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Restrict the search for
dimethyl fumarate
to a specific field?
Status:
Investigational
Source:
NCT01543919: Phase 2 Interventional Completed Pulmonary Disease, Chronic Obstructive
(2012)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
PH-797804 is a diarylpyridinone inhibitor of p38alpha mitogen-activated protein. The drug was developed by Pfizer for the treatment of inflammatory diseases. PH-797804 is being tested in phase II of clinical trials in patients with COPD, osteoarthritis, rheumatoid arthritis and post-herpetic neuralgia.
Status:
Investigational
Source:
NCT04313166: Phase 2 Interventional Completed Amyotrophic Lateral Sclerosis
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02977065: Phase 2 Interventional Completed Dyslipidemias
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT03711162: Phase 3 Interventional Terminated Idiopathic Pulmonary Fibrosis
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02993250: Phase 2 Interventional Completed Hepatitis C, Chronic
(2016)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Odalasvir (previously known as ACH-3102) is a second-generation inhibitor of the nonstructural protein 5A (NS5A) of hepatitis C virus (HCV). It was reported that HCV NS5A is associated with interferon signaling related to HCV replication and hepatocarcinogenesis. HCV NS5A inhibitors efficiently inhibited HCV replication. It is known that HCV is a leading cause of hepatocellular carcinoma (HCC) in Japan and is one of the major causes of end-stage liver disease, HCC, and liver transplantation in the United States and Europe. Odalasvir completed phase II clinical trial, where was evaluated efficacy and safety of its combinations with AL-335, and simeprevir in the treatment of chronic hepatitis C Infection.
Status:
Investigational
Source:
NCT02121301: Phase 2 Interventional Completed Keratoconjunctivitis Sicca
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT01236352: Phase 1/Phase 2 Interventional Terminated Cancer
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
BMS 911543 is a selective orally administered small molecule inhibitor of Janus kinase 2 (JAK2), developed by BristolMyers Squibb for the myelofibrosis treatment. BMS 911543 displayed potent antiproliferative effects in mutated JAK2expressing cell lines. A superior antiproliferative response occurred in primary progenitor cells isolated from patients with JAK2positive myeloproliferative disease (MPD) compared with those isolated from healthy volunteers. In vivo, a single oral dose of BMS 911543 resulted in durable JAK2phosphorylated STAT signalling pathway inhibition in multiple species. In a JAK2expressing xenograft model (SET2), BMS 911543 displayed a minimally effective dose of <2 mg/kg on phosphorylated STAT5 pathway inhibition.
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:
NCT00322517: Phase 2 Interventional Completed Breast Neoplasms
(2006)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
SU-14813 is an oral, multitargeted tyrosine kinase inhibitor (TKI) targeting vascular endothelial growth factor receptors (VEGFR), platelet-derived growth factor receptors (PDGFR), KIT, and fms-like tyrosine kinase 3 (FLT-3). SU-14813 was developed as a next-generation TKI agent following sunitinib (SU-11248) designed to demonstrate optimized pharmacokinetic (PK) and tolerability profiles. SU14813 demonstrated broad and potent antitumor activity equivalent to that of sunitinib, which resulted in tumor regression, growth arrest, growth delay, and prolonged survival in established xenograft cancer models in mice. A phase II trial of SU-14813 in patients with breast cancer was completed. However, according to the Pfizer pipeline development has been discontinued.
Status:
Investigational
Source:
NCT03671564: Phase 1 Interventional Completed Acute Myeloid Leukemia
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
DS-3032 (Milademetan) is an orally available, potent and selective inhibitor of the p53-MDM2 (murine double minute 2) interaction. Milademetan binds to, and prevents the binding of MDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. Milademetan is 10-fold more potent than the first-generation inhibitor nutlin-3a. By preventing this MDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This results in the restoration of p53 signaling and leads to the p53-mediated induction of tumor cell apoptosis. DS-3032 is currently being evaluated in three phase 1 clinical trials for solid and hematological malignancies, including acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML) in blast phase, lymphoma and myelodysplastic syndrome (MDS).
