BEZ235 (NVP-BEZ235, Dactolisib) 化学構造
分子量: 469.55

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Quality Control & MSDS

製品説明

  • Compare PI3K Inhibitors
    PI3K製品生物活性の比較
  • 研究分野
  • Combination Therapy
    併用療法

製品の説明

生物活性

製品説明 BEZ235 (NVP-BEZ235, Dactolisib)は競争性的なPI3K、mTOR 阻害剤、 p110α, p110γ, p110δ と p110β を作用すると、 IC50 がぞれぞれ 4 nM, 5 nM, 7 nM と 75 nMになる.
ターゲット

p110α

p110γ

p110δ

p110β

ATR

IC50

4 nM

5 nM

7 nM

75 nM [1]

21 nM [8]

In vitro試験 BEZ235 significantly reduces the phosphorylation levels of the mTOR activated kinase p70S6K. BEZ235 results in a reduction of S235/S236P-RPS6 levels with IC50 of 6.5 nM. The activity of BEZ235 against mTOR is determined using a biochemical mTOR K-LISA assay with IC50 of 20.7 nM. BEZ235 shows slightly lower activity against its β paralogue with IC50 of 75 nM. The PI3K/Akt/mTOR pathway is often constitutively activated in human tumor cells. BEZ235 blocks PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. Both PTEN-null cell lines PC3M and U87MG show a dose-dependent reduction in cell proliferation when treated with increasing concentrations of BEZ235 with an average GI50 of 10-12 nM. [1] BEZ235 is an mTORC1/2 catalytic inhibitor. [2]
Cell Data
Cell LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
Trypanosoma brucei brucei M3jUZWFvfGmvaXPyc4Jq[WxiQYPzZZk> NYjXVIdlOThiaB?= NEDid2xFVVOR NEPldHFCdnSrdIL5dIFvd3OxbXHsJIFkfGm4aYT5JJdqfGhiRVO1NEBw\iByLkCwNlUh|ryP M4fhdlI1QDB3OUS2
MCF7 NYezUoRwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3[xdFAvODFvMUCwJO69VQ>? NF;RXpg1QCCq M3rrfGROW09? M4Tme2lEPTB;MD63N{DPxE1? NVn5e4tuOjN6N{G5NFQ>
HCT116 M3HBSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\FNE4xOS1zMECg{txO NXnqSWlNPDhiaB?= NEXB[lFFVVOR MWPJR|UxRTFwMU[g{txO M1m5WlI{QDdzOUC0
U87MG MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmL0NE4xOS1zMECg{txO MXe0PEBp NWTmWHF5TE2VTx?= MXLJR|UxRTFwM{Kg{txO MXSyN|g4OTlyNB?=
HBC4 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGPsPYcxNjBzLUGwNEDPxE1? NU\NTHo4PDhiaB?= M4S0fWxw\yCJSUWwQU05NjZzIF2= Mo\JNlI{OzZ{NE[=
BSY1 M4nOdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Moe1NE4xOS1zMECg{txO NHS0WoQ1QCCq NXPDOnVvVG:pIFfJOVA:NThwNEigUS=> MmX1NlI{OzZ{NE[=
HBC5 MonsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUmwMlAyNTFyMDFOwG0> NV[4[mV7PDhiaB?= M2fkWWxw\yCJSUWwQU04Njh5IF2= NFrYdnozOjN|NkK0Oi=>
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MDA-MB-231 NYP3XIZPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWGwMlAyNTFyMDFOwG0> MorrOFghcA>? M{LOc2xw\yCJSUWwQU05NjB7IF2= MmTCNlI{OzZ{NE[=
U251 MknkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXTCeoNTOC5yMT2xNFAh|ryP NF;tSpE1QCCq NFnLSJNNd2diR1m1NF0uPy54NjDN M4PaeVIzOzN4MkS2
SF268 NVn0fnNoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUjRN48{OC5yMT2xNFAh|ryP Mly4OFghcA>? MX7Mc4chT0l3ME2tO{46OiCP MnPNNlI{OzZ{NE[=
SF295 M3nOWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NI\MUmYxNjBzLUGwNEDPxE1? NVfSdWtpPDhiaB?= NH;XNpZNd2diR1m1NF0uQC5|MTDN NFj4cW0zOjN|NkK0Oi=>
SF539 NWnwOpdGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NY\DSY5wOC5yMT2xNFAh|ryP MmXVOFghcA>? NFn5VnhNd2diR1m1NF0uQC53OTDN MkTlNlI{OzZ{NE[=
SNB75 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXzT[YpSOC5yMT2xNFAh|ryP MkPVOFghcA>? NVf3eXZbVG:pIFfJOVA:NThwNUigUS=> MlvXNlI{OzZ{NE[=
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NCI-H23 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1HsVFAvODFvMUCwJO69VQ>? NF7tXlI1QCCq NFrsWoxNd2diR1m1NF0uPy54NDDN MVmyNlM{PjJ2Nh?=
NCI-H226 NFLyXWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MW[wMlAyNTFyMDFOwG0> MorQOFghcA>? MWnMc4chT0l3ME2tPE41PCCP NWDHbWo{OjJ|M{[yOFY>
NCI-H522 NWr6UW5qT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV[wMlAyNTFyMDFOwG0> NXLLdplKPDhiaB?= MXrMc4chT0l3ME2tPE41PSCP MXiyNlM{PjJ2Nh?=
