Gibberellic acid was first discovered in Japan in 1935 as a result of the study of a condition common in rice plants called "foolish seedling" disease, which caused the plants to grow much taller than normal. The effects of gibberellins weren't widely understood until years later. Gibberellic acid, GA3 is a naturally occurring plant hormone that regulates the growth of plants, including triggering seed germination. Gibberellic Acid is not manufactured; it's a natural product extracted from the Gibberella fujikuroi fungus. There are over 100 known forms of gibberellic acid; GA3 is the most effective. Gibberellic acid (GA3) is used extensively in Egypt and other countries, to increase the growth of many fruits (such as strawberries and grapes) and vegetables (such as tomatoes, cabbages and cauliflower). Carcinogenic effect of Gibberellic acid has being demonstrated in several studies. Gibberellic acid increased the activity of testicular 3β-HSD and 17β-HSD and elevated testosterone content in rats, acting as an agonist of steroidogenesis in male rats. Gibberellic acid has being suggested to promote ulcer-healing, healing of surgical wounds or open fractures and treatment of bronchitis or thrombophlebitis in animals including humans.

Quinic acid is an acid obtained from cinchona bark, coffee beans, tobacco leaves, carrot leaves, apples, etc. For over 50 years, hippuric/quinic acids were believed to have no biological efficacy, but in 2009th these components were identified as major dietary components, and not simply originating from environmental pollution as previously had been thought. Quinic acid has been shown to possess radioprotection, anti-neuroinflammatory, and anti-oxidant activities. It also inhibits the TNF-α-stimulated induction of vascular cell adhesion molecule-1 (VCAM-1) by inhibiting the MAP kinase and NF-κB signaling pathways, which may explain the ability of QA to inhibit vascular inflammation such as atherosclerosis.

Tauroursodeoxycholic acid (TUDCA) is an endogenous hydrophilic bile acid used clinically to treat certain liver diseases. It is approved in Italy and Turkey for the treatment of cholesterol gallstones and is an investigational drug in China, Unites States, and Italy. Tauroursodeoxycholic acid is being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. Tauroursodeoxycholate (TUDC) promote choleresis by triggering the insertion of transport proteins for bile acids into the canalicular and basolateral membranes of hepatocytes. In addition, Tauroursodeoxycholate exerts hepatoprotective and anti-apoptotic effects, can counteract the action of toxic bile acids and reduce endoplasmic reticulum stress. Tauroursodeoxycholate can also initiate the differentiation of multipotent mesenchymal stem cells (MSC) including hepatic stellate cells and promote their development into hepatocyte-like cells. Although the hepatoprotective and choleretic action of TUDC is empirically used in clinical medicine since decades, the underlying molecular mechanisms remained largely unclear.

Lesinurad (brand name Zurampic) is a urate transporter inhibitor for treating hyperuricemia associated with gout in patients who have not achieved target serum uric acid levels with a xanthine oxidase inhibitor alone. In gout patients, Lesinurad lowered serum uric acid levels and increased renal clearance and fractional excretion of uric acid. Following single and multiple oral doses of Lesinurad to gout patients, dose-dependent decreases in serum uric acid levels and increases in urinary uric acid excretion were observed. Lesinurad reduces serum uric acid levels by inhibiting the function of transporter proteins involved in uric acid reabsorption in the kidney. Lesinurad inhibited the function of two apical transporters responsible for uric acid reabsorption, uric acid transporter 1 (URAT1) and organic anion transporter 4 (OAT4), with IC50 values of 7.3 and 3.7 µM, respectively. URAT1 is responsible for the majority of the reabsorption of filtered uric acid from the renal tubular lumen. OAT4 is a uric acid transporter associated with diuretic-induced hyperuricemia. Lesinurad does not interact with the uric acid reabsorption transporter SLC2A9 (Glut9), located on the basolateral membrane of the proximal tubule cell. Based on in vitro studies, lesinurad is an inhibitor of OATP1B1, OCT1, OAT1, and OAT3; however, lesinurad is not an in vivo inhibitor of these transporters. In vivo drug interaction studies indicate that lesinurad does not decrease the renal clearance of furosemide (substrate of OAT1/3), or affect the exposure of atorvastatin (substrate of OATP1B1) or metformin (substrate of OCT1). Based on in vitro studies, lesinurad has no relevant effect on P-glycoprotein.

Cystine is the oxidized dimer form of the amino acid cysteine. Cystine serves two biological functions, a site of redox reactions and a mechanical linkage that allows proteins to retain their 3-dimensional structure. It is common in many foods such as eggs, meat, dairy products, and whole grains as well as skin, horns and hair. Human hair and skin contain approximately 10–14% cystine by mass. Cysteine supplements are sometimes marketed as anti-aging products with claims of improved skin elasticity. Cysteine is more easily absorbed by the body than cystine, so most supplements contain cysteine rather than cystine. N-acetyl-cysteine (NAC) is better absorbed than other cysteine or cystine supplements.