ZM323881|2mg|K1289-上海高创化学科技有限公司

ZM323881

报价：¥1100

供货周期：

7天

品牌：

型号：

2mg

货号：

K1289

CAS号：

193000-39-4

SKU:K1289		M. Wt:411.86
Formula:C22H18FN3O2.HCl		Solubility:DMSO 10 mg/mL, Water <1 mg/mL, Ethanol <1 mg/mL
Purity:99%		Storage:2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
CAS No.:193000-39-4		Synonyms:N/A
Chemical Name4-fluoro-2-methyl-5-[(7-phenylmethoxyquinazolin-4-yl)amino]phenol

Description	ZM323881 inhibits VEGF-A-induced endothelial cell proliferation with IC50 of 8 nM.
Targets	VEGFR2
IC50	2 nM
In vitro	ZM323881 inhibits VEGF-A-induced endothelial cell proliferation with IC50 of 8 nM and VEGF-R2 tyrosine phosphorylation in vitro. VEGF-A-mediated increases in vascular permeability in perfused mesenteric microvessels in vivo can be reversibly abolished by ZM323881. ZM323881 inhibits activation of VEGFR-2, but not of VEGFR-1, epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), or hepatocyte growth factor (HGF) receptor. SCC-9 cells express the VEGF receptors Flk-1 and neuropilin-1 (Np-1), with VEGF treatment increasing VEGF promoter activity and VEGF secretion that was attenuated by the Flk-1 tyrosine kinase inhibitor, ZM 323881. VEGF significantly increases VEGF promoter activity. Treatment of cells with the ﬂk-1 tyrosine kinase inhibitor ZM323881 completely blocks this effect. VEGF can stimulate Hif-1alpha protein accumulation was blocked by treatment with ZM323881. The effects of ZM 323881 were speciﬁc based on its lack of effect on IGF-1 stimulated Hif-1alpha accumulation. ZM 323881 treatment alone reduces the basal expression of Hif-1alpha, consistent with the presence of a VEGF: VEGFR-2 autocrine loop in quiescent SCC-9 cells.
In vivo	N/A.
Clinical Trials	N/A
Features	N/A

Description

ZM323881 inhibits VEGF-A-induced endothelial cell proliferation with IC50 of 8 nM.

Targets

VEGFR2

IC50

2 nM

In vitro

ZM323881 inhibits VEGF-A-induced endothelial cell proliferation with IC50 of 8 nM and VEGF-R2 tyrosine phosphorylation in vitro. VEGF-A-mediated increases in vascular permeability in perfused mesenteric microvessels in vivo can be reversibly abolished by ZM323881. ZM323881 inhibits activation of VEGFR-2, but not of VEGFR-1, epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), or hepatocyte growth factor (HGF) receptor. SCC-9 cells express the VEGF receptors Flk-1 and neuropilin-1 (Np-1), with VEGF treatment increasing VEGF promoter activity and VEGF secretion that was attenuated by the Flk-1 tyrosine kinase inhibitor, ZM 323881. VEGF significantly increases VEGF promoter activity. Treatment of cells with the ﬂk-1 tyrosine kinase inhibitor ZM323881 completely blocks this effect. VEGF can stimulate Hif-1alpha protein accumulation was blocked by treatment with ZM323881. The effects of ZM 323881 were speciﬁc based on its lack of effect on IGF-1 stimulated Hif-1alpha accumulation. ZM 323881 treatment alone reduces the basal expression of Hif-1alpha, consistent with the presence of a VEGF: VEGFR-2 autocrine loop in quiescent SCC-9 cells.

In vivo

N/A.

Clinical Trials

N/A

Features

N/A