MK-2206 dihydrochloride

カタログ番号 T1952 CAS 1032350-13-2

別名: MK-2206 2HCl

MK-2206 dihydrochloride (MK-2206 2HCl) is a variant Akt inhibitor that inhibits Akt1, Akt2, and Akt3 (IC50=8/12/65 nM) with orally active, highly potent and selective potency. MK-2206 dihydrochloride exhibits antitumor activity.

TargetMolの製品は全て研究用試薬です。人体にはご使用できません。また、個人の方への販売は行っておりません。

MK-2206 dihydrochloride, CAS 1032350-13-2

パッケージサイズ	在庫状況	単価(税別)
サンプルについてお問い合わせ
2 mg	在庫あり	￥ 7,000
5 mg	在庫あり	￥ 11,000
10 mg	在庫あり	￥ 15,000
25 mg	在庫あり	￥ 22,500
50 mg	在庫あり	￥ 34,000
100 mg	在庫あり	￥ 52,500
200 mg	在庫あり	￥ 85,500
500 mg	在庫あり	￥ 141,000
1 mL * 10 mM (in DMSO)	在庫あり	￥ 12,000

バルクのお問い合わせ

バッチを選択

純度: 99.91%

COA DATASHEET SDS HNMR HPLC

純度: 99.69%

COA DATASHEET SDS HNMR HPLC

純度: 99.59%

COA DATASHEET SDS HPLC HNMR

純度: 99.228%

COA DATASHEET SDS HPLC HNMR

COA DATASHEET SDS HNMR

COA DATASHEET SDS

バッチの詳細情報はお問い合わせください

生物学的特性に関する説明

化学的特性

保存条件 & 溶解度情報

説明	MK-2206 dihydrochloride (MK-2206 2HCl) is a variant Akt inhibitor that inhibits Akt1, Akt2, and Akt3 (IC50=8/12/65 nM) with orally active, highly potent and selective potency. MK-2206 dihydrochloride exhibits antitumor activity.
ターゲット＆IC50	Akt3:65 nM (cell free), Akt2:12 nM (cell free), Akt1:8 nM (cell free)
In vitro	METHODS: Fourteen tumor cells were treated with MK-2206 dihydrochloride for 72 h. Cell viability was measured by CellTiter-Glo assay. RESULTS: MK-2206 dihydrochloride inhibited the growth of tumor cells with IC50 ranging from 0.1 to 28.6 μmol/L. [1] METHODS: Human nasopharyngeal carcinoma cell lines CNE-2 and HONE-1 were treated with MK-2206 dihydrochloride (0.625-10 μM) for 24-48 h, and the cell cycle was detected by Flow Cytometry. RESULTS: MK-2206 dihydrochloride caused a dose-dependent increase in the percentage of cells in G0/G1 phase and a decrease in the number of cells in S phase.MK-2206 dihydrochloride induced cell cycle arrest in G1 phase. MK-2206 dihydrochloride induces cell cycle arrest in the G1 phase. [2]
In vivo	METHODS: To detect anti-tumor activity in vivo, MK-2206 dihydrochloride (120 mg/kg three times per week or 360 mg/kg once per week, 30% Captisol) and erlotinib (50 mg/kg five times per week, 0.5% methylcellulose + 0.1% Tween 80) were orally administered to CD1 mice bearing human lung cancer tumor NCI-H292 for two weeks. RESULTS: Three-times-weekly MK-2206 monotherapy was ineffective, and the once-weekly regimen mediated only moderate antitumor efficacy. Although erlotinib alone mediated significant tumor growth inhibition, combination therapy with MK-2206 significantly enhanced its antitumor efficacy, including tumor regression. [1] METHODS: To assay antitumor activity in vivo, MK-2206 dihydrochloride (120 mg/kg in 30% captisol) was administered by gavage to NSG mice bearing human endometrial cancer tumors twice a week for three weeks. RESULTS: MK-2206 dihydrochloride treatment resulted in significant inhibition of the growth of three different types and grades of PDX tumors. [3]
細胞研究	Cells were seeded at a density of 2 to 3 × 103 per well in 96-well plates. Twenty-four hours after plating, varying concentrations of the drug, either as a single agent or in combination, were added to the wells. Cell proliferation was determined by using the CellTiter-Glo assay at 72 or 96 hours after dosing. The nature of the drug interaction was evaluated by using the combination index (CI) according to the method of Chou and Talalay. A commercial software package was obtained from Calcusyn. In combination with docetaxel, we tested three treatment sequences: (a) MK-2206 followed by docetaxel—cells were exposed to MK-2206 for 24 hours, and then after washout of MK-2206, cells were treated with docetaxel for an additional 72 hours; (b) docetaxel followed by MK-2206—cells were exposed to docetaxel for 24 hours, and then after washout of docetaxel, cells were treated with MK-2206 for an additional 72 hours; and (c) concurrent treatment—cells were exposed to both MK-2206 and docetaxel for 72 hours [2].
動物実験	When the mean tumor size reached 0.13 cm3 for the SK-OV-3 or 0.2 cm3 for the NCI-H292, HCC70, PC-3, and NCI-H460 models, the mice were randomized into control and treatment groups with approximately equivalent ranges of tumor volume between groups (n = 5 animals per group). The following vehicles were used to dose the compounds: 30% Captisol (Cydex) for MK-2206; 0.5% methylcellulose + 0.1% Tween 80 for erlotinib; distilled water for lapatinib; 0.73% ethanol in saline for docetaxel; and saline for carboplatin and gemcitabine. The control group received vehicle only. Tumor volume was measured with calipers twice a week. Animal body weight and physical signs were monitored during the experiments. Tumor volume was calculated, taking length to be the longest diameter across the tumor and width to be the perpendicular diameter, by using the following formula: (length × width)2 × 0.5. Relative tumor volume was assessed by dividing the tumor volume on different observation days with the starting tumor volume. Statistical significance was evaluated by using the two-way repeated ANOVA test followed by Dunnett's test or an unpaired t-test [2].

