MK-2206 free base

Name: MK-2206 free base
Brand: MedChemExpress
SKU: HY-10357
Rating: 5.0 (462 reviews)

Cat. No.: HY-10357: Data Sheet Handling Instructions
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MK-2206 free base is an orally active pan-AKT inhibitor, with IC₅₀ values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 free base inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 free base induces G1-phase cell cycle arrest, apoptosis (apoptosis), epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 free base causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 free base can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia.

For research use only. We do not sell to patients.

CAS No. : 1032349-93-1

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5 mg	Get quote 5 - 7 weeks 4 - 6 weeks 6 - 8 weeks 4 - 6 weeks	Estimated Time of Arrival: December 31
10 mg	Get quote 5 - 7 weeks 4 - 6 weeks 6 - 8 weeks 4 - 6 weeks	Estimated Time of Arrival: December 31
25 mg	Get quote 5 - 7 weeks 4 - 6 weeks 6 - 8 weeks 4 - 6 weeks	Estimated Time of Arrival: December 31
50 mg	Get quote 5 - 7 weeks 4 - 6 weeks 6 - 8 weeks 4 - 6 weeks	Estimated Time of Arrival: December 31
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Based on 462 publication(s) in Google Scholar

Other Forms of MK-2206 free base:

MK-2206 dihydrochloride In-stock
MK-2206 In-stock

462 Publications Citing Use of MCE MK-2206 free base

In Vivo Imaging

Cell Proliferation/Viability Assay

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Nat Cancer. 2024 Jul;5(7):1082-1101. [Abstract]; AKT phosphorylation levels by western blot in OCI-AML2 cells either infected with PIK3CG- and PIK3R5-directed sgRNAs for 72 hours or treated with 500nM IPI-549, AZ2, or the AKT inhibitor, MK-2206, for one and 72 hours.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Nat Cancer. 2024 Jul;5(7):1082-1101. [Abstract]; AKT phosphorylation levels by western blot of OCI-AML2 cells treated for one hour, 72 hours, or 72 hours followed by fresh addition of 500nM IPI-549, AZ2, or MK-2206 for one hour.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Nat Commun. 2024 Jun 17;15(1):5144. [Abstract]; Representative Western blots from isolated tubule suspensions cultured for 30 min in indicated K+ concentrations with or without the AKT inhibitor MK2206 (10 μM).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2024 Jul;11(26):e2306348. [Abstract]; MK‐2206 (5 µM; 18 h) significantly suppresses IL11‐induced upregulation of PDL1, but did not affect the level of p‐EGFR.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]; Representative images of immunofluorescence analysis of Nrf2 expression in microglia treated with the AKT inhibitor MK2206 (5 μM，6 h), the GSK3β activator sodium nitroprusside (SNP, 100 μM， 6h), and the GSK3β inhibitor TDZD-8 (5 μM，6 h). Nrf2 (red), nuclei (blue).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]; Representative western blots and quantitative data for the expression of Nrf2 in the nucleus and the downstream proteins of Nrf2 pathway, including HO-1 and NQO1, with different treatments (MK2206: 5 μM，6 h; SNP: 100 μM， 6h; TDZD-8: 5 μM，6 h).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]; Nrf2 knockout abolished neurological function improvement mediated by combined curcumin-hUC-MSC treatment. TTC-stained brain sections (A) and quantitative analysis (B) showed the decreased infarct volume with combined therapy in MCAO mice (MK2206, SNP or TDZD-8 :5 mg/kg， intraperitoneally，3 consecutive days after MCAO).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Nov:120:155074. [Abstract]; SUDHL-4 cells were pretreated with the pan-PI3K inhibitor LY294002 (20 µM), the Akt inhibitor MK2206 (HY-108232; 4 µM), or the GSK3β inhibitor AR-A014418 (HY-10512; 10 µM) for 1 h followed by treating with FKB (Flavokawain B; HY-N2132) at 2.5 µg/ml for 24 h. Cell viability was measured using the MTS assay and results were shown as the percentage relative to the vehicle-treated control. *p < 0.05, #p < 0.01, and †p < 0.001.