Proline (L-Proline) is one of the twenty amino acids used in living organisms as the building blocks of proteins. Proline is a non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. Proline is used in pharmaceuticals as an excipient and as an active substance in nutritional supplements. Proline is not commonly used in pharmaceuticals as an excipient. It is approved for use in Privigen (IVIg) and Hizentra (SCIg) solution for injection as a stabiliser for IgG. Proline is also contained in low amounts in several vaccines, e.g. Havrix 720 Kinder (Hepatitis A).

Laquinimod is a new orally available carboxamide derivative, which is currently developed for relapsing remitting (RR) and chronic progressive (CP) forms of multiple sclerosis (MS; RRMS or CPMS) as well as neurodegenerative diseases. The mechanism of action of laquinimod is not fully elucidated because the molecular target is not known. Treatment with laquinimod led to a significant and persistent increase in brain-derived neuroprotective factor (BDNF) serum levels compared to placebo treatment. In human studies, a decrease of pro-inflammatory and an increase of anti-inflammatory cytokines have been measured. After commercial launch the unexpected severe cardiac adverse events (AEs) such as serositis, pericarditis, and myocardial infarction were detected.

Brivudine (trade names Zostex, Mevir, Brivir, among others) is an antiviral drug used in the treatment of herpes zoster ("shingles"). Brivudine is an analog of the nucleoside thymidine. The active compound is brivudine 5'-triphosphate, which is formed in subsequent phosphorylations by viral (but not human) thymidine kinase and presumably by the nucleoside-diphosphate kinase. Brivudine 5'-triphosphate works because it is incorporated into the viral DNA, but then blocks the action of DNA polymerases, thus inhibiting viral replication. Brivudine is used for the treatment of herpes zoster in adult patients. It is taken orally once daily, in contrast to aciclovir, valaciclovir, and other antivirals. A study has found that it is more effective than aciclovir, but this has been disputed because of a possible conflict of interest on part of the study authors. The drug is contraindicated in patients undergoing immunosuppression (for example because of an organ transplant) or cancer therapy, especially with fluorouracil (5-FU) and chemically related (pro)drugs such as capecitabine and tegafur, as well as the antimycotic drug flucytosine, which is also related to 5-FU. It has not been proven to be safe for children and pregnant or breastfeeding women. The drug is generally well tolerated. The only common side effect is nausea (in 2% of patients). Less common side effects (<1%) include a headache, increased or lowered blood cell counts (granulocytopenia, anemia, lymphocytosis, monocytosis), increased liver enzymes, and allergic reactions. Brivudine is approved for use in a number of European countries including Austria, Belgium, Germany, Greece, Italy, Portugal, Spain, and Switzerland.

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.

Morinidazole is a novel third generation 5-nitroimidazole-class antimicrobial agent indicated for the treatment of anaerobic bacterial infections including appendicitis and pelvic inflammatory disease. Morinidazole is administered as a racemate. Morinidazole was approved by China Food and Drug Administration (CFDA) on February, 2014. The bactericidal activity of morinidazole, depends on the formation of a redox intermediate metabolite in the bacterium that causes DNA strand breakage, inhibits repair, and, ultimately leads to cell death. The main adverse effects (all are mild) relate to the drug are dizziness, drowsiness and nausea. Recent in vitro assays have demonstrated that higher antiparasitic potency is observed in S- morinidazole than in R-morinidazole.

Ethyl cysteinate is derivative of semi-essential proteinogenic amino acid Cysteine. Ethyl cysteinate is widely used in food additive, cosmetic, pharmaceutical area. Ethyl cysteinate is membrane-permeable, readily enters peripheral tissues and the brain, and increases intracellular pools of cysteine in these tissues via a membrane-associated carboxylesterase. The increased availability of cysteine directly alters the redox status of cells and enhances glutathione production. The enhanced biovailability of L-cysteine and L-glutathione would also promote the direct formation of the S-nitrosothiols, L-S-nitrosocysteine and L-S-nitrosoglutathione and the overall S-nitrosylation status of functional proteins in cells.

(S)-Sulindac is the (S)-enantiomer of nonsteroidal anti-inflammatory drug (NSAID) Sulindac, that is marketed in the U.S. by Merck as Clinoril. Sulindac is a prodrug, derived from sulfinyl-indene, that is converted in vivo to an active sulfide compound by liver methionine sulfoxide reductases (Msr). The (Msr) family of enzymes includes two major classes, MsrA and MsrB, that specifically reduce the S- and R-epimers of Sulindac. Reduction of (S)-Sulindac to Sulindac Sulfide catalyzed by methionine sulfoxide reductase (Msr)-A. The oxidation of both epimers to sulindac sulfone is catalyzed primarily by the microsomal cytochrome P450 (P450) system. (S)-Sulindac increases the activity of the P450 system better than (R)-sulindac, but both epimers increase primarily the enzymes that oxidize (R)-sulindac. Both epimers can protect normal lung cells against oxidative damage and enhance the killing of lung cancer cells exposed to oxidative stress.

Icotinib is an orally available quinazoline-based inhibitor of epidermal growth factor receptor. It selectively inhibits the wild-type and several mutated forms of EGFR tyrosine kinase. The major organ of icotinib metabolism is the liver, with the primarily enzymes being CYP2C19 and CYP3A4 from the cytochrome P450 monooxygenase system. Icotinib Hydrochloride was approved for the treatment of patients with advanced stage Nonsmall cell lung cancer by the State Food and Drug Administration (SFDA) of China. The major drug related adverse reactions of the traditional cytotoxic agents include rash, diarrhea, severe bone marrow suppression, neuropathy, hair loss, and gastrointestinal reactions. Icotinib is under investigation as an active agent against other EGFR mutation-positive cancers, like lung adenocarcinoma, oesophageal cancer, nasopharyngeal cancer and others.

D-Methionine is a stereoisomer of an essential proteinogenic sulfur-containing amino-acid L-methionine. D-methionine is an antioxidant, it demonstrated protective effects on cisplatin-induced anorexia and renal injury, and protected normal cells from radiation-induced cell death and from radiation-induced mucosal injury. In animal models, it protected against hearing loss induced by cisplatin, carboplatin, aminoglycosides, or noise exposure. A phase 3 clinical trial of D-methionine for prevention of hearing loss was conducted by the US Army, the study was terminated and no results were reported.