別名	MK-2206 2HCl
分子量	480.39
分子式	C25H23Cl2N5O
CAS No.	1032350-13-2

保存条件

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度情報

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 7.5 mg/mL (15.61 mM)

参考文献

1. Hirai H, et al. MK-2206, an allosteric Akt inhibitor, enhances antitumor efficacy by standard chemotherapeutic agents or molecular targeted drugs in vitro and in vivo. Mol Cancer Ther. 2010 Jul;9(7):1956-67. 2. Zhao YY, et al. Effects of an oral allosteric AKT inhibitor (MK-2206) on human nasopharyngeal cancer in vitro and in vivo. Drug Des Devel Ther. 2014 Oct 10;8:1827-37. 3. Winder A, et al. The allosteric AKT inhibitor, MK2206, decreases tumor growth and invasion in patient derived xenografts of endometrial cancer. Cancer Biol Ther. 2017 Dec 2;18(12):958-964. 4. Jin J, Zhao Y, Guo W, et al. Thiocoraline mediates drug resistance in MCF-7 cells via PI3K/Akt/BCRP signaling pathway[J]. Cytotechnology. 2019 Feb;71(1):401-409. 5. He J, Zhang A, Song Z, et al. The resistant effect of SIRT1 in oxidative stress-induced senescence of rat nucleus pulposus cell is regulated by Akt-FoxO1 pathway[J]. Bioscience reports. 2019 May 10;39(5). pii: BSR20190112. 6. Lv W, Huan M, Yang W, et al. Snail promotes prostate cancer migration by facilitating SPOP ubiquitination and degradation[J]. Biochemical and Biophysical Research Communications. 2020, 529(3): 799-804. 7. Lv, Wei, et al. Snail promotes prostate cancer migration by facilitating SPOP ubiquitination and degradation. Biochemical and Biophysical Research Communications . 529.3 (2020): 799-804. 8. Li Z, Zhou Z, Wu X, et al. LMP1 promotes nasopharyngeal carcinoma metastasis through NTRK2-mediated anoikis resistance[J]. American journal of cancer research . 2020, 10(7): 2083. 9. Zhou C, Du J, Zhao L, et al. GLI1 reduces drug sensitivity by regulating cell cycle through PI3K/AKT/GSK3/CDK pathway in acute myeloid leukemia[J]. Cell Death & Disease. 2021, 12(3): 1-14. 10. Zhang L, Zhou Q, Qiu Q, et al. CircPLEKHM3 acts as a tumor suppressor through regulation of the miR-9/BRCA1/DNAJB6/KLF4/AKT1 axis in ovarian cancer[J]. Molecular Cancer. 2019, 18(1): 1-19.

