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Fig. 1 · Structure
Cat. No.
A10133
CAS No.
915019-65-7
Formula
C30H23N5O
Mol. Weight
469.6

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Dactolisib (BEZ235, NVP-BEZ235)

PI3K/mTOR Inhibitor

BEZ235 (NVP-BEZ235) inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes.

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Publications for Dactolisib

5 publications citing this product

  1. Kohei Maruyama, .et al. , NPJ Precis Oncol, 2025, Jan 6;9(1):4 PMID: 39762482
  2. Lijuan Chen, .et al. , Behav Neurol, 2023, May 9;2023:6991826 PMID: 37200987
  3. Makoto Koyama, .et al. , Int J Oncol, 2020, Sep 2 PMID: 32901840
  4. Tzeng SF, .et al. , FASEB J, 2018, Jun 15:fj201800687 PMID: 29906246
  5. Dominik Schulz, .et al. , Am J Cancer Res, 2016, 6(9): 1963-1975 PMID: 27725902
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Biological Activity

Bioactivity / Mechanism

BEZ235 has been used to suppress PI3K/AKT/mTOR pathway readouts in glioblastoma cells. It reduced AKT S473 phosphorylation and inhibited phosphorylation of the mTOR substrates S6K1 and 4EBP1. Responses depended on concentration and phosphorylation site; AKT T308 was not reduced in the U87/P3 study. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
p110α IC50 4nM
p110γ IC50 5nM
mTOR(p70S6K) IC50 6nM
p110δ IC50 7nM
ATR IC50 21nM
p110β IC50 75nM
EGFR/ErbB1 IC50 >8.5μM
VEGFR1/FLT1 IC50 >10μM
FLT3 IC50 >10μM
IGF-1R IC50 >10μM
EphB4 IC50 >10μM
RET IC50 >10μM
Tie-2 IC50 >10μM
c-Met IC50 >10μM
FGFR(K650E) IC50 >10μM
FAK IC50 >10μM
JAK2 IC50 >10μM
c-Abl IC50 >10μM
c-Src IC50 >10μM
PKA IC50 >10μM
Akt1/PKBα IC50 >10μM
PDK-1 IC50 >10μM
B-Raf(V599E) IC50 >10μM
CDK1 IC50 >10μM

24 targets · Scroll to view more

Cellular Effect

Cell Line Activity Value Description Reference
A-375 IC50 0.58 μM Antiproliferative activity against human A375 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 31228810]
A-431 IC50 12.5 μM Cytotoxicity against human A431 cells after 24 hrs by MTT assay [PMID: 25062005]
A549 IC50 0.1 μM Antiproliferative activity against human A549 cells after 72 hrs by MTT assay [PMID: 24878359]
A549 IC50 0.28 μM Cytotoxicity against human A549 cells after 72 hrs by MTT assay [PMID: 26210161]
A549 IC50 0.38 μM Antiproliferative activity against human A549 cells assessed as reduction in cell viability after 48 hrs by MTT assay [PMID: 31446244]
A549 IC50 0.62 μM Cytotoxicity against human A549 cells after 72 hrs by SRB assay [PMID: 29407971]
A549 IC50 0.62 μM Antiproliferative activity against human A549 cells after 72 hrs by sulforhodamine B assay [PMID: 29475582]
A549 IC50 0.76 μM Antiproliferative activity against human A549 cells incubated for 72 hrs by MTT assay [PMID: 26321603]
A549 IC50 1.08 μM Antiproliferative activity against human A549 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay [PMID: 31228810]
A549 IC50 6.5 μM Cytotoxicity against human A549 cells after 24 hrs by MTT assay [PMID: 25062005]
A549 IC50 6.5 μM Cytotoxicity against human A549 cells after 48 hrs by MTT assay [PMID: 25088398]
BT-549 IC50 0.74 μM Cytotoxicity against human BT549 cells after 72 hrs by SRB assay [PMID: 29407971]
COLO 205 IC50 0.085 μM Cytotoxicity against human COLO205 cells after 24 hrs by MTT assay [PMID: 25062005]
COLO 205 IC50 0.085 μM Cytotoxicity against human COLO205 cells after 48 hrs by MTT assay [PMID: 25088398]
HCC827 IC50 0.53 μM Antiproliferative activity against human HCC827 cells assessed as reduction in cell viability measured after 72 hrs by flow cytometry analysis [PMID: 34403956]
HCT-116 IC50 0.044 μM Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay [PMID: 25062005]
HCT-116 IC50 0.044 μM Cytotoxicity against human HCT116 cells after 48 hrs by MTT assay [PMID: 25088398]
HCT-116 IC50 0.14 μM Antiproliferative activity against human HCT116 cells after 72 hrs by SRB assay 10.1039/C5MD00401B
HCT-116 IC50 0.2 μM Cytotoxicity against human HCT116 cells after 72 hrs by SRB assay [PMID: 26596710]
HCT-116 IC50 0.22 μM Antiproliferative activity against human HCT116 cells after 72 hrs by SRB assay [PMID: 28109945]

