Ephedrine (l-form) is an alkaloid, which was initially purified from Ephedra plant. The extract form Ephedra has been used in China for medicinal purposes for several thousand years. Ephedrine acts as an agonist at alpha- and beta-adrenergic receptors and indirectly causes the release of norepinephrine from sympathetic neurons. The drug crosses the blood brain barrier and stimulates the central nervous system. Ephedrine products are now banned in many countries, as they are a major source for the production of the addictive compound methamphetamine. FDA has approved ephedrine only for the treatment of clinically important hypotension occurring in the setting of anesthesia.

Menthol, (+)- is a fragrance ingredient used in decorative cosmetics, fine fragrances, shampoos, toilet soaps and other toiletries as well as in non-cosmetic products such as household cleaners and detergents. Recent investigations have provided evidence for menthol to increase cough thresholds. Racementhol is used as a topical analgesic.

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.

Epinephrine is a sympathomimetic catecholamine. It acts as a naturally occurring agonist at both alpha and beta-adrenergic receptors. Three pharmacologic types have been identified: alpha 1-, alpha 2-, and beta-adrenergic receptors. Each of these has three subtypes, characterized by both structural and functional differences. The alpha 2 and beta receptors are coupled negatively and positively, respectively, to adenylyl cyclase via Gi or Gs regulatory proteins, and the alpha 1 receptors modulate phospholipase C via the Go protein. Subtype expression is regulated at the level of the gene, the mRNA, and the protein through various transcriptional and postsynthetic mechanisms. Through its action on alpha-adrenergic receptors, epinephrine lessens the vasodilation and increased vascular permeability that occurs during anaphylaxis, which can lead to loss of intravascular fluid volume and hypotension. Through its action on beta-adrenergic receptors, epinephrine causes bronchial smooth muscle relaxation and helps alleviate bronchospasm, wheezing and dyspnea that may occur during anaphylaxis. Epinephrine also alleviates pruritus, urticaria, and angioedema and may relieve gastrointestinal and genitourinary symptoms associated with anaphylaxis because of its relaxer effects on the smooth muscle of the stomach, intestine, uterus and urinary bladder. Epinephrine increases glycogenolysis, reduces glucose up take by tissues, and inhibits insulin release in the pancreas, resulting in hyperglycemia and increased blood lactic acid.

Roxifiban (also known as DMP754), a potent antiplatelet agent in inhibiting platelet aggregation, and has a high specificity and affinity for human platelet glycoprotein IIb/IIIa complex (GPIIb/IIIa) receptors. Roxifiban participated in clinical trials phase III for the treatment of peripheral arterial disorders. This drug was also well tolerated in patients with chronic stable angina pectoris and was studied in the treatment of heparin-induced thrombocytopenia, and thrombosis. However, the development of this drug appears to have been discontinued.

Ezatiostat (TLK199) [γ-glutamyl-S-(benzyl)cysteinyl-R-phenyl glycine diethyl ester] is an inhibitor of Glutathione S-transferase P1–1 (GSTπ). The drug is a peptidomimetic of GSH (glutathione), esterified to enhance cellular uptake and designed to bind to the “G-site” of GSTP1–1. Independent of catalysis inhibition, TLK199 also disrupts the protein:protein interaction site(s) between GSTP1–1 and JNK1. Telik Inc was developing TLK-199 for the potential prevention of myelosuppression in blood diseases, namely myelodysplastic syndrome.