引用文献

1. Jiang Y, Zhao X, Chen J, et al.PM2. 5 induces cardiac malformations via PI3K/akt2/mTORC1 signaling pathway in zebrafish larvae.Environmental Pollution.2023: 121306. 2. Zhao W, Xu C, Peng L, et al.cAMP/PKA signaling promotes AKT deactivation by reducing CIP2A expression, thereby facilitating decidualization.Molecular and Cellular Endocrinology.2023: 111946. 3. Mavrogonatou E, Angelopoulou M, Rizou S V, et al. Activation of the JNKs/ATM-p53 axis is indispensable for the cytoprotection of dermal fibroblasts exposed to UVB radiation. Cell death & disease. 2022, 13(7): 1-14. 4. Hou X, Liu Q, Gao Y, et al. Mesencephalic astrocyte-derived neurotrophic factor reprograms macrophages to ameliorate acetaminophen-induced acute liver injury via p38 MAPK pathway. Cell Death & Disease. 2022, 13(2): 1-13. 5. Zhang P, Zhang J, Quan H, et al. Effects of butein on human osteosarcoma cell proliferation, apoptosis, and autophagy through oxidative stress. Human & Experimental Toxicology. 2022, 41: 09603271221074346. 6. Lv W, Huan M, Yang W, et al. Snail promotes prostate cancer migration by facilitating SPOP ubiquitination and degradation. Biochemical and Biophysical Research Communications. 2020, 529(3): 799-804 7. Li Z, Zhou Z, Wu X, et al. LMP1 promotes nasopharyngeal carcinoma metastasis through NTRK2-mediated anoikis resistance. American journal of cancer research. 2020, 10(7): 2083. 8. Zhou C, Du J, Zhao L, et al. GLI1 reduces drug sensitivity by regulating cell cycle through PI3K/AKT/GSK3/CDK pathway in acute myeloid leukemia. Cell Death & Disease. 2021, 12(3): 1-14. 9. Liu Y, Wang J, Chen J, et al. Upregulation of miR-520c-3p via Hepatitis B Virus Drives Hepatocellular Migration and Invasion through the PTEN/AKT/NF-κB Signaling Pathway. Molecular Therapy-Nucleic Acids. 2022 10. Zhang L, Zhou Q, Qiu Q, et al. CircPLEKHM3 acts as a tumor suppressor through regulation of the miR-9/BRCA1/DNAJB6/KLF4/AKT1 axis in ovarian cancer. Molecular Cancer. 2019, 18(1): 1-19

11. Zhang H, Xia P, Liu J, et al. ATIC inhibits autophagy in hepatocellular cancer through the AKT/FOXO3 pathway and serves as a prognostic signature for modeling patient survival. International Journal of Biological Sciences. 2021, 17(15): 4442-4458. 12. He J, Zhang A, Song Z, et al. The resistant effect of SIRT1 in oxidative stress-induced senescence of rat nucleus pulposus cell is regulated by Akt-FoxO1 pathway. Bioscience Reports. 2019 May 10;39(5). pii: BSR20190112 13. Jin J, Zhao Y, Guo W, et al. Thiocoraline mediates drug resistance in MCF-7 cells via PI3K/Akt/BCRP signaling pathway. Cytotechnology. 2019 Feb;71(1):401-409.

