{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Search results for l root_names_stdName in Standardized Name (approximate match)
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:lefleuganan [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01187836: Phase 1/Phase 2 Interventional Completed Heart Failure
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
TRV-120027 is a novel β-arrestin biased ligand of the angiotensin II type 1 receptor; it antagonizes canonical G-protein-mediated coupling while, in contrast to classical angiotensin II type 1 receptor antagonists, it engages β-arrestin-mediated signaling. Consequently, TRV-120027 inhibits angiotensin II-mediated vasoconstriction while, via β-arrestin coupling, it increases cardiomyocyte contractility. In preclinical studies, TRV-120027 not only produced vasodilation by antagonizing the AT1R-Gαq pathway but also enhanced cardiac performance by activating AT1R-β-arrestin signaling. Because of this unique pharmacological profile, TRV-120027 is now being evaluated in a phase II clinical trial as a novel therapeutic for acute heart failure (AHF).
Status:
Investigational
Source:
INN:yttrium (⁹⁰Y) anditixafortide [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
JAN:LYSINE SULFITE [JAN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:zosurabalpin [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02753699: Phase 3 Interventional Completed Hepatitis C
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Alisporivir (DEBIO-025) is a first-in-class synthetic cyclophilin inhibitor, in development with Debiopharm as an oral treatment for hepatitis C virus (HCV) infections. Alisporivir has the potential to be used for the treatment of additional diseases such as other viral infections, certain muscular dystrophies, and myocardial infarction. Alisporivir has potent anti-hepatitis C virus (HCV) activity both in vitro and in vivo. It is currently being evaluated in phase II clinical trials.
Status:
Investigational
Source:
INN:levomoprolol [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Levomoprolol (L-moprolol) is a beta-adrenergic blocker which was introduced as an oral medication for treatment of systemic hypertension. It was found to be effective in 2% eyedrops in reducing the intraocular pressure in glaucoma. Observations on glaucoma patients treated with the eyedrop for 1.5 to 2.5 years was without undesirable side effects. L-moprolol and dipivefrin had an equivalent effect in lowering the intraocular pressure. The association of the two drugs caused a further reduction of intraocular pressure.
Status:
Investigational
Source:
JAN:TRETINOIN TOCOFERIL [JAN]
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
INN:desglugastrin [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Desglugastrin is a gastric acid secretion stimulator. It dose dependently stimulated gastric acid secretion in anaesthetized rats. In view of the trophic action of gastrointestinal hormones on the exocrine pancreas, the effects of desglugastrin on the growth of hamster pancreatic well differentiated adenocarcinoma were investigated in vitro. Desglugastrin exhibited the greatest effect on thymidine incorporation into these cells after a lag period of 96 h. Doses of desglugastrin caused a significant and dose-dependent increase in thymidine incorporation.