Miransertib (ARQ 092) HCl

For research use only.

Catalog No.S8339 Synonyms: Miransertib

5 publications

Miransertib (ARQ 092) HCl Chemical Structure

Molecular Weight(MW): 468.98

ARQ 092 is a novel, orally bioavailable and selective AKT pathway inhibitor exhibiting a manageable safety profile among patients with advanced solid tumors.

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Selleck's Miransertib (ARQ 092) HCl has been cited by 5 publications

1 Customer Review

  • ARQ-092, a novel pan-AKT inhibitor, promotes axonal recovery when applied pre- and post-OGD. ARQ-092, which is an inhibitor of activated AKT, promoted axon function recovery when applied as a pre-treatment and as a post-treatment. A) Pre-treatment with ARQ-092 (500 nM, dark blue) applied before OGD promoted consistent and sustained CAP area recovery. B) ARQ-092 improved CAP area recovery at 250 nM and 500 nM when compared to control CAP area recovery. C) ARQ-092 (500 nM, brown) applied after OGD promoted consistent and sustained CAP area recovery. D) ARQ-092 improved CAP area recovery at 250 and 500 nM compared to control CAP area recovery. *p < 0.05 and **p < 0.01, one-way ANOVA with Newman-Keuls post hoc test. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

    Neurobiol Dis, 2018, pii: S0969-9961(18)30149-9. Miransertib (ARQ 092) HCl purchased from Selleck.

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Biological Activity

Description ARQ 092 is a novel, orally bioavailable and selective AKT pathway inhibitor exhibiting a manageable safety profile among patients with advanced solid tumors.
Akt2 [1]
(Cell-free assay)
Akt1 [1]
(Cell-free assay)
Akt3 [1]
(Cell-free assay)
4.5 nM 5 nM 16 nM
In vitro

ARQ 092 blocks membrane translocation of inactive AKT and even dephosphorylates the membrane-associated active form, thereby perturbing AKT activity. Treatment with 50-500 nM ARQ 092 significantly blocks αMβ2 integrin function in neutrophils and reduces P-selectin exposure and glycoprotein Ib/IX/V-mediated agglutination in platelets[2]. In a large panel of diverse cancer cell lines, ARQ 092 inhibits proliferation across multiple tumor types but are most potent in leukemia, breast, endometrial, and colorectal cancer cell lines. Moreover, inhibition by ARQ 092 is more prevalent in cancer cell lines containing PIK3CA/PIK3R1 mutations compared to those with wt-PIK3CA/PIK3R1 or PTEN mutations[1]. ARQ 092 targets the PI3K/AKT pathway and AKT specifically and reduces phosphorylation of GSK3α and GSK3β in mutation-positive cells[3].

Methods Test Index PMID
Growth inhibition assay
Cell viability; 

PubMed: 30399177     

dTHP-1 cells (human macrophages) were infected with L. donovani promastigotes for 24 hours and then treated with indicated concentrations of Miransertib for an additional 24 hours. At the end of the experiment, infected cells with and without Miransertib treatment were washed, and internalized parasites were released by lysing the cells using a mild concentration of SDS, followed by transfer to transformation medium as described in “Materials and Methods”. Transformed motile promastigotes were counted. The data was compiled from three independent experiments done in duplicates.

Western blot
p-AKT / AKT / p-PRAS40 / PRAS40 / p-ERK / ERK / p-FOXO1 / p-GSKβ(S9) / pAS160(S318) / pBAD / pS6 / p-4EBP1 ; 

PubMed: 26469692     

MDA-MB 453 breast cancer cell line (PIK3CAH1047R; Her2 amp) were treated with various concentrations (1 = 0, 2 = 0.012, 3 = 0.037, 4 = 0.11, 5 = 0.33, and 6 = 1 μM) of ARQ 092, ARQ 751, MK-2206 or GDC-0068 for 2 hours. pAKT(S473), pAKT(T308), pPRAS40(T246), pFOXO1(T24) /3a(T36), pGSK3β(S9), pAS160(S318), pBAD(S136), pS6(S235/236) and p4E-BP1(S65) and phospho ERK were assessed by western blot analysis.

In vivo Short-term oral administration of ARQ 092 or hydroxyurea, a main therapy for sickle cell disease, diminishes heterotypic cell-cell interactions in venules of sickle cell disease mice challenged with TNF-α. ARQ 092 is well tolerated at a continuous daily dose of 60 mg or a dose of 600 mg when administered once a week, for several months. ARQ 092 is likely to inhibit the activity of all AKT isoforms in intravascular cells and thereby attenuates the process of thrombosis and inflammation in SCD patients[2]. ARQ 092 is highly active in a subset of endometrial tumors that harbor PI3K pathway gene mutations[1].


Cell Research:[1]
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  • Cell lines: MDA-MB-453 cells; NCI-H1650 cells; KU-19-19 cells
  • Concentrations: 0, 0.012, 0.037, 0.11, 0.33, and 1 μM
  • Incubation Time: 2 h
  • Method: Cells (MDA-MB-453: 1.5×106; NCI-H1650: 1×106; KU-19-19: 0.7×106) are plated into 6 well plates, left overnight, and then treated with full media containing different concentrations (0, 0.012, 0.037, 0.11, 0.33, and 1 μM) of AKT inhibitors (ARQ 092, ARQ 751, MK-2206, GDC-0068) for 2 hours. Cells are treated under designated conditions and lysates are extracted. Proteins are resolved from extracts using SDS-PAGE followed by immunoblotting.
    (Only for Reference)
Animal Research:[2]
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  • Animal Models: Male SCD mice
  • Dosages: 100 mg/10ml/kg
  • Administration: oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 75 mg/mL (159.92 mM)
Ethanol 4 mg/mL (8.52 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 468.98


CAS No. 1313883-00-9
Storage powder
in solvent
Synonyms Miransertib
Smiles Cl.NC1=NC=CC=C1C2=NC3=CC=C(N=C3[N]2C4=CC=C(C=C4)C5(N)CCC5)C6=CC=CC=C6

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID