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Restrict the search for
tyrosine
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Status:
Investigational
Source:
NCT03037645: Phase 1/Phase 2 Interventional Terminated Chronic Lymphocytic Leukemia
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
Investigational
Source:
NCT03564288: Phase 1 Interventional Completed Acute Myeloid Leukemia
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
G749 is a Fms-like tyrosine receptor kinase 3 (FLT3) inhibitor and a promising next-generation drug candidate for the treatment of relapsed and refractory acute myeloid leukemia (AML) patients with various FLT3-ITD/FLT3-TKD mutants that shows the ability to overcome drug resistance. It demonstrated potent and sustained inhibition of the FLT3 wild type and mutants including FLT3-ITD, FLT3-D835Y, FLT3-ITD/N676D, and FLT3-ITD/F691L in cellular assays. G749 retained its inhibitory potency in various drug-resistance milieus such as patient plasma, FLT3 ligand surge, and stromal protection. It also displayed potent antileukemic activity in bone marrow blasts from AML patients regardless of FLT3 mutation status, including those with little or only minor responses to AC220 or PKC412. Oral administration of G749 yielded complete tumor regression and increased life span in animal models.
Status:
Investigational
Source:
NCT01168882: Phase 1 Interventional Withdrawn Hematological Malignancies
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
RGB-286638 is a multi-targeted protein kinase inhibitor currently in Phase 1 clinical testing. In vitro cell-free kinase assays indicated that RGB-286638 inhibits CDK1, 2, 3, 4, 5, and 9 and is less active against CDK6 and 7. The RGB-286638 compound has been shown to inhibit the processes controlling cell division in cancer cells by targeting multiple cyclin-dependent kinase proteins involved in regulating the cell cycle. RGB-286638 has also been shown to induce apoptosis (programmed cell death) and to inhibit other important protein kinases involved in the proliferation of cancer cells. RGB-286638 treatment results in tumor regression and increased survival in a number of pre-clinical models of solid and hematological tumors.
Status:
Investigational
Source:
NCT00096239: Phase 2 Interventional Completed Fallopian Tube Cancer
(2004)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Pfizer's CP-547632 is a selective inhibitor of VEGFR-2 tyrosine kinase that was discovered during Pfizer's collaboration with OSI Pharmaceuticals. CP-547632, was identified as a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC(50) = 11 and 9 nM, respectively). It is selective relative to epidermal growth factor receptor, platelet-derived growth factor beta, and other related TKs. It also inhibits VEGF-stimulated autophosphorylation of VEGFR-2 in a whole cell assay with an IC(50) value of 6 nM. After oral administration of CP-547632 to mice bearing NIH3T3/H-ras tumors, VEGFR-2 phosphorylation in tumors was inhibited in a dose-dependent fashion (EC(50) = 590 ng/ml). CP-547,632 is a well-tolerated, orally-bioavailable inhibitor presently under clinical investigation for the treatment of human malignancies. CP-547632 is in phase I for the treatment of diabetic retinopathy and age-related macular degeneration.
Status:
Investigational
Source:
NCT02040623: Phase 2 Interventional Completed Chronic Graft-versus-host Disease
(2014)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Investigational
Source:
NCT03230318: Phase 2 Interventional Completed Intrahepatic Cholangiocarcinoma
(2017)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Derazantinib (ARQ 087) is an investigational, oral, multi-kinase inhibitor designed to preferentially inhibit the FGFR family of kinases with demonstrated activity in FGFR2 genetic alterations, including fusions. In human cancers, FGFRs have been found to be dysregulated by multiple mechanisms, including aberrant expression, mutations, chromosomal rearrangements, and amplifications. FGFR dysregulation has been identified as a driver in a number of cancers, including iCCA, cholangiocarcinoma, bladder, endometrial, breast, gastric, lung and ovarian. Current scientific literature suggests FGFR alterations exist in anywhere from 5% to 40% of these cancers. Derazantinib is a potent FGFR inhibitor that shows strong anti-proliferative activity in cell lines harboring FGFR2 alterations. In clinical testing, the molecule has demonstrated activity in cancerous tumors harboring FGFR2 fusions in iCCA and bladder cancers.