20 records · Scroll to view more

In Vitro Studies

In a 72-hour MTS assay, dactolisib had reported viability IC50 values of 15.8 nM in U87 cells and 12.7 nM in patient-derived P3 glioblastoma cells. These assay-specific measurements do not define a general working concentration. [2]

Concentration-dependent mTOR substrate inhibition

Cell-based study · PTEN-null U-87 MG human glioblastoma cells [1]

BEZ235 at 250 nM suppressed phosphorylation of S6K1 T389 and 4EBP1 T37/46. At 20 nM, inhibition was evident for S6K1 but limited for 4EBP1; adding 20 nM RAD001 enhanced 4EBP1 inhibition.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
S6K1 T389 and 4EBP1 T37/46 phosphorylationQualitative immunoblot response 250 nM BEZ235: both phosphoprotein signals reduced; 20 nM BEZ235: S6K1 inhibition with limited 4EBP1 inhibition[1]

Literature-Reported Treatment Conditions

Treatment concentration
BEZ235: 20 or 250 nM; RAD001 comparator/combination: 20 nM
Exposure duration
6, 24 and 48 h
Method
Cell-culture exposure
Vehicle
DMSO
Co-treatment
Separate BEZ235 monotherapy, RAD001 monotherapy and BEZ235 20 nM + RAD001 20 nM conditions
Reported limits
Final DMSO fraction and independent immunoblot replicate count not stated for Figure 1A.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: NVP-BEZ235

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figure 1A (viewed); Results: RAD001 and BEZ235 synergistically inhibit mTOR signaling and tumorigenesis; Methods: Antibodies and inhibitors, Immunoblotting

S6K1 T389 and 4EBP1 T37/46 phosphorylation: Western blot with total S6K1, total 4EBP1 and β-actin controls — Figure 1A (viewed); Results: RAD001 and BEZ235 synergistically inhibit mTOR signaling and tumorigenesis; Methods: Antibodies and inhibitors, Immunoblotting

Glioblastoma cell viability and AKT phosphorylation

Cell-based study · U87 cells and P3 patient-derived glioblastoma xenograft cells in monolayer [2]

After 72 h, reported MTS IC50 values were 15.8 nM in U87 and 12.7 nM in P3 cells. AKT S473 phosphorylation decreased, while AKT T308 phosphorylation and total AKT showed no reported reduction.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
U87 relative cell viabilityIC50 15.8 nM[2]
P3 relative cell viabilityIC50 12.7 nM[2]
AKT phosphorylation and total AKTQualitative response pAKT S473 decreased; pAKT T308 and total AKT not reduced[2]

