For research use only. Not Intended for Therapeutic Use!
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is a synthetic, orally bioavailable inhibitor of Src kinase and tubulin polymerization, with IC50 of 20 nM for Scr kinase autophosphorylation.
IC50: 20 nM (Scr kinase)
in vitro: KX2-391 has been shown to potently inhibit Src-catalyzed trans-phosphorylation of focal adhesion kinase (FAK), Shc, paxillin, and Src kinase autophosphorylation with an IC50 of approximately 20 nM. It also induces p53 expression and stimulates caspase-3 and PARP cleavage in vitro, leading to tumor cell apoptosis. KX2-391 is potent against a broad range of solid tumor cell types as well as many leukemia subtypes, including those resistant to imatinib and/or dasatinib. It is highly selective without effects on PDGFR, EGFR, JAK1, JAK2, Lck and ZAP70. KX2-391 targets the substrate binding pocket of Src and had more broad spectrum activity and higher potency than dasatinib.
in vovo: KX2-391 demonstrates potent antineoplastic activity across a wide spectrum of tumor cell lines (including several prostate cancer cell lines) and inhibits primary tumor growth as well as metastasis in an orthotopic prostate cancer mouse model.
. /Naing A, et al. A phase I trial of KX2-391, a novel non-ATP competitive substrate-pocket- directed SRC inhibitor, in patients with advanced malignancies. Invest New Drugs.?2013 Aug;31(4):967-73. /
. /Antonarakis ES, et al. A phase 2 study of KX2-391, an oral inhibitor of Src kinase and tubulin polymerization, in men with bone-metastatic castration-resistant prostate cancer. Cancer Chemother Pharmacol.?2013 Apr;71(4):883-92 /