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Nov:120:155074. [Abstract]; Raji and Jeko-1 cells were pretreated with the pan-PI3K inhibitor LY294002 (20 µM), the Akt inhibitor MK2206 (HY-108232; 4 µM), or the GSK3β inhibitor AR-A014418 (HY-10512; 10 µM) for 1 h followed by treating with FKB (Flavokawain B; HY-N2132) at 2.5 µg/ml for 24 h. Cell viability was measured using the MTS assay and results were shown as the percentage relative to the vehicle-treated control. *p < 0.05, #p < 0.01, and †p < 0.001.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Nat Commun. 2021 Jun 30;12(1):4050. [Abstract]; Total and phosphorylated AKT (pAKT Ser473) immunoblotting in isogenic control (+vehicle) and mutant NPCs (+vehicle or MK-2206 AKT inhibitor) and quantification as pAKT/AKT ratio.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2021 Jun;11(6):1592-1606. [Abstract]; HCCLM3 cells were pretreated with or without 10 μmol/L MK2206 (a PI3K/AKT inhibitor) and then with HYD-PEP06 (200 μg/mL) for 24 h. The protein expression of p-AKT, AKT, the epithelial and mesenchymal markers was determined by Western blot.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Mol Cell. 2021 Jan 21;81(2):370-385.e7. [Abstract]; Lack of differential inhibition of mTORC1 signaling in wild-type versus RIPK1^−/− HT-29 cells upon inhibition of Akt by MK-2206 and mTORC1 by rapamycin or Torin-1. Cells were treated for indicated time points, and cell lysates were immunoblotted with indicated antibodies.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2021 Jan;11(1):71-88. [Abstract]; Protein phosphorylation of PKB (Ser473) and GSK-3β (Ser9) in cardiomyocytes treated with DT or MK-2206 or DIF-3, either alone or in combination (n = 5).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Proc Natl Acad Sci U S A. 2019 Feb 19;116(8):2996-3005. [Abstract]; HT22 cells were pretreated with the indicated inhibitors (CDDO (Bardoxolone, HY-14909); T0070907 (HY-13202); Troglitazone (HY-50935 ); TPCA-1 (HY-10074); JAKi; STAT3i; AV-412 (HY-10346); and MK2206 (HY-10358)) and then treated with T/Z, T/S/Z, T/C/Z for 9 h or Glutamate, Erastin (T: 20 ng/ml; Z: 50 μM; S: 20 nM; C: 1 μg/ml; Glutamate: 50 mM; Erastin 10 μM) for 12 h. Cell viability was measured by CellTiterGlo assay.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Oncogene. 2019 Jun;38(26):5250-5264. [Abstract]; Western blotting analysis shows the effect of AKT inhibitor MK2206 (AKT i) and SET7 inhibitor (R)-PFI-2 on the levels of SOX2 proteins. The cells are treated with 1 μM MK2206 for 24 h and 10 μM (R)-PFI-2 for 12 h before being harvested for analysis.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Invest Dermatol. 2019 Jan;139(1):71-80. [Abstract]; HEKa (left) and HaCaT (right) cells are seeded in six-cell plates and pretreated with MK2206 for 6 hours, and then stimulated with M5 (2.5 ng/mL) for 48 hours before measuring the protein levels of cyclin D1, Akt, and phosphoAkt by Western blot analysis.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Cancer Cell. 2018 Jun 11;33(6):1061-1077.e6. [Abstract]; Dih10 cells are treated with CDDP (20 μM) in the presence or absence of the Akt inhibitor MK2206 (5 μM).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Nat Commun. 2018 May 8;9(1):1816. [Abstract]; Representative western blot analysis of p-ERK1/2, p-p90 RSK, p-AKT, p-AKT p-PRAS40, p-FOXO1/3a/4, p-GSK3β, p-mTOR, p-p70 S6K, and p-S6 protein in MCF-10A^P and MCF-10A^H1047R cells stably expressing empty vector (EV) or mutant HRAS^Q61R treated with 2 µM MK2206 (AKTi) at different time points.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2018 Oct 3;9(10):1015. [Abstract]; Representative western blot images are showing the LC3, and the phosphorylated and total protein expression of Akt and ERK1/2 after treatment with H₂O₂ in the presence and absence of MK2206 (5 μM) and U0126 (25 μM).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2018 Nov;39(11):1787-1796. [Abstract]; Effects of LY294002 or AKT siRNA on the levels of total AKT, pAKT, phosphorylated PRAS40 and pMDM2 are examined by Western blot analysis in MCF-7 cells when HBXIP was overexpressed. Effects of MK-2206 or HBXIP siRNA on the levels of total AKT, pAKT, pPRAS40, and pMDM2 are examined by Western blot analysis in MCF-7-HBXIP cells.