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MK-2206 2HCl

Catalog No.S1078
12 Reviews 57 Product Citations

MK-2206 2HCl is a highly selective inhibitor of Akt1/2/3 with IC50 of 8 nM/12 nM/65 nM, respectively; no inhibitory activities against 250 other protein kinases observed. Phase 2.

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MK-2206 2HCl Chemical Structure

MK-2206 2HCl Chemical Structure
Molecular Weight: 480.39

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Product Citations(57)

Customer Reviews(12)

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MK-2206 2HCl is available in the following compound libraries:

Inhibitor Library Kinase Inhibitor Library Bioactive Compound Library Cambridge Cancer Compound Library

Product Information

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Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description MK-2206 2HCl is a highly selective inhibitor of Akt1/2/3 with IC50 of 8 nM/12 nM/65 nM, respectively; no inhibitory activities against 250 other protein kinases observed. Phase 2.
Targets Akt1 Akt2 Akt3
IC50 8 nM 12 nM 65 nM [1]
In vitro MK-2206 is an allosteric inhibitor and is activated by the pleckstrin homology domain. MK-2206 inhibits auto-phosphorylation of both Akt T308 and S473. MK-2206 also prevents Akt-mediated phosphorylation of downstream signaling molecules, including TSC2, PRAS40 and ribosomal S6 proteins. [1] MK-2206 inhibits Ras wild-type (WT) cell lines (A431, HCC827, and NCI-H292) more potently when compared to Ras-mutant cell lines (NCI-H358, NCI-H23, NCI-H1299, and Calu-6). MK-2206 also shows synergistic responses in combination with cytotoxic agents such as erlotinib or lapatinib in lung NCI-H460 or ovarian A2780 tumor cells. [2] MK-2206 or siRNA-mediated Akt inhibition strongly activates autophagy in human glioma cells. However, eukaryotic elongation factor-2 (eEF-2) silencing suppresses MK-2206-induced-autophagy, with a promotion of apoptotic cell death. [3]
If your cell culture is contaminated by mycoplasma, please use our new product MycoClean™ Mycoplasma Removal Kit (Catalog No. K9000). This is a novel, efficient and safe kit to remove mycoplasma.
In vivo MK-2206 shows 60% TGI and inhibits more than 70 % of phospho-Akt1/2 (T308 and S473) in A2780 ovarian cancer xenografts at a dose of 240 mg/kg. [1] MK-2206 exhibits significant antitumor activity in NCI-H292 xenograft in combination with erlotinib or lapatinib. [2]
Features MK-2206 is the first allosteric small molecule inhibitor of Akt to enter clinical development.

Protocol(Only for Reference)

Kinase Assay: [4]

Akt kinases assay Akt kinases are assayed by a GSK-derived biotinylated peptide substrate. The extent of peptide phosphorylation is determined by Homogeneous Time Resolved Fluorescence (HTRF) using a lanthanide chelate (Lance)-coupled monoclonal antibody specific for the phosphopeptide in combination with a streptavidin-linked allophycocyanin (SA-APC) fluorophore which will bind to the biotin moiety on the peptide. When the Lance and APC are in proximity, a non-radiative energy transfer takes place from the Lance to the APC, followed by emission of light from APC at 655 nm. Working Solution: 100X protease inhibitor cocktail (PIC): 1mg/mL benzamidine, 0.5 mg/mL pepstatin, 0.5 mg/mL leupeptin, 0.5 mg/mL aprotinin; 10X assay buffer: 500 mM HEPES, pH7.5, 1% PEG, 16.6 mM EDTA, 1 mM EGTA, 1% BSA, 20 mM 9-glycerol phosphate; Quench buffer 50 mM HEPES pH 7.3, 16.6 mM EDTA, 0.1% BSA, 0.1% Triton X-100, 0.17 nM labeled monoclonal antibody, 0.0067 mg/mL SA-APC; ATP/MgCl2 working solution: 1X Assay buffer, 1 mM DTT, 1X PIC, 5% glycerol, active Akt; Peptide working solution: 1X Assay buffer, 1 mM DTT, 1X PIC, 5% glycerol, 2 TM GSK biotinylated peptide. The reaction is assembled by adding 16 µL of ATP/MgCl2 working solution to the appropriate wells. MK-2206 or vehicle (1.0 µL) is added followed by 10 µL of peptide working solution. The reaction is started by adding 13 μL of the enzyme working solution and mixing. The reaction is allowed to proceed for 50 min and then stopped by the addition of 60 µL HTRF quench buffer. The stopped reactions are incubated at room temperature for at least 30 min and then read in the instrument.

