| Field | Specification |
|---|---|
| Target | |
| Alternative names | BEZ235; NVP-BEZ235 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C30H23N5O |
| Purity | |
| Activity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Dactolisib (BEZ235), also known as NVP-BEZ235, is an orally active, dual pan-class I PI3K and mTOR kinase inhibitor, with IC50 values of 4 nM for p110α, 5 nM for p110γ, 7 nM for p110δ, 75 nM for p110β, and 20.7 nM for mTOR. It inhibits both mTORC1 and mTORC2. It is supplied as a white to light yellow solid (C30H23N5O, MW 469.54) at 99.94% purity.
Physical & Chemical Properties
| CAS Number | 915019-65-7 |
|---|---|
| Molecular Formula | C30H23N5O |
| Molecular Weight | 469.54 g/mol |
| Purity | 99.94% |
| Appearance | Solid |
| Color | White to light yellow |
| SMILES | CN(C1=C2C3=CC(C4=CC5=CC=CC=C5N=C4)=CC=C3N=C1)C(N2C6=CC=C(C=C6)C(C)(C#N)C)=O |
| Target | p110α, p110α-H1047R, p110α-E545K, p110γ, p110δ, p110β, mTOR, mTORC1, mTORC2 |
| Signaling Pathway | PI3K/Akt/mTOR; Autophagy |
| Bioactivity Class | Autophagy |
| Solubility | In Vitro: 5% TFA: 8.33 mg/mL (17.74 mM; Requires sonication and warming and heat to 60°C) DMF: 2 mg/mL (4.26 mM; Requires sonication) DMSO: 1 mg/mL (2.13 mM; Requires sonication and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target[1]
|
p110α 4 nM (IC50) |
p110α-H1047R 4.6 nM (IC50) |
p110α-E545K 5.7 nM (IC50) |
p110γ 5 nM (IC50) |
p110δ 7 nM (IC50) |
p110β 75 nM (IC50) |
mTOR 20.7 nM (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 |
|---|---|---|
| 5% TFA | 8.33 mg/mL (17.74 mM) | requires sonication and warming and heat to 60°C |
| DMF | 2 mg/mL (4.26 mM) | requires sonication |
| DMSO | 1 mg/mL (2.13 mM) | requires sonication and warming and heat to 60°C; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); 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 | ≥ 0.52 mg/mL (1.11 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 0.52 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (5.2 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% Corn Oil |
|---|---|
| Result | ≥ 0.52 mg/mL (1.11 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 0.52 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (5.2 mg/mL) to 900 μL corn oil. |
Direct preparation of the working solution
These formulations are prepared directly, without a DMSO stock; use them promptly after preparation.
Protocol 3
| Composition | 50% PEG300 + 50% saline |
|---|---|
| Result | 12.5 mg/mL (26.62 mM); suspension; requires sonication |
Protocol 4
| Composition | 10% 1-Methyl-2-pyrrolidinone + 90% PEG300 |
|---|---|
| Result | ≥ 1.1 mg/mL (2.34 mM); clear solution |
Data provided by the manufacturer.
In Vitro
Dactolisib (BEZ235) potently inhibits PI3K in an ATP-competitive manner. At 250 nM, Dactolisib (BEZ235) significantly lowers the phosphorylation levels of the mTOR-activated kinase p70S6K. Dactolisib (BEZ235) also reduces S235/S236P-RPS6 levels with an IC50 of 6.5 nM, which suggests that Dactolisib (BEZ235) can directly inhibit the mTOR kinase, since the kinase domain of mTOR is highly homologous to that of class IA PI3K. Activity of Dactolisib (BEZ235) against mTOR is confirmed in a biochemical mTOR K-LISA assay (IC50, 20.7 nM)[1]. In HCT116, DLD-1, and SW480 cell lines, the IC50s of Dactolisib (BEZ235) are 14.3±6.4, 9.0±1.5, and 12.0±1.6 nM, respectively[2].
