Pyridoxamine (PM) is one of three natural forms of vitamin B6. It is a critical transient intermediate in catalysis of transamination reactions by vitamin B6-dependent enzymes. In preclinical or clinical trials PM has demonstrated pharmacological potential for treatment of diabetic nephropathy, diabetic retinopathy, and hyperlipidemia, and for use in kidney stone preventive therapies. Although its precise mode of action in vivo is not yet clear, it is likely that at least three mechanisms are at play: inhibition of post-Amadori steps of the Maillard reaction; scavenging of reactive carbonyl compounds; and inhibition of toxic effects of ROS. Pyridoxamine was marketed as a dietary supplement, often as the hydrochloride salt, pyridoxamine dihydrochloride. However, in the United States, the FDA ruled in January 2009 that pyridoxamine must be regulated as a pharmaceutical drug because it is the active ingredient in Pyridorin, a drug designed to prevent the progression of diabetic nephropathy.

Sodium glycerol 2-phosphate (Disodium beta-glycerophosphate) is used for the preparation of thermo-sensitive chitosan hydrogen as a scaffold to construct tissue engineered injectable nucleus pulposus (NP). Since Sodium glycerol 2-phosphate (6 g/day) reduced the lithogenic index of bile in human subjects with cholesterol gallstones in a short-term study and facilitated dissolution of cholesterol gallstones in mice, Sodium glycerol 2-phosphate may have potential to help dissolve cholesterol gallstones in man. Sodium glycerol 2-phosphate is an alkaline phosphate inhibitor. Sodium β-glycerophosphate pentahydrate is used as a phosphatase inhibitor. It promotes bone matrix mineralization while delivering to osteoblasts by providing a source of phosphate ions. It is used in the development of hydrogels and scaffolds, which finds applications in tissue engineering and cell growth. It is used as an additive in isolation mediums by providing phosphate ions to isolate. It is utilized to promote mineralization in vitro by modulating bone cell metabolic activity.

Pyridoxamine (PM) is one of three natural forms of vitamin B6. It is a critical transient intermediate in catalysis of transamination reactions by vitamin B6-dependent enzymes. In preclinical or clinical trials PM has demonstrated pharmacological potential for treatment of diabetic nephropathy, diabetic retinopathy, and hyperlipidemia, and for use in kidney stone preventive therapies. Although its precise mode of action in vivo is not yet clear, it is likely that at least three mechanisms are at play: inhibition of post-Amadori steps of the Maillard reaction; scavenging of reactive carbonyl compounds; and inhibition of toxic effects of ROS. Pyridoxamine was marketed as a dietary supplement, often as the hydrochloride salt, pyridoxamine dihydrochloride. However, in the United States, the FDA ruled in January 2009 that pyridoxamine must be regulated as a pharmaceutical drug because it is the active ingredient in Pyridorin, a drug designed to prevent the progression of diabetic nephropathy.

Alpha-ketoglutarate (AKG), an endogenous intermediary metabolite in the Krebs cycle, is a molecule involved in multiple metabolic and cellular pathways. As an intermediate of the tricarboxylic acid cycle, AKG is essential for the oxidation of fatty acids, amino acids, and glucose. Extracellular AKG is a significant source of energy for cells of the gastrointestinal tract. As a precursor for the synthesis of glutamate and glutamine in multiple tissues (including liver, skeletal muscle, heart, brain, and white adipose tissue), AKG bridges carbohydrate and nitrogen metabolism for both conservation of amino acids and ammonia detoxification. Additionally, emerging evidence shows that AKG is a regulator of gene expression and cell signaling pathways (including the mammalian target of rapamycin and AMPactivated protein kinase). Thus, AKG is an attractive dietary supplement in animal and human nutrition to improve cellular energy status, immunity, and health.AKG can decrease protein catabolism and increase protein synthesis to enhance bone tissue formation in the skeletal muscles and can be used in clinical applications. In addition to these health benefits, a recent study has shown that AKG can extend the lifespan of adult Caenorhabditis elegans by inhibiting ATP synthase and TOR. Orally, AKG is used for kidney disease, gastrointestinal disorders, bacterial overgrowth, intestinal toxemia, liver dysfunction, and chronic candidiasis. It is also used for improving peak athletic performance, improving amino acid metabolism in hemodialysis patients, and cataracts. Intravenously, AKG is used for preventing ischemic injury during heart surgery, improving renal blood flow after heart surgery, and preventing muscle protein depletion after surgery or trauma.

Debrisoquin is an antihypertensive drug having guanethidine-like properties, which inhibits monoamine oxidase (MAO) and does not enter the brain. Debrisoquine was used for the treatment of hypertension. Debrisoquine hydroxylation phenotype has been the most used test in humans to evaluate CYP2D6 activity. Two debrisoquine hydroxylation phenotypes have been described: poor and extensive metabolizers. A group with a very low debrisoquine metabolic ratio within the extensive metabolizers, named ultrarapid metabolizers, has also been distinguished. This CYP2D6 variability can be for a large part alternatively determined by genotyping, which appears to be of clinical importance given CYP2D6 involvement in the metabolism of a large number of commonly prescribed drugs.