Cell Assay: [2]

Cell lines A431, HCC827, NCI-H292, NCI-H358, NCI-H23, NCI-H1299, Calu-6 and NCI-H460 cells
Concentrations 0, 0.3, 1 and 3 μM
Incubation Time 72 or 96 hours
Method MK-2206 is dissolved in DMSO as a stock solution and diluted by culture media before use. Cells are seeded at a density of 2-3 × 103 in 96-well plates and incubated for 24 hours. Then MK-2206 (0, 0.3, 1 and 3 μM) is added to the cells. Cell proliferation is determined after 72 or 96 hours.

Animal Study: [2]

Animal Models SK-OV-3, NCI-H292, HCC70, PC-3, and NCI-H460 models in male CD1-nude mice
Formulation Formulated in 30% Captisol
Dosages 120 mg/kg
Administration Orally administered
1

References

Chemical Information

Download MK-2206 2HCl SDF
Molecular Weight (MW) 480.39
Formula

C25H21N5O.2HCl
CAS No. 1032350-13-2
Synonyms N/A
Solubility (25°C)

* <1 mg/ml means slightly soluble or insoluble
  • DMSO 14 mg/mL
  • Water 1 mg/mL
  • Ethanol <1 mg/mL
Storage 2 years -20°CPowder
6 months-80°Cin DMSO
Chemical Name 8-(4-(1-aminocyclobutyl)phenyl)-9-phenyl-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3(2H)-one

Preparing Stock Solutions

Stock Solution (1ml DMSO) 1mM 10mM 20mM 30mM
Mass(mg) 0.48039 4.8039 9.6078 14.4117
Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (12)


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Source Biochim Biophys Acta, 2012, 1823(5), 987-96. MK-2206 2HCl purchased from Selleck
Method Immunofluorescence
Cell Lines HC11 cells
Concentrations 10 µM
Incubation Time 1 h
Results whole ADRP levels, estimated by Western blot , decreased only in the presence of MK -2206 and LY294002. In most cases, ADRP decorated the surface of small lipid droplets and appeared as little patches on large cytoplasmic lipid droplets. With the exception of SP600125, which induced a strong ADRP coating of almost all cytoplasmic lipid droplets (although this inhibitor did not increase ADRP synthesis), variation in the distribution of ADRP at the surface of lipid droplet was difficult to estimate, notably because the signal was faint and uneven.

Click to enlarge 		Rating
Source Oncotarget, 2011, 2(12), 1109-26.. MK-2206 2HCl purchased from Selleck
Method Western blot/ Wst-1 assay
Cell Lines ATC/ FTC cell lines
Concentrations 500 nM
Incubation Time 1 h/72 h
Results One-hour treatment with the AKT inhibitor MK-2206 (0.5 μM) or with the MEK inhibitor U0126 (10 μM) effectively abolished AKT and ERK1/2 phosphorylation in all cell lines.

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Source Gynecol Oncol, 2011, 123(1), 13-8.. MK-2206 2HCl purchased from Selleck
Method Western blot
Cell Lines ovarian cancer cell lines
Concentrations 1-6 μM
Incubation Time 1 h/72 h
Results Activation of pAKT by IGF-1 in the low-grade cell line HOC-7 was blocked by the AKT inhibitor MK-2206.

Click to enlarge 		Rating
Source FASEB J, 2013, 27(4), 1644-56.. MK-2206 2HCl purchased from Selleck
Method Clonogenic growth assay
Cell Lines U2OS cells
Concentrations 1 μM
Incubation Time 9 d
Results Specific inhibition of PKB activity using MK-2206 or triciribine also significantly reduced cell growth, although to a lesser extent compared to PI-103, suggesting that both the PKB and mTOR pathways are important for anchorage-dependent growth.

