Vistusertib (AZD2014)

For research use only.

Catalog No.S2783

71 publications

Vistusertib (AZD2014) Chemical Structure

CAS No. 1009298-59-2

Vistusertib (AZD2014) is a novel mTOR inhibitor with IC50 of 2.8 nM in a cell-free assay; highly selective against multiple PI3K isoforms (α/β/γ/δ). AZD2014 showed no or weak binding to the majority of kinases when tested at 1 μM. AZD2014 induces proliferation suppression, apoptosis, cell cycle arrest, and autophagy in HCC cells with antitumor activity.

Selleck's Vistusertib (AZD2014) has been cited by 71 publications

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Biological Activity

Description Vistusertib (AZD2014) is a novel mTOR inhibitor with IC50 of 2.8 nM in a cell-free assay; highly selective against multiple PI3K isoforms (α/β/γ/δ). AZD2014 showed no or weak binding to the majority of kinases when tested at 1 μM. AZD2014 induces proliferation suppression, apoptosis, cell cycle arrest, and autophagy in HCC cells with antitumor activity.
mTOR [1]
(Cell-free assay)
P-Akt (S473) [1]
(Cell-free assay)
pS6 (S235/236) [1]
(Cell-free assay)
2.8 nM 80 nM 200 nM
In vitro

AZD2014 is a close analogue of AZD8055 and a selective inhibitor of mTOR kinase. AZD2014 has greater inhibitory activity against mTORC1 compared to rapamycin: AZD2014 decreases p4EBP1 Thr37/46, inhibits the translation initiation complex and decreases overall protein synthesis while rapamycin has no effect. AZD2014 also inhibits the mTORC2 biomarkers pAKTSer473 and pNDRG1Thr346. AZD2014 has broad antiproliferative activity across multiple tumour cell lines. In particular, AZD2014 induces growth inhibition and cell death in breast cancer cell lines, including ER+ cell lines with acquired resistance to hormone therapy. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 MVPGeY5kfGmxbjDhd5NigQ>? MnfPTY5pcWKrdHnvckBw\iC{ZXPvcYJqdmGwdDDGUGFINXSjZ3fl[EBuXE:UIDixN|YzKHSxIEK1OFkqKCi3bnvuc5dvKG:{aXfpckkh\XiycnXzd4VlKGmwIFjFT|I6OyClZXzsd{whUUN3MDC9JFAvODB{ODFOwG0v NFW4T3c9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{M{O3OVc6Oyd-MkOzO|U4QTN:L3G+
MDA-MB-468 NHL6T5RHfW6ldHnvckBie3OjeR?= MUOyJIhzew>? MWHJcohq[mm2aX;uJI9nKG2WT2LDNkBqdiCqdX3hckBOTEFvTVKtOFY5KGOnbHzzJIF{e2W|c3XkJIF{KHKnZIXjeIlwdiCxZjDBT3QheGixc4Doc5J6dGG2aX;uJIF1KFOnckS3N{Bi\nSncjCyJIhzeyxiSVO1NEA:KDBwMEig{txONg>? M3jqSlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|M{e1O|k{Lz5{M{O3OVc6OzxxYU6=
MDA-MB-468 MUDGeY5kfGmxbjDhd5NigQ>? NW\MTnhNOiCqcoO= MUjJcohq[mm2aX;uJI9nKG2WT2LDNUBqdiCqdX3hckBOTEFvTVKtOFY5KGOnbHzzJIF{e2W|c3XkJIF{KHKnZIXjeIlwdiCxZjDwV|YheGixc4Doc5J6dGG2aX;uJIF1KFOnckKzOU8zOzZiYX\0[ZIhOiCqcoOsJGlEPTBiPTCwMlIh|ryPLh?= M{fmRlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|M{e1O|k{Lz5{M{O3OVc6OzxxYU6=
MCF7 M4fr[GZ2dmO2aX;uJIF{e2G7 NWDHbmd6UW6qaXLpeIlwdiCxZjDtWG9TSzJiaX6gbJVu[W5iTVPGO{Bk\WyuczD4[Y5w\3KjZoTl[EBud3W|ZTDhd5Nme3OnZDDhd{Bud2S3bHH0bY9vKHO3YoP0doF1\Q>? MWm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zOzN5NUe5N{c,OjN|N{W3PVM9N2F-
MCF7 NITMZYtHfW6ldHnvckBie3OjeR?= MlPsTY5pcWKrdHnvckBw\iCvVF;SR|EhcW5iaIXtZY4hVUOINzDj[YxteyC6ZX7v[5Ji\nSnZDDtc5V{\SCjc4Pld5Nm\CCjczDtc4R2dGG2aX;uJJN2[nO2cnH0[S=> NVq2ZWxYRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkOzO|U4QTNpPkKzN|c2Pzl|PD;hQi=>
MCF7 NEDtVIlEgXSxdH;4bYNqfHliYYPzZZk> NUnRVpFMPSCmYYnz M4PvSGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1ETjdiY3XscJMh[W[2ZYKgOUBl[Xm|IHL5JHBz\XO2bzDicJVmKHKnYXflcpQu[mG|ZXSg[ox2d3Knc3PlcoNmKGGwYXz5d4l{ MW[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyyN|M3OzJ3Lze+R4hGVUKOPD;hQi=>

