{{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}}
Restrict the search for
m nalidixic acid
to a specific field?
Status:
Investigational
Source:
NCT02045095: Phase 1 Interventional Terminated Advanced Malignant Solid Tumors
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
TAK-243 (MLN7243) is a small molecule inhibitor of ubiquitin-activating enzyme (UAE), with potential antineoplastic activity, which was developed by Takeda Oncology, Millennium. MLN7243 binds to and inhibits UAE, which prevents both protein ubiquitination and subsequent protein degradation by the proteasome. This inhibits tumor cell proliferation and survival. UAE, also called ubiquitin E1 enzyme (UBA1; E1), is more active in cancer cells than in normal, healthy cells. Currently, TAK-243 is in phase I clinical trial evaluating safety, tolerability, pharmacokinetics, pharmacodynamics against advanced malignant solid tumors phase.
Status:
Investigational
Source:
NCT01358981: Phase 1 Interventional Completed Diabetes Mellitus, Type 2
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT00454233: Phase 2 Interventional Completed Diabetes Mellitus Type 2
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
ASP-543 (also known as YM-543), a selective inhibitor of the sodium-glucose cotransporter 2. This protein is specifically expressed in the kidney that plays an important role in renal glucose reabsorption, and its inhibition may present a novel therapeutic strategy for treating diabetes. ASP-543 participated in phase II clinical trials in Europe and in the USA for the treatment of Type 2 diabetes mellitus but these studies were discontinued.
Status:
Investigational
Source:
NCT04083339: Phase 3 Interventional Active, not recruiting Diabetic Cardiomyopathies
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
INN:quazomotide [INN]
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01332552: Phase 1 Interventional Terminated Hepatitis C
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00849134: Phase 1 Interventional Completed Pain, Inflammatory
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
GSK-1482160 is being evaluated for treatment of inflammatory pain (such as arthritis). This compound acts on P2X7 receptors, expressed by cells of innate and adaptive immunity. P2X7 receptors are involved in the production of pro-inflammatory cytokines that are thought to be an important mediator of inflammation. By blocking P2X7 receptors, less inflammatory chemicals are released, which possibly results in less inflammatory pain. Because of its ability to target P2X7R with high selectivity and to be radiolabelled with 11C, GSK-1482160 was suggested to be a useful biomarker for neuroinflammation via positron emission tomography (PET).
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT01347203: Phase 1 Interventional Completed Deep Vein Thrombosis Leg
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00847197: Phase 2 Interventional Completed Dyslipidemia
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
MK-1903 is a potent and selective hydroxycarboxylic acid receptor 2 (HCA2, GPR109A) full agonist. Exhibits no binding at the GRP109B receptor. This drug had been in phase II clinical trial for the treatment of atherosclerosis and Dyslipidemia. But then, according to Merck, elevation of HDL cholesterol relative to placebo did not meet the trial's pre-specified primary objective for efficacy; no safety signals were implicated as drivers of the decision to discontinue development.