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Restrict the search for
m nalidixic acid
to a specific field?
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.
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
NCT04629443: Phase 1/Phase 2 Interventional Completed Acute Myeloid Leukaemia
(2021)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT00784290: Phase 1/Phase 2 Interventional Completed Hepatocellular Carcinoma
(2003)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Orantinib (SU-6668) is an orally bioavailable receptor tyrosine kinase inhibitor. Orantinib binds to and inhibits the autophosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), thereby inhibiting angiogenesis and cell proliferation. Orantinib also inhibits the phosphorylation of the stem cell factor receptor tyrosine kinase c-kit, often expressed in acute myelogenous leukemia cells. Orantinib was in phase II clinical trials for the treatment of breast cancer. It was also in phase III clinical trials for the treatment of hepatocellular carcinoma. However, this research was terminated in 2014. The compound was originally developed by Sugen (subsidiary of Pfizer). In 1998, a co-development agreement took place between Sugen and Taiho for the compound.
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:
NCT04229394: Phase 1 Interventional Completed Osteoarthritis (OA) of the Knee
(2018)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Investigational
Source:
NCT02173457: Phase 3 Interventional Completed Type 2 Diabetes
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT00626626: Phase 1/Phase 2 Interventional Terminated Leukemia
(2007)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02483182: Phase 2 Interventional Completed Herpes Labialis
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
SIS Shulov Innovative Science is developing ZEP 3, a short synthetic peptide. This drug was studied in phase II clinical trial for the treatment of cold sores (Herpes labialis). In addition, was shown that ZEP-3 exhibited analgesic activity in various indications such as osteoarthritis, herpes labialis and ocular pain. In parallel, the company is planning a phase II clinical study in atopic dermatitis.
Status:
Investigational
Source:
NCT01760525: Phase 1 Interventional Completed Solid Tumor With p53 Wild Type Status
(2013)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
CGM-097, a novel, highly optimized, and selective inhibitor of the p53-Mdm2 interaction. CGM-097 binds to human Mdm2 protein with a Ki value of 1.3 nM, activates p53 in human cells and induces robust p53-dependent cell cycle arrest and apoptosis in human p53 wild-type tumor cells. Its activity and selectivity has been tested and confirmed across a large panel of cancer cell lines from the Cancer Cell Line Encyclopedia. CGM-097 displays desirable pharmacokinetic and pharmacodynamic profiles in animals together with excellent oral bioavailability, which triggers rapid and sustained activation of p53-dependent pharmacodynamic biomarkers resulting in tumor regression in multiple xenografted models of p53 wild-type human cancer. The validation and understanding of its mechanism of action, the overall favorable drug-like properties and the characterization of its on-target toxicological profile in preclinical species strongly supported the initiation of Phase I clinical trials with CGM-097 in pre-selected patients with p53 wild-type tumors.