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Clin Epigenetics. 2018 May 23:10:69. [Abstract]; The expression levels of E-cadherin, vimentin, pan-AKT, p-AKTser473, MMP-2, MMP-7, MMP-9, and actin (control) are detected by Western blot in RAI2 un-expressed and re-expressed RKO and LOVO cells as well as in the control group, shRAI2 knockdown group, and shRAI2 knockdown plus MK2206 treated group.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Cancer Sci. 2018 Apr;109(4):944-955. [Abstract]; Western blotting of Sox2 and b-actin in A549 cells with or without IGF2 treated in the presence or absence of MK-2206.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Cancer. 2018 Jun 14;9(14):2480-2491. [Abstract]; Analysis of indicated proteins in Cry1 silencing osteosarcoma cells after MK-2206 treatment. Data are expressed as the mean±standard deviation.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Int J Biochem Cell Biol. 2018 Jun:99:43-51. [Abstract]; Western blot analysis of NDRG2, p-ATK, XIAP, E-cadherin and Vimentin in TE-13 cells shows NDRG2 negatively regulates the expressions of AKT, XIAP, E-cadherin and Vimentin proteins.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: J Cell Biochem. 2018 May;119(5):3885-3891. [Abstract]; Western blot showed the protein expression of P-gp,MRP1, PTEN, p-AKT, Bax, Bcl-2, and cleaved caspase-3.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Radiat Res. 2018 Aug;190(2):204-215. [Abstract]; When 6 Gy irradiation is combined with AKT2 inhibitor MK-2206 treatment, the protein levels in phosphorylated AKT2, mTOR and IKBa are decreased, and the downstream proapoptotic proteins, caspase 3 and caspase 8, are increased.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Br J Cancer. 2017 Sep 26;117(7):974-983. [Abstract]; The effect of the AKT inhibitor MK2206 (10 μM) on the expression levels of phosphor-AKT, AKT, and STMN1 in TKI-pretreated NCI-H460 cells. β-actin is used as a loading control.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Hum Mol Genet. 2017 Sep 15;26(18):3553-3563. [Abstract]; Immunofluorescence analysis for expression of the I-cell marker ΔNP63 on proximal sections of ureters explanted from E12.5 wildtype (control) embryos and cultured for 6 d in the presence of solvent (DMSO) (A), the AKT inhibitor (AKT-i) MK2206 (B), the P38 inhibitor (P38-i) SB203580 (C), the ERK1/2 inhibitor (ERK1/2-i) PD98059 (D) or combinations as indicated (E and F).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Jan 31;8(5):8536-8549. [Abstract]; Western blot analysis of cyclin D1 and cyclin E in OE19 cells treated with the control, BIBR 277 alone, MK-2206 alone, or BIBR 277 combined with MK-2206 for 48 h.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Jul 18;8(29):47642-47654. [Abstract]; Akt/JNK signal pathway is impaired in the inhibition of αMSH on adipocyte inflammation and FoxOs expressions. Mouse adipocytes are pretreated with αMSH and MK-2206, respectively. Relative protein levels of Akt, p-Akt^ser473, JNK, p-JNK^Thr183 with or without MK-2206 (n=3).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Modern Oncology. 2017,25(01):0009-0013.; The related protein expression of Bcl-2, Bax, Caspase-3, PARP, GSK-3β, p65 gene in each intervention group. Western blot assay:1:Control group; 2:MK2206 positive group; 3:0.3g/L Mat; 4: 0.6g/L Mat; 5:1.2g/LMat.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Proc Natl Acad Sci U S A. 2016 Jul 26;113(30):E4338-47. [Abstract]; HCC1937 cells are treated for 16 h with inhibitors as indicated. Immunoblotting of total cell lysates is performed with antibodies as indicated. Induction of PAR and H2ax phosphorylation (γH2ax) following treatment with inhibitors of pan-PI3K (BKM120, 1.5 μM), PI3Kα (BYL719, 3 μM; PIK75, 0.5 μM), PI3Kβ (TGX221, 30 μM), AZD2281 (5 μM), and inhibitors of AKT (MK2206, 1 μM), SGK (GSK650394, 10 μM), or MAPKK (GSK1120212, 5 nM).

