MK-2206 2HCl 别名：MK-2206 dihydrochloride

目录号 M1837

MK-2206是一种高度选择性的Akt1/2/3抑制剂，IC50分别为8 nM/12 nM/65 nM；对250种其他蛋白激酶没有抑制活性。

CAS No.：1032350-13-2

规格	价格	库存状态
Free Sample (0.5-1 mg)	¥ 0	现货
10mM*1mL in DMSO	¥ 756	现货
2mg	¥ 430	现货
5mg	¥ 686	现货
10mg	¥ 980	现货
50mg	¥ 2240	现货

*AbMole所有产品仅供有资质的科研机构或医药企业进行科学研究或药证申报用途，不能被用于人体和任何其它用途。我们不向任何个人或非科研性质的机构提供产品和服务。

客户使用AbMole的MK-2206 2HCl发表的文献

Cell Rep. 2023 Apr 14;42(4):112378.

AKT activity orchestrates marginal zone B cell development in mice and humans

Cell Rep. 2023 Jun 27;42(7):112690.

Identification of XAF1 as an endogenous AKT inhibitor

Front Immunol. 2023 Mar 15;14:1127552.

Giardia duodenalis-induced G0/G1 intestinal epithelial cell cycle arrest and apoptosis involve activation of endoplasmic reticulum stress in vitro

PLoS Pathog. 2022 Sep 6;18(9):e1010808.

White spot syndrome virus directly activates mTORC1 signaling to facilitate its replication via polymeric immunoglobulin receptor-mediated infection in shrimp

Sci Rep. 2022 Jul 6;12(1):11444.

PD-L1 regulates cell proliferation and apoptosis in acute myeloid leukemia by activating PI3K-AKT signaling pathway

Anticancer Res. 2022 Jul;42(7):3325-3340.

PI3K/Akt and Wnt/β-catenin Signaling Cross-regulate NF-κB Signaling in TNF-α-induced Human Lgr5+ Intestinal Stem Cells

Cells. 2021 Feb 18;10(2):430.

Knockdown of AKT3 Activates HER2 and DDR Kinases in Bone-Seeking Breast Cancer Cells, Promotes Metastasis In Vivo and Attenuates the TGFβ/CTGF Axis

BMC Biol. 2021 May 20;19(1):108.

Very long intergenic non-coding (vlinc) RNAs directly regulate multiple genes in cis and trans

Biochem Biophys Res Commun. 2021 Sep 10;569:1-9.

Rapid tumor recurrence in a novel murine GBM surgical model is associated with Akt/PD-L1/vimentin signaling

Anticancer Res. 2021 May;41(5):2257-2275.

Combined Targeting of AKT and mTOR Synergistically Inhibits Formation of Primary Colorectal Carcinoma Tumouroids In Vitro: A 3D Tumour Model for Pre-therapeutic Dгυg Screening

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Cell Biol Int. 2020 Mar 17.

Fluid Shear Stress Induces Runx-2 Expression via Upregulation of PIEZO1 in MC3T3-E1 Cells

Cell. 2019 Mar 7;176(6):1379-1392.e14.

Lateral Inhibition in Cell Specification Mediated by Mechanical Signals Modulating TAZ Activity.

ACS Nano. 2019 Aug 27;13(8):8597-8608.

Gadofullerene Nanoparticles Reverse Dysfunctions of Pancreas and Improve Hepatic Insulin Resistance for Type 2 Diabetes Mellitus Treatment.

Mol Med Rep. 2019 May;19(5):3519-3526.

Overexpression of ribonuclease inhibitor induces autophagy in human colorectal cancer cells via the Akt/mTOR/ULK1 pathway.

Int J Biol Sci. 2018 Oct 3;14(13):1769-1781.

Inhibition of AKT suppresses the initiation and progression of BRCA1-associated mammary tumors.

Am J Pathol. 2017 Jun;187(6):1301-1312.

Tight Junction Proteins Claudin-1 and Occludin Are Important for Cutaneous Wound Healing

Oncotarget. 2016 Feb 22.

Mechanosensitive caveolin-1 activation-induced PI3K/Akt/mTOR signaling pathway promotes breast cancer motility, invadopodia formation and metastasis in vivo.

Biochem Pharmacol. 2015 Aug 15;323-36.

Arctigenin exerts anti-colitis efficacy through inhibiting the differentiation of Th1 and Th17 cells via an mTORC1-dependent pathway.

Cell Signal. 2015 Nov;2191-200.

Discontinuing MEK inhibitors in tumor cells with an acquired resistance increases migration and invasion.

J Cancer. 2015 Sep 16;1195-205.

