Golvatinib is a highly potent, small-molecule, ATP-competitive inhibitor of c-Met and multiple members of the Eph receptor family plus c-Kit and Ron. Eisai was developing an oral formulation of golvatinib, which acts as both a c-Met inhibitor and a vascular endothelial growth factor receptor 2 antagonist with potential antineoplastic activity. Golvatinib binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis. Clinical trials involving several forms of cancer are currently underway.

Lixazinone selectively inhibits the high-affinity form of cyclic AMP phosphodiesterase (type IV) isolated from human platelets with only weak effects on both the nonspecific and cyclic GMP-sensitive phosphodiesterases. The inhibitor reduces both maximum velocity and substrate affinity of the type IV enzyme. Lixazinone exhibits marked selectively for the platelet high-affinity enzyme. It also has significant inhibitory effects on cardiac membrane-bound phosphodiesterase. Lixazinone may be useful as an agent to increase cardiac output in the treatment of congestive heart failure. It is a potent PDE3 inhibitor. Lixazinone suppresses folic acid-induced proliferation of rat tubular epithelial cells in vivo.

Dersalazine is a locally-acting compound. It is a potent platelet activating factor (PAF)-antagonist. Dersalazine inhibited IL-1beta or TNF-alpha production in THP-1 or U937 cells, respectively. Dersalazine sodium reduced colonic proinflammatory cytokines IL-1b, IL-6, and IL-17 in dextran sodium sulphate (DSS)–induced colitis. After oral administration, dersalazine sodium is mostly unabsorbed until it reaches the large bowel where the azo bond is reduced by bacteria releasing the active compound. Dersalazine had been in phase I clinical trial for the treatment of ulcerative colitis. No serious adverse reactions were detected in clinical trial. However, no recent development has been reported.

Ravidasvir (RDV, ASC16) is a second‐generation, pan‐genotypic non‐structural (NS) 5A inhibitor, which inhibits viral replication and assembly. Ravidasvir exhibits high antiviral potency with EC50 0.04–1.14 nM for HCV GT1–GT6. The pharmacokinetics results indicated that steady status achieved quickly after the first dose. Metabolism studies utilizing human clinical samples showed that Ravidasvir was very stable, with only modest (~2%) metabolite formation. Biliary excretion of Ravidasvir appears to be the primary route of elimination of the absorbed dose, while renal excretion of the intact drug appears to be negligible. In clinical trans twelve-week Ravidasvir and ritonavir-boosted Danoprevir in combination with ribavirinfor 12 weeks achieve the sustained virologic response rate of 100% in treatment-naïve non-cirrhotic Asian patients with HCV GT1 infection. Ravidasvir for treatment‐naïve, non‐cirrhotic HCV GT1 patients was safe and well tolerated. There was no death, treatment‐related serious adverse events, and discontinued cases due to adverse events.

Tosedostat is a proprietary orally bioavailable inhibitor of the M1 family of aminopeptidases with potential antineoplastic activity. Tosedostat is converted intracellularly into a poorly membrane-permeable active metabolite (CHR-79888) which inhibits the M1 family of aminopeptidases, particularly puromycin-sensitive aminopeptidase (PuSA), and leukotriene A4 (LTA4) hydrolase; inhibition of these aminopeptidases in tumor cells may result in amino acid deprivation, inhibition of protein synthesis due to a decrease in the intracellular free amino acid pool, an increase in the level of the proapoptotic protein Noxa, and cell death. There are several ongoing Phase 2 cooperative group-sponsored trials and investigator-sponsored trials evaluating the clinical activity of Tosedostat in combination with standard agents in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).

P276-00 (also known as riviciclib) is a novel, potent, small-molecule, flavone-derived inhibitor of cyclin-dependent kinases (Cdk), Cdk 4 D1, Cdk1 B, and Cdk9 T, with potent cytotoxic effects against chemosensitive and chemoresistant cancer cell lines. P276-00 was in phase II clinical trial for the treatment mantle cell lymphoma, but that study was terminated based on interim results and all subjects were off study at that time. Although, there were not the major safety or tolerability concerns. However, this drug successfully passed phase II clinical trial for the treatment Melanoma, squamous cell carcinoma of head and neck, malignant melanoma and in combination with Gemcitabine in the treatment of advanced pancreatic cancer.

FLEROBUTEROL is a beta-adrenoceptor agonist with potential antidepressant activity.

AstraZeneca was developing AZD-2066, a metabotropic glutamate receptor 5 (mGLUR5) antagonist, for the oral treatment of pain indications (e.g. chronic neuropathic pain and painful diabetic neuropathies), depressive disorders and gastro-oesophageal reflux disease. AZD-2066 had been in phase II clinical trials by AstraZeneca for the treatment of diabetic neuropathic pain and phase I for the treatment of gastrooesophageal reflux disease (GERD). However, this reasearch had being discontinued.