Vascular Endothelial Growth Factor Receptor (VEGFR)

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PZ0264 CP-547632 hydrochloride ≥98% (HPLC) CP-547632 hydrochloride is a well-tolerated, orally-bioavailable ATP-competitive kinase inhibitor. It is currently in clinical trials for the treatment of human malignancies.
CP-547632 is a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC50 = 11 and 9 nM, respectively). The compound CP-547632 inhibits VEGF and basic FGF-induced angiogenesis in animal models, and inhibits growth of xenograft tumors in mice.
SML0509 JK-P3 ≥98% (HPLC) JK-P3 is a VEGFR-2 inhibitor.
JK-P3 is a pyrazole-based inhibitor of VEGFR-2 (IC50 = 7.8 μM). JK-P3 inhibits FGFR 1/3 kinase activity in vitro, but has no effect on FGFR signaling in cell-based assays. The compound blocks wound healing and tube formation in HUVEC without effecting endothelial cell proliferation.
SML0957 KRN633 ≥98% (HPLC) KRN633 is a cell-permeable; reversible and ATP-competitive inhibitor of vascular endothelial growth factor receptor tyrosine kinase (VEGFR) with IC50 values of 170, 160, and 125 nM for VEGFR-1, -2, -3, respectively. Krn633 inhibits PDGFR-α and c-Kit only at higher concentrations (IC50 = 0.97 and 4.33 μM, respectively) and is inactive towards a panel of 17 other kinases (IC50 >/= 10 μM).
SML1693 Pz-1 ≥98% (HPLC) Pz-1 is a cell-permeable, non-cytotoxic (up to 0.1 μM and 6 days; NIH/3T3 cells), and highly potent type II kinase inhibitor that potently inhibits RET and VEGFR2 tyrosine kinase activity (IC50 <1 nM; [ATP] = 190 μM) by targeting the kinases in their inactive DFG-out conformation, displaying significant affinity (Kd <50 nM) toward only TRKB, TRKC, GKA, FYN, SRC, TAK1, MUSK from a panel of 96 other kinases. Pz-1 inhibits cellular RET mutants (C634R, C634Y, V804L, V804M, M918T) and VEGFR2 phosphorylations, and selectively inhibits the growth of RET C634Y- than HRas G12V-transformed NIH/3T3 cultures (IC50 = 0.5 vs. 34.4 nM). Likewise, Pz-1 completely abrogated tumor formation from RET C634Y-transformed NIH/3T3 cells in mice in vivo (1 mg/kg/d, p.o.), while only up to 70% tumor suppression of HRas G12V-transformed cells was achieved with 10 mg/kg daily oral dosage.
SML0858 SC-1 ≥98% (HPLC) SC-1 is a derivative of the multiple tyrosine kinase inhibitor sorafenib with no kinase-inhibition activity. SC-1 blocks STAT3 phosphorylation and activation with similar potency to sorafenib, and induces apoptosis in hepatocellular carcinoma cell lines.
S1195 ST638 ≥98% (HPLC), solid Protein tyrosine kinase inhibitor (IC50 = 370 nM). Also inhibits HGF-induced MAP kinase activation in hepatocytes and inhibits phospholipase D activity in human neutrophils.
S8442 SU 5416 ≥98% (HPLC) SU 516 inhibits the activity of neuronal nitric oxide synthase and protects the neuronal cells from nitric oxide-mediated neurotoxicity.1 It also acts an agonist of aryl hydrocarbon receptor and is an effective clinical agent for treating autoimmune diseases and transplant rejection.2
SU 5416 is a vascular endothelial growth factor (VEGF) receptor protein tyrosine kinase 1/2 inhibitor.
PZ0012 Sunitinib malate ≥98% (HPLC) Sunitinib has greater bioavailability and potency compared to other inhibitors. It prevents angiogenesis.
Sunitinib malate is a receptor tyrosine kinase inhibitor, which targets VEGF-R1, VEGF-R2, VEGF-R3, PDGF-Rα, PDGF-Rβ, KIT, FLT3, CSF-1R, and RET. Sunitinib malate is an anticancer drug.
SML1691 ZM323881 hydrochloride ≥98% (HPLC) ZM323881 is a selective inhibitor of VEGFR-2 with an IC50 value of 2 nM. ZM323881 is selective for VEGFR-2 over VEGFR-1 and other receptor tyrosine kinases including PDGFRβ, FGFR1, EGFR and erbB2. ZM323881 inhibited VEGF-A-induced endothelial cell proliferation with an IC50 value of 8 nM.
ZM323881 is also known as (5‐{[7‐(benzyloxy) quinazolin‐4‐yl]amino}‐4‐fluoro‐2‐methylphenol). It is capable of blocking the efflux function and altering breast cancer resistant protein (BCRP)-related multidrug resistance (MDR).