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Restrict the search for
tyrosine
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Status:
Investigational
Source:
NCT02349633: Phase 1/Phase 2 Interventional Terminated Non-Small Cell Lung Cancer
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
PF-06747775 is an irreversible pyrrolopyrimidine inhibitor of epidermal growth factor receptor (EGFR) T790M mutants which provides potent EGFR activity against the four common mutants (exon 19 deletion (Del), L858R, and double mutants T790M/L858R and T790M/Del), selectivity over wild-type EGFR, and desirable ADME properties. The third-generation class of EGFR tyrosine kinase inhibitors PF-06747775 is a clinical candidate drug for treatment of non-small-cell lung cancer (NSCLC) driven by mutant EGFR.
Status:
Investigational
Source:
NCT00427349: Phase 2 Interventional Completed Gastrointestinal Carcinoid Tumor
(2008)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Motesanib (AMG 706), a novel nicotinamide, was identified as a potent, orally bioavailable inhibitor of the VEGFR1/Flt1, VEGFR2/kinase domain receptor/Flk-1, VEGFR3/Flt4 and Kit receptors. Motesanib was expected to reduce vascular permeability and blood flow in human tumours. A phase III trial of motesanib in combination with paclitaxel and carboplatin in non-squamous NSCLC has been terminated by Takeda and subsequently the development was discontinued. Motesanib has also been investigated up to phase II in breast, thyroid, colorectal and gastrointestinal stromal tumours. However, development has been discontinued in these indications.
Status:
Investigational
Source:
NCT02442414: Phase 1 Interventional Completed Advanced Solid Tumors
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT02335814: Phase 1 Interventional Terminated Acute Myeloid Leukemia
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
AMG-925, a dual FLT3/CDK4 inhibitor, has been developed to overcome resistance to FLT3 inhibitors, which is a serious clinical issue in treating acute myelogenous leukemia (AML). AMG-925 inhibits FLT3, including many FLT3 mutants reported to date. AMG-925 inhibits the proliferation of a panel of human tumor cell lines including Colo205 (Rb(+)) and U937 (FLT3(WT)) and induced cell death in MOLM13 (FLT3(ITD)) and even in MOLM13 (FLT3(ITD, D835Y)), which exhibits resistance to a number of FLT3 inhibitors currently under clinical development. At well-tolerated doses, AMG-925 leads to significant growth inhibition of MOLM13 xenografts in nude mice, and the activity correlates with inhibition of STAT5 and Rb phosphorylation. AMG-925 is in Phase I clinical trials for the treatment of Acute myeloid leukaemia.
Status:
Investigational
Source:
NCT03091192: Phase 3 Interventional Active, not recruiting Carcinoma
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Savolitinib (AZD6094, HMPL-504) has been demonstrated to inhibit the growth of tumors in a series of preclinical disease models, selectively for those tumors with aberrant c-Met signaling. Phase I dose escalation studies were initiated in Australia and China in 2012 and 2013 respectively. Savolitinib has demonstrated good safety and tolerability and favorable pharmacokinetic properties in late stage cancer patients, and has shown encouraging anti-tumor activity in several tumor-types, in particular for metastatic Papillary Renal Cell Cancer (PRCC). Phase II, study designed to evaluate the efficacy and safety of savolitinib in patients with locally advanced or metastatic PRCC. Approximately 20 centers in the United States, Canada, and Europe will participate in the study. The primary objective of this study is to assess the anti-tumor activity in patients with PRCC as measured by overall response rate according to Response Evaluation Criteria in Solid Tumours (“RECIST”). The secondary objectives for this study are to: assess the progression free survival and duration of response in patients with PRCC according to RECIST; assess the safety and tolerability in the treatment of patients with PRCC; characterize the pharmacokinetics and pharmacodynamics of savolitinib and metabolites following administration to steady state after multiple dosing when given orally.
Status:
Investigational
Source:
NCT02589821: Phase 3 Interventional Completed Neuroendocrine Tumors
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Sulfatinib (previously known as HMPL-012) was developed as a small-molecule inhibitor targeting vascular endothelial growth factor receptors 1 and 3, fibroblast growth factor receptor 1 and colony-stimulating factor 1 receptor with potential antineoplastic and anti-angiogenic activities. Sulfatinib has shown encouraging antitumor activity and manageable toxicities in patients with advanced neuroendocrine tumors (NET). The drug is participating in two ongoing phases III studies, validating the efficacy of surufatinib in patients with NETs. In addition, in November 2018, Hutchison MediPharma completed a phase II trial of sulfatinib, for the treatment of patients with biliary tract cancer. This drug is also participating in the phase II trial that is currently in recruiting status in treating advanced medullary thyroid carcinoma.
Status:
Investigational
Source:
NCT04488081: Phase 2 Interventional Recruiting COVID-19
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT04416516: Phase 2 Interventional Completed Basal Cell Carcinoma
(2020)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03908242: Phase 1 Interventional Unknown status Diabetes
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT04586023: Phase 3 Interventional Active, not recruiting Relapsing Multiple Sclerosis
(2021)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
G-0853 (also GDC-0853, or Fenebrutinib) is a potent, selective, orally administered, and noncovalent Bruton's tyrosine kinase (Btk) inhibitor currently in clinical development. Upon administration, G-0853 inhibits the activity of Btk and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and Btk-mediated activation of downstream survival pathways, which leads to the inhibition of the growth of malignant B-cells that overexpress BTK. BTK is overexpressed in B-cell malignancies, and plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival. G-0853 suppresses B cell- and myeloid cell-mediated components of disease and demonstrates dose-dependent activity in an in vivo rat model of inflammatory arthritis. G-0853 demonstrates highly favorable safety, pharmacokinetic (PK), and pharmacodynamic (PD) profiles in preclinical and Phase 2 studies ongoing in patients with rheumatoid arthritis, lupus, and chronic spontaneous urticaria.
