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Restrict the search for
phenyl aminosalicylate
to a specific field?
Status:
Investigational
Source:
NCT00273936: Phase 1 Interventional Completed Acute Leukemia
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
AVN-944 is an IMPDH (inosine 5-monophosphate dehydrogenase) inhibitor which is now being tested in phase I of clinical trials for the treatment of hematologic malignancies and solid tumors and in phase II for pancreatic cancer (in combination with gemcitabine). The drug showed good inhibition of IMPDH isoforms I and II with Ki=6-10 nM.
Class (Stereo):
CHEMICAL (ABSOLUTE)
Trecetilide is a class III antiarrhythmic agent developed for the treatment of atrial flutter and fibrillation. Trecetilide probably has effects on the cardiac myocyte membrane that are similar to ibutilide. It is being developed for both oral and intravenous administration. Unlike ibutilide, trecetilide has good oral bioavailability. Trecetilide has a good metabolic stability. As with ibutilide, its mechanism of class III action may involve both rectifier K+ current blockade and other mechanisms of prolonging repolarization.
Status:
Investigational
Source:
INN:fenaftic acid [INN]
Source URL:
Class (Stereo):
CHEMICAL (MIXED)
Fenaftic acid is a choleretic agent.
Status:
Investigational
Source:
NCT00525941: Phase 3 Interventional Withdrawn Insomnia
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Indiplon is a nonbenzodiazepine, hypnotic sedative that was proposed for the treatment of insomnia. It is a high-affinity allosteric potentiator of GABAA responses that demonstrates preference for α1 subunit-containing GABAA receptors. There is minimal potential for adverse effects, residual daytime sedation, tolerance, respiratory depression. The simultaneous administration of indiplon and alcohol did not result in any significant pharmacokinetic changes. There is little risk of pharmacokinetic interaction between indiplon and any co-administered drugs. Developer (Neurocrine) decided to discontinue all clinical and marketing development of Indiplon in the United States.
Status:
Investigational
Source:
INN:carmoxirole [INN]
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Carmoxirole is a dopamine D2 receptor agonist with limited central activity that modulates sympathetic activation and subsequently reduces pre-load and afterload in animals. It was shown, that carmoxirole induced beneficial effects on hemodynamic and neurohumoral parameters in heart failure. In addition, experimental evidence showed that carmoxirole lowered blood pressure in various models of hypertension mainly or exclusively through inhibition of noradrenaline release from sympathetic nerve endings. That effect of carmoxirole was mediated by presynaptic dopamine receptors with the characteristic that release inhibition was restricted to low rates of sympathetic nerve discharge.
Status:
Investigational
Source:
NCT00003914: Phase 2 Interventional Completed Kidney Cancer
(1999)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dolastatin 10 is an unusual peptide of marine origin which binds to tubulin, inhibits microtubule assembly, resulting in the formation of tubulin aggregates and inhibition of mitosis. Dolastatin 10 has been used in trials phase II studying the treatment of Sarcoma, Leukemia, Lymphoma, Liver Cancer, among others. In case of hormone-refractory prostate cancer, it lacks significant clinical activity as a single agent and also dolastatin-10 is inactive against hepatobiliary and pancreatic carcinomas.
Status:
Investigational
Source:
NCT00106808: Phase 3 Interventional Completed Type 2 Diabetes Mellitus
(2005)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Muraglitazar previously known as BMS-298585 has been identified as a non-thiazolidinedione dual agonist of peroxisome proliferator-activated receptor alpha/gamma. Muraglitazar is currently in clinical trial phase III development for the treatment of type 2 diabetes and dyslipidemia.
Status:
Investigational
Source:
NCT01227265: Phase 3 Interventional Completed Parkinson Disease
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Preladenant (SCH-420814) is an adenosine A(2A) receptor antagonist with a high affinity and very high selectivity for adenosine A(2A) receptors, which is being developed by Merck & Co Inc (following its acquisition of Schering-Plough Corp) for the potential treatment of Parkinson's disease. Preladenant is a potent competitive antagonist of the human A2Areceptor (Ki = 1.1 nM) and has >1000-fold selectivity over all other adenosine receptors, making this compound the most selective A2A receptor antagonist reported to date. Preladenant was being researched as a potential treatment for Parkinson's disease. Positive results were reported in Phase II clinical trials in humans, but it did not prove itself to be more effective than a placebo during Phase III trials, and so was discontinued in May 2013.
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
The novel compounds clamikalant (HMR 1883) or its sodium salt HMR 1098) have been shown to block selectively Kir6.2/SUR1-composed K(ATP) channels. Clamikalant is under development by Aventis Pharma (formerly Hoechst Marion Roussel) for the potential treatment of heart arrest and ventricular arrhythmias. Nevertheless, clamikalant and its sodium salt did not pass the clinical trials
Status:
Investigational
Source:
NCT00389779: Phase 3 Interventional Completed Hypertension
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
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.