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DMS114 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUGwMlAyNTFyMDFOwG0> MlTPOFghcA>? NX63ZY5mVG:pIFfJOVA:NThwM{mgUS=> NUDOVIczOjJ|M{[yOFY>
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MKN28 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW[4OGFqOC5yMT2xNFAh|ryP MV60PEBp MWHMc4chT0l3ME2tO{4xPyCP M1XVblIzOzN4MkS2
MKN45 NGnHd3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnPaNE4xOS1zMECg{txO M{DVN|Q5KGh? MUjMc4chT0l3ME2tPE4{PCCP NWrRcWVLOjJ|M{[yOFY>
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Trypanosoma brucei brucei NHHsfJFHfW6ldHnvckBCe3OjeR?= NEj1WnUyQCCq NH3oXo9FVVOR MVTJcohq[mm2aX;uJI9nKHKnY3XweI9zNW2nZHnheIVlKGWwZH;jfZRwe2m|IHHzd4V{e2WmIHHzJIRm[3KnYYPlJIlvKHS{YX7z[oVzemmwIIXweIFs\Q>? MUeyOFgxPTl2Nh?=
Trypanosoma brucei brucei NX3WcmtjTnWwY4Tpc44hSXO|YYm= M4fxeVIxOCCwTR?= M3nVO|EzKGh? Ml\uSG1UVw>? NUHZfpR7TW[oZXP0JI9vKHOyaHnu[49ugWynaX6gcIV3\Wx? NUnJXWt7OjR6MEW5OFY>
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UM-UC-3 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV3JR|UxRTNzNTDwUS=> NVTrcFVUW0GQR1XS
SBC-1 M{TzUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEW0eZBKSzVyPUe0NkBxVQ>? M2fDdXNCVkeHUh?=
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LU-139 M2L3Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2PTOmlEPTB;Nz63O{BvVQ>? NIXKb4ZUSU6JRWK=
ETK-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1zwSGlEPTB;Nz64PEBvVQ>? MnvVV2FPT0WU
Ramos-2G6-4C10 Ml\vS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkHxTWM2OD16LkS5JI5O NXnCSoVJW0GQR1XS
MHH-PREB-1 NXPt[2w3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnTETWM2OD17LkGyJI5O MXPTRW5ITVJ?
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MFE-280 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M17hN2lEPTB;OT65PUBvVQ>? MVTTRW5ITVJ?
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HH NGG5dGRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3zuV2lEPTB;MUWuO{BvVQ>? M3rlfXNCVkeHUh?=
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MOLT-16 MoHpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4S2bmlEPTB;MUeuNVUhdk1? MVLTRW5ITVJ?
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T84 NGLhTpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTZwOUi2OEDPxE1? MXHTRW5ITVJ?
CAPAN-1 MnjZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NI\a[ZpKSzVyPUeuOlIzOzNizszN Mnn5V2FPT0WU
SW1417 Mn;OS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NELGbHRKSzVyPUeuPVE4OzFizszN NGXpOlNUSU6JRWK=
BALL-1 NHW4UnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHHTTZJKSzVyPUiuOVA1ODlizszN NUTRe3BkW0GQR1XS
HT-29 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRTlwMEe1PVkh|ryP M4LtPHNCVkeHUh?=
C3A NWf5e45GT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkXHTWM2OD17Lki4N|k1KM7:TR?= NUXaRlRDW0GQR1XS
NCI-H1993 Ml7KS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmntTWM2OD1zMD61NFgyKM7:TR?= NXO2eod7W0GQR1XS
SK-MEL-1 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYj6VHRnUUN3ME2xNU43Ojh7IN88US=> NHLlXnhUSU6JRWK=
DU-145 M2Twd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFji[XBKSzVyPUG0MlUxPTJizszN M2D1c3NCVkeHUh?=
KP-N-YN MlrHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlnkTWM2OD1zND61NVA{KM7:TR?= NYDoNJlOW0GQR1XS
CCRF-CEM NXrWV3RZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEfqWnRKSzVyPUG0Mlc5ODlizszN NEXKe3FUSU6JRWK=
ZR-75-30 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3vXbmlEPTB;MU[uN|MxOyEQvF2= NXzJN3ppW0GQR1XS
A673 M1nYWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVnJR|UxRTJyLkW1NFch|ryP MkXNV2FPT0WU
K-562 MoPaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M164cmlEPTB;MkiuOFE5OyEQvF2= M3L2S3NCVkeHUh?=

