Vildagliptin, previously identified as LAF237, is a new oral anti-hyperglycemic agent (anti-diabetic drug) of the new dipeptidyl peptidase-4 (DPP-4) inhibitor class of drugs. Vildagliptin inhibits the inactivation of GLP-1 and GIP by DPP-4, allowing GLP-1 and GIP to potentiate the secretion of insulin in the beta cells and suppress glucaon release by the alpha cells of the islets of Langerhans in the pancreas. It is currently in clinical trials in the U.S. and has been shown to reduce hyperglycemia in type 2 diabetes mellitus. While the drug is still not approved for use in the US, it was approved in Feb 2008 by European Medicines Agency for use within the EU and is listed on the Australian PBS with certain restrictions. Vildagliptin is marketed under the trade names Galvus, Zomelis.

Heliomycin was isolated as a stable polyketide antibiotic substance produced by Streptomyces resistomycificus. Heliomycin has been shown to demonstrate antibacterial activity against gram-positive bacteria and mycobacteria. Heliomycin preferentially inhibits RNA synthesis in comparison to DNA and protein synthesis in intact bacterial cells. Heliomycin is indicated for the treatment of various dermatological pathologies, including pyoderma, pemphigus or pemphigus of newborns, trophic ulcers infected secondarily, microbial eczema, cracked nipples in women breastfeeding a baby, pseudofurunculosis and others. Since heliomycin is low in toxicity, the only contraindication is increased individual intolerance to the components of the ointment. It is cytotoxic to gastric adenocarcinoma HMO2 cells and hepatic carcinoma HePG2 cells.

Docarpamine (marketed under the tradename Tanadopa) is a dopamine prodrug developed in Japan for the treatment of chronic heart failure. The drug does not cross the blood-brain barrier and shows no effect on CNS activity. It is supposed that the drug exerts its action by activating dopamine receptor D1.

Roxithromycin is a semi-synthetic macrolide antibiotic, which was developed by Roussel Uclaf and is available in Australia. Roxithromycin prevents bacteria from growing, by interfering with their protein synthesis. Roxithromycin binds to the subunit 50S of the bacterial ribosome, and thus inhibits the translocation of peptides. It can treat respiratory tract, urinary and soft tissue infections.

Dilevalol, the RR-stereoisomer of labetalol, is a non-cardioselective β-adrenoceptor antagonist with substantial partial β2-agonist and negligible α1-blocking activity. Reduction in blood pressure during dilevalol administration is associated with peripheral vasodilatation, and heart rate remains essentially unchanged. Following oral administration, dilevalol is completely absorbed. Once-daily administration is possible, due to a long elimination half-life. In vitro and in vivo animal studies and results obtained in humans reveal that dilevalol is a nonselective blocker of β1- and β2-adrenoceptors, with a similar potency to propranolol, but has negligible antagonistic activity at α1-receptors. Dilevalol, the R,R′ stereoisomer, makes up 25% of racemic labetalol, the drug, approved by FDA for the treatment of hypertension. The relaxing potency of dilevalol was approximately 4.7 times more potent than that of labetalol. Dilevalol markedly reduced the diastolic blood pressure with only a slight increase of heart rate In pithed rats, while isoproterenol and pindolol caused moderate to marked positive chronotropic effects in proportion to their hypotensive effects. These results suggest that dilevalol has more potent ISA than labetalol. In contrast to labetalol, dilevalol possesses little, if any, alpha-adrenergic blocking activity. The compound is 3 to 10 times less potent than labetalol at α1-adrenergic receptors under a variety of experimental conditions. Moreover, it is 300- to 1000-fold less potent at alpha1-adrenergic receptors compared with β1-adrenergic receptors. The pA2 values for dilevalol as an α antagonist range from 5.9 to 6.4. Because maximal plasma concentrations of the drug after administration of a 400-mg dose are approximately 0.5 pmol, it is doubtful that alpha blockade is involved in the antihypertensive response to dilevalol in humans.

Cyproterone acetate is a steroid drug which was developed by Schering A.G (now Bayer). Cyproterone acetate was approved in Canada, Asia, Latin America and Europe for the treatment of sever acne under the name Diane-35 (ethinyl estradiol) and its mechanism of action in this condition is explained by competitive inhibition of androgen receptor AR. In Canada cyproterone acetate is widely used as a contraceptive, however its usage is associated with liver toxicity and clots formation. In the UK the drug is marketed for the treatment of prostate cancer (Cyproterone acetate brand name).