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Harvard University. 2016 Aug.; Mouse embryonic fibroblasts (MEFs) are deprived of Arginine and treated with 2 µM MK2206 for up to 6 hours.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Okayama University. 2015.; Expression of Sema4D and PlexinB1 in various oral squamous cell carcinoma cell lines following the addition of IGF-I. Notably, the addition of IGF-I resulted in increased expression of Sema4D, particularly in HSC-2 and SAS cells. This increase was suppressed when IGF-I was administered in the presence of inhibitors targeting its receptor or downstream signaling pathways. No changes in PlexinB1 expression were observed following the addition of IGF-I.

: MK-2206 free base purchased from MedChemExpress. Usage Cited in: Cell. 2014 Feb 13;156(4):771-85. [Abstract]; (A) Effects of inhibiting PI3K and Akt in MEFs. Serum starved (16 hr) MEFs are pretreated (30 min) with Wortmannin (100 nM), MK2206 (2 μM) or vehicle (DMSO). Immunoblots of lysates are probed with the indicated antibodies. (B) PTEN null MEFs exhibit constitutive Akt, TSC2 and S6K phosphorylation, which are reversed by the Akt inhibitor MK2206.

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GSK-3 GSK-3α GSK-3β

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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

Biological Activity
Purity & Documentation
References
Customer Review

Description

IC₅₀ & Target^[1]

Akt1

8 nM (IC₅₀)

Akt2

12 nM (IC₅₀)

Akt3

65 nM (IC₅₀)

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	8.1 μM Compound: MK2206	Antiproliferative activity against human A549 cells after 48 hrs by MTT assay Antiproliferative activity against human A549 cells after 48 hrs by MTT assay	[PMID: 30777660]
AN3-CA	EC₅₀	972 nM Compound: MK-2206	Antiproliferative activity against human AN3-CA cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human AN3-CA cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]
AN3-CA	EC₅₀	972 nM Compound: MK-2206	Antiproliferative activity against human AN3-CA cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay Antiproliferative activity against human AN3-CA cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay	[PMID: 31584233]
BT-474	EC₅₀	1682 nM Compound: MK-2206	Antiproliferative activity against human BT-474 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human BT-474 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]
HCT-116	IC₅₀	7.5 μM Compound: MK-2206	Growth inhibition of human HCT116 cells after 72 hrs by coulter counter method Growth inhibition of human HCT116 cells after 72 hrs by coulter counter method	[PMID: 24900862]
KU-19-19	EC₅₀	7054 nM Compound: MK-2206	Antiproliferative activity against human KU-19-19 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human KU-19-19 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]
MCF7	EC₅₀	571 nM Compound: MK-2206	Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human MCF7 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]
NCI-H1666	CC₅₀	58.5 μM Compound: 57; MK2206	Cytotoxicity against human NCI-H1666 cells Cytotoxicity against human NCI-H1666 cells	[PMID: 33539089]
NCI-H358	IC₅₀	< 0.1 μM Compound: A2-NH2; MK2206	Antiproliferation activity against human NCI-H358 cells incubated for 3 days in presence of trametinib by MTT assay Antiproliferation activity against human NCI-H358 cells incubated for 3 days in presence of trametinib by MTT assay	[PMID: 38457912]
NCI-H460	IC₅₀	5.4 μM Compound: MK-2206	Growth inhibition of human NCI-H460 cells after 72 hrs by coulter counter method Growth inhibition of human NCI-H460 cells after 72 hrs by coulter counter method	[PMID: 24900862]
SK-MEL-2	IC₅₀	1 μM Compound: MK-2206	Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of LY3214996 by MTT assay Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of LY3214996 by MTT assay	[PMID: 36961300]
SK-MEL-2	IC₅₀	1 μM Compound: MK-2206	Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of MEK-162 by MTT assay Synergistic cytotoxicity against human SK-MEL-2 cells expressing NRAS mutant assessed as cell growth inhibition measured for 48 hrs in presence of MEK-162 by MTT assay	[PMID: 36961300]
T47D	EC₅₀	411 nM Compound: MK-2206	Antiproliferative activity against human T47D cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay Antiproliferative activity against human T47D cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay	[PMID: 31584233]
T47D	EC₅₀	583 nM Compound: MK-2206	Antiproliferative activity against human T47D cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human T47D cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]
ZR-75-1	EC₅₀	571 nM Compound: MK-2206	Antiproliferative activity against human ZR-75-1 cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay Antiproliferative activity against human ZR-75-1 cells assessed as reduction of cell growth measured after 5 days by CellTiter-Glo assay	[PMID: 31584233]
ZR-75-1	EC₅₀	63 nM Compound: MK-2206	Antiproliferative activity against human ZR-75-1 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay Antiproliferative activity against human ZR-75-1 cells assessed as reduction in cell viability incubated for 5 days by celltiter-glo assay	[PMID: 30996949]

