Sopitazine is an anticholinergic agent.

Spirgetine is an adrenergic agonist.

Spiroglumide (CR2194) is a potent and specific cholecystokinin-B (CCKB)/gastrin receptor antagonist structurally similar to lorglumide. Gastrin receptor blockade with CR2194 alters gastric acid secretion in response to food ingestion or to sham feeding. The results support a physiological role for gastrin in regulating acid secretion in humans. In healthy volunteers, intravenous infusion of spiroglumide was shown to reduce basal and postprandial intragastric acidity. These data also support the thesis that CCK2 receptor antagonism is an effective means to suppression gastric acid secretion. Although the oral bioavailability of spiroglumide was an improvement over L-365,260, it was not very potent and had little selectivity for the CCK2 receptor over the CCK1 receptor. These factors seem likely to have contributed to the decision not to continue its development

Stibamine Glucoside is a nitrogen glucoside of p-aminophenylstibinate of sodium useful for the treatment of leishmaniasis and visceral leishmaniasis also known as kala-azar black fever Stibamine Glucoside is administered by slow i.v or deep i.m. injection. Some 80% of a dose is recov¬ered in the urine on 24 h. Elimination from the plasma is biphasic, the half-life of the initial phase being 2 h and that of the subsequent phase 76 h. In high dose car¬diac, renal or hepatic toxicity may occur. Stibamine Glucoside is no longer marketed due to safety reason.

Spiroxepin is a dioxolane derivative patented by Delalande S. A. as an antidepressant and spasmolytic agent.

MKC-1 is an orally available cell cycle inhibitor with downstream targets that include tubulin and the importin-β family. MKC-1 has shown broad antitumor activity in preclinical models. MKC-1 and its metabolites inhibit tubulin polymerization, blocking the formation of the mitotic spindle, which may result in cell cycle arrest at the G2/M phase and apoptosis. In addition, this agent has been shown to inhibit the activities of the oncogenic kinase Akt, the mTOR pathway, and importin-beta, a protein essential to the transport of other proteins from the cytosol into the nucleus. MKC-1 had been in phase II clinical trials for the treatment of ovarian cancer, endometrial cancer, pancreatic cancer and breast cancer. This compound was originally discovered by Roche, then licensed to EntreMed (now CASI Pharmaceuticals) the exclusive worldwide rights to develop and commercialize. However, no recent development has been reported.

Cethromycin is a ketolide antibiotic derived from erythromycin A being investigated for use in community-acquired pneumonia and other respiratory tract infections. Cethromycin possesses reliable activity against the bacteria most commonly associated with community-acquired pneumonia including S. pneumoniae, H. influenzae, M. catarrhalis, M. pneumoniae, C. pneumoniae, and L. pneumophila. Unlike fluoroquinolones, cethromycin has a narrower spectrum of activity against gram-negative bacteria, which may reduce the risk of collateral damage and the incidence of Clostridium difficile infection. It offers an advantage over telithromycin in that hepatotoxicity does not seem to be a concern. The FDA denied approval of cethromycin for the treatment of CAP in 2009, requesting more efficacy data.

Darusentan is an orally active, propanoic acid-based endothelin receptor antagonist (ERA) that selectively blocks endothelin-1 (ET-1) binding to the endothelin type-A (ETA) receptor. Darusentan exhibited subnanomolar binding affinity and approximately 1000-fold selectivity for the ETA receptor in binding experiments conducted in vitro under steady-state conditions. Darusentan is orally bioavailable and, when administered to humans, maximum plasma concentrations are observed within 1–2 h post dosing. The mean elimination half-life is relatively long (>15 h), which is consistent with once-daily dosing. Darusentan is primarily glucuronidated by Phase II enzymes in the liver, and the major route of elimination of Darusentan and its metabolites is via the bile. Some glucuronidated metabolites of Darusentan are also excreted in the urine. Darusentan doses up to 300 mg/day were well tolerated and associated with a manageable safety profile in patients with resistant hypertension (RHTN). The most frequently reported adverse events in Ddarusentan-treated subjects were peripheral edema (17%) and headache (11%), which were mostly mild or moderate in severity. Other commonly reported adverse events in the Darusentan treatment group were sinusitis (8%), dizziness (7%), upper respiratory tract infection (5%) and gastroenteritis (5%). In phase III clinical trial the mean reductions in clinic systolic and diastolic blood pressures were 9/5 mm Hg with placebo, 17/10 mm Hg with Darusentan 50 mg, 18/10 mm Hg with Darusentan 100 mg, and 18/11 mm Hg with Darusentan 300 mg. Unfortunately, phase III clinical trial evaluating Darusentan did not achieve its co-primary efficacy endpoints of achieving a change in systolic and diastolic blood pressure after 14 weeks compared to a placebo. Perhaps for this reason, shortly after the top-line results of this study became known, the sponsor announced that Darusentan would not be developed further for resistant hypertension.

Feneritrol is a hypocholesteraemic agent.

Namirotene [CBS-211A] is a retinoic acid analogue which was undergoing phase II trials with Chauvin in France as 0.02% eye drops for corneal ulcer. It was discontinued later. Namirotene is a synthetic analogue of retinoic acid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, namirotene binds to and activates retinoic acid receptors (RARs), thereby altering the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells. When it was associated with 1 alpha,25(OH)2D3, CBS-211A strongly potentiated the 1 alpha,25(OH)2D3-induced inhibition of U937 cell proliferation and caused a dramatic increase in their differentiation toward monocytes/macrophages. The co-inducing effect of CBS-211A was restricted to U937 cells. Our data suggest that CBS-211A may have therapeutic implications in the treatment of certain kinds of myelomonocytic leukemia. CBS-211A also provides an interesting tool to understand the mechanisms involved in the differentiation of myelomonocytic cells.