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MK-2206 dihydrochloride Catalog No.GC16304

Akt1/2/3 inhibitor

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Sample solution is provided at 25 µL, 10mM.

Quality Control

Quality Control & SDS

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Cell experiment:[1]

Cell lines

Endometriotic stromal cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reaction Conditions

100 nM, 2h


Inhibiting AKT with MK-2206 or MEK1/2 with U0126 for 24 hours in the absence of R5020 increased total and nuclear PRA and PRB protein levels in OSIS but not in eutopic endometrial stromal cells from disease-free patients from disease-free patients. MK-2206 and R5020 decreased OSIS viability and increased apoptosis. Trends toward decreased volumes of sc grafted endometriosis tissues were demonstrated with MK-2206 and progesterone.

Animal experiment:[1]

Animal models

5-week-old CD-1 nude mice

Dosage form

360 mg/kg/d, 15 days, oral Gavage


No significant interaction between MK-2206 and progesterone (P=0.628). Trends toward decreased tumor volume were noted with MK-2206 (P=0.077) and progesterone (P=0.087). Treatment with MK-2206 decreased levels of Ki67. Levels of cleaved caspase-3 (CC3) were very low in E and E +P-treated grafts, whereas MK-2206 increased CC3 levels, especially in the presence of P.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


1. Eaton JL1, Unno K, Caraveo M et al. Increased AKT or MEK1/2 activity influences progesterone receptor levels and localization in endometriosis. J Clin Endocrinol Metab. 2013 Dec;98(12):E1871-9.

Chemical Properties

Cas No. 1032350-13-2 SDF
Synonyms MK-2206,MK2206,MK 2206
Chemical Name 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-2H-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3-one;dihydrochloride
Canonical SMILES C1CC(C1)(C2=CC=C(C=C2)C3=C(C=C4C(=N3)C=CN5C4=NNC5=O)C6=CC=CC=C6)N.Cl.Cl
Formula C25H21N5O.2HCl M.Wt 480.39
Solubility ≥ 12.01mg/mL in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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MK-2206 dihydrochloride (MK-2206 (2HCl)) is an orally active allosteric AKT inhibitor with IC50s of 5 nM, 12 nM, and 65 nM for AKT1, AKT2, and AKT3, respectively[1].

MK-2206 dihydrochloride (MK-2206 (2HCl)) (0-10 μM; 72 and 96 hours) inhibits the nasopharyngeal carcinoma (NPC) cell lines CNE-1, CNE-2, HONE-1, and SUNE-1 proliferation in dose- and time-dependent manner[1]. MK-2206 dihydrochloride (0-10 μM; 24 and 48 hours) results in a dose-dependent increase in the percentage of cells in G0/G1 phase and a concomitant reduction of cell numbers in S phase in CNE-2 and HONE-1 cells[1]. MK-2206 dihydrochloride (0-10 μM; 24 hours) attenuates phosphorylation levels of PRAS40 and S6 in a dose-dependent manner. MK-2206 does not effect phosphorylation of GSKα/β and AKT[1]. MK-2206 dihydrochloride (0-10 μM; 24 hours) increases the appearance of LC3-II in CNE-2 cells dose-dependently. Microtubule-associated protein 1 LC3 is an essential autophagy protein[1].

Both MK-2206 dihydrochloride (MK-2206 (2HCl)) doses (oral gavage; 480 mg/kg once a week and 240 mg/kg three times a week; for 2 weeks) can inhibit the growth of human CNE-2 xenografts in nude mice. In the two MK-2206 dihydrochloride groups, the tumor weights are much lighter than the control group. Temporal body weight reduction is observed after receiving the MK-2206 dihydrochloride treatment[1]. No other obvious toxicity is observed in mice[1]. MK-2206 dihydrochloride (orally; 120 mg/kg; alternate days; for 3 weeks) significantly inhibits tumor growth[2].

[1]. 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.
[2]. Agarwal E, et al. Akt inhibitor MK-2206 promotes anti-tumor activity and cell death by modulation of AIF and Ezrin in colorectal cancer. BMC Cancer. 2014 Mar 1;14:145.