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Restrict the search for
vitamin a
to a specific field?
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.
Status:
Investigational
Source:
NCT01145989: Phase 2 Interventional Completed Multiple Myeloma
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
AT-9283 was being developed by Astex Pharmaceuticals as a treatment for cancer and myelofibrosis. AT-9283 is an inhibitor of mitosis (cell division) and is the second most progressed drug candidate in the Astex portfolio of novel molecularly targeted cancer drugs. All of Astex’s current products have been discovered internally using its proprietary drug discovery approach. AT9283 is a potent inhibitor of the Aurora A and B kinases and has been shown to arrest tumour growth in a range of tumour models. Aurora kinases play a key role in mitotic checkpoint control in cell division. Both Aurora A and B are over-expressed in many human tumours and are believed to be excellent targets for anti-cancer therapy.
Status:
Investigational
Source:
NCT03585296: Phase 2 Interventional Completed Atopic Dermatitis
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT01167244: Phase 2 Interventional Completed Non-Small-Cell Lung Carcinoma
(2010)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
BMS-690514 is a potent, reversible oral inhibitor of epidermal growth factor receptor (EGFR/HER-1), HER-2 and -4, and vascular endothelial growth factor receptors (VEGFRs)-1 to -3 offering targeted inhibition of tumour growth and vascularisation in a single agent. Bristol-Myers Squibb was developing BMS 690514, as an oral treatment for cancer. BMS-690514 had being in phase II for the treatment of breast cancer; non-small cell lung cancer, but later these studies were discontinued.
Status:
Investigational
Source:
NCT01515358: Phase 1 Interventional Completed Healthy Volunteers
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
LY-3000328 is a Cathepsin S inhibitor with excellent in vitro potency and selectivity against other cysteine proteases. LY-3000328 is currently in clinical trials. Cathepsin S (Cat S) plays an important role in many pathological conditions, including abdominal aortic aneurysm (AAA). Inhibition of Cathepsin S may provide a new treatment for AAA.