In Vitro

MK-2206 free base inhibits Akt1 kinase activity in various human cancer cell lines with an IC₅₀ of approximately 20 nM, blocks the downstream signaling pathway of Akt, and exerts potent antiproliferative effects on cancer cell lines with specific PI3K pathway gene defects, while activation of the Ras pathway predicts no response^[1].
MK-2206 free base exerts additive or synergistic antiproliferative and pro-apoptotic sensitizing effects when combined with various chemotherapeutic agents and targeted inhibitors in relevant human cancer cell lines^[1].
MK-2206 (72 h) free base potently inhibits the growth of U937, OCI/AML3, MV-4-11 and MOLM-13 acute myeloid leukemia (AML) cell lines, with IC₅₀ values ranging from 0.6 to 2.5 μM, while it exhibits only extremely low cytotoxicity against normal human peripheral blood mononuclear cells (PBMCs)^[2].
MK-2206 (1-10 μM; 24 h) free base induces dose-dependent G₁ cell cycle arrest in OCI/AML3, MOLM-13 and MV-4-11 AML cell lines^[2].
MK-2206 (1-10 μM; 24 h) free base induces dose-dependent apoptosis in OCI/AML3, MOLM-13 and MV-4-11 acute myeloid leukemia (AML) cell lines, with a significant increase in apoptotic cell populations at higher doses^[2].
MK-2206 (0.1-10 μM; 2-24 h) free base induces apoptosis in MV-4-11 acute myeloid leukemia (AML) cells via caspase-3 and PARP cleavage, downregulates Mcl-1 protein levels in MV-4-11, OCI/AML3 and U937 AML cells in a dose-dependent manner, and inhibits the phosphorylation of Akt at Ser⁴⁷³ and GSK3β at Ser⁹ after 2 to 24 h of treatment, respectively^[2].
MK-2206 (10 μM; 1-4 h) free base induces downregulation of Mcl-1 in MV-4-11 acute myeloid leukemia (AML) cells via a GSK3β-mediated proteasome-dependent mechanism^[2].
Combined administration of MK-2206 (200 nM; 72 h) free base and Cytarabine (HY-13605) synergistically enhances cytotoxicity in MV-4-11, MOLM-13 and OCI/AML3 acute myeloid leukemia (AML) cell lines (ED₅₀ CI value < 1), but exhibits antagonistic effects in U937 AML cells (ED₅₀ CI value = 1.13)^[2].
MK-2206 (0.5-5 μM; 48 h) free base inhibits TGF-β1-induced fibrosis, epithelial-mesenchymal transition (EMT), and activation of the Akt/mTOR signaling pathway in HK-2 cells. The effective concentration is 1 μM, which reduces the mRNA expression of Collagen I and Fibronectin, restores E-cadherin levels, and suppresses the expression of mesenchymal markers and phosphorylated Akt/mTOR proteins^[3].
MK-2206 (0.5-20 μM; 2-24 h) free base upregulates LDLR protein levels in HepG2 cells treated with sterol feeding or sterol starvation. The maximum induction effect is observed in the sterol starvation group treated with 5 μM for 14 h, while that in the sterol feeding group is achieved with 10 μM treatment for 14 h. Moreover, a significant induction effect occurs within 4 h of treatment with 5 μM^[4].
MK-2206 (2.5-5 μM; 2-6 h) free base inhibits the activity of AKT kinase in sterol-fed HepG2 cells. At concentrations ≥2.5 μM, it reduces the phosphorylation levels of AKT and its downstream target PRAS40 within 2 h^[4].
MK-2206 (5 μM; 14 h) free base increases cell-surface LDLR expression and stimulates LDL uptake in HepG2 cells under both sterol-fed and sterol-starved conditions^[4].
MK-2206 (5-12 μM; 2-24 h) free base induces LDLR mRNA expression in sterol-fed HepG2 cells within 2 h through a mechanism that enhances transcription (rather than mRNA stabilization) and is independent of de novo protein synthesis^[4].
MK-2206 (5-10 μM; 14 h) free base upregulates LDLR protein levels in sterol-fed IHH, HeLa, IMH, and Hepac1c7 cells^[4].
MK-2206 (5 μM; 24 h) free base inhibits de novo cholesterol biosynthesis in HepG2 cells under sterol starvation conditions^[4].
MK-2206 (5 μM; 14 h) free base upregulates LDLR protein levels in CHO cells and HMGCR-deficient UT-2 cells, indicating that this effect is independent of HMGCR activity^[4].
MK-2206 (0.5-4 μM; 38 h) free base enhances the LDLR (low-density lipoprotein receptor)-inducing effect of Mevastatin (HY-17408) in sterol-starved HepG2 cells^[4].
MK-2206 (5 μM; 2-24 h) free base upregulates the mRNA expression of PCSK9, HMGCR, SREBP-2 and HMGCS1 in sterol-fed HepG2 cells, exerts only minor effects on ACACA, FASN and SCD1, and has no effect on IDOL^[4].
MK-2206 (2.5-5 μM; 14-24 h) free base stimulates LDLR promoter activity in sterol-fed HepG2 cells in an SRE-1-dependent manner^[4].
MK-2206 (5 μM; 14-24 h) free base upregulates LDLR mRNA levels in sterol-fed HepG2 cells in an SREBP-2-dependent manner^[4].
MK-2206 (5 μM; 2-6 h) free base stimulates proteolytic cleavage of FL-SREBP-2 to generate the active NTF-SREBP-2 in sterol-fed HepG2 cells^[4].
MK-2206 (2.5-10 μM; 14 h) free base upregulates LDLR protein levels in primary adult hepatocytes^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[2]