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-mTOR(S2448) / mTOR / p-S6(235/236) / S6; 

PubMed: 26176608     

AZD2014 and rapamycin inhibited mTOR signaling in A549 cells as shown by the decreased phosphorylation of mTORand S6 after treatment for 24h.

p-4EBP1 / 4EBP1 / p-S6K / S6K / p-AKT S473 / AKT; 

PubMed: 25628925     

Biochemical activity of AZD2014 and rapamycin in blocking mTORC1 and mTORC2 signaling. HCC cells were treated with DMSO or increasing concentrations of AZD2014 or rapamycin for 1 hour before lysis and immunoblotting.

26176608 25628925
E-cadherin / Vimentin ; 

PubMed: 25628925     

Immunofluorescence staining in Huh-7 and SMMC-7721 cells. bars, 30 μm

Growth inhibition assay
Cell viability; 

PubMed: 26219339     

Dose-response curve for AZD2014 was determined for NF2-deficient primary (MN521, MN527, MN580) and immortalized (Ben-Men-1) meningioma cells lines, as well as primary (AC028) and immortalized arachnoid (AC007) cell lines. AZD2014 in a 10 point, 4-fold serial dilution series (0-20μM).

In vivo AZD2014 induces tumour growth inhibition against several xenograft models including a human primary explant model of ER+ breast cancer refractory to tamoxifen. The antitumour activity is associated with modulation of both mTORC1 and mTORC2 substrates. [1]


Solubility (25°C)

In vitro DMSO 38 mg/mL (82.15 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+30% PEG 300+ddH2O
For best results, use promptly after mixing.

* 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 462.54


CAS No. 1009298-59-2
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02780830 Withdrawn Drug: AZD2014|Drug: Ibrutinib Core: Relapsed or Refractory Diffuse Large B-Cell Lymphoma|Module 1: Non-GCB Diffuse Large B-Cell Lymphoma AstraZeneca June 2016 Phase 1
NCT02730923 Active not recruiting Drug: AZD2014|Drug: Anastrozole Endometrial Carcinoma|Metastatic Carcinoma|Hormone Receptor Positive Tumor Centre Leon Berard April 2016 Phase 1|Phase 2
NCT02619864 Completed Drug: AZD2014 Glioblastoma Multiforme Canadian Cancer Trials Group|AstraZeneca January 13 2016 Phase 1
NCT02599714 Active not recruiting Drug: AZD2014|Drug: Palbociclib|Drug: Fulvestrant Advanced and Metastatic Breast Cancer AstraZeneca December 7 2015 Phase 1
NCT02752204 Completed Drug: AZD 2014|Drug: Rituximab Diffuse Large B-Cell Lymphoma University of Birmingham|Bloodwise|AstraZeneca|Cancer Research UK October 2015 Phase 2

Tech Support

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.

Handling Instructions

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Frequently Asked Questions

  • Question 1:

    I am looking for a i.p. or i.v. formula of AZD2014. Any suggestion?

  • Answer:

    S2783 AZD2014 can be dissolved in 5% DMSO/30% PEG 300/ddH2O at 5 mg/ml as a clear solution for I.P. use.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID