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Restrict the search for
alpha-tocopherol
to a specific field?
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:
NCT04629443: Phase 1/Phase 2 Interventional Completed Acute Myeloid Leukaemia
(2021)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02173457: Phase 3 Interventional Completed Type 2 Diabetes
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02965885: Phase 1 Interventional Completed Advanced Solid Tumors
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
TAS-116 is a highly potent oral HSP90 inhibitor with unique tissue distribution properties. TAS-116 has the potential to demonstrate antitumor activity, while being designed to limit certain adverse events by unique tissue distribution. Phase-II clinical trials in gastrointestinal stromal tumours are ongoing in Japan.
Status:
Investigational
Source:
NCT03593421: Phase 2 Interventional Withdrawn Panel Reactive Antibodies
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02734615: Phase 1 Interventional Terminated Advanced or Metastatic ER+ Breast Cancer
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Status:
Investigational
Source:
NCT04176198: Phase 1/Phase 2 Interventional Recruiting Myelofibrosis
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT01580644: Phase 1 Interventional Completed Healthy
(2012)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
GLPG0187 is a compound that belongs to the class of organic compounds known as naphthyridines, and has been studied as a potential drug in the treatment of solid tumors. GLPG0187 is a broad spectrum integrin receptor antagonist that inhibits αvβ1 integrin. In vitro, this compound was found to diminish the size of the aldehyde dehydrogenase high subpopulation of prostate cancer cells dose-dependently. It also significantly reduced tumor cell migration and cell proliferation. In vivo, it reduced metastatic tumor growth, and inhibited the progression of bone metastases as well as the formation of new bone metastases. Phase I studies have been completed to study safety and drug tolerance of GLPG0187. The drug was well tolerated, but continuous infusion of GLPG0187 did not show signs of monotherapy efficacy.
Status:
Investigational
Source:
NCT00003403: Phase 1 Interventional Completed Unspecified Adult Solid Tumor, Protocol Specific
(1999)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
13-deoxyadriamycin hydrochloride (13-Deoxydoxorubicin hydrochloride, GPX-100) is an anthracycline similar to doxorubicin. GPX-100 is unique among anthracyclines because it is not converted to doxorubicinol during metabolism in the body. This metabolite has been shown to be a major cause of damage to the heart (cardiotoxicity) in laboratory studies. GPX-100 belongs to the class of reactive oxygen species stimulants; RNA synthesis inhibitors and Type II DNA topoisomerase inhibitors. It was in phase II clinical trial for the treatment of cancer.
