Tartaric acid is found in many plants such as grapes, tamarinds, pineapples, mulberries and so on. Wine lees (called mud in the US), the sediment collected during the fermentation of grapes, contains potassium bitartrate (potassium hydrogen tartrate) as its major component. L-(+)-tartaric acid is an enantiomer of tartaric acid. Twenty five years before the tetrahedral structure for carbon was proposed in 1874 to explain the optical activity and other properties of organic compounds, Louis Pasteur discovered the existence of enantiomerism in tartaric acid. L-(+)-tartaric acid is widely used in food and beverage as acidity regulator with E number E334.

Benzocaine is a local anesthetic. It acts by blocking voltage-gated sodium ion channels in nerve endings. Benzocaine is available over-the counter for local anesthesia of oral and pharyngeal mucous membranes (sore throat, cold sores, mouth ulcers, toothache, sore gums, denture irritation), otic pain, and as a local anesthetic for surgical or diagnostic procedures. As a spray, benzocaine is used for temporary relief of pain and itching associated with minor burns, sunburn, minor cuts or scrapes, insect bites, or minor skin irritations. Topical application of benzocaine to gums or mouth may cause rare, but serious and potentially fatal adverse effect methemoglobinemia.

Methyl salicylate (or methyl 2-hydroxybenzoate), also known as wintergreen oil, is a natural product and is present in white wine, tea, porcini mushroom Boletus edulis, Bourbon vanilla, clary sage, red sage and fruits including cherry, apple, raspberry, papaya and plum. Methyl salicylate is topically used in combination with methanol and under brand name SALONPAS to temporarily relieves mild to moderate aches and pains of muscles and joints associated with: strains, sprains, simple backache, arthritis, bruises. The precise mechanism of action of methyl salicylate is not known, but there is suggested, that it cause dilation of the capillaries thereby increasing blood flow to the area.

Dalvastatin is a synthetic HMG-CoA reductase inhibitor developed by Rhône-Poulenc Rorer. Dalvastatin is a prodrug and is itself an inactive lactone. After oral ingestion, the drug is hydrolyzed in vivo to the corresponding beta-hydroxy acid, which is the pharmacologically active form. HMG-CoA reductase is the rate-limiting enzyme in the cholesterol biosynthetic pathway. An active form of dalvastatin inhibits HMG-CoA reductase with IC50 of 3.4 nM. In ex vivo assay, orally administered dalvastatin inhibited cholesterol biosynthesis in rat liver slices with an ED50 value of 0.9. The efficacy of dalvastatin to lower cholesterol was investigated in the clinical trials in the 1990s, but no results were reported.

Rivenprost (ONO-4819) is a potent and selective EP4 receptor agonist. This compound can increase bone formation by stimulating osteoblast differentiation and function, possibly by modulating mesenchymal cell differentiation. Rivenprost has also been studied for its potential to prevent bone loss (in osteoporosis) and stabilize bone implants. Combined with risedronate, rivenprost may be an effective treatment for osteoporosis. A phase II study evaluating rivenprost in ulcerative colitis was terminated in 2009.

Arhalofenate is a uricosuric drug which lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney. Arhalofenate activity is mediated by inhibition of URAT1, OAT4 and OAT10. Additionally, arhalofenate has been suggested to exert potent anti-inflammatory activity. Arhalofenate has completed Phase 2 and is ready to advance to Phase 3 as a novel potential treatment for gout. The drug was also tested in patients with type 2 diabetes mellitus (phase III study), where it demonstrated its ability to lower glucose level, acting as a selective, partial PPAR-gamma agonist. However, the development of arhalofenate as an anti-diabetic drug was terminated.

QGC-001 (also known as RB-150) is an aminobutane-1-sulfonic acid derivative patented by Institut National de la Sante et de la Recherche Medicale as antihypertensive agent. QGC-001 acts as aminopeptidase A inhibitor and suppress conversion of angiotensin II to angiotensin III in brain tissues Oral administration of RB150 in conscious deoxycorticosterone acetate (DOCA)–salt rats inhibited brain aminopeptidase A activity, resulting in values similar to those obtained with the brains of normotensive rats, demonstrating the central bioavailability of RB150. Oral RB150 treatment resulted in a marked dose-dependent reduction in blood pressure in DOCA-salt but not in normotensive rats. In clinical trials single oral administration of QGC001 up to 1,250 mg in healthy volunteers was well-tolerated. Following oral administration, QGC001 is absorbed via the gastrointestinal tract and converted partially into its active metabolite EC33 in plasma. As in animal experiments, in normotensive subjects QGC001 had no effect on the systemic renin-angiotensin-aldosterone parameters and on PCop concentrations, a marker of vasopressin release.