| Field | Specification |
|---|---|
| Target | |
| Alternative names | AZD2014 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C25H30N6O3 |
| Purity | |
| Activity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Vistusertib, also known as AZD2014, is an ATP-competitive mTOR inhibitor with an IC50 of 2.81 nM that inhibits both the mTORC1 and mTORC2 complexes. It is supplied as a yellow to orange solid (C25H30N6O3, MW 462.54) at 99.70% purity.
Physical & Chemical Properties
| CAS Number | 1009298-59-2 |
|---|---|
| Molecular Formula | C25H30N6O3 |
| Molecular Weight | 462.54 g/mol |
| Purity | 99.70% |
| Appearance | Solid |
| Color | Yellow to orange |
| SMILES | O=C(NC)C1=CC=CC(C2=CC=C3C(N=C(N4[C@@H](C)COCC4)N=C3N5[C@@H](C)COCC5)=N2)=C1 |
| Target | mTOR, mTORC1, mTORC2, PI3Kα |
| Signaling Pathway | PI3K/Akt/mTOR; Autophagy; Apoptosis |
| Bioactivity Class | Autophagy |
| Solubility | In Vitro: DMSO: ≥ 50 mg/mL (108.10 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) * "≥" means soluble, but saturation unknown. |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 1 year; -20°C, 6 months. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
mTOR 2.81 nM (IC50) |
PI3Kα 3.766 μM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | ≥ 50 mg/mL (108.10 mM) | use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 1 year) or -20°C (up to 6 months); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (5.40 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | 2.5 mg/mL (5.40 mM); suspension; requires sonication and warming |
| How to prepare | Gives a suspension at 2.5 mg/mL. The suspension is suitable for oral and intraperitoneal dosing. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 5% DMSO + 40% PEG300 + 5% Tween-80 + 50% saline |
|---|---|
| Result | 2.5 mg/mL (5.40 mM); suspension; requires sonication |
Protocol 4
| Composition | 5% DMSO + 95% (20% SBE-β-CD in saline) |
|---|---|
| Result | 2.5 mg/mL (5.40 mM); suspension; requires sonication |
Data provided by the manufacturer.
In Vitro
Vistusertib (AZD2014) is evaluated for inhibitory effects against isolated recombinant mTOR enzyme (IC50 of 2.81 nM) and in cellular assays that measure both mTORC1 and mTORC2 activities. In MDAMB468 cells, Vistusertib (AZD2014) lowers phosphorylation of ribosomal protein S6 (Ser235/236), an mTORC1 substrate, with a mean IC50 value of 210 nM, and of AKT (Ser473), an mTORC2 substrate, with a mean IC50 value of 78 nM[1].
In Vivo
Vistusertib (AZD2014) induces dose-dependent tumor growth inhibition across several xenograft and primary explant models. In addition, the antitumor activity of Vistusertib (AZD2014) is linked to modulation of both mTORC1 and mTORC2 substrates, in line with its mechanism of action. For pharmacokinetics in mice, Vistusertib (AZD2014) is tested at doses between 7.5 and 15 mg/kg. Cmax and AUC increase dose-dependently after single dose and repeat dosing of AZD2014, with Cmax from 1 to 16 μM and AUC from 220 to 5,042 μM·h across the dose range. In SCID mice bearing MCF7 xenografts, the pharmacodynamic effect of Vistusertib (AZD2014) on a biomarker of mTORC1 (phosphorylation of S6) and a biomarker of mTORC2 (phosphorylation of AKT) is assessed after administration of 3.75, 7.5, and 15 mg/kg AZD2014. Plasma drug concentrations correlate well with biomarker levels (p-AKT IC50 estimated at 0.119 μM total, 53% SE; p-S6 IC50 estimated at 0.392 μM, 28.8% SE)[1].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Animal Administration[1]
Mice[1] MCF7 experiments: Inject male SCID mice s.c. with 5×106 MCF7 cells in 0.1 mL, and split the animals at random into control and treatment groups once tumors reach 0.2 cm3. Dissolve Vistusertib (AZD2014) in captisol, then dilute until the final captisol concentration is 30% (w/v). Give Vistusertib (AZD2014) by oral gavage (0.1 mL/10 g body weight). Treat the control group with vehicle alone. Record tumor volumes (by calliper), animal body weight and condition twice weekly throughout the study. Calculate tumor volume with the formula (length×width)×√(length×width)×(π/6), where length is the longest diameter across and width is the corresponding perpendicular diameter.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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The target landscape of clinical kinase drugs. Science 2017 Dec 1;358(6367):eaan4368.
Single-Cell Lineage Tracing Uncovers Resistance Signatures and Sensitizing Strategies to FLT3 Inhibitors in Acute Myeloid Leukemia. Cancer Res 2025 Nov 21:10.1158/0008-5472.CAN-24-3753. PMID: 41270153
The anti-cancer drug ABTL0812 induces ER stress-mediated cytotoxic autophagy by increasing dihydroceramide levels in cancer cells. Autophagy 2021 Jun;17(6):1349-1366.
Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. Nat Commun 2026 Feb 12;17(1):1214. PMID: 41680175
An ErbB2/c-Src axis links bioenergetics with PRC2 translation to drive epigenetic reprogramming and mammary tumorigenesis. Nat Commun 2019 Jul 1;10(1):2901.
Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance. Nat Commun 2017 Jun 8:8:15617.
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. Sci Transl Med 2018 Jul 18;10(450):eaaq1093.
Response to mTOR and PI3K inhibitors in enzalutamide-resistant luminal androgen receptor triple-negative breast cancer patient-derived xenografts. Theranostics 2020 Jan 1;10(4):1531-1543.
Atractylenolide I inhibits colorectal cancer cell proliferation by affecting metabolism and stemness via AKT/mTOR signaling. Phytomedicine 2020 Mar:68:153191. PMID: 32135457
Evidence of promoting effects of 6:2 Cl-PFESA on hepatocellular carcinoma proliferation in humans: An ideal alternative for PFOS in terms of environmental health?. Environ Int 2024 Apr:186:108582. PMID: 38513556
