Pyridoxal is a pyridinecarbaldehyde and a form of vitamin B 6 which is converted to pyridoxal phosphate. Pyridoxal 5'-phosphate is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemoglobin, sphingomyelin, and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA). Pyridoxal is one of the natural forms available of vitamin B6, therefore, it is used for nutritional supplementation and for treating dietary shortage or imbalances. Some medically relevant bacteria, such as those in the genera Granulicatella and Abiotrophia, require pyridoxal for growth. This nutritional requirement can lead to the culture phenomenon of satellite growth. In in vitro culture, these pyridoxal-dependent bacteria may only grow in areas surrounding colonies of bacteria from other genera ("satellitism") that are capable of producing pyridoxal.

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.

Bilirubin is an orange-yellow pigment made during the normal breakdown of red blood cells. Bilirubin passes through the liver and is excreted out of the body. Occasionally, higher bilirubin levels may indicate an increased rate of destruction of red blood cells (hemolysis). A high level of bilirubin in the blood is called hyperbilirubinemia. High bilirubin levels can cause jaundice. Jaundice makes the skin and the whites of the eyes appear yellow, due to the brown and yellow bilirubin in the blood. Phototherapy for neonatal is one of the treatment methods against hyperbilirubinemia. Light absorption by bilirubin in the skin transforms the native Z,Z-bilirubin to conformational photoisomers Z,E-bilirubin and E,Z-bilirubin and structural photoisomers E,Z-lumirubin and E,E-lumirubin. Formation and excretion of Z,E-bilirubin and E,Z-lumirubin are both important routes of elimination of bilirubin through bile and urine, although the precise contributions of the various photoisomers to the overall elimination of bilirubin are still unknown.

Cinnamic acid is a polyphenol found in cinnamon oil and used in commercial flavorings. Recent studies have shown the pharmacological properties of cinnamic acid and its derivatives, including hepatoprotective, anti-oxidant, and anti-diabetic activities. In preclinical studies cinnamic acid demonstrated to be a promising candidate for the treatment ob obesity and diabetes. The mechanism of action of cinnamic acid in obesity is explained by its ability to inhibit lipases and ACE (angiotensin-converting enzyme). However, there are several hypotesis regarding the effect of cinnamic acid in diabetes: cinnamic acid enhances glucose-induced insulin secretion, prevents palmitic acid-induced lipotoxicity, inhibits palmitic acid-induced alteration of lipogenic gene and protein expression (AMPK, SREBP-1c, FAS, ACC), inhibits DPP IV, exhibits an additive effect on the uptake of glucose, stimulates adiponectin secretion, etc.

Uric acid, generated from the metabolism of purines, has proven and emerging roles in human disease. Humans produce large quantities of uric acid. Excess serum accumulation of uric acid can lead to a type of arthritis known as gout. Hyperuricemia may increase risk factors for cardiovascular disease. High serum uric acid was associated with higher risk of type 2 diabetes and other diseases.

Sulfaquinoxaline is a veterinary drug, which can be given to animals to treat coccidiosis and Acute Fowl cholera. It has often used in combinations with others drugs. It had its origins in the chemical synthetic program that sprang from the introduction of sulfonamide drugs into human medicine in the 1930s. The program was sustained through the years of World War II despite declining clinical use of that chemical class. Several sulfa drugs were known to be active against the sporozoan parasite (Plasmodium spp.) that causes malaria, but were not satisfactory in clinical practice. A sulfonamide that had a long plasma half-life would ipso facto be considered promising as an antimalarial drug. Sulfaquinoxaline, synthesized during the war, was such a compound. It proved too toxic to be used in human malaria, but was found to be a superior agent against another sporozoan parasite, Eimeria spp., the causative agent of coccidiosis in domestic chickens. In 1948 sulfaquinoxaline was introduced commercially as a poultry coccidiostat. The action mechanism of sulfaquinoxaline is to inhibit the dihydrofolate synthetase to encumber the nucleate synthesis of bacterium and coccidian its active peak to coccidian is at the second schizont stage (the fourth day of coccidial life cycle), so it will not affect the anti-coccidial immunity in chicken.

Glyoxal refers to the reactive electrophilic species (RES) and is formed during different processes, e.g., lipid peroxidation, DNA oxidation. RES cause the damage of proteins and nucleotides and thus can cause different diseases in human, e.g., diabetes. Glyoxal reacting with free guanines in RNAs can be is used for chemical probing of RNA structure.