Literature-Reported Treatment Conditions

Treatment concentration
MTS: 0, 1, 10, 20, 30, 40, 50 and 250 nM; immunoblot: 0, 50 and 250 nM
Exposure duration
72 h
Method
Cell-culture exposure
Vehicle
DMSO stock diluted in culture medium
Co-treatment
Single-agent dactolisib
Reported limits
Final DMSO fraction and IC50 confidence intervals not reported. Figure 1 summarizes three independent experiments; Figure 2 reports three U87 and two P3 immunoblot experiments.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: Dactolisib

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figures 1A and 2B–C (viewed); Methods: Cell viability (MTS assay), Immunoblotting; Results: Dactolisib inhibits cell proliferation and Dactolisib inhibits phosphorylation of Akt

U87 relative cell viability: 72-h MTS assay, relative to untreated controls — Figure 1A (U87 panel, viewed); Methods: Cell viability (MTS assay); Results first subsection

P3 relative cell viability: 72-h MTS assay, relative to untreated controls — Figure 1A (P3 panel, viewed); Methods: Cell viability (MTS assay); Results first subsection

AKT phosphorylation and total AKT: 72-h immunoblot and densitometric analysis at 0, 50 and 250 nM — Figure 2B–C (viewed); Results: Dactolisib inhibits phosphorylation of Akt

In Vivo Studies

Animal findings were model- and regimen-dependent. BEZ235 plus RAD001 significantly inhibited subcutaneous U-87 MG tumor growth, whereas BEZ235 alone at 10 mg/kg did not. Dactolisib at 10 mg/kg did not improve survival in rats bearing orthotopic P3 glioblastoma. In a separate study, measurable brain exposure after 25 mg/Kg intraperitoneal NVP-BEZ235 did not establish efficacy: NVP-BEZ235 combined with irradiation failed to improve survival in the COMI orthotopic model. [1,2,3]

U-87 MG xenograft response to BEZ235 and RAD001

Animal study · Female nude mice bearing subcutaneous U-87 MG tumors; randomized groups of 10 [1]

The combination inhibited tumor growth more strongly than either monotherapy under this regimen. BEZ235 alone did not significantly inhibit growth.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Change in tumor volume relative to controlT/C BEZ235: 59%; RAD001: 31%; combination: 0% (p<0.001)[1]

Conditions shared by the study groups

Route
Oral
Frequency
Once daily
Treatment course
4 weeks; T/C assessed after 26 days
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
BEZ235 monotherapy
10 mg/kg BEZ235		Vehicle-treated tumor-bearing miceT/C 59%; tumor-growth inhibition was not statistically significant.[1]
RAD001 comparator
2.5 mg/kg RAD001		Vehicle-treated tumor-bearing miceT/C 31%; tumor-growth inhibition was not statistically significant.[1]
BEZ235 plus RAD001
10 mg/kg BEZ235 + 2.5 mg/kg RAD001		Vehicle-treated tumor-bearing mice; single-agent groups also includedT/C 0%; tumor-growth inhibition p<0.001.[1]
BEZ235 monotherapy
Model: Female nude mice bearing subcutaneous U-87 MG xenografts; n=10/group
Reported limits: In-vivo vehicle composition not reported.
RAD001 comparator
Model: Same U-87 MG xenograft design; n=10/group
Reported limits: In-vivo vehicle composition not reported.
BEZ235 plus RAD001
Model: Same U-87 MG xenograft design; n=10/group
Reported limits: In-vivo vehicle composition not reported.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: NVP-BEZ235

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figure 2E (viewed); Results first subsection; Methods: RAD001 and BEZ235 in vivo experiments

Change in tumor volume relative to control: T/C = (ΔT/ΔC) × 100; day 1 to day 26; Kruskal–Wallis with Dunn multiple-comparison test — Figure 2E (viewed); Results first subsection; Methods: RAD001 and BEZ235 in vivo experiments

BEZ235 monotherapy · Figure 2E (viewed); Results first subsection; Methods: RAD001 and BEZ235 in vivo experiments

RAD001 comparator · Figure 2E (viewed); Results first subsection; Methods: RAD001 and BEZ235 in vivo experiments