Status:
Investigational
Source:
NCT01423851: Phase 1/Phase 2 Interventional Completed Primary Myelofibrosis
(2011)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
NS-018 is a potent inhibitor of Janus kinase 2 (JAK2) enzyme activity and Src-family kinases. It was developed as an oral therapy for the treatment of myelofibrosis. Overall NS-018 has been used in trials studying the treatment of primary myelofibrosis, post-polycythemia vera myelofibrosis, and post-essential thrombocythemia. NS-018 is a highly active JAK2 inhibitor, with an IC50 of 0.72 nM, 46-, 54-, and 31-fold selectivity for JAK2 over JAK1 (IC50, 33 nM), JAK3 (IC50, 39 nM), and Tyk2 (IC50, 22 nM). NS-018 also inhibits Src-family kinases, especially SRC and FYN, and weakly inhibits ABL and FLT3 with 45- and 90-fold selectivity for JAK2, respectively. NS-018 shows potent inhibitory activity against cell lines JAK2V617F or MPLW515L mutations or the TEL-JAK2 fusion gene.
Status:
Investigational
Source:
NCT03598699: Phase 2 Interventional Completed Dry Eye
(2018)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Investigational
Source:
NCT02179814: Not Applicable Interventional Suspended Bulimia Nervosa
(2012)
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Racemetirosine is an orally active inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamine. At dosages of 600 to 3500mg daily, it is effective in controlling the hypertensive episodes and symptoms of catecholamine excess in phaeochromocytoma during preparation for surgery. Oral Racemetirosine is well absorbed and absorption appears constant in each individual over a wide dosage range. The drug is largely excreted via the kidneys, but extrarenal elimination has not been studied. Case reports on the clinical use of Racemetirosine in phaeochromocytoma indicate that the drug controls hypertension and symptoms of catecholamine excess in most patients during preparation for surgical removal of a tumor. In some cases, the addition of Racemetirosine to phenoxybenzamine plus propranolol has resulted in adequate control of symptoms previously unresponsive to the adrenergic blocking regimen. Drowsiness and sedation have been the most frequently reported side effects of Racemetirosine treatment.
Status:
Investigational
Source:
NCT03906071: Phase 3 Interventional Active, not recruiting Metastatic Non-Squamous Non-Small Cell Lung Cancer
(2019)
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Sitravatinib (MGCD516) is a receptor tyrosine kinases (RTK) inhibitor that blocks a wide array of RTKs known to be amplified/overexpressed in sarcomas, which are key regulators of signaling pathways that lead to cell growth, survival and tumor progression. It is involved in driving sarcoma cell growth with IC50 of 3980 nM and is superior to other multi-kinase inhibitors in inhibiting cell proliferation, RTK phosphorylation, and phosphorylation of downstream effectors. The efficacy of sitravatinib was tested using a wide panel of sarcoma cell lines, including malignant peripheral nerve sheath tumor (MPNST), Ewing sarcoma (A673), osteosarcoma (Saos2), and liposarcoma (DDLS, LS141). Both in vitro and in vivo efficacy sitravatinib was significantly better that the other two multi-kinase inhibitors, imatinib and crizotinib. Sitravatinib treatment not only inhibits tumor cell proliferation at low nanomolar concentrations in vitro but also results significant tumor growth suppression in vivo in mouse xenograft models. Sitravatinib is being evaluated in a Phase 1b dose expansion cohort in selected patients with specific genetic alterations that are drivers of tumor growth, with an initial focus on Non-Small-Cell Lung carcinoma (NSCLC) and in other solid tumors where sitravatinib may confer a benefit. Its efficacy and safety is also being tested in Phase II clinical trials in patients with advanced liposarcoma as a monotherapy and NSCLC in combination with nivolumab.
