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MK-2206 dihydrochloride

(Synonyms: MK-2206 (2HCl))
484 Cited Publications
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Based on 484 publication(s) in Google Scholar

MK-2206 dihydrochloride (MK-2206 2HCl) 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 dihydrochloride inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia.

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  • Pureté: 99.94%
  • CAS No.: 1032350-13-2
  • Formule: C25H23Cl2N5O
  • Masse moléculaire:480.39
  • Stockage:

    4°C, sealed storage, away from moisture

    * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

  • MK-2206 dihydrochloride Chemical Structure
    MK-2206 dihydrochloride Chemical Structure
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
  • Experimental Validation Results for MK-2206 dihydrochloride
CAS No.: 1032350-13-2
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  • MK-2206 dihydrochloride Chemical Structure
    MK-2206 dihydrochloride Chemical Structure
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    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Nat Cancer. 2024 Jul;5(7):1082-1101. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Nat Cancer. 2024 Jul;5(7):1082-1101. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Nat Commun. 2024 Jun 17;15(1):5144. [Abstract]

    Customer Validation
     Representative Western blots from isolated tubule suspensions cultured for 30 min in indicated K+ concentrations with or without the AKT inhibitor MK2206 (10 μM).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2024 Jul;11(26):e2306348. [Abstract]

    Customer Validation
     MK‐2206 (5 µM; 18 h) significantly suppresses IL11‐induced upregulation of PDL1, but did not affect the level of p‐EGFR.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Neuroinflammation. 2023 Feb 24;20(1):49. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Nov:120:155074. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Phytomedicine. 2023 Nov:120:155074. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Nat Commun. 2021 Jun 30;12(1):4050. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Mol Cell. 2021 Jan 21;81(2):370-385.e7. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2021 Jan;11(1):71-88. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharm Sin B. 2021 Jun;11(6):1592-1606. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Proc Natl Acad Sci U S A. 2019 Feb 19;116(8):2996-3005. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Oncogene. 2019 Jun;38(26):5250-5264. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Invest Dermatol. 2019 Jan;139(1):71-80. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Cancer Cell. 2018 Jun 11;33(6):1061-1077.e6. [Abstract]

    Customer Validation
     Dih10 cells are treated with CDDP (20 μM) in the presence or absence of the Akt inhibitor MK2206 (5 μM).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Nat Commun. 2018 May 8;9(1):1816. [Abstract]

    Customer Validation
     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-10AP and MCF-10AH1047R cells stably expressing empty vector (EV) or mutant HRASQ61R treated with 2 µM MK2206 (AKTi) at different time points.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2018 Oct 3;9(10):1015. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2018 Nov;39(11):1787-1796. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Clin Epigenetics. 2018 May 23:10:69. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Cancer Sci. 2018 Apr;109(4):944-955. [Abstract]

    Customer Validation
     Western blotting of Sox2 and b-actin in A549 cells with or without IGF2 treated in the presence or absence of MK-2206.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Int J Biochem Cell Biol. 2018 Jun:99:43-51. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Cancer. 2018 Jun 14;9(14):2480-2491. [Abstract]

    Customer Validation
     Analysis of indicated proteins in Cry1 silencing osteosarcoma cells after MK-2206 treatment. Data are expressed as the mean±standard deviation.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: J Cell Biochem. 2018 May;119(5):3885-3891. [Abstract]

    Customer Validation
     Western blot showed the protein expression of P-gp,MRP1, PTEN, p-AKT, Bax, Bcl-2, and cleaved caspase-3.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Radiat Res. 2018 Aug;190(2):204-215. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Br J Cancer. 2017 Sep 26;117(7):974-983. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Hum Mol Genet. 2017 Sep 15;26(18):3553-3563. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Jan 31;8(5):8536-8549. [Abstract]

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Oncotarget. 2017 Jul 18;8(29):47642-47654. [Abstract]

    Customer Validation
     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-Aktser473, JNK, p-JNKThr183 with or without MK-2206 (n=3).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Modern Oncology. 2017,25(01):0009-0013.

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Proc Natl Acad Sci U S A. 2016 Jul 26;113(30):E4338-47. [Abstract]

    Customer Validation
     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).

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Harvard University. 2016 Aug.

    Customer Validation
     Mouse embryonic fibroblasts (MEFs) are deprived of Arginine and treated with 2 µM MK2206 for up to 6 hours.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Okayama University. 2015.

    Customer Validation
     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.

  • 1/16

    MK-2206 dihydrochloride purchased from MedChemExpress. Usage Cited in: Cell. 2014 Feb 13;156(4):771-85. [Abstract]

    Customer Validation
     (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.

  • MK-2206 dihydrochloride