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Source Cancer Res, 2013, 73(7), 2189-98.. MK-2206 2HCl purchased from Selleck
Method Western blot
Cell Lines SKNAS/SJNB8/IMR32/GIMEN/SHEP2/KCNR/NGP/LAN1/LAN5/TR14/UHGNP cell lines
Concentrations 8 μM
Incubation Time 48 h
Results The 8 μM MK-2206 treatments resulted in effective pathway inhibition in all cell lines as shown by western blot for phosphoryl ated FOXO3a and PRAS40 as well as AKT serine 473 phosphorylation.

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Source MK-2206 2HCl purchased from Selleck
Method Western blot analysis
Cell Lines MCF-7 cells
Concentrations 0 nM/100 nM/250 nM/1000 nM
Incubation Time 24 h
Results The effect of MK-2206 on the serine 473 phosphorylation mark of AKT 1 was uneven and did not correlate with inhibition of AKT activity, but the AKT1 mutant cells maintained higher levels of AKT1 serine 473 phosphorylation with increasing concentrations of MK-2206. Of note, MK-2206 completely inhibited AKT2 activation at 100 nM, a concentration where PIK3CA E545K mutant, but not AKT1 mutant cells were already strongly growth inhibited. MK-2206 treatment up to 1 μM did not have strong effects on other protein biomarkers such as ribosomal protein S6, ev en though growth was suppressed by approximately 80% in MCF-7 cells at this concentration.

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Source J Cell Biochem, 2010, 112, 924–932. MK-2206 2HCl purchased from Selleck
Method Confocal microscopy
Cell Lines platelets
Concentrations 1μM
Incubation Time
Results Upon treatment with increasing concentrations of AEA from 0.1 to 10 mM (Fig. B–D) platelets were fully fluorescently marked as compared to control (Fig. A) and the increase in DAF 2 fluorescence intensity appears to be dose-dependent. In agreement with data shown in Figure 4, SR1(Fig. E) and MK2206 (Fig. F) abolished fluorescence intensity induced by AEA, while LY294002 (Fig. 5G) was less potent.

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Source Radiat Oncol, 2009, 4, 43. MK-2206 2HCl purchased from Selleck
Method Western blot, clonogenic survival assay
Cell Lines U87MG cells
Concentrations 1 μM
Incubation Time 1 h
Results Akt inhibitor MK-2206 showed similar effect. MK-2206 is a potent allosteric Akt inhibitor with IC50 at 8 nm, 2 mM, 65 mM for Akt1, Akt2 and Akt3 respectively. U87MG cells were preincubated with 1 μM MK-2206 for 1 hr, followed by irradiation at 0 - 9 Gy. As shown in Fig C, MK-2206 treatment abolished IR-induced Akt phosphorylation. Moreover, treatment with MK-2206 also increased the radiosensitivity of U87MGcells (Fig. D)

Click to enlarge 		Rating
Source J Cell Biochem, 2010, 112, 924–932. MK-2206 2HCl purchased from Selleck
Method Western blot
Cell Lines platelets
Concentrations 1 μM
Incubation Time
Results eNOSser1177 phosphorylation was greatly reduced by LY294002 and cancelled by MK2206 but it was not modified by platelet pretreatment with EGTA or BAPTA/AM.

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Source Sci Signal, 2011, 4, rs9. MK-2206 2HCl purchased from Selleck
Method ELISA
Cell Lines HeLa cells
Concentrations 1 μM
Incubation Time
Results Treatment of infected cells with kinase inhibitors directed at Akt (MK-2206), MEK(PD 98059), PKC(CEC), or Pim family kinases identified a dominant role for Pim family kinases in the release of IL-8 from Salmonella-infected epithelial cells.

Click to enlarge 		Rating
Source Dr. Zhang of Tianjin Medical University. MK-2206 2HCl purchased from Selleck
Method Western blot
Cell Lines Breast cancer cells
Concentrations 0-10 nM
Incubation Time 3 h
Results Breast cancer cells were serum starved for 24 h, pretreated with the indicated concentrations of MK-2206 for 3 h, and then treated with 100ng/ml EGF for 15 min.

