1. PI3K/Akt/mTOR
  2. Akt
  3. Miransertib

Miransertib (Synonyms: ARQ-092)

Cat. No.: HY-19719 Purity: 99.77%
Handling Instructions

Miransertib (ARQ-092) is an orally bioavailable, selective, and potent allosteric Akt inhibitor with IC50s of 2.7 nM, 14 nM and 8.1 nM for Akt1, Akt2, Akt3, respectively.

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

Miransertib Chemical Structure

Miransertib Chemical Structure

CAS No. : 1313881-70-7

Size Price Stock Quantity
10 mM * 1  mL in DMSO USD 137 In-stock
Estimated Time of Arrival: December 31
1 mg USD 96 In-stock
Estimated Time of Arrival: December 31
5 mg USD 144 In-stock
Estimated Time of Arrival: December 31
10 mg USD 252 In-stock
Estimated Time of Arrival: December 31
50 mg USD 1092 In-stock
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100 mg USD 2040 In-stock
Estimated Time of Arrival: December 31
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Miransertib (ARQ-092) is an orally bioavailable, selective, and potent allosteric Akt inhibitor with IC50s of 2.7 nM, 14 nM and 8.1 nM for Akt1, Akt2, Akt3, respectively.

IC50 & Target[1]


2.7 nM (IC50)


8.1 nM (IC50)


14 nM (IC50)

In Vitro

Miransertib (ARQ-092; Compound 21a) demonstrates high enzymatic potency against Akt1, Akt2 and Akt3, as well as potent cellular inhibition of Akt activation and the phosphorylation of the downstream target PRAS40. Miransertib shows strong affinity for un-phosphorylated fulllength Akt1 and potently inhibited the phosphorylated form of full-length Akt isoforms. In a large panel of cell lines derived from various tumor types, Miransertib shows potent anti-proliferative activity in cell lines containing PIK3CA/PIK3R1 mutations compared to those with wild-type (wt) PIK3CA/PIK3R1 or PTEN loss. Miransertib shows excellent inhibition of p-Akt (S473) and p-Akt (T308) in both AN3CA and A2780 cells. The inhibition of the downstream protein p-PRAS40 (T246) is observed with Miransertib (IC50=0.31 μM)[1].

In Vivo

In a mouse pharmacokinetic study, (po at 100 mg/kg, iv at 5 mg/kg), Miransertib (ARQ-092; Compound 21a) shows an oral bioavailability of 23%. Miransertib results in 99%, 95% and 58% reductions in p-Akt (S473), p-Akt (T306) and p-PRAS40 (T246), respectively, after tumor-bearing mice are treated with 100 mg/kg po. The inhibition of phosphorylation is sustained at eight hours. The plasma concentration of Miransertib at one hour is 2.1 μM and decreased to 0.26 μM at 8 hours, while in the tumor, the concentration is 21.0 μM at one hour and 9.6 μM at 8 hours[1]. To determine the effects of Miransertib (ARQ-092) on cardiac function, echocardiographic analysis of SHP2+/+ and SHP2Y279C/+ littermates is conducted, either in the presence of orally administered vehicle or Miransertib (100 mg/kg/day), at 12, 14, and 16 weeks of age. By 12 weeks of age, SHP2Y279C/+ mice show significant left ventricular hypertrophy, as indicated by decreased chamber dimension and increased posterior wall thickness compared with those of littermate controls; hypertrophy in these mice continued to progress over the 4 week time period. Treatment of the SHP2Y279C/+ mice with Miransertib normalizes the hypertrophic cardiomyopathy (HCM) phenotype as early as 2 weeks following treatment, with levels comparable to those in SHP2+/+ at this time point[2].

Clinical Trial
Molecular Weight









Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 12.5 mg/mL (28.90 mM; Need ultrasonic)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.3120 mL 11.5602 mL 23.1203 mL
5 mM 0.4624 mL 2.3120 mL 4.6241 mL
10 mM 0.2312 mL 1.1560 mL 2.3120 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 1.25 mg/mL (2.89 mM); Clear solution

*All of the co-solvents are provided by MCE.
Cell Assay

Anti-proliferative cellular assays are conducted using the CellTiter Non-Radioactive Cell Proliferation Assay, which utilizes the production of formazan from a tetrazolium compound by live cells. AN3CA and A2780 cells are obtained from the ATCC. AN3CA cells are cultured in DMEM, and A2780 cells are cultured in RPMI. Cells are plated in 96-well plates at 2,000-10,000 cells/well, cultured for 24 h, and treated with the test compound for 72 h at a final DMSO concentration no greater than 0.5% v/v. PMS stock reagent (0.92 mg/mL in DPBS) is diluted 20-fold in MTS stock reagent (2 mg/mL in DPBS), and this MTS/PMS mixture is diluted 5-fold into each well of the 96-well plate. The plates are incubated for 3-4 h, and the absorbance of formazan is measured at 490 nm. The data are normalized to the untreated controls, the dose-response curves are fit to a four-parameter logistic equation, and the IC50 values are determined. All IC50 values reported are the geometric mean of at least two independent determinations[1].

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

Animal Administration

SHP2Y279C/+ mice are used. Only male progeny are used for the experiments herein and all mice are maintained on outbred C57BL6/J backgrounds, backcrossed for more than 10 generations. Either vehicle or Miransertib (100 mg/kg body weight) is then daily administered by oral gavage for 4 weeks. Administration began at 12 weeks of age (after established hypertrophy is indicated), and continued for 4 weeks, until the mice reach 16 weeks of age. As controls, SHP2+/+ and SHP2Y279C/+ mice are treated with vehicle alone.

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

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MiransertibARQ-092ARQ092ARQ 092AktPKBProtein kinase BInhibitorinhibitorinhibit

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