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Enzymes for Research, Diagnostic and Industrial Use

MK2206(dihydrochloride)

Cat No.
CEI-0143
Description
MK-2206 can inhibit Akt1, Akt2, and Akt3 with IC50 of 8 nM, 12 nM, and 65 nM.
CAS No.
1032350-13-2
Molecular Weight
480.39
Purity
>99%
Storage
2 years at -20centigrade Powder
Targets
Akt1, Akt2, Akt3
Molecular Formula
C25H21N5O.2HCL
Chemical Name
8-(4-(1-aminocyclobutyl)phenyl)-9-phenyl-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3(2H)-one
Solubility
DMSO 14 mg/mL Water 1 mg/ml Ethanol
In vitro
MK-2206 can inhibit Akt1, Akt2, and Akt3 with IC50 of 8 nM, 12 nM, and 65 nM. As a novel allosteric Akt inhibitor, MK-2206 can synergistically inhibited cell proliferation of human cancer cell lines. MK-2206 causes growth inhibition of the eight cell lines with an IC50 that ranges between 3.4 and 28.6 umol/L. MK-2206 alone more potently inhibited the cell growth of Ras wild-type (WT) cell lines (A431, HCC827, and NCI-H292; IC50 s of 5.5, 4.3, and 5.2 umol/L, respectively) as compared with Ras-mutant cell lines (NCI-H358, NCI-H23, NCI-H1299, and Calu-6; IC50 s of 13.5, 14.1, 27.0, and 28.6 umol/L, respectively), with the exception of NCI-H460, which has a PIK3CA E545K mutation (IC50, 3.4 umol/L).In acute lymphoblastic leukemia, MK-2206 decreased T-ALL cell line viability by blocking leukemic cells in the G0/G1 phase of the cell cycle and inducing apoptosis. MK-2206 also induced autophagy. In acute lymphoblastic leukemia, MK-2206 lead to a concentration-dependent dephosphorylation of Akt and its downstream targets, GSK-3alpha/beta and FOXO3A. In Neuroblastoma, MK-2206 treatment inhibited NB cell proliferation which was accompanied by a cell line selective G1 arrest of cell cycle or production of ROS.
In vivo
Mice with xenografted tumors treated with MK-2206 alone or with progesterone alone exhibited modest reductions in their tumor volume. The Akt inhibitor (MK-2206) also inhibits increased NCC phosphorylation in db/db mice.
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