Cell Line:	OCI/AML3, MOLM-13, MV-4-11 human AML cell lines
Concentration:	1, 5 and 10 μM
Incubation Time:	24 h
Result:	Caused a dose-dependent increase in the percentage of cells in the G₁ phase and a corresponding decrease in cells in the S and G₂/M phases across all three cell lines. Increased G₁ phase cells in OCI/AML3 cells from ~45% (control) to ~75% (10 μM MK-2206). Increased G₁ phase cells in MOLM-13 cells from ~45% to ~75%. Increased G₁ phase cells in MV-4-11 cells from ~60% to ~90%.

Apoptosis Analysis^[2]

Cell Line:	OCI/AML3, MOLM-13, MV-4-11 human AML cell lines
Concentration:	1-10 μM
Incubation Time:	24 h
Result:	Caused a dose-dependent increase in the percentage of apoptotic cells in all three cell lines. Increased apoptotic cells in OCI/AML3 cells from ~4% (control) to ~11.5% (10 μM MK-2206). Increased apoptotic cells in MOLM-13 cells from ~3% to ~9.5%. Increased apoptotic cells in MV-4-11 cells from ~0.5% to ~14.5%.

Western Blot Analysis^[2]

Cell Line:	MV-4-11, OCI/AML3, U937 human AML cell lines
Concentration:	0.1, 1, 5 and 10 μM (24 h incubation in MV-4-11 cells); 0.1, 1, 5 and 10 μM (2 h incubation in MV-4-11, OCI/AML3, U937 cells)
Incubation Time:	24 h (MV-4-11 cells); 2 h (MV-4-11, OCI/AML3, U937 cells)
Result:	Induced dose-dependent cleavage of caspase-3 and PARP, and reduced Mcl-1 protein levels to 51% of control at 10 μM in MV-4-11 cells treated for 24 h, with no effect on Bak, Bcl-2, or Bcl-XL levels. Reduced Akt phosphorylation at Ser473, reduced GSK3β phosphorylation at Ser9, and reduced Mcl-1 protein levels to 35% of control in MV-4-11, 26% in OCI/AML3, and 33% in U937 at 10 μM in cells treated for 2 h, with no effect on total Akt, total GSK3β, Bcl-2, or Bcl-XL levels.