Vertical Targeting of AKT and mTOR as Well as Dual Targeting of AKT and MEK Signaling Is Synergistic in Hepatocellular Carcinoma.

2015 Apr.

THE MECHANOBIOLOGICAL MECHANISMS OF CAVEOLAE/CAVEOLIN-1 IN LOW SHEAR STRESS-INDUCED BREAST CARCINOMA CELL MIGRATION AND INVASION

Invest New Drugs. 2014 Dec;32(6):1144-54.

Dual Inhibition of PI3K-AKT-mTOR- and RAF-MEK-ERK-signaling is synergistic in cholangiocarcinoma and reverses acquired resistance to MEK-inhibitors.

Int J Cancer. 2013 Nov;133(9):2065-76.

Combined targeting of AKT and mTOR using MK-2206 and RAD001 is synergistic in the treatment of cholangiocarcinoma.

质量标准及产品资料

纯度：99.59%
COA
H-NMR
HPLC

化学性质/溶解性/储存

分子量	480.39
分子式	C25H21N5O.2HCl
CAS号	1032350-13-2
溶解性	DMSO 12 mg/mL
储存条件	粉末型式 -20°C 3年；4°C 2年溶于溶剂 -80°C 6个月；-20°C 1个月
运输方式	冰袋运输，根据产品的不同，可能会有相应调整。

生物活性

MK-2206是一种高度选择性的Akt1/2/3抑制剂，IC50分别为8 nM/12 nM/65 nM；对250种其他蛋白激酶没有抑制活性。MK-2206抑制Akt的苏氨酸308位点和丝氨酸473位点的自身磷酸化作用。另外，MK-2206阻止Akt调节的下游信号分子（包括TSC2, PRAS40，及核糖体S6蛋白）的磷酸化作用。与抑制Ras 突变型细胞系(如NCI-H358, NCI-H23, NCI-H1299, 和Calu-6)相比，MK-2206 更有效地抑制Ras野生型细胞系(如A431, HCC827, 和NCI-H292)。MK-2206和细胞毒素药剂如erlotinib 和lapatinib联用作用于肺部NCI-H460肿瘤细胞或者卵巢A2780肿瘤细胞，MK-2206也显示出协同效应。

实验参考

蛋白/细胞实验

下述溶液配置方法仅为基于分子量计算出的理论值。不同产品在配置溶液前，需考虑其在不同溶剂中的溶解度限制。

浓度/溶剂体积/质量	1 mg	5 mg	10 mg
1 mM	2.0816 mL	10.4082 mL	20.8164 mL
5 mM	0.4163 mL	2.0816 mL	4.1633 mL
10 mM	0.2082 mL	1.0408 mL	2.0816 mL

*吸湿的DMSO对产品的溶解度有显著影响，请使用新开封的DMSO；
请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。

质量		浓度		体积		分子量*
	=		x		x

细胞系	CNE-1,CNE-2,HONE-1,SUNE-1
方法	MK-2206 is dissolved in DMSO as a stock solution and diluted by culture media before use. Cells are seeded at an appropriate density per well in 96-well plates and incubated for 24 hours. Then MK-2206 (0~10μM) is added to the cells. Cell proliferation is determined after 72 or 96 hours.
浓度	0,0.08,0.16,0.31,0.63,1.25,2.5,5,10μM
处理时间	72 or 96 hours

* 上述方法来自公开文献，仅供相同目的实验参考。如实验目的、材料、方法不同，请参考其他文献。

动物实验

建议您制定动物给药及实验方案时，尽量参考已发表的相关实验文献（溶剂种类及配比众多，简单地溶解目的化合物，并不能解决动物给药依从性、体内生物利用度、组织分布等相关问题，未必能保证目的化合物在动物体内充分发挥生物学效用）。
体内实验的工作液，建议您现用现配，当天使用；如在配制过程中出现沉淀、析出现象，可以通过超声和（或）加热的方式助溶。
切勿一次性将产品全部溶解。

动物实验方案计算器

请在下面的计算器中，输入您的动物实验相关数据并点击计算，即可得到该实验的总需药量和工作液终浓度。
例如您给药剂量是10 mg/kg，平均每只动物的体重为20 g，每只动物的给药体积是100 μL，动物数量为20只，则该动物实验的总需药量为4 mg，工作液终浓度为2 mg/mL。

1：鉴于实验过程的损耗，建议您至少多配1-2只动物的量；
2：为该产品最终给药时的浓度。

动物模型	CNE-2 model in male BALB/c nude mice
配制	Formulated in 30% Captisol
剂量	MK-2206 (240 mg/kg, three times a week), MK-2206 (480 mg/kg, once a week), and 30% Captisol (Cydex) diluents
给药处理	Oral gavage for 2 weeks