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Restrict the search for
vitamin a
to a specific field?
Status:
Investigational
Source:
NCT00952198: Phase 1 Interventional Completed Type 2 Diabetes
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
AMG-151 [AMG 151, ARRY-403] was under development with Amgen for the treatment of type 2 diabetes mellitus (T2DM). AMG 151 binds to glucose-bound glucokinase distinctly from glucose- or adenosine triphosphate–binding sites
to activate glucokinase selectively. AMG 151 was in a phase I trial for the treatment of Type 2 diabetes. AMG 151 in a twice-daily dosing regimen decreased fasting
and postprandial glucose in patients with type 2 diabetes inadequately controlled with metformin. In all AMG 151 once-daily
dose groups and in the AMG 151 200-mg twice-daily dose
group, significant reductions were observed in glucose
AUC0–240 in after a MTT from baseline to day 28 compared with placebo. However, Amgen disconinued the development of AMG-151.
Status:
Investigational
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03997838: Phase 3 Interventional Completed Pain, Postoperative
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
Clin Nephrol. Feb 1986;25(2):70-4.: Not Applicable Human clinical trial Completed Hyperlipidemias/complications
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Pantetheine is the mercaptoethyl conjugated amide analog of pantothenic acid (Vitamin B5), an intermediate in the production of coenzyme A by the body. Pantetheine is part of two larger compounds (coenzyme A and acyl-carrier protein) that promote a large number of metabolic reactions essential for the growth and well-being of animals. Pantetheine has been found to ameliorate symptoms in various disease models but specifically in Pantothenate Kinase-Associated Neurodegeneration (PKAN). Pantetheine is usually administered in its disulfide form (i.e. pantethine) since pantethine is commercially available and is reduced to pantetheine in biological systems and pantethine was hydrolyzed to pantetheine and pantothenic acid prior to absorption. The applicability and efficacy of pantethine (therefore also pantetheine) as a clinical therapeutic however is hampered since both forms can be degraded by pantetheine present in the body.
Status:
Investigational
Source:
NCT01332695: Phase 2 Interventional Completed Essential Tremor
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
ST-101 (also known as ZSET1446) is an azaindolizinone derivative patented by Zenyaku Kogyo Kabushiki Kaisha for the treatment of Alzheimer's disease and improvement of cerebral function. In preclinical models, ST-101 stimulates acetylcholine release and improves methamphetamine-induced impairment of recognition memory in mice by activating extracellular signal-regulated kinase 1/2. Impaired neurogenesis observed in olfactory bulbectomized mice was significantly improved by chronic administration with ST-101. We confirmed that administration with mecamylamine, a nicotinic acetylcholine receptor antagonist, inhibits ST-101-enhanced neurogenesis in the dentate gyrus. ST-101 administration also restored decreased phosphorylation of Akt and extracellular signal-regulated kinase in the dentate gyrus of olfactory bulbectomized mice.
Status:
Investigational
Source:
NCT02518113: Phase 1/Phase 2 Interventional Completed T-cell Acute Lymphoblastic Leukemia
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
LY-3039478 is an orally bioavailable, novel small molecule inhibitor of Notch signaling pathway, developed Eli Lilly and Company for cancer treatment. The Notch receptor, on the surfaces of progenitor cells and cancer cells, binds neighboring cell-surface ligands DLL or JAGGED. On ligand binding, the intramembrane protease γ-secretase cleaves the Notch intracellular domain (NICD). LY-3039478 is an exquisitely potent inhibitor of Notch-1 intracellular domain (N1ICD) cleavage with an IC50 of ∼1nM in most of the tumor cell lines tested. LY3039478 also potently inhibits mutant Notch receptor activity. Treatment with a gamma-secretase inhibitor, LY3039478, significantly inhibited the growth of 2 CCRCC(Clear cell renal cell carcinoma) cell lines in a concentration-dependent manner. LY3039478 treatment also led to decreased expression of Myc and Cyclin A1, two genes that were part of the NOTCH driven proliferative signature in murine and human model systems. LY3039478 treatment also led to G0/G1 cell cycle arrest in CCRCC cells. In a xenograft tumor model, LY3039478 inhibited N1ICD cleavage and expression of Notch-regulated genes in the tumor microenvironment. The inhibition of Notch cleavage also resulted in the induction of apoptosis in a Notch-dependent xenograft model. In immunodeficient NSG mice xenografted with 769-P CCRCC cells, LY3039478 treatment resulted in significantly increased survival and delayed tumor growth in independent cohorts of mice demonstrating in vivo efficacy in CCRCC. LY3039478 is being investigated in a clinical trial in patients with T-cell acute lymphoblastic leukemia or T-cell lymphoblastic lymphoma in combination with Dexamethasone.
Status:
Investigational
Source:
NCT03731026: Phase 3 Interventional Unknown status Breast Cancer
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02722018: Phase 1 Interventional Completed Healthy Volunteer
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
ARN-810 (GDC-0810) is a novel, orally bioavailable, estrogen receptor antagonist that induces proteasomal estrogen receptor degradation in breast cancer cell lines at picomolar concentrations and tumor regression in tamoxifen-sensitive and resistant BC xenograft models. Results from a first-in-human phase I/IIa study of ARN-810 indicate that it is tolerable and may benefit some postmenopausal women with advanced estrogen receptor-positive breast cancer. Development of ARN-810 was discontinued.
Status:
Investigational
Source:
NCT02607280: Phase 3 Interventional Completed Diabetic Peripheral Neuropathic Pain
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Mirogabalin, a selective alpha 2 delta ligand binds to the α2δ subunits of voltage-dependent calcium channels and thus blocks the channel. This drug was developed by Daiichi Sankyo and in January 2019 was approved in Japan for the treatment of neuropathic pain and for the postherpetic neuralgia.
Status:
Investigational
Source:
NCT02335814: Phase 1 Interventional Terminated Acute Myeloid Leukemia
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
AMG-925, a dual FLT3/CDK4 inhibitor, has been developed to overcome resistance to FLT3 inhibitors, which is a serious clinical issue in treating acute myelogenous leukemia (AML). AMG-925 inhibits FLT3, including many FLT3 mutants reported to date. AMG-925 inhibits the proliferation of a panel of human tumor cell lines including Colo205 (Rb(+)) and U937 (FLT3(WT)) and induced cell death in MOLM13 (FLT3(ITD)) and even in MOLM13 (FLT3(ITD, D835Y)), which exhibits resistance to a number of FLT3 inhibitors currently under clinical development. At well-tolerated doses, AMG-925 leads to significant growth inhibition of MOLM13 xenografts in nude mice, and the activity correlates with inhibition of STAT5 and Rb phosphorylation. AMG-925 is in Phase I clinical trials for the treatment of Acute myeloid leukaemia.