Click to enlarge 		Rating
Source J Cell Biochem, 2010, 112, 924–932. MK-2206 2HCl purchased from Selleck
Method Nitriter+Nitrate(NOX) measurement, cGMP detection
Cell Lines platelets
Concentrations 1 μM
Incubation Time 1 min
Results As shown in Figure 4 SR1 significantly reduced both NOx and cGMP formation, while SR2 failed to affect these parameters.

Product Citations (57)

  • Direct Reversal of Glucocorticoid Resistance by AKT Inhibition in Acute Lymphoblastic Leukemia. [Piovan E, et al Cancer Cell 2013;10.1016/j.ccr.2013.10.022]

    PubMed: 24291004

  • Expansion of oligodendrocyte progenitor cells following SIRT1 inactivation in the adult brain. [Rafalski VA, et al. Nat Cell Biol 2013;15(6):614-24]

    PubMed: 23644469

  • The Akt-SRPK-SR Axis Constitutes a Major Pathway in Transducing EGF Signaling to Regulate Alternative Splicing in the Nucleus. [Zhou Z, et al. Mol Cell 2012;47(3):422-33]

    PubMed: 22727668

  • Deubiquitylation and stabilization of PTEN by USP13. [Zhang J, et al Nat Cell Biol 2013;10.1038/ncb2874]

    PubMed: 24270891

  • Human Merkel cell polyomavirus small T antigen is an oncoprotein targeting the 4E-BP1 translation regulator. [Shuda M, et al. J Clin Invest 2011;121(9), 3623-3634]

    PubMed: 21841310

  • Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice. [Cheung R, et al. J Clin Invest 2011;121(11):4446-61]

    PubMed: 22005300

  • MTORC1 functions as a transcriptional regulator of autophagy by preventing nuclear transport of TFEB. [Martina JA, et al. Autophagy 2012;8(6), 903-914]

    PubMed: 22576015

  • Cytotoxic activity of the novel Akt inhibitor, MK-2206, in T-cell acute lymphoblastic leukemia. [Simioni C, et al. Leukemia 2012;26(11):2336-42]

    PubMed: 22614243

  • Epithelial to mesenchymal transition rewires the molecular path to PI3-Kinase-dependent proliferation. [Salt MB, et al Cancer Discov 2013;10.1158/2159-8290.CD-13-0520]

    PubMed: 24302555

  • Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors. [Ercan D, et al. Cancer Discov 2012;2(10), 934-947]

    PubMed: 22961667

  • The TSC-mTOR pathway regulates macrophage polarization. [Byles V, et al Nat Commun 2013;2013;4:2834]

    PubMed: 24280772

  • Relaxin increases human endothelial progenitor cell NO and migration and vasculogenesis in mice. [Segal MS, et al. Blood 2012;119(2):629-36]

    PubMed: 22028476

  • Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition. [Shi H, et al. Cancer Res 2011;71(15), 5067-5074]

    PubMed: 21803746

  • FOXO3a Is A Major Target Of Inactivation By PI3K/AKT Signaling In Aggressive Neuroblastoma. [Santo EE, et al. Cancer Res 2013;ahead of print]

    PubMed: 23378341

  • Antitumor activity of BRAF inhibitor vemurafenib in preclinical models of BRAF-mutant colorectal cancer. [Yang H, et al. Cancer Res 2012;72(3), 779-789]

    PubMed: 22180495

  • Resistance to selective BRAF inhibition can be mediated by modest upstream pathway activation. [Su F, et al. Cancer Res 2012;72(4), 969-978]

    PubMed: 22205714

  • Effects of Akt inhibitor MK2206 on proliferation and apoptosis of breast cancer cells. [Sangai T, et al. Clin Cancer Res 2012;18(20):5816-28]

    PubMed: 22932669

  • Akt Inhibitors MK-2206 and Nelfinavir Overcome mTOR Inhibitor Resistance in Diffuse Large B-cell Lymphoma. [Petrich AM, et al. Clin Cancer Res 2012;18(9):2534-44]

    PubMed: 22338016

  • PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system. [Beaver JA, et al. Clin Cancer Res 2013;ahead of print]

    PubMed: 23888070

  • Phosphoproteomic analysis of salmonella-infected cells identifies key kinase regulators and SopB-dependent host phosphorylation events. [Rogers LD, et al. Sci Signal 2011;4(191), rs9]

