Mecarbinate is a chemical intermediate of arbidol hydrochloride. Dimecarbin is used in the treatment of hypertension in Russia.

Fenclozic acid emerged in the late 1960s as a promising carboxylic acid non-steroidal anti-inflammatory drug candidate that demonstrated potent anti-inflammatory, anti-pyretic and analgesic properties. Whole body autoradiography showed fenclozic acid distribution into all tissues except the brain, with radioactivity still detectable in blood, kidney and liver at 72 h post-dose. Fenclozic acid was compared with aspirin in a double-blind, crossover trial in patients with rheumatoid arthritis. It was concluded that fenclozic acid afforded symptomatic relief and was comparable to aspirin. Unfortunately, hepatotoxicity was observed in subsequent trials and the drug was withdrawn from the clinic.

Nordazepam (INN; marketed under brand names Nordaz, Stilny, Madar, Vegesan, and Calmday) is a 1,4-benzodiazepine derivative with amnesic, anticonvulsant, anxiolytic, muscle relaxant, and sedative properties. Nordazepam is an active metabolite of diazepam, chlordiazepoxide, clorazepate, prazepam, pinazepam, and medazepam, used primarily in the treatment of anxiety disorders. Nordazepam is a partial agonist at the GABAA receptor, which makes it less potent than other benzodiazepines, particularly in its amnesic and muscle-relaxing effects. Nordazepam’s elimination half-life is between 36 and 200 hours, with wide variation among individuals; factors such as age and gender are known to impact it. The variation of reported half-life are attributed to differences in nordazepam metabolism and that of its metabolites as nordazepam is hydroxylated to active metabolites such as oxazepam, before finally being glucuronidated and excreted in the urine. Common side effects of nordazepam include somnolence, which is more common in elderly patients and/or people on high-dose regimens. Hypotonia, which is much less common, is also associated with high doses and/or old age.

Cefalonium is a 1st generation cephalosporin with a broad spectrum of actvity against Gram-positive and Gram-negative bacterias. The drug inhibits the bacterial cell wall synthesis by binding to penicillin binding proteins. Cefalonium is approved for routine dry cow therapy to treat existing sub-clinical infections and to prevent new infections which occur during the dry period.

Canrenone, a spironolactone metabolite, is a mineralocorticoid receptor antagonist. Canrenone is used as a diuretic in Europe and, in particular, in Italy under brand name Luvion. Luvion is a tablet for oral application which is effective for the treatment Hyperaldosteronism primary, secondary hyperaldosteronism from edematous states ( heart failure congestive, cirrhosis of the liver in phase ascites, nephrotic syndrome) and arterial hypertension essential where other therapies were not sufficiently effective or tolerate. In addition was suggested that canrenone might represent an effective therapy for idiopathic post-puberal hirsutism and it normalizds the cardiac response to the postural challenge in patients with preascitic cirrhosis. Canrenone seems to be effective in reducing blood pressure in patients with metabolic syndrome. Moreover, canrenone seems also to improve MPO, Lp(a), and metalloproteinases in these patients.

Diloxanide (used in the form of furoate) was developed for the treatment of intestinal amoebiasis. The effectiveness of the drug was proved in clinical trials, however, the mechanism of its action is unknown. The drug is not marketed in the United States, athough it is available in India.

Nitrendipine is a calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, nitrendipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.

Metochalcone is a chalcone. It was isolated from heartwood of Pterocarpus marsupium. It has been approved for clinical use as choleretic and diuretic agent. It was made from 2,4-dihydroxybenzaldehyde (beta-resorcaldehide).

Atamestane is a new, competitive, and irreversible inhibitor of estrogen biosynthesis. It is an aromatase inhibitor. Atamestane lacks other intrinsic hormonal or antihormonal activities and shows no inhibition of other cytochrome-P450 dependent enzymes of adrenal steroidogenesis. It had been in phase III clinical trial for the treatment of breast cancer and phase II for the treatment of benign prostatic hyperplasia. It was discontinued from development after an 865-patient trial in breast cancer showed no improvement in efficacy over letrozole.

Pipofezine (Azafen or Azaphen) is a tricyclic antidepressant (TCA) approved in Russia for the treatment of depression. It was introduced in the late 1960s and is still used today. Pipofezine has been shown to act as a potent inhibitor of the reuptake of serotonin. In addition to its antidepressant action, pipofezine has sedative effects as well, suggesting antihistamine activity. Other properties such as anticholinergic or antiadrenergic actions are less clear but are likely. The main advantage of Azafen compared with other tricyclic antidepressants is that this drug has a low toxic effect on the body, including the heart, and it does not block cholinergic receptors and does not change the activity of monoamine oxidase. The maximum concentration in the blood is reached after 1-2 hours after taking the drug. Absorbed in the gastrointestinal tract, metabolism occurs in the liver, and is excreted by Azaphene kidneys.