| Field | Specification |
|---|---|
| Target | |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C25H22ClN5O |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
MK-2206 is an orally active pan-AKT inhibitor, showing IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. It suppresses Akt/mTOR signaling and lowers downstream GSK3β and Mcl-1 levels through proteasomal degradation, and it triggers G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. In animals, MK-2206 produces transient hyperglycemia and hyperinsulinemia, and it can be used in research on solid tumors, renal fibrosis and hypercholesterolemia[1][2][3][4]. It is supplied as an off-white to light yellow solid (C25H22ClN5O, MW 443.93) at 99.72% purity.
Physical & Chemical Properties
| CAS Number | 1032349-77-1 |
|---|---|
| Molecular Formula | C25H22ClN5O |
| Molecular Weight | 443.93 g/mol |
| Purity | 99.72% |
| Appearance | Solid |
| Color | Off-white to light yellow |
| SMILES | O=C1NN=C2C3=C(N=C(C4=CC=C(C5(N)CCC5)C=C4)C(C6=CC=CC=C6)=C3)C=CN21.[H]Cl |
| Target | Akt1, Akt2, Akt3 |
| Signaling Pathway | Apoptosis; Stem Cell/Wnt; PI3K/Akt/mTOR |
| Solubility | In Vitro: DMSO: 100 mg/mL (225.26 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | 4°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
Akt1 8 nM (IC50) |
Akt2 12 nM (IC50) |
Akt3 65 nM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under 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.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (225.26 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (5.63 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (5.63 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (5.63 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
MK-2206 inhibits Akt1 kinase activity in various human cancer cell lines (IC50 approximately 20 nM), blocks downstream Akt signaling, and strongly inhibits proliferation of cancer cell lines carrying specific PI3K pathway gene defects, whereas Ras pathway activation predicts no response[1]. In relevant human cancer cell lines, combining MK-2206 with various chemotherapeutic agents and targeted inhibitors produces additive or synergistic antiproliferative and pro-apoptotic sensitizing effects[1]. In the acute myeloid leukemia (AML) cell lines U937, OCI/AML3, MV-4-11 and MOLM-13, MK-2206 (72 h) potently inhibits growth (IC50 values ranging from 0.6 to 2.5 μM), while being very weakly cytotoxic to normal human peripheral blood mononuclear cells (PBMCs)[2]. In OCI/AML3, MOLM-13 and MV-4-11 AML cell lines, MK-2206 (1-10 μM; 24 h) causes dose-dependent G1 cell cycle arrest[2]. MK-2206 (1-10 μM; 24 h) triggers apoptosis in a dose-dependent manner in the acute myeloid leukemia (AML) cell lines OCI/AML3, MOLM-13 and MV-4-11, with apoptotic cell populations rising significantly at higher doses[2]. In MV-4-11 acute myeloid leukemia (AML) cells, MK-2206 (0.1-10 μM; 2-24 h) induces apoptosis through caspase-3 and PARP cleavage; it also lowers Mcl-1 protein levels dose-dependently in MV-4-11, OCI/AML3 and U937 AML cells and, after 2 to 24 h of treatment, inhibits phosphorylation of Akt at Ser473 and of GSK3β at Ser9, respectively[2]. In MV-4-11 acute myeloid leukemia (AML) cells, MK-2206 (10 μM; 1-4 h) downregulates Mcl-1 through a GSK3β-mediated, proteasome-dependent mechanism[2]. Combining MK-2206 (200 nM; 72 h) with Cytarabine synergistically increases cytotoxicity in the acute myeloid leukemia (AML) cell lines MV-4-11, MOLM-13 and OCI/AML3 (ED50 CI value < 1), whereas antagonistic effects occur in U937 AML cells (ED50 CI value = 1.13)[2]. In HK-2 cells, MK-2206 (0.5-5 μM; 48 h) suppresses TGF-β1-induced fibrosis, epithelial-mesenchymal transition (EMT), and Akt/mTOR signaling pathway activation. At the effective concentration of 1 μM, Collagen I and Fibronectin mRNA expression is reduced, E-cadherin levels are restored, and expression of mesenchymal markers and phosphorylated Akt/mTOR proteins is suppressed[3]. In HepG2 cells under sterol feeding or sterol starvation, MK-2206 (0.5-20 μM; 2-24 h) raises LDLR protein levels. Induction peaks in the sterol starvation group at 5 μM for 14 h and in the sterol feeding group at 10 μM for 14 h. A significant induction effect is also seen within 4 h of treatment with 5 μM[4]. In sterol-fed HepG2 cells, MK-2206 (2.5-5 μM; 2-6 h) inhibits AKT kinase activity. At concentrations ≥2.5 μM, phosphorylation of AKT and its downstream target PRAS40 is reduced within 2 h[4]. In HepG2 cells under both sterol-fed and sterol-starved conditions, MK-2206 (5 μM; 14 h) raises cell-surface LDLR expression and stimulates LDL uptake[4]. In sterol-fed HepG2 cells, MK-2206 (5-12 μM; 2-24 h) induces LDLR mRNA expression within 2 h by enhancing transcription (rather than mRNA stabilization), independently of de novo protein synthesis[4]. In sterol-fed IHH, HeLa, IMH, and Hepac1c7 cells, MK-2206 (5-10 μM; 14 h) increases LDLR protein levels[4]. Under sterol starvation conditions, MK-2206 (5 μM; 24 h) suppresses de novo cholesterol biosynthesis in HepG2 cells[4]. In CHO cells and HMGCR-deficient UT-2 cells, MK-2206 (5 μM; 14 h) increases LDLR protein levels, which indicates that the effect does not depend on HMGCR activity[4]. In sterol-starved HepG2 cells, MK-2206 (0.5-4 μM; 38 h) strengthens the LDLR (low-density lipoprotein receptor)-inducing effect of Mevastatin[4]. In sterol-fed HepG2 cells, MK-2206 (5 μM; 2-24 h) raises mRNA expression of PCSK9, HMGCR, SREBP-2 and HMGCS1, has only minor effects on ACACA, FASN and SCD1, and does not affect IDOL[4]. In sterol-fed HepG2 cells, MK-2206 (2.5-5 μM; 14-24 h) stimulates LDLR promoter activity in an SRE-1-dependent manner[4]. In sterol-fed HepG2 cells, MK-2206 (5 μM; 14-24 h) raises LDLR mRNA levels in an SREBP-2-dependent manner[4]. In sterol-fed HepG2 cells, MK-2206 (5 μM; 2-6 h) stimulates proteolytic cleavage of FL-SREBP-2, generating the active NTF-SREBP-2[4]. In primary adult hepatocytes, MK-2206 (2.5-10 μM; 14 h) increases LDLR protein levels[4].
In Vivo
In preclinical ovarian cancer xenograft models, MK-2206 enhances the anti-tumor efficacy of multiple chemotherapeutic agents and in animals also induces mild, transient hyperglycemia and hyperinsulinemia, which resolve after treatment[1]. In mice, MK-2206 (120 mg/kg; p.o.; alternate days; 4 total doses) relieves UUO-induced renal fibrosis through reduced inflammation, inhibited epithelial-mesenchymal transition, suppressed myofibroblast activation and extracellular matrix deposition, and blocked activation of the Akt/mTOR signaling pathway[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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