BEZ235 plus RAD001 · Figure 2E (viewed); Results first subsection; Methods: RAD001 and BEZ235 in vivo experiments

No survival benefit in a patient-derived glioblastoma rat model

Animal study · Nude rats with orthotopic P3 patient-derived GBM xenografts [2]

Dactolisib did not improve survival or inhibit tumor growth in this model. The trend toward shorter survival was not statistically significant.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Survival versus vehicleLog-rank p 0.0845[2]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Once daily, 5 days/week
Treatment course
Started after MRI confirmation 3 weeks after implantation; monitored to humane endpoint
Vehicle
0.5% methyl cellulose + 0.5% Tween20
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Dactolisib in orthotopic P3 tumors
10 mg/kg		Same vehicle orallyNo survival improvement (log-rank p=0.0845); MRI showed comparable tumor sizes after 1 and 2 weeks of treatment.[2]
Dactolisib in orthotopic P3 tumors
Model: Athymic homozygous nude rats (Han: nru/nru Rowett); n=5 treated, n=6 controls
Reported limits: Sex and fixed total course not specified for this comparison.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: Dactolisib

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figure 4A–B (viewed); Results: Dactolisib does not inhibit tumour growth or prolong survival for rats carrying orthotopic GBM xenografts; Methods: Animal medication, Statistical analysis

Survival versus vehicle: Kaplan–Meier comparison; treated n=5, control n=6 — Figure 4A–B (viewed); Results: Dactolisib does not inhibit tumour growth or prolong survival for rats carrying orthotopic GBM xenografts; Methods: Animal medication, Statistical analysis

Dactolisib in orthotopic P3 tumors · Figure 4A–B (viewed); Results: Dactolisib does not inhibit tumour growth or prolong survival for rats carrying orthotopic GBM xenografts; Methods: Animal medication, Statistical analysis

Brain and blood exposure after a single dose

Animal study · Tumor-free CD-1 mice, 8 weeks old [3]

NVP-BEZ235 was detected in brain and blood after intraperitoneal administration. These measurements establish tissue exposure under this regimen; they do not establish free-brain concentrations, target inhibition or antitumor efficacy.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Brain NVP-BEZ235 concentrations at 1, 2, 6 and 8 hConcentration 36, 111, 44 and 12 × 10−9 M[3]
Blood NVP-BEZ235 concentrations at 1, 2, 6 and 8 hConcentration 146, 32, 28 and 12 × 10−9 M[3]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Single administration
Treatment course
Samples at 1, 2, 6 and 8 h
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Single-dose brain distribution
25 mg/Kg body weight		Analytical calibration; AZD6738 tested separatelyNVP-BEZ235 detected in brain; highest sampled brain concentration at 2 h.[3]
Single-dose brain distribution
Model: Tumor-free 8-week-old CD-1 mice
Reported limits: PK vehicle, sex and explicit biological replicate count per time point not reported in the selected methods/legend.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: NVP-BEZ235

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figure 1a,b,e–g (viewed); Methods: Chemicals, Pharmacokinetics of ATRi after intraperitoneal delivery; Results: Pharmacokinetics

Brain NVP-BEZ235 concentrations at 1, 2, 6 and 8 h: HPLC/MS; reported quantitation limit 10 × 10−9 M; average procedural SD ±31% — Figure 1e labels (viewed), Figure 1 legend; Results: Pharmacokinetics

Blood NVP-BEZ235 concentrations at 1, 2, 6 and 8 h: HPLC/MS; reported quantitation limit 10 × 10−9 M; average procedural SD ±31% — Figure 1g labels (viewed), Figure 1 legend; Results: Pharmacokinetics

Single-dose brain distribution · Figure 1a,b,e–g (viewed); Methods: Chemicals, Pharmacokinetics of ATRi after intraperitoneal delivery; Results: Pharmacokinetics