Real Time qPCR^[2]

Cell Line:	MV-4-11 human AML cell line
Concentration:	0.1, 1, 5 and 10 μM
Incubation Time:	24 h
Result:	Had no significant effect on Mcl-1 mRNA transcript levels in MV-4-11 cells at any tested concentration.

Western Blot Analysis^[2]

Cell Line:	MV-4-11 human AML cell line
Concentration:	10 μM MK-2206 (following 30 min pretreatment with 10 μM MG-132 or 20 mM lithium chloride)
Incubation Time:	1 h, 2 h, 4 h
Result:	Pretreatment with MG-132 prevented MK-2206-associated downregulation of Mcl-1, maintaining Mcl-1 levels at near-control values across all incubation times. Pretreatment with lithium chloride prevented MK-2206-induced Mcl-1 downregulation and maintained GSK3β phosphorylation at Ser9 at levels comparable to control cells.

Cell Viability Assay^[2]

Cell Line:	U937, OCI/AML3, MV-4-11, MOLM-13 human AML cell lines
Concentration:	200 nM MK-2206 (co-administered with varying cytarabine concentrations)
Incubation Time:	72 h
Result:	Significantly reduced the IC₅₀ of cytarabine in MV-4-11, OCI/AML3, and MOLM-13 cells, but not in U937 cells. Produced ED₅₀ CI values of 0.59 (MV-4-11), 0.37 (MOLM-13), 0.38 (OCI/AML3), and 1.13 (U937), indicating synergistic effects in the first three cell lines and an antagonistic effect in U937 cells.

Western Blot Analysis^[4]

Cell Line:	human hepatoma HepG2 cells (sterol-fed and sterol-starved conditions)
Concentration:	0.5, 1, 2.5, 5, 10 and 20 μM (for 14 h); 5 μM (for time-course analysis)
Incubation Time:	14 h (dose-response); 2-24 h (time-course with 5 μM)
Result:	Induced LDLR protein expression in a dose-responsive manner, with 5 μM and 10 μM exerting maximal effects in sterol-starved and sterol-fed cells, respectively; concentrations above 10 μM mitigated the LDLR-inducing effect. Significantly increased LDLR levels within 4 h of 5 μM treatment, reaching maximum levels at 14 h (sterol-starved) and 18 h (sterol-fed), followed by a slight decline by 24 h.

Western Blot Analysis^[4]

Cell Line:	sterol-fed human hepatoma HepG2 cells
Concentration:	2.5, 5 μM (for 2 h); 2.5, 5 μM (for 6 h)
Incubation Time:	2 h; 6 h
Result:	Potently inhibited AKT activity, as shown by reduced pAKT and pPRAS40 levels within 2 h of treatment with concentrations as low as 2.5 μM.

Real Time qPCR^[4]

Cell Line:	sterol-fed human hepatoma HepG2 cells
Concentration:	5 μM
Incubation Time:	2-24 h; 12 h (followed by actinomycin D treatment for 2-6 h); 5 h (with 1 h cycloheximide preincubation)
Result:	Induced LDLR mRNA levels in a time-dependent manner, with significant increases observed within 2 h of treatment. Had no significant stabilizing effect on LDLR mRNA. Inhibition of protein synthesis with cycloheximide did not reduce MK-2206-mediated induction of LDLR mRNA.

Western Blot Analysis^[4]

Cell Line:	sterol-fed immortalized human hepatocytes (IHH), HeLa, immortalized mouse hepatocytes (IMH), and Hepac1c7 cells
Concentration:	5, 10 μM
Incubation Time:	14 h
Result:	Induced LDLR protein expression in all tested cell lines, with significant increases observed at 5 μM and 10 μM.

Western Blot Analysis^[4]

Cell Line:	Chinese hamster ovary (CHO) cells and UT-2 cells (HMGCR-deficient CHO cells)
Concentration:	5 μM
Incubation Time:	14 h
Result:	Induced LDLR protein expression in both CHO and UT-2 cells, with significant increases relative to vehicle-treated cells.