    PubMed: 21934108

  • Snail1 controls TGF-β responsiveness and differentiation of mesenchymal stem cells. [Batlle R, et al. Oncogene 2012;ahead of print]

    PubMed: 22869142

  • Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors. [Antico Arciuch VG, et al. Oncotarget 2011;2(12):1109-26]

    PubMed: 22190384

  • Metabolic biomarkers for response to PI3K inhibition in basal-like breast cancer. [Moestue SA, et al. Breast Cancer Res 2013;ahead of print]

    PubMed: 23448424

  • Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase. [Ruisanchez E, et al FASEB J 2013;10.1096/fj.13-234997 fj.13-234997]

    PubMed: 24249637

  • PtdIns5P is an oxidative stress-induced second messenger that regulates PKB activation. [Jones DR, et al. FASEB J 2012;ahead of print]

    PubMed: 23241309

  • Selective Cox-2 inhibitor celecoxib induces epithelial-mesenchymal transition in human lung cancer cells via activating MEK-ERK signaling. [Wang ZL, et al. Carcinogenesis 2013;34(3):638-46]

    PubMed: 23172668

  • PERK Utilizes Intrinsic Lipid Kinase Activity To Generate Phosphatidic Acid, Mediate Akt Activation, and Promote Adipocyte Differentiation. [Bobrovnikova-Marjon E, et al. Mol Cell Biol 2012;32(12):2268-78]

    PubMed: 22493067

  • Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells. [Grabinski N, et al. Mol Cancer 2012;11, 85]

    PubMed: 23167739

  • Preventing the calorie restriction-induced increase in insulin-stimulated Akt2 phosphorylation eliminates calorie restriction's effect on glucose uptake in skeletal muscle. [Sharma N, et al. Biochim Biophys Acta 2012;1822(11):1735-40]

    PubMed: 22846604

  • Prolactin and epidermal growth factor stimulate adipophilin synthesis in HC11 mouse mammary epithelial cells via the PI3-kinase/Akt/mTOR pathway. [Pauloin A, et al. Biochim Biophys Acta 2012;1823(5), 987-996]

    PubMed: 22426621

  • Prolactin and epidermal growth factor stimulate adipophilin synthesis in HC11 mouse mammary epithelial cells via the PI3-kinase/Akt/mTOR pathway. [Pauloin A, et al. Biochim Biophys Acta 2012;1823(5):987-96]

    PubMed: 22426621

  • Relaxin induces rapid dilation of rodent small renal and human subcutaneous arteries via PI3 kinase and nitric oxide. [McGuane JT, et al. Endocrinology 2011;152(7):2786-96]

    PubMed: 21558316

  • Dual regulation of Glycogen Synthase Kinase 3 (GSK3)α/β by Protein Kinase C (PKC)α and Akt promotes thrombin-mediated integrin αIIbβ3 activation and granule secretion in platelets. [Moore SF, et al. J Biol Chem 2012;ahead of print]

    PubMed: 23239877

  • MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes. [Dey N, Das F, et al. J Biol Chem 2011;286(29):25586-603]

    PubMed: 21613227

  • FOG2 Protein Down-regulation by Transforming Growth Factor-β1-induced MicroRNA-200b/c Leads to Akt Kinase Activation and Glomerular Mesangial Hypertrophy Related to Diabetic Nephropathy. [Park JT, et al. J Biol Chem 2013;288(31):22469-80]

    PubMed: 23788640

  • IKBKE protein activates Akt independent of phosphatidylinositol 3-kinase/PDK1/mTORC2 and the pleckstrin homology domain to sustain malignant transformation. [Guo JP, et al. J Biol Chem 2011;286(43), 37389-37398]

    PubMed: 21908616

  • P90 RSK arranges Chk1 in the nucleus for monitoring of genomic integrity during cell proliferation. [Li P, Goto H, et al. Mol Biol Cell 2012;23(8):1582-92]

    PubMed: 22357623

  • The insulin-like growth factor 1 pathway is a potential therapeutic target for low-grade serous ovarian carcinoma. [King ER, Zu Z, et al. Gynecol Oncol 2011;123(1):13-8]