Doxepin is a dibenzoxepin tricyclic antidepressant marketed worldwide. It is a white crystalline solid readily soluble in water, lower alcohols and chloroform. The mechanism of action of doxepin is not definitely known. It is not a central nervous system stimulant nor a monoamine oxidase inhibitor. The current hypothesis is that the clinical effects are due, at least in part, to influences on the adrenergic activity at the synapses so that deactivation of norepinephrine by reuptake into the nerve terminals is prevented. Antidepressants may increase risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (18–24 years of age) with major depressive disorder and other psychiatric disorders. Drowsiness is the most commonly noticed side effect. This tends to disappear as therapy is continued. Other infrequently reported CNS side effects are confusion, disorientation, hallucinations, numbness, paresthesias, ataxia, extrapyramidal symptoms, seizures, tardive dyskinesia, and tremor. : Cardiovascular effects including hypotension, hypertension, and tachycardia have been reported occasionally. Skin rash, edema, photosensitization, and pruritus have occasionally occurred. Eosinophilia has been reported in a few patients. There have been occasional reports of bone marrow depression manifesting as agranulocytosis, leukopenia, thrombocytopenia, and purpura. Doxepin is used to treat depression, anxiety disorders, itchiness, trouble sleeping, and as a second-line treatment of chronic idiopathic urticaria (hives). Its oral formulations are FDA-approved for the treatment of depression, anxiety, and insomnia and its topical formulations are FDA-approved the short-term management (up to 8 days) of atopic dermatitis and lichen simplex chronicus. Whereas in Australia and the UK, the only licensed indication(s) is/are in the treatment of major depression and pruritus in eczema, respectively.

Synthetic glycerophosphates have been known for many years and have been prepared in several ways. The acid may exist in two isomeric forms, alpha and beta. The L-a-acid is the naturally occurring form; the b-acid, present in hydrolyzates of lecithins from natural sources, arises from migration of the phosphoryl group from the a-carbon atom. Dehydrogenation of L-glycerol 3-phosphate produces Dihydroxyacetone phosphate and is part of the entry of glycerol (sourced from triglycerides) into the glycolytic pathway.

Glucose is a sugar with the molecular formula C6H12O6. The D-isomer (D-glucose), also known as dextrose, occurs widely in nature, but the L-isomer (L-glucose) does not. Glucose is made during photosynthesis from water and carbon dioxide, using energy from sunlight. The reverse of the photosynthesis reaction, which releases this energy, is a very important source of power for cellular respiration. Glucose is stored as a polymer, in plants as starch and in animals as glycogen, for times when the organism will need it. Glucose circulates in the blood of animals as blood sugar. Glucose can be obtained by hydrolysis of carbohydrates such as milk, cane sugar, maltose, cellulose, glycogen etc. It is however, manufactured by hydrolysis of cornstarch by steaming and diluting acid. Glucose is the human body's key source of energy, through aerobic respiration, providing about 3.75 kilocalories (16 kilojoules) of food energy per gram. Breakdown of carbohydrates (e.g. starch) yields mono- and disaccharides, most of which is glucose. Use of glucose as an energy source in cells is by either aerobic respiration, anaerobic respiration, or fermentation. All of these processes follow from an earlier metabolic pathway known as glycolysis. The insulin reaction, and other mechanisms, regulate the concentration of glucose in the blood. Glucose supplies almost all the energy for the brain, so its availability influences psychological processes. When glucose is low, psychological processes requiring mental effort (e.g., self-control, effortful decision-making) are impaired. Ingested glucose is absorbed directly into the blood from the intestine and results in a rapid increase in the blood glucose level. Glucose is used to manage hypoglycemia and for intravenous feeding. Nausea may occur after ingesting glucose, but this also may be an effect of the hypoglycemia which is present just prior to ingestion. Other adverse effects include increased blood glucose, injection site leakage of fluid (extravasation), injection site inflammation, and bleeding in the brain.

Lactose is the most important carbohydrate in the milk of most species. Its biosynthesis takes place in the mammary gland. The molecular structures of α- and β -lactose differ in the orientation of a hydrogen- and a hydroxyl group on carbon atom no.1 in the glucose moiety. Both forms change into one another continuously. At room temperature, the equilibrium results in a ratio of about 40% α-lactose and 60% β-lactose. The fact that two forms of lactose exist which differ in molecular structure has profound effects on various properties of lactose such as crystallization behavior, crystal morphology, solid-state properties, and solubility. The intestine does not actively absorb lactose unless it is split into its two-monosaccharide components, i.e. glucose and galactose. This hydrolysis of lactose is affected by the enzyme lactase, which is produced by the epithelium cells in the brush-border of the small intestine. Thus, the capacity of mammals to digest lactose is dependent on the lactase activity in the intestine. The maximum activity of the enzyme occurs shortly after birth and declines during the weaning period, after which it remains at a relatively constant level. Genetically determined factors governing residual lactase activity also exist. Individuals having low lactase activity are called lactose malabsorbers. Lactose intolerance is a condition in which people have symptoms due to the decreased ability to digest lactose. The principal symptom of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear one-half to two hours after consumption.

Aconitic Acid found in leaves and tubers of Aconitum napellus L., Ranunculaceae, in various species of Achillea (Compositae) and Equisetum (Equisetaceae), in beet root, and in sugar cane. It is indicated for the temporary relief of symptoms of chronic illness including fatigue, effects of toxin buildup, slowed metabolism, weakened constitution. The limited data on trans-aconitic acid indicate it to be less toxic than citric acid. Trans-aconitate salts appear to be excreted readily by the kidneys. There is no direct evidence that trans-aconitic acid is utilized as is the cis-aconitic acid isomer in mammalian metabolism although non-specific oxidation probably occurs.