Western Blot Analysis^[4]

Cell Line:	sterol-starved human hepatoma HepG2 cells treated with mevastatin
Concentration:	0.5, 1, 2, 4 μM
Incubation Time:	14 h (following 24 h mevastatin pretreatment)
Result:	Combination treatment with MK-2206 and mevastatin markedly increased LDLR protein levels relative to treatment with either agent alone.

Real Time qPCR^[4]

Cell Line:	sterol-fed human hepatoma HepG2 cells
Concentration:	5 μM
Incubation Time:	2-24 h
Result:	Induced mRNA expression of PCSK9, HMGCR, SREBP-2, and HMGCS1 in a time-dependent manner, with significant increases observed at multiple time points. Had no effect on IDOL mRNA levels, and only modestly induced ACACA, FASN, and SCD1 mRNA levels with significant increases at 8 h.

Real Time qPCR^[4]

Cell Line:	sterol-fed human hepatoma HepG2 cells with SREBP-2 knockdown
Concentration:	5 μM
Incubation Time:	14 h (24 h post-transfection)
Result:	Knockdown of SREBP-2 significantly diminished the LDLR-inducing effect of MK-2206 on LDLR mRNA levels.

Western Blot Analysis^[4]

Cell Line:	sterol-fed human hepatoma HepG2 cells
Concentration:	5 μM
Incubation Time:	2, 4, 6 h
Result:	Increased levels of CTF-SREBP-2 (membrane fraction) and NTF-SREBP-2 (nuclear extract), with a concomitant reduction in FL-SREBP-2 levels, indicating enhanced proteolytic cleavage of SREBP-2.

In Vivo

MK-2206 free base enhances the anti-tumor efficacy of multiple chemotherapeutic agents in preclinical ovarian cancer xenograft models and induces mild, transient hyperglycemia and hyperinsulinemia in animals that resolves post-treatment^[1].
MK-2206 (120 mg/kg; p.o.; alternate days; 4 total doses) free base alleviates UUO-induced renal fibrosis in mice by reducing inflammation, inhibiting epithelial-mesenchymal transition, suppressing myofibroblast activation and extracellular matrix deposition, and blocking activation of the Akt/mTOR signaling pathway^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	strain not specified (n=6 per group)^[3]
Dosage:	120 mg/kg
Administration:	p.o.; alternate days; 4 total doses
Result:	Reduced renal tubular injury and interstitial collagen fiber deposition compared to untreated UUO mice. Lowered renal mRNA expression of inflammatory factors TGF-β1, IL-1β, and IL-6. Restored renal E-cadherin expression, reduced expression of myofibroblast markers α-SMA and Vimentin, and downregulated EMT-associated transcription factors Twist and Snail in UUO kidneys. Decreased renal protein expression of extracellular matrix components Collagen I and Fibronectin. Inhibited UUO-induced phosphorylation of Akt and mTOR in kidney tissue, reducing the p-Akt/Akt ratio and p-mTOR/mTOR ratio compared to untreated UUO mice.

Molecular Weight

407.47

Formula

C₂₅H₂₁N₅O

CAS No.

1032349-93-1

SMILES

O=C1N2C(C3=CC(C4=CC=CC=C4)=C(C(C=C5)=CC=C5C6(CCC6)N)N=C3C=C2)=NN1

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Yan L. Abstract# DDT01-1: MK-2206: A potent oral allosteric AKT inhibitor. Cancer research. 2009 May 1;69(9_Supplement):DDT01-1.

[2]. Lu JW, et al. MK-2206 induces apoptosis of AML cells and enhances the cytotoxicity of cytarabine. Med Oncol. 2015;32(7):206.

[3]. Chen M, et al. MK-2206 Alleviates Renal Fibrosis by Suppressing the Akt/mTOR Signaling Pathway In Vivo and In Vitro. Cells. 2022;11(21):3505. Published 2022 Nov 5. [Content Brief]

[4]. Bjune K, et al. MK-2206, an allosteric inhibitor of AKT, stimulates LDLR expression and LDL uptake: A potential hypocholesterolemic agent. Atherosclerosis. 2018;276:28-38.

MK-2206 free base Related Classifications

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