No survival improvement with NVP-BEZ235 plus irradiation

Animal study · Orthotopic COMI glioblastoma in NOD/SCID mice; 7 animals per treatment group [3]

NVP-BEZ235 plus irradiation did not prolong survival relative to vehicle plus irradiation. The shorter median survival was described as a trend, not a demonstrated toxic mechanism.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Median survival after tumor implantationMedian survival 86 days (NVP-BEZ235 + IR); 99 days (DMSO + IR)[3]

Conditions shared by the study groups

Route
Intraperitoneal drug; irradiation directed to the head
Frequency
Once daily on days 22, 23 and 24 after tumor implantation
Treatment course
Three treatments; irradiation 4 h after each drug dose
Vehicle
DMSO
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
NVP-BEZ235 plus irradiation
25 mg/Kg body weight NVP-BEZ235 + 0.5 Gy irradiation		DMSO plus the same irradiation scheduleMedian survival 86 days versus 99 days with vehicle plus irradiation; no significant survival improvement.[3]
NVP-BEZ235 plus irradiation
Model: NOD/SCID mice bearing orthotopic COMI glioma-initiating-cell tumors; n=7/group
Reported limits: Final DMSO formulation details not reported; no drug-only arm in this comparison.
Methods and source locations

Compound reported in the paper: BEZ235 (NVP-BEZ235, dactolisib); Compound label in the paper: NVP-BEZ235

Published compound-level research; study formulations and model-specific effects do not establish performance of an Adooq batch.

Figure 2b (viewed) and legend; Results: Radiosensitization; Methods: RT and Statistics

Median survival after tumor implantation: Kaplan–Meier; log-rank and Gehan–Breslow–Wilcoxon comparisons; no significant difference reported — Figure 2b (viewed) and legend; Results: Radiosensitization; Methods: RT and Statistics

NVP-BEZ235 plus irradiation · Figure 2b (viewed) and legend; Results: Radiosensitization; Methods: RT and Statistics

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 915019-65-7
Applications PI3K/mTOR Inhibitor
Formula C30H23N5O
Molecular Weight 469.6
Synonyms BEZ235; NVP-BEZ235
SMILES
CC(C)(C#N)C1=CC=C(C=C1)N2C3=C4C=C(C=CC4=NC=C3N(C2=O)C)C5=CC6=CC=CC=C6N=C5

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO <1 mg/mL
Water Insoluble
Ethanol Warmed: 16 mg/mL (34.07 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
NMP+PEG300 (10+90, v+v)

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Nyfeler B, Chen Y, Li X, et al. RAD001 enhances the potency of BEZ235 to inhibit mTOR signaling and tumor growth. PloS one (2012). PMID: 23155392 DOI: 10.1371/journal.pone.0048548 Source material
  2. [2] Netland IA, Førde HE, Sleire L, et al. Dactolisib (NVP-BEZ235) toxicity in murine brain tumour models. BMC cancer (2016). PMID: 27542970 DOI: 10.1186/s12885-016-2712-4 Source material
  3. [3] Fròsina G, Profumo A, Marubbi D, et al. ATR kinase inhibitors NVP-BEZ235 and AZD6738 effectively penetrate the brain after systemic administration. Radiation oncology (London, England) (2018). PMID: 29685176 DOI: 10.1186/s13014-018-1020-3 Source material

Publications

5 publications citing this product

  1. Kohei Maruyama, .et al. , NPJ Precis Oncol, 2025, Jan 6;9(1):4 PMID: 39762482
  2. Lijuan Chen, .et al. , Behav Neurol, 2023, May 9;2023:6991826 PMID: 37200987
  3. Makoto Koyama, .et al. , Int J Oncol, 2020, Sep 2 PMID: 32901840
  4. Tzeng SF, .et al. , FASEB J, 2018, Jun 15:fj201800687 PMID: 29906246
  5. Dominik Schulz, .et al. , Am J Cancer Res, 2016, 6(9): 1963-1975 PMID: 27725902

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