貨號(hào)	規(guī)格	價(jià)格	上海	北京	武漢	南京
S80831-5mg	99.6%	￥120.00 S80831-5mg ￥120.00 現(xiàn)貨	8 8	-	-	-
S80831-10mg	99.6%	￥180.00 S80831-10mg ￥180.00 現(xiàn)貨	5 5	-	-	-
S80831-25mg	99.6%	￥350.00 S80831-25mg ￥350.00 現(xiàn)貨	6 6	-	-	-
S80831-50mg	99.6%	￥610.00 S80831-50mg ￥610.00 現(xiàn)貨	5 5	-	-	-
S80831-100mg	≥98%	￥1030.00 S80831-100mg ￥1030.00 2-3天	0 貨期：2-3天	-	-	-

產(chǎn)品介紹

Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM.

產(chǎn)品描述：

Binimetinib (MEK162) is an oral and selective MEK1/2 inhibitor. Binimetinib (MEK162) inhibits MEK with an IC50 of 12 nM.

靶點(diǎn)：

MEK:12 nM (IC50);Autophagy ;MEK;Autophagy

體內(nèi)研究：

Treatment with Binimetinib (ARRY-438162) reduces disease severity in a dose-related manner in both animal models. ARRY-438162 in the CIA model inhibits increases in ankle diameter by 27% and 50% at 1 and 3 mg/kg, while Ibuprofen has 46% inhibition. When combined with Ibuprofen, these same two doses result in 74% and 72% inhibition, respectively. Microscopic examination of the ankle joints show Binimetinib (ARRY-438162) significantly inhibits lesions (inflammation, cartilage damage, pannus formation and bone resorption) by 32% and 60% at 1 and 3 mg/kg, while treatment with Ibuprofen alone results in 17% inhibition, which is not significantly different from the controls. When these two doses of Binimetinib (ARRY-438162) are combined with ibuprofen, the result is 54% and 77% inhibition of joint destruction. In AIA, 3 and 10 mg/kg of Binimetinib (ARRY-438162) inhibit AIA ankle diameter 11% and 34%, while MTX has 33% inhibition. When combined with MTX, 3 and 10 mg/kg of Binimetinib (ARRY-438162) result in 55% and 71% inhibition. Microscopic examination of ankle joints for inflammation and bone resorption also shows improved efficacy versus either compound alone. When Binimetinib (MEK162) is combined with BEZ235, a significant reduction of tumor growth is observed (P=0.01). This increase in antitumor activity is accompanied by a decrease in phospho-ERK and phospho-S6 staining. No significant changes are observed in phospho-4EBP1 staining, a direct target of mTOR activity

參考文獻(xiàn)：

1. J Pheneger, et al. 2006, ACR Annual Scientific Meeting. Abst 794. 2. Serra V, et al. RSK3/4 mediate resistance to PI3K pathway inhibitors in breast cancer. J Clin Invest, 2013, 123(6), 2551-2563. 3. Kiessling MK, et al. Mutant HRAS as novel target for MEK and mTOR inhibitors. Oncotarget. 2015 Dec 8;6(39):42183-96. 4. Cheng H, et al. PIK3CA(H1047R)- and Her2-initiated mammary tumors escape PI3K dependency by compensatory activation of MEK-ERK signaling. Oncogene. 2016 Jun 9;35(23):2961-70. 5. Seip K, et al. Fibroblast-induced switching to the mesenchymal-like phenotype and PI3K/mTOR signaling protects melanoma cells from BRAF inhibitors. Oncotarget. 2016 Apr 12;7(15):19997-20015.

溶解性：

DMSO : 50 mg/mL (113.32 mM; Need ultrasonic)

保存條件：

-20℃

配置溶液濃度參考：

	1mg	5mg	10mg
1 mM	2.266 ml	11.332 ml	22.664 ml
5 mM	0.453 ml	2.266 ml	4.533 ml
10 mM	0.227 ml	1.133 ml	2.266 ml
50 mM	0.045 ml	0.227 ml	0.453 ml

注意：

部分產(chǎn)品我司僅能提供部分信息，我司不保證所提供信息的權(quán)威性，僅供客戶參考交流研究之用。

參考文獻(xiàn)

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MEK162 (ARRY-162, ARRY-438162)