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Vemurafenib (PLX4032, RG7204)BRAF激酶抑制剂

Vemurafenib (PLX4032, RG7204)

产品编号:A3004
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规格 单价 库存 订购数量
10mM (in 1mL DMSO) ¥550.00 现货
10mg ¥500.00 现货
50mg ¥1,200.00 现货
200mg ¥3,000.00 现货
500mg ¥4,400.00 现货
1000mg ¥10,000.00 现货

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Sample solution is provided at 25 µL, 10mM.

引用文献

质量控制

化学结构

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

相关生物数据

PLX4032

Vemurafenib (PLX4032, RG7204) Dilution Calculator

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Vemurafenib (PLX4032, RG7204) Molarity Calculator

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化学性质

CAS号 918504-65-1 SDF Download SDF
别名 Vemurafenib,Zelboraf,PLX-4032,RG7204,RO5185426,
化学名 N-[3-[5-(4-chlorophenyl)-1H-pyrrolo[2,3-b]pyridine-3-carbonyl]-2,4-difluorophenyl]propane-1-sulfonamide
SMILES CCCS(=O)(=O)NC1=C(C(=C(C=C1)F)C(=O)C2=CNC3=NC=C(C=C23)C4=CC=C(C=C4)Cl)F
分子式 C23H18ClF2N3O3S 分子量 489.93
溶解度 ≥24.5mg/mL in DMSO 储存条件 Store at -20°C
物理性状 A solid 运输条件 试用装:蓝冰运输。
其他可选规格:常温运输或根据您的要求用蓝冰运输。
一般建议 为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。

生物活性

描述 Vemurafenib (PLX4032, RG7204)是一种新型有效的B-Raf V600E抑制剂,IC50值为31 nM。
靶点 B-RafV600E C-Raf MAP4K5 (KHS1) SRMS ACK1 FGR
IC50 31 nM 48 nM 51 nM 18 nM 19 nM 63 nM

实验操作

细胞实验:

细胞系

MALME-3M黑色素瘤细胞系

溶解方法

在DMSO中的溶解度>10 mM。为了获得更高的浓度,可以将离心管在37℃加热10分钟和/或在超声波浴中震荡一段时间。原液可以在-20℃以下储存几个月。

反应时间

24 h;10 μM

应用

在黑色素瘤细胞系中,RG7204在表达BRAF V600E而非BRAF WT的细胞中有效抑制细胞增殖。RG7204也有效抑制表达其它密码子600 BRAF突变(V600D、V600 K和V600R)的黑色素瘤细胞的增殖。

动物实验:

动物模型

无胸腺裸鼠

剂量

100 mg/kg;口服给药。

应用

在Colo829肿瘤异种移植小鼠中,RG7204以100 mg/kg的剂量口服给药21天,在肿瘤细胞植入后第38天研究结束时,与对照相比,RG7204极大提高了抗肿瘤活性(P = 0.001)。所有10只RG7204处理的小鼠均出现完全的肿瘤消退,其存活率与对照相比也显著提高(P = 0.0008)。

注意事项

请测试所有化合物在室内的溶解度,实际溶解度和理论值可能略有不同。这是由实验系统的误差引起的,属于正常现象。

References:

[1] Yang H, Higgins B, Kolinsky K, et al. RG7204 (PLX4032), a selective BRAFV600E inhibitor, displays potent antitumor activity in preclinical melanoma models[J]. Cancer research, 2010, 70(13): 5518-5527.

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研究更新

1. Impact of P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) on the brain distribution of a novel BRAF inhibitor: vemurafenib (PLX4032). J Pharmacol Exp Ther. 2012 Jul;342(1):33-40. doi: 10.1124/jpet.112.192195. Epub 2012 Mar 27.
Abstract
Vemurafenib is a BRAF inhibitor that has been approved by FDA for the treatment of metastatic melanoma patients with a BRAF(V600E) mutation. Active efflux by P-gp and BCRP significantly restricted the brain distribution of vemurafenib at the blood-brain barrier, where active efflux by P-gp and BCRP restricted intracellular accumulation of vemurafenib and altered bidirectional net flux of vemurafenib.
2. Vemurafenib (RG67204, PLX4032): a potent, selective BRAF kinase inhibitor. Future Oncol. 2012 May;8(5):509-23. doi: 10.2217/fon.12.31.
Abstract
Vemurafenib is a mutated BRAF kinase inhibitor that showed response rates of >50% in metastatic melanoma patients with BRAF mutation. In a Phase III study, the treatment of vemurafenib in previously untreated patients led to over survival of 84%, response rates of 48% and prolonged progression-free survival with largely reduced risk of death and disease progression.
4. Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutations. J Transl Med. 2011 May 24;9:76. doi: 10.1186/1479-5876-9-76.
Abstract
The combined MAPK oncogene inhibition and metabolic modulation of AMPK is an effective treatment of melanoma cells due to a molecular linkage between the MAPK and the LKB1-AMPK pathways.
5. Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas. J Invest Dermatol. 2013 Aug;133(8):2041-9. doi: 10.1038/jid.2013.32. Epub 2013 Jan 23.
Abstract
Although the treatment of vemurafenib, a Braf inhibitor, in melanoma patients with Braf(V600E) mutations resulted in dramatic improvement with decreased risk of death and tumor progression, melanoma cells rapidly acquire vemurafenib resistance, which can be overcome by targeting Stat3-PAX3 signaling pathway.

产品描述

Vemurafenib是BRAF激酶的抑制剂,它可以抑制突变型BRAF V600E的活性,同时也可以抑制CRAF、ARAF和野生型BRAF激酶的活性。Vemurafenib是一个竞争性的小分子抑制剂,针对丝氨酸-苏氨酸激酶,靶向结合突变型BRAF的ATP结合域。在无BRAF突变的细胞中,Vemurafenib可以增强由RAF同源或异源二聚体对下游MEK的激活,这是由于在BRAF-CRAF异源二聚体和CRAF-CRAF同源二聚体中非药物结合伴侣的反式激活引起的。

参考文献:
Keith.  T Flaherty, Uma Yasothan and Peter Kirkpatrick. Vemurafenib. Nature Reviews Drug Discovery. 2011; 10: 811 – 812.
Jason J.  Luke, F. Stephen Hodi. Vemurafenib and BRAF Inhibition: A New Class of Treatment for Metastatic Melanoma. Clinical Cancer Research. 2012; 18: 9 – 14.