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Restrict the search for
beta carotene
to a specific field?
Status:
Investigational
Source:
NCT00853450: Phase 1 Interventional Completed Antiplatelet Effect
(2009)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
AZD-6482 is being developed by AstraZeneca to evaluate its therapeutic effects in the treatment of thrombosis. AZD-6482 is essentially a PI3K-beta inhibitor. It is a PI3Kβ inhibitor with IC50 of 10 nM, 8-, 87- and 109-fold more selective to PI3Kβ than PI3Kδ, PI3Kα and PI3Kγ in cell-free assays. by targeting PI3Kβ, AZD-6482 specifically inhibits thrombosis without interfering with normal haemostasis. Therefore, AZD-6482 is used as an anti-thrombotic drug for the prophylaxis of thrombotic disorders. AZD-6482 was in phase I trials by AstraZeneca for the prevention of thrombosis. However, the study was discontinued.
Status:
Investigational
Source:
NCT01741116: Phase 2 Interventional Completed Hormone Refractory Prostate Cancer
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Dovitinib is an orally active small molecule that exhibits potent inhibitory activity against multiple receptor tyrosine kinases (RTK) involved in tumor growth and angiogenesis. Dovitinib strongly binds to fibroblast growth factor receptor 3 (FGFR3) and inhibits its phosphorylation, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell death. In addition, this agent may inhibit other members of the RTK superfamily, including the vascular endothelial growth factor receptor; fibroblast growth factor receptor 1; platelet-derived growth factor receptor type 3; FMS-like tyrosine kinase 3; stem cell factor receptor (c-KIT); and colony-stimulating factor receptor 1; this may result in an additional reduction in cellular proliferation and angiogenesis, and the induction of tumor cell apoptosis. There are several ongoing Phase I/III clinical trials for dovitinib.
Status:
Investigational
Source:
NCT02914639: Phase 1/Phase 2 Interventional Completed Age-Related Macular Degeneration
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT00040404: Phase 2/Phase 3 Interventional Terminated Parkinson Disease
(2002)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02209753: Phase 2 Interventional Completed Psoriasis
(2001)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Doramapimod (BIRB-796) is a p38 MAPK inhibitor, relatively potent against alpha isoform. Oral doramapimod exerts anti-inflammatory potential in humans in vivo. Doramapimod has entered clinical trials for the treatment of autoimmune diseases.
Status:
Investigational
Source:
NCT02145468: Phase 3 Interventional Completed Acute Coronary Syndrome
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Losmapimod (GW856553, GSK-AHAB) is a selective, potent, and orally active p38 MAPK (p38α and p38β isoforms) inhibitor that acts by competing for the kinase ATP binding site. GlaxoSmithKline (GSK) is developing oral losmapimod for the treatment of acute coronary syndromes (phase III), chronic obstructive pulmonary disease (phase II) and primary focal segmental glomerulosclerosis (phase II). Oral losmapimod was in phase II development for the treatment of rheumatoid arthritis and major depressive disorder; however, it appears that development for these indications has been discontinued. No further development was reported for atherosclerosis, dyslipidaemia and neuropathic pain.
Status:
Investigational
Source:
NCT00666081: Phase 1 Interventional Withdrawn Cancer
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
GSK690693 is an aminofurazan derivative, a novel ATP-competitive, low-nanomolar pan-Akt kinase inhibitor. It is selective for the Akt isoforms versus the majority of kinases in other families; however, it does inhibit additional members of the AGC kinase family. GlaxoSmithKline was developing this compound for the treatment of lymphoma solid tumours but the clinical development of this compound was terminated due to the associated side-effect of transient hyperglycemia.
Status:
Investigational
Source:
NCT01648010: Not Applicable Interventional Completed Carcinoma of Urinary Bladder, Invasive
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02400255: Phase 2 Interventional Completed Acute Myeloid Leukemia
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Crenolanib is an orally active, highly selective, small molecule, next generation inhibitor of platelet-derived growth factor receptor (PDGFR) tyrosine kinase. Crenolanib, manufactured by Arog Pharmaceuticals in Dallas, is taken orally with chemotherapy. The compound is currently being evaluated for safety and efficacy in clinical trials for various types of cancer, including acute myeloid leukemia (AML), gastrointestinal stromal tumor (GIST), and glioma. Crenolanib is an orally bioavailable, selective small molecule inhibitor of type III tyrosine kinases with nanomolar potencies against platelet-derived growth factor receptors (PDGFR) (isoforms PDGFRα and PDGFRβ) and Fms-related tyrosine kinase 3 (FLT3). Besides PDGFR and FLT3, crenolanib does not inhibit any other known receptor tyrosine kinase (RTK) (e.g. VEGFR and FGFR) or any other serine/threonine kinase (e.g., Abl, Raf) at clinically achievable concentrations. Preclinical trials have shown Crenolanib to be active in inhibiting both wild-type and mutant FLT3. Crenolanib is cytotoxic to the FLT3/ITD-expressing leukemia cell lines Molm14 and MV411, with IC50s of 7 nM and 8 nM, respectively. In immunoblots, crenolanib inhibited phosphorylation of both the wild-type FLT3 receptor (in SEMK2 cells) and the FLT3/ITD receptor (in Molm14 cells) in culture medium with IC50s of 1-3 nM. Importantly, the IC50 of crenolanib against the D835Y mutated form of FLT3 was 8.8 nM in culture medium. Furthermore, crenolanib had cytotoxic activity against primary samples that were obtained from patients who had developed D835 mutations while receiving FLT3 TKIs. In vitro, the IC50 of crenolanib for inhibition of FLT3/ITD in plasma was found to be 34 nM, indicating a relatively low degree of plasma protein binding. From pharmacokinetic studies of crenolanib in solid tumor patients, steady state trough plasma levels of roughly 500 nM were found to be safe and tolerable, suggesting that crenolanib could potentially inhibit the target in vivo. Crenolanib has no significant activity against c-KIT, which may be an advantage in that myelosuppression can be avoided.1Furthermore, there was no evidence of QTc prolongation in patients treated with crenolanib. In summary, crenolanib offers a number of advantages over other FLT3 TKIs. Clinical trials of crenolanib in AML patients with FLT3 activating mutations are being planned.
Status:
Investigational
Source:
NCT00354042: Phase 1 Interventional Completed Asthma
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