In Vivo
Dactolisib (BEZ235) (45 mg/kg, p.o.) treatment causes colonic tumor regression in a GEM model of sporadic PIK3CA wild-type CRC[2]. MENX rats (n=2 each group) receive Dactolisib (BEZ235) (45 mg/kg) by oral gavage and are sacrificed 1 or 6 hours post-treatment. P-AKT and P-S6 immunostains show a considerable reduction of both proteins, particularly P-S6, 6 hours after administration of Dactolisib (BEZ235) compared with PEG-treated rats. At 6 hours after treatment, pituitary adenomas from Dactolisib (BEZ235)-treated rats have a proteomic profile significantly different from tumors of placebo-treated rats[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Cell Assay[2]
Maintain the human CRC cell lines (ATCC) HCT116 (PIK3CA kinase domain mutant, H1047R), DLD-1 (PIK3CA helical domain mutant, E545K), and SW480 (PIK3CA wild-type) in DMEM, together with isogenic DLD-1 PIK3CA mutant and wild-type cells. To account for differential growth kinetics, plate cells at different initial densities: HCT116 with 3,000 cells/well, DLD-1 with 5,500 cells/well, SW480 with 4,500 cells/well, DLD-1 PIK3CA mutant with 7,000 cells/well, and DLD-1 PIK3CA wild-type with 9,000 cells/well. After 16 hours, treat the cells with increasing concentrations of BEZ235 (10, 100, 1000 nM), and replace the drug-containing growth medium every 24 hours. Assess cell viability 16 hours after the initial plating and 48 hours after drug treatment begins, using the CellTiter 96 AQueous One Solution Cell Proliferation Assay, a colorimetric MTS assay. Normalize cell viability after drug treatment to that of untreated cells also grown for 48 hours. Calculate IC50 values by 4 parameter nonlinear regression in GraphPad Prism 5[2].
Animal Administration[2][3]
Mice[2] Randomly assign tumor-bearing Apc CKO mice to treatment with either vehicle alone as control (n=8) or BEZ235 at 45 mg/kg body weight in 10% 1-methyl-2-pyrrolidone/90% PEG 300 (n=8), given as daily oral gavage over 28 days. Choose the dose according to literature showing that 40-50 mg/kg body weight BEZ235 treats murine tumor models effectively and without adverse effects. Based on pharmacokinetic studies showing maximal tissue concentration one hour after NVP-BEZ235 administration, sacrifice tumor-bearing mice one hour after the final treatment dose. Assess colonic tumor volume with calipers (width×length×height) and harvest tumors for both western blot analysis and immunohistochemistry. Rats[3] Use MENX-affected rats. Test three doses of BEZ235 in MENX rats: 20, 30, and 45 mg/kg. Because the two higher doses cause a weight loss >10% after 10 days of treatment, use the 20 mg/kg dose for further studies. For MRI studies, for 14 days, treat MENX-affected rats aged 7 to 8 months (sizeable adenomas, but still in good general health) with BEZ235 (20 mg/kg) or placebo (PEG), administered daily per oral gavage.
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Selective depletion of tumor-associated SAMHD1 enhances chemotherapeutic efficacy and antitumor immune responses. Signal Transduct Target Ther 2025 Dec 15;10(1):406. PMID: 41392286
Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature 2018 Aug;560(7719):499-503. PMID: 30051890
Innate immune and metabolic signals induce mitochondria-dependent membrane lysis via mitoxyperiosis. Cell 2025 Dec 11;188(25):7155-7174.e25. PMID: 41317732
Endothelial CDS2 deficiency causes VEGFA-mediated vascular regression and tumor inhibition. Cell Res 2019 Nov;29(11):895-910.
Suz12 inactivation cooperates with JAK3 mutant signaling in the development of T-cell acute lymphoblastic leukemia. Blood 2019 Oct 17;134(16):1323-1336.
H4K20me3-Mediated Repression of Inflammatory Genes Is a Characteristic and Targetable Vulnerability of Persister Cancer Cells. Cancer Res 2025 Jan 2;85(1):32-51. PMID: 39476057
Intrinsic resistance to RAS inhibitors is driven by dysregulation of KRAS degradation. Nat Commun 2025 Dec 15. PMID: 41397976
Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance. Nat Commun 2017 Jun 8:8:15617.
Effects of molecularly targeted therapies on murine thymus: highly selective mTOR inhibitors induce reversible thymic involution. Exp Hematol Oncol 2016 Jul 29:5:22. PMID: 27478685
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. Sci Transl Med 2018 Jul 18;10(450):eaaq1093.
