Radalbuvir (also known as GS-9669 ) is a Hepatitis C virus NS 5 protein inhibitor for the treatment of hepatitis C virus (HCV) infection developed by Gilead Sciences. Radalbuvir is a highly optimized thumb site II nonnucleoside inhibitor, with a binding affinity of 1.35 nM for the genotype (GT) 1b protein. It is a selective inhibitor of HCV RNA replication, with a mean 50% effective concentration of ≤ 11 nM in genotype 1 and 5 replicon assays, but lacks useful activity against genotypes 2 to 4. In preclinical Radalbuvir exhibited at least additive activity in combination with agents encompassing four other direct modes of action (NS3 protease, NS5A, NS5B via an alternative allosteric binding site, and NS5B nucleotide) as well as with alpha interferon or ribavirin in replicon assays. It exhibited high metabolic stability in vitro human liver microsomal assays, which, in combination with its pharmacokinetic profiles in rat, dog, and two monkey species, is predictive of good human pharmacokinetics. In clinical trials, Radalbuvir shows highly effective inhibition of wild-type HCV.

Stercuronium is a conessine derivative patented by Koninklijke Nederlandsche Gist-en Spiritusfabriek N. V. as a competitive neuromuscular blocking agent with antimuscarinic activity. In preclinical models, Stercuronium produced significantly greater inhibition (P < 0.05) of the bradycardia than of the vasodepressor response produced by carbachol. In guinea-pig atria, the negative chronotropic response to carbachol was inhibited to a similar degree to the negative inotropic response by Stercuronium, whereas in bladder and ileum Stercuronium was 17 fold less active as an antimuscarinic drug. The affinity of Stercuronium for the prejunctional muscarinic receptor on sympathetic nerve endings in the rabbit ear artery was similar to that for the muscarinic receptor mediating negative inotropic responses to carbachol in the rabbit left atrium. Unfortunately, in clinical trials Stercuronium producing marked tachycardia in some patients when used as a muscle relaxant.

MK-571 is a selective, orally active leukotriene D4/E4 (LTD4/E4) receptor antagonist patented by Merck Frosst Canada, Inc. for the treatment bronchoconstriction. In ex vivo models MK-571 competitively antagonizes contractions of guinea pig trachea and ileum induced by leukotriene (LT) D4 and LTE4 and contractions of human trachea induced by LTD4. MK-571 antagonizes bronchoconstriction induced in anesthetized guinea pigs by i.v. LTC4, LTD4, and LTE4 but do not block bronchoconstriction to arachidonic acid. In clinical trials, MK-571 is a potent antagonist of LTD4-induced bronchoconstriction in both normal volunteers and asthmatic patients.

JNJ-39393406 is a positive allosteric alpha-7 nicotinic acetylcholine receptor modulator. It was under development for the treatment of smoking cessation, schizophrenia, Alzheimer's disease, but development for these indications was discontinued.

PF-00446687 is the highly selective, brain-penetrant, melanocortin 4 receptor (MC4R) agonist. PF-00446687 induced partner preferences formation in females prairie voles after a 6-h cohabitation without mating. PF-00446687 had been in phase I clinical trial for the treatment of sexual function disorders.

Kintor Pharma is developing proxalutamide (developmental code GT-0918), an androgen receptor antagonist, for the treatment of metastatic castrate-resistant prostate cancer and AR-positive triple-negative breast cancer. Proxalutamide is involved in phase III clinical trials in China and in phase II in the USA for patients with metastatic castrate-resistant prostate cancer. In addition, the drug participates in phase I clinical trials for the treatment of AR-positive triple-negative breast cancer. Proxalutamide is expected to become a more effective, less toxic second-generation AR antagonist, which will have a bright prospect once it receives approval for coming on the market.