KRN 633|2mg|K1383-上海高创化学科技有限公司

KRN 633

参考价：¥1298

供货周期：

一周

品牌：

规格：

2mg

货号：

K1383

CAS号：

286370-15-8

SKU:K1383		M. Wt:416.86
Formula:C20H21ClN4O4		Solubility:No
Purity:>99%		Storage:2 years at -20 degrees centigrade
CAS No.:286370-15-8		Synonyms:N/A
Chemical NameN/A

Description	KRN 633
Targets	VEGFR-2
IC50	1.16 nM
In vitro	KRN633 can inhibit tyrosine phosphorylation of VEGFR-2 with IC50 of 1.16 nM in human umbilical vein endothelial cells.KRN633 is highly selective for VEGFR-1, VEGFR-2, and VEGFR-3. KRN633 also can block the activation of mitogen-activated protein kinases by VEGF, along with human umbilical vein endothelial cell proliferation and tube formation. The propagation of various cancer cell lines in vitro was not inhibited by KRN633.[1] KRN633 also shows suppression on HIF-1alpha accumulation under the hypoxic condition. The VEGFR tyrosine kinase inhibitors, KRN633, possess dual functions:inhibition of VEGFR signaling and HIF-1alpha expression under the hypoxic condition. KRN633 suppresses HIF-1alpha expression through inhibition of both Akt and ERK phosphorylation signaling pathways.[2] Administration of KRN633 can decreases the alkaline phosphatase (ALP) activity during the osteoblastic differentiation of cultured human periosteal-derived cells.[3]
In vivo	P.o. administration of KRN633 inhibits tumor growth in several in vivo tumor xenograft models with diverse tissue origins, including lung, colon, and prostate, in athymic mice and rats. KRN633 also causes the regression of some well-established tumors and those that has regrown after the cessation of treatment. In these models, the trough serum concentration of KRN633 has a more significant effect than the maximum serum concentration on antitumor activity. Tumor xenografts treated with KRN633 shows a reduction in the number of endothelial cells in non-necrotic areas and a decrease in vascular permeability. KRN633 is well tolerated and had no significant effects on body weight or the general health of the animals. [1]Pregnant mice daily treated with the VEGF receptor-2 (VEGFR-2) tyrosine kinase inhibitor KRN633 (300 mg/kg, p.o.) suppresses vascular growth of both the placenta and fetus without obvious health impairments of mother mice and increases the risk of induction of intrauterine growth restriction.[3]
Clinical Trials	N/A
Features	N/A

Description

KRN 633

Targets

VEGFR-2

IC50

1.16 nM

In vitro

KRN633 can inhibit tyrosine phosphorylation of VEGFR-2 with IC50 of 1.16 nM in human umbilical vein endothelial cells.KRN633 is highly selective for VEGFR-1, VEGFR-2, and VEGFR-3. KRN633 also can block the activation of mitogen-activated protein kinases by VEGF, along with human umbilical vein endothelial cell proliferation and tube formation. The propagation of various cancer cell lines in vitro was not inhibited by KRN633.[1] KRN633 also shows suppression on HIF-1alpha accumulation under the hypoxic condition. The VEGFR tyrosine kinase inhibitors, KRN633, possess dual functions:inhibition of VEGFR signaling and HIF-1alpha expression under the hypoxic condition. KRN633 suppresses HIF-1alpha expression through inhibition of both Akt and ERK phosphorylation signaling pathways.[2] Administration of KRN633 can decreases the alkaline phosphatase (ALP) activity during the osteoblastic differentiation of cultured human periosteal-derived cells.[3]

In vivo

P.o. administration of KRN633 inhibits tumor growth in several in vivo tumor xenograft models with diverse tissue origins, including lung, colon, and prostate, in athymic mice and rats. KRN633 also causes the regression of some well-established tumors and those that has regrown after the cessation of treatment. In these models, the trough serum concentration of KRN633 has a more significant effect than the maximum serum concentration on antitumor activity. Tumor xenografts treated with KRN633 shows a reduction in the number of endothelial cells in non-necrotic areas and a decrease in vascular permeability. KRN633 is well tolerated and had no significant effects on body weight or the general health of the animals. [1]Pregnant mice daily treated with the VEGF receptor-2 (VEGFR-2) tyrosine kinase inhibitor KRN633 (300 mg/kg, p.o.) suppresses vascular growth of both the placenta and fetus without obvious health impairments of mother mice and increases the risk of induction of intrauterine growth restriction.[3]

Clinical Trials

N/A

Features

N/A