation by phospholipase B of the essential phospholipid phosphatidylinositol. Glycerophosphoinositols are involved in control of signalling enzymes (e.g. adenylyl cyclase), in actin cytoskeleton organization, in invasion of the extracellular matrix by melanoma and breast carcinoma cell lines, and in the control of cell proliferation in epithelial cells.

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.

Glucose-6-phosphate belongs to the class of organic compounds known as monosaccharide phosphates. It lies at the start of two major metabolic pathways: glycolysis and the pentose phosphate pathway. It is a glucose-6-phosphatase substrate. Hexokinase is inhibited by its product, glucose 6-phosphate. The non-enzymatic glycation of myosin by glucose 6-phosphate is probably the primary cause for the observed loss of the ATPase activity of myosin.