Unithiol was developed in the Soviet Union in the late 1950s. It only became more widely used in America and Western Europe since the mid-1970s, and particularly since the late 1970s when the Heyl Company in Germany began production. It remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century. Unithiol has been used in the management of acute and chronic poisoning with a number of different metals and metalloids, and is particularly useful for arsenic, bismuth and mercury. Unithiol can be given parenterally or orally depending on the clinical situation and severity of poisoning. Its action mechanism is close that of complexones. Active sulfhydryl groups enter into reactions with thiol poisons present in blood and tissues, form not toxic complex with them eliminated with urine. The poisons fixation results in the body enzyme systems changed under the poisons effect functions restoration. It is efficient as an antidote in case of intoxications by arsenic and heavy metals salts.

Anethole trithione or anetholtrithione is a drug used in the treatment of dry mouth. Anethole trithione is a bile secretion-stimulating drug that restores salivation. It is listed in the U.S. National Cancer Institute's Dictionary of Cancer Terms as being studied in the treatment of cancer. Anethol has also been identified as a treatment for improving medium and severe dry eye symptoms. The mechanism of action for the chemopreventive and xerostomia properties have not been fully elucidated.

Warfarin, (R)- is R-enantiomer of warfarin, an oral anticoagulant, with relatively low potency compared to S-enantiomer. Clinically available warfarin is a racemic mixture of (R)- and (S)-warfarin, and the (S)-enantiomer has 3 to 5 times greater anticoagulation potency than its optical congener. Both enantiomers are eliminated extensively via hepatic metabolism with low clearance relative to hepatic blood flow. The scientific debate on the contribution of the R- Warfarin -to-S- Warfarin effect is a long and conflictual story. It has shown that the pharmacodynamic response to (R/S)-Warfarin 25 mg (a mixture of equal amounts of S-Warfarin and R- Warfarin) was nearly twice that of S-Warfarin 12.5 mg given alone, thus indicating the substantial contribution of R-Warfarin to the (R/S)-Warfarin effect. (R/S)-Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism. It is also indicated for the prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of vitamin K1 epoxide.

Androstenedione (Δ4-Androstenedione, 4-androstene-3,17-dione or 17-ketotestosterone) is an endogenous androgen steroid hormone and intermediate in the biosynthesis of testosterone from dehydroepiandrosterone (DHEA). In turn, Androstenedione is also a precursor of dihydrotestosterone (DHT), estrogens such as estradiol and estrone, and the neurosteroid 3α-androstanediol. Androstenedione is used to increase the production of the hormone testosterone to enhance athletic performance, increase energy, keep red blood cells healthy, enhance recovery and growth from exercise, and increase sexual desire and performance. Androstenedione has been shown to increase serum testosterone levels over an eight-hour period in men when taken as a single oral dose of 300 mg per day, but a dose of 100 mg had no significant effect on serum testosterone. However, serum levels of estradiol increased following both the 100 mg and 300 mg doses. The study also reported that the serum level of estrogens and testosterone produced varied widely among individuals. Androstenedione is currently used as a nutritional supplement to grow bigger muscles and stronger bones. This implies that androstenedione may have anabolic properties. Even though it has not been convincingly demonstrated yet that androstenedione is an anabolic steroid, its anabolic properties are likely based on its proven ability to increase testosterone levels. The role of testosterone in building stronger muscles and bones is widely accepted. Thus, high doses of testosterone-boosting drugs combined with strength training have been shown to increase muscle size and strength even in normal young men. This confirms what thousands of athletes who take anabolic steroids have known for decades. Yet androstenedione is different from testosterone-boosting drugs in a number of important aspects. To begin with, androstenedione is a naturally occurring substance that is produced by the body itself. In contrast to synthetic anabolic steroids, androstenedione is right at home in the human body, and perfectly complements the complex hormonal network in the body. Information about possible side effects and risks of androstenedione is very limited. Also, recent studies show that the drug's actions don't support manufacturer's claims. While a few individuals have shown increased levels of testosterone, most failed to achieve increases in blood testosterone levels. Initial medical research has raised concerns about this supplement's safety. Doctors worry that androstenedione may increase the risk of heart disease or liver cancer. In addition, research also associates androstenedione use with increases in estradiol, a female estrogen.