もっと見る隠し

投与量変換

You can also refer to dose conversion for different animals. 詳細

In vivo投与量計算 (透明溶液)

ステップ1: 以下の情報を入力してください

投与量

mg/kg

動物の平均体重

動物あたりの投与量

動物数

溶媒の組成を入力してください

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

計算するリセット

計算結果:

作業濃度: mg/ml;

DMSO溶液の作成方法: mg あらかじめ溶解した薬剤 μL DMSO (マスター溶液の濃度 mg/mL)，濃度がそのバッチの薬剤のDMSO溶解度を超える場合は、まずご連絡ください。

生体内薬剤の調合法：取る μL DMSO マスター溶液、次に追加 μL PEG300，確実に混ぜてから加える μL Tween 80，確実に混ぜてから加える μL ddH₂O, 確実に混ぜる

お問合せ内容:

必ず順番通りに溶媒を加えてください。ボルテックスミキサーや超音波、湯煎することで溶解しやすくなります

計算器

モル濃度計算機

希釈計算機

再構成計算

分子量計算機

質量

濃度

体積

分子量

モル度計算機では以下の計算が可能です

既知の体積と濃度の溶液を調製するために必要な化合物の質量
質量が既知の化合物を目的の濃度まで溶解させるのに必要な溶液の量
特定の体積の中に既知の質量の化合物を入れて得られる溶液の濃度

参考例

モル濃度計算機を使用したモル濃度計算の例
化合物の分子量が197.13g/molである場合、10mlの水に10mMのストック溶液を作るのに必要な化合物の質量はどれくらいですか？
［分子量（MW）］の欄に［197.13］と入力してください
[濃度]ボックスに10と入力し、正しい単位（millimolar）を選択します
[容量]ボックスに10と入力し、正しい単位（milliliter）を選択します
計算を押します
答えの19.713mgが質量欄に表示されます

濃度 (開始)

体積 (開始)

濃度 (終了)

体積 (終了)

溶液を作るのに必要な希釈率の計算

溶液の調製に必要な希釈率の算出
希釈計算機は、既知の濃度の原液をどのように希釈するかを計算することができる便利なツールです。V1を計算するためにC1、C2＆V2を入力します。

参考例

Tocrisの希釈計算器を用いた希釈計算の一例
50μMの溶液を20ml作るためには、10mMの原液を何ml必要ですか？
C1V1=C2V2という式を用いて、C1=10mM、C2=50μM、V2=20ml、V1を未知数とします。
濃度（開始）ボックスに10を入力し正しい単位(millimolar)を選択してください
濃度（終了）ボックスに50を入力し正しい単位(millimolar)を選択してください
体積（終了）ボックスに20を入力し正しい単位(millimolar)を選択してください
計算を押します
100 microliter (0.1 ml) という答えが体積（開始）ボックスに表示されます。

分子式

分子量 g/mol

化合物の化学式を入力して、そのモル質量や元素組成を計算します

Tヒント：化学式は大文字と小文字を区別します。: C10H16N2O2 c10h16n2o2

化合物のモル質量（分子量）を計算する手順:
化学物質のモル質量を計算するには、その化学式を入力し、「計算」をクリックしてください。.
分子質量、分子量、モル質量、モル重量の定義:
分子質量（分子量）とは、物質の1分子の質量であり、統一された原子質量単位（u）で表されます。(1uは炭素12の1原子の質量の1/12に等しい）
モル質量（molar weight）とは、ある物質の1モルの質量のことで、単位はg/molです。

bottom

技術サポート

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.

Keywords

MK-2206 dihydrochloride 1032350-13-2 Apoptosis Autophagy Cytoskeletal Signaling PI3K/Akt/mTOR signaling Akt mutant Inhibitor MK 2206 cancer inhibit MK-2206 (2HCl) MK2206 dihydrochloride PIK3CA selective MK-2206 Dihydrochloride Protein kinase B loss PKB PTEN MK-2206 2HCl sensitive oral MK 2206 Dihydrochloride breast MK-2206 MK2206 MK 2206 dihydrochloride MK2206 Dihydrochloride inhibitor

本ウェブサイトに掲載されている製品は全て研究用試薬です。研究目的以外の用途にはご使用できません。

MK-2206 dihydrochloride

保存条件

溶解度情報

参考文献

引用文献

関連化合物ライブラリー

関連製品

投与量変換

In vivo投与量計算 (透明溶液)

計算器

モル度計算機では以下の計算が可能です

溶液を作るのに必要な希釈率の計算

バイアルを再構成するのに必要な溶媒の量を計算する.

化合物の化学式を入力して、そのモル質量や元素組成を計算します

技術サポート

Keywords