    PubMed: 21726895

  • Casitas B-lineage lymphoma mutants activate AKT to induce transformation in cooperation with class III receptor tyrosine kinases. [Polzer H, et al. Exp Hematol 2013;41(3), 271-280.e4]

    PubMed: 23127761

  • CBL mutants activate AKT to induce transformation in cooperation with class III receptor tyrosine kinases. [Polzer H, et al. Exp Hematol 2013;41(3):271-280.e4]

    PubMed: 23127761

  • A switch from canonical to noncanonical Wnt signaling mediates drug resistance in colon cancer cells. [Bordonaro M, et al. PLoS One 2011;6(11):e27308]

    PubMed: 22073312

  • K-RAS mutant pancreatic tumors show higher sensitivity to MEK than to PI3K inhibition in vivo. [Hofmann I, et al. PLoS One 2012;7(8):e44146]

    PubMed: 22952903

  • Expression of SLP-2 Was Associated with Invasion of Esophageal Squamous Cell Carcinoma. [Cao W, et al. PLoS One 2013;8(5):e63890]

    PubMed: 23667687

  • Akt Regulates TNFα Synthesis Downstream of RIP1 Kinase Activation during Necroptosis. [McNamara CR, et al. PLoS One 2013;8(3):e56576]

    PubMed: 23469174

  • AKT Signaling as a Novel Factor Associated with In Vitro Resistance of Human AML to Gemtuzumab Ozogamicin. [Rosen DB, et al. PLoS One 2013;8(1), e53518]

    PubMed: 23320091

  • Activation of AKT by hypoxia: a potential target for hypoxic tumors of the head and neck. [Stegeman H, et al. BMC Cancer 2012;12, 463]

    PubMed: 23046567

  • Propionyl-L-carnitine induces eNOS activation and nitric oxide synthesis in endothelial cells via PI3 and Akt kinases. [Ning WH, et al. Vascul Pharmacol 2013;ahead of print]

    PubMed: 23850990

  • ATM-depletion in breast cancer cells confers sensitivity to PARP inhibition. [Gilardini Montani MS, et al J Exp Clin Cancer Res 2013;10.1186/1756-9966-32-95.]

    PubMed: 24252502

  • The Anandamide effect on NO/cGMP pathway in human platelets. [Signorello MG, et al. J Cell Biochem 2011;112(3), 924-932]

    PubMed: 21328466

  • Activation of Human Platelets by 2-Arachidonoylglycerol: Role of PKC in NO/cGMP Pathway Modulation. [Signorello MG, et al. Curr Neurovasc Res 2011;8(3):200-9]

    PubMed: 21675954

  • MK-2206 induces cell cycle arrest and apoptosis in HepG2 cells and sensitizes TRAIL-mediated cell death. [Jiao P, et al. Mol Cell Biochem 2013;ahead of print]

    PubMed: 23797319

  • Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells. [Li HF, et al. Radiat Oncol 2009;4, 43]

    PubMed: 19828040

  • Anandamide enhances expression of heat shock protein 72 to protect against ischemia-reperfusion injury in rat heart. [Li Q, et al. J Physiol Sci 2013;63(1):47-53]

    PubMed: 23007622

  • Combining radiotherapy with MEK1/2, STAT5 or STAT6 inhibition reduces survival of head and neck cancer lines. [Stegeman H, et al. Mol Cancer ;12(1):133]

    PubMed: 24192080

  • Injury-triggered Akt phosphorylation of Cx43: a ZO-1-driven molecular switch that regulates gap junction size. [Dunn CA, et al. J Cell Sci ;10.1242/jcs.142497]

    PubMed: 24213533

  • Neuropilin-2 is upregulated in lung cancer cells during TGFβ1-induced epithelialmesenchymal transition. [Nasarre P, et al. Cancer Res ;10.1158/0008-5472]

    PubMed: 24121493

  • Akt and Rac1 signaling are jointly required for insulin-stimulated glucose uptake in skeletal muscle and downregulated in insulin resistance. [Sylow L, et al. Cell Signal ;10.1016/j.cellsig.2013.11.007]

    PubMed: 24216610

Tech Support & FAQs

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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