Stigmasterol (also known as Wulzen anti-stiffness factor) is a plant sterol, or phytosterol. Recent investigation discovered that this compound could be new promising anti- Methicillin-resistant Staphylococcus aureus agent.

Nelociguat, a soluble guanylate cyclase (sGC) activator, has been in phase II clinical trials by Bayer for the treatment of erectile dysfunction and heart failure. However, no recent development has been reported. Nelociguat is a direct soluble guanylate cyclase (sGC) stimulator that acts independently of nitric oxide (NO); has an EC50 of 353 nM on P-VASP formation in rat aortic smooth muscle cells. BAY 60-4552 is pharmacologically active major metabolite of Riociguat.

Lorediplon is a novel non-benzodiazepine, the hypnotic drug acting as a GABAA receptor modulator, differentially active at the alpha1-subunit, associated with promoting sleep. As compared with other selective benzodiazepine receptor agonists, lorediplon has demonstrated in pre-clinical studies a potent hypnotic profile with potential advantages in sleep maintenance and sleep architecture preservation associated with a good safety profile, that is, no induction of tolerance, lack of next-day hangover effect, weak effect on muscular tone, and weak interaction with ethanol. Lorediplon demonstrated a minimum of 10-fold and the 6-fold increase in potency (respectively) in the spontaneous motor activation studies, compared with the currently marketed hypnotics (zolpidem and zaleplon). Additionally, when the electroencephalogram (EEG) effects of lorediplon and zolpidem were compared in the sleep-wake cycle in the mouse, lorediplon demonstrated a 10-fold increase in potency compared with zolpidem in the sleep-wake cycle and 13% greater possibility of fewer wake episodes than zolpidem. At concentrations of 1.2mg/kg, lorediplon demonstrated a 57%increased effect on Slow Wave Sleep (SWS), when compared with a placebo. In clinical trials, the clinical safety and tolerability were excellent for all doses tested. In pharmacokinetic studies, after oral administration, lorediplon is rapidly absorbed from the gastrointestinal tract reaching maximum plasma concentrations at approximately 2 h. Lorediplon demonstrated a dose-dependent improvement in sleep, whereas zolpidem showed a more sustained wake after sleep onset effect. No next-day hangover effects were observed. These sleep effects are also consistent with the pharmacokinetic profile of lorediplon.

Delanzomib (CEP-18770), a proteasome inhibitor, was being developed by Cepahlon (a subsidiary of Teva) for the treatment of cancer and immunological disorders. Delanzomib (CEP-18770) induces apoptotic cell death in multiple myeloma (MM) cell lines and in primary purified CD138-positive explant cultures from untreated and bortezomib-treated MM patients. In vitro, Delanzomib (CEP-18770) has a strong antiangiogenic activity and potently represses RANKL-induced osteoclastogenesis. Delanzomib represses the proteasomal degradation of a variety of proteins, including inhibitory kappaBalpha (IkappaBalpha), resulting in the cytoplasmic sequestration of the transcription factor NF-kappaB; inhibition of NF-kappaB nuclear translocation and transcriptional up-regulation of a variety of cell growth-promoting factors; and apoptotic cell death in susceptible tumor cell populations. In vitro studies indicate that this agent exhibits a favorable cytotoxicity profile toward normal human epithelial cells, bone marrow progenitors, and bone marrow-derived stromal cells relative to the proteasome inhibitor bortezomib. Delanzomib has been in phase II clinical trials for the treatment of multiple myeloma (MM). However, this research has been discontinued. Currently Delanzomib is on Phase I clinical trial for Non-Hodgkin's lymphoma and Solid tumours.

Atecegetran metoxil (more widely known as AZD0837), an anticoagulant and a prodrug, converted to a selective and reversible direct thrombin inhibitor (AR-H067637). Atecegetran metoxil participated in phase II clinical trials to prevent the stroke and systemic embolism in patients with non-valvular atrial fibrillation. The development of atecegetran metoxil was discontinued, due to a limitation identified in the long-term stability of the extended-release drug product.

BCX-4430 hydrochloride is a salt of an antiviral adenosine analog BCX4430 (Immucillin-A) that acts as a viral RNA-dependent RNA polymerase (RdRp) inhibitor. It was developed as a potential treatment for deadly filovirus infections such as Ebola virus disease and Marburg virus disease but also demonstrated broad-spectrum antiviral effectiveness against a range of other RNA virus families, including, bunyaviruses, arenaviruses, paramyxoviruses, and coronaviruses. Biochemical, reporter-based and primer-extension assays indicate that BCX4430 inhibits viral RNA polymerase function, acting as a non-obligate RNA chain terminator. BCX4430 inhibits infection of distinct filoviruses in human cells. Post-exposure administration of BCX4430 protects rodents against Ebola and Marburg virus disease and cynomolgus macaques from Marburg virus when administered as late as 48 hours after infection. BCX4430 is highly active in a Syrian golden hamster model of yellow fever, even when treatment is initiated at the peak of viral replication. BCX4430 also showed efficacy against Zika virus in a mouse model.

ENMD-2076 is an orally-active, Aurora A/angiogenic kinase inhibitor. urora kinases are key regulators of mitosis (cell division), and are often over-expressed in human cancers. ENMD-2076 also targets the VEGFR, Flt-3 and FGFR3 kinases, which have been shown to play important roles in the pathology of several cancers. ENMD-2076 is tested in phase 2 clinical trials against ovarian cancer, breast cance, hepatocellular carcinoma and other malignancies.

Aflatoxin B1 is a very potent carcinogen produced by Aspergillus flavus and related fungi that grow on improperly stored food such as corn, rice, and peanuts. Dietary exposure to aflatoxin B1 is associated with an increased incidence of hepatocellular carcinoma, especially given co-infection with hepatitis B virus. Mechanism of carcinogenicity involves metabolic activation to aflatoxin B1-8,9 exo-epoxide by cytochrome p450 and formation of adducts with guanine DNA base.