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Restrict the search for
vitamin a palmitate
to a specific field?
Status:
Investigational
Source:
NCT04053803: Phase 2 Interventional Active, not recruiting Sickle Cell Disease
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01314885: Phase 1 Interventional Completed Chronic Obstructive Pulmonary Disease (COPD)
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
PF-03715455 is a potent p38 inhibitor, showing some selectivity for p38-alpha over p38-beta. PF-03715455 inhibited IL-6, MCP-1, MIP1β, CC16 and CRP levels in plasma of healthy subjects. PF-03715455 was optimized for delivery by inhalation. PF-03715455 substantially reduced tobacco-smoke--induced lung neutrophilia and inflammatory damage to the lungs. PF-03715455 had been in phase II clinical trial for the treatment of asthma and phase I clinical trial for the treatment of chronic obstructive pulmonary disease. However, these investigations were discontinued.
Status:
Investigational
Source:
NCT04141670: Phase 1 Interventional Completed RYR-1 Myopathy
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03903211: Phase 2 Interventional Completed Cognitively Normal
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03711162: Phase 3 Interventional Terminated Idiopathic Pulmonary Fibrosis
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT00519662: Phase 1 Interventional Completed Advanced Solid Tumors
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
SNS 314 is a selective small molecule inhibitor of Aurora kinases A, B and C. The compound was being developed by Sunesis Pharmaceuticals for the treatment of cancer. Proliferating cells treated with SNS-314 bypass the mitotic spindle checkpoint and fail to undergo cytokinesis, leading to multiple rounds of endoreduplication and eventually cell death. SNS-314 inhibits tumor growth in a variety of preclinical models, and it was being tested in single agent Phase 1 studies in patients with advanced solid tumours.
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:
NCT00557193: Phase 3 Interventional Completed Acute Lymphoblastic Leukemia
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Lestaurtinib (CEP-701, KT-5555) is an orally bio-available polyaromatic indolocarbazole
alkaloid derived from K-252a. Lestaurtinib is a multi-targeted tyrosine kinase inhibitor which has been shown to potently inhibit FLT3 at nanomolar concentrations in preclinical studies, leading to its rapid development as a potential targeted agent for treatment of AML. Phase I studies have shown lestaturtinib to be an active agent particularly when used in combination with cytotoxic drugs. Currently, Phase II and Phase III studies are underway aiming to establish the future of this agent as a treatment option for patients with FLT3-ITD AML.
Status:
Investigational
Source:
NCT03025308: Phase 3 Interventional Active, not recruiting Rheumatoid Arthritis
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Filgotinib (GLPG0634) is a highly selective JAK1 inhibitor. GLPG0634 is a promising drug candidate for the future treatment of autoimmune and inflammatory disorders. It is in phase III clinical trials (initiated mid-2016) for the treatment of rheumatoid arthritis, Crohn's disease and ulcerative colitis. Most common adverse events observed were infections, gastrointestinal disorders and nervous system disorders.
Status:
Investigational
Source:
NCT01830985: Phase 2/Phase 3 Interventional Completed Rheumatoid Arthritis
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Decernotinib is an oral JAK3 kinase inhibitor developed by Vertex for the treatment of rheumatoid arthritis. Although the drug demonstrated a good potency in vitro and in phases I and II of clinical trials, its development was terminated.
