Home>>Signaling Pathways>> Ubiquitination/ Proteasome>> Autophagy>>MK-2206 dihydrochloride

MK-2206 dihydrochloride (Synonyms: MK-2206,MK2206,MK 2206)

Catalog No.GC16304

An allosteric Akt inhibitor

Products are for research use only. Not for human use. We do not sell to patients.

MK-2206 dihydrochloride Chemical Structure

Cas No.: 1032350-13-2

Size Price Stock Qty
10mM (in 1mL DMSO)
$84.00
In stock
10mg
$69.00
In stock
50mg
$162.00
In stock
100mg
$220.00
In stock
500mg
$902.00
In stock
1g
$1,114.00
In stock

Tel:(909) 407-4943 Email: sales@glpbio.com

Customer Reviews

Based on customer reviews.

  • GlpBio Citations

    GlpBio Citations
  • Bioactive Compounds Premium Provider

    Bioactive Compounds Premium Provider

Sample solution is provided at 25 µL, 10mM.

Product has been cited by 8 publications

Product Documents

Quality Control & SDS

View current batch:

Protocol

Cell experiment [1]:

Cell lines

NCI-H292 NSCLC cells

Preparation Method

Cells were treated with MK-2206 (0, 0.3, 1, and 3 μmol/L) in the presence or absence of erlotinib (0, 0.6, 2.5, 10, and 20 μmol/L) for 48 h. Apoptosis was evaluated by measuring the caspase-3/7 activity.

Reaction Conditions

MK-2206 (0, 0.3, 1, and 3 μmol/L), 48h

Applications

Caspase activation became apparent at 2.5 μmol/L erlotinib and 3 μmol/L MK-2206 or higher.

Animal experiment [2]:

Animal models

female nu/nu mice

Preparation Method

1 × 107 ZR75-1 breast cancer cells were inoculated in the mammary fat pads of female nu/nu mice. Mice were subcutaneously implanted with 17β-estradiol pellets. Mice bearing ZR75-1 xenografts were randomized into 3 groups (vehicle, MK-2206 240 mg/kg, or 480 mg/kg, n = 5–6). Tumor measurements were followed to assess antitumor efficacy, and RPPA was utilized to assess the effect on cell signaling as described above.

Dosage form

240 mg/kg, or 480 mg/kg, p.o.

Applications

MK-2206 (240 mg/kg, or 480 mg/kg) inhibits tumor growth in ZR75-1 xenografts.

References:

[1]. Hirai H, et al. MK-2206, an allosteric Akt inhibitor, enhances antitumor efficacy by standard chemotherapeutic agents or molecular targeted drugs in vitro and in vivo. Mol Cancer Ther. 2010 Jul;9(7):1956-67.

[2]. Xing Y, et al. Phase II trial of AKT inhibitor MK-2206 in patients with advanced breast cancer who have tumors with PIK3CA or AKT mutations, and/or PTEN loss/PTEN mutation. Breast Cancer Res. 2019 Jul 5;21(1):78.

Background

MK-2206 dihydrochloride is an orally active allosteric Akt inhibitor used in treatment of solid tumors.[1]

IIn vitro experiment it shown that MK-2206 is equally potent toward purified recombinant human Akt1 and Akt2 enzyme with IC50 of 5 nmol/L and 12 nmol/L, respectively; and approximately 5-fold less potent against human Akt3 (IC50, 65 nmol/L). MK-2206 potently inhibited the cell growth of Ras wild-type (WT) cell lines (A431, HCC827, and NCI-H292 with IC50s of 5.5, 4.3, and 5.2 μmol/L, respectively. The combination of 2.5 μmol/L erlotinib and 3 μmol/L MK-2206 or higher obviously activated the caspase.[1] In vitro, Akt inhibitor (MK 2206 dihydrochloride, 2.5 nM) reduces the effects of anti-microRNA-320a on the apoptosis of MDA-MB-231 cells.[2] In vitro, treatment with 0.1 and 1 μM for 48 h MK-2206 reduced the expression p-Akt in all pancreatic cancer cell lines suggesting that MK-2206 inhibited Akt phosphorylation in pancreatic cancer cells.[3] In vitro the colony formation assay confirmed that 1 μM of MK-2206 significantly inhibited the proliferation of SGC-7901 cells.[4]

In vivo test displayed it that treatment with 120 mg/kg MK-2206 orally 2 hours after erlotinib (50 mg/kg), and tumors were isolated 14 hours after erlotinib administration to verify the inhibition of phospho-Akt for the PI3K pathway and phospho-Erk for the Ras/Erk pathway. In vivo efficacy studies it demonstrated that the antitumor efficacy of MK-2206 with once a week at 360 mg/kg intermittently dosing was quite similar to the efficacy of three times a week at 120 mg/kg dosing when MK-2206 was combined with erlotinib.[1].

References:
[1]. Hirai H, et al. MK-2206, an allosteric Akt inhibitor, enhances antitumor efficacy by standard chemotherapeutic agents or molecular targeted drugs in vitro and in vivo. Mol Cancer Ther. 2010 Jul;9(7):1956-67.
[2]. Guan J, et al. MicroRNA 320a suppresses tumor cell growth and invasion of human breast cancer by targeting insulin like growth factor 1 receptor. Oncol Rep. 2018 Aug;40(2):849-858.
[3]. Wang Z, et al. Akt inhibitor MK-2206 reduces pancreatic cancer cell viability and increases the efficacy of gemcitabine. Oncol Lett. 2020 Mar;19(3):1999-2004.
[4]. Jin P, et al. MK-2206 co-treatment with 5-fluorouracil or doxorubicin enhances chemosensitivity and apoptosis in gastric cancer by attenuation of Akt phosphorylation. Onco Targets Ther. 2016 Jul 19;9:4387-96.

Chemical Properties

Cas No. 1032350-13-2 SDF
Synonyms MK-2206,MK2206,MK 2206
Chemical Name 8-[4-(1-aminocyclobutyl)phenyl]-9-phenyl-2H-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3-one;dihydrochloride
Canonical SMILES C1CC(C1)(C2=CC=C(C=C2)C3=C(C=C4C(=N3)C=CN5C4=NNC5=O)C6=CC=CC=C6)N.Cl.Cl
Formula C25H21N5O.2HCl M.Wt 480.39
Solubility ≥ 12.01mg/mL in DMSO Storage Store at -20°C
General tips Please select the appropriate solvent to prepare the stock solution according to the solubility of the product in different solvents; once the solution is prepared, please store it in separate packages to avoid product failure caused by repeated freezing and thawing.Storage method and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored at -20°C, please use it within 1 month.
To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time.
Shipping Condition Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request.

Complete Stock Solution Preparation Table

Prepare stock solution
1 mg 5 mg 10 mg
1 mM 2.0816 mL 10.4082 mL 20.8164 mL
5 mM 0.4163 mL 2.0816 mL 4.1633 mL
10 mM 0.2082 mL 1.0408 mL 2.0816 mL
  • Molarity Calculator

  • Dilution Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
**When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / CoA (available online).

Calculate

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.

Related Video

    MK-2206 dihydrochloride-GlpBio

Reviews

Review for MK-2206 dihydrochloride

Average Rating: 5 ★★★★★ (Based on Reviews and 30 reference(s) in Google Scholar.)

5 Star
100%
4 Star
0%
3 Star
0%
2 Star
0%
1 Star
0%
Review for MK-2206 dihydrochloride

GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.

Required fields are marked with *

You may receive emails regarding this submission. Any emails will include the ability to opt-out of future communications.