Vistusertib (AZD2014)

Catalog No.S2783

For research use only.

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.

Vistusertib (AZD2014) Chemical Structure

CAS No. 1009298-59-2

Selleck's Vistusertib (AZD2014) has been cited by 75 publications

Purity & Quality Control

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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 NWflO3pCTnWwY4Tpc44h[XO|YYm= MWPJcohq[mm2aX;uJI9nKHKnY3;tZolv[W62IF\MRWcufGGpZ3XkJI1VV1JiKEGzOlIhfG9iMkW0PUkhMHWwa37ve44hd3KrZ3nuLUBmgHC{ZYPz[YQhcW5iSFXLNlk{KGOnbHzzMEBKSzVyIE2gNE4xODJ6IN88UU4> MlO1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjN|N{W3PVMoRjJ|M{e1O|k{RC:jPh?=
MDA-MB-468 MVzGeY5kfGmxbjDhd5NigQ>? MnvINkBpenN? M1HmN2lvcGmkaYTpc44hd2ZibWTPVmMzKGmwIHj1cYFvKE2GQT3NRk01PjhiY3XscJMh[XO|ZYPz[YQh[XNicnXkeYN1cW:wIH;mJGFMXCCyaH;zdIhwenmuYYTpc44h[XRiU3XyOFc{KGGodHXyJFIhcHK|LDDJR|UxKD1iMD6wPEDPxE1w M4XROFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|M{e1O|k{Lz5{M{O3OVc6OzxxYU6=
MDA-MB-468 NELKVpNHfW6ldHnvckBie3OjeR?= MonFNkBpenN? M2fiVWlvcGmkaYTpc44hd2ZibWTPVmMyKGmwIHj1cYFvKE2GQT3NRk01PjhiY3XscJMh[XO|ZYPz[YQh[XNicnXkeYN1cW:wIH;mJJBUPiCyaH;zdIhwenmuYYTpc44h[XRiU3XyNlM2NzJ|NjDh[pRmeiB{IHjyd{whUUN3MDC9JFAvOiEQvF2u MkLNQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjN|N{W3PVMoRjJ|M{e1O|k{RC:jPh?=
MCF7 M{jicmZ2dmO2aX;uJIF{e2G7 NIDkVo1KdmirYnn0bY9vKG:oIH3UU3JEOiCrbjDoeY1idiCPQ1[3JINmdGy|IIjlco9oemGodHXkJI1wfXOnIHHzd4V{e2WmIHHzJI1w\HWuYYTpc44he3Wkc4TyZZRm M2G4UFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ|M{e1O|k{Lz5{M{O3OVc6OzxxYU6=
MCF7 M3viPWZ2dmO2aX;uJIF{e2G7 NIfPdYlKdmirYnn0bY9vKG:oIH3UU3JEOSCrbjDoeY1idiCPQ1[3JINmdGy|IIjlco9oemGodHXkJI1wfXOnIHHzd4V{e2WmIHHzJI1w\HWuYYTpc44he3Wkc4TyZZRm NYD5RWRpRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkOzO|U4QTNpPkKzN|c2Pzl|PD;hQi=>
MCF7 NFfQ[YxEgXSxdH;4bYNqfHliYYPzZZk> NFizS3I2KGSjeYO= MUjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNR2Y4KGOnbHzzJIFnfGW{IEWg[IF6eyCkeTDQdoV{fG9iYnz1[UBz\WGpZX70MYJie2WmIH\seY9z\XOlZX7j[UBidmGueYPpdy=> MlT3QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNlM{PjN{NT:nQmNpTU2ETEyvZV4>
Methods Test Index PMID
Western blot p-mTOR(S2448) / mTOR / p-S6(235/236) / S6 ; p-4EBP1 / 4EBP1 / p-S6K / S6K / p-AKT S473 / AKT 26176608 25628925
Immunofluorescence E-cadherin / Vimentin 25628925
Growth inhibition assay Cell viability 26219339
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]

Protocol (from reference)

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 3 years -20°C powder
2 years -80°C in solvent

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

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.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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

(data from, updated on 2021-09-06)

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?

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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