... Click to View More Cell Line Experimental Data

In vivo試験 BEZ235 induces regression of the tumors (69%) without statistically significant effect on body weight gain. Altogether, these preliminary in vivo efficacy results show that BEZ235 causes disease stasis when administered orally as a single agent and can enhance the efficacy of other anticancer agents when used in combination studies. [1]
臨床試験
特集

プロトコル (参考用のみ)

キナーゼアッセイ:

[1]

In vitro Protein Kinase, PI3K, and mTOR Assays PI3Kα, β, and δ proteins are composed of the iSH2 domain of p85 NH2-terminally fused to the full-length protein p110 protein, with the exception of α that also does not contain the last 20 amino acids. PI3Kγ is produced as full-length protein deleted for its first 144 amino acids. All constructs are fused to a COOH-terminal His tag for convenient purification and then cloned into the pBlue-Bac4.5 (for α, β, and δ isoforms) or pVL1393 (for γ isoform) plasmids. The different vectors are then cotransfected with BaculoGold WT genomic DNA using methods recommended by the vendor for production of the respective recombinant baculoviruses and proteins. BEZ235 are tested for their activity against PI3K using a Kinase-Glo assay. The kinase reaction is done in 384-well black plate. Each well is loaded with 50 μL of test items (in 90% DMSO) and 5 μL reaction buffer containing 10 μg/mL PI substrate (l-α-phosphatidylinositol; Avanti Polar Lipids; prepared in 3% octyl-glucoside) and the PI3K proteins (10, 25, 10, and 150 nM of p110α, p110β, p110δ, and p110γ, respectively) are then added to it. The reaction is started by the addition of 5 μL of 1 μM ATP prepared in the reaction buffer and is incubated for either 60 (for p110α, p110β, and p110δ) or 120 min (for p110γ). It is terminated by the addition of 10 μL Kinase-Glo buffer. The plates are then read in a Synergy 2 reader for luminescence detection.

細胞アッセイ:

[2]

細胞株 HCT116, DLD-1 and SW480 cells
濃度 0-1 μM
反応時間 48 hours
実験の流れ

The human CRC cell lines, HCT116 (PIK3CA mutant; kinase domain at H1047R), DLD-1 (PIK3CA mutant; helical domain at E545K), and SW480 (PIK3CA wild-type) and isogenic DLD-1 PIK3CA mutant as well as wild-type cells are maintained in DMEM with 10% FBS and 1 × Penicillin/Streptomycin. Cells are plated at different initial densities (HCT116: 3 × 103 cells/well, DLD-1: 5.5 × 103 cells/well, SW480: 4.5 × 103 cells/well, DLD-1 PIK3CA mutant: 7 × 103 cells/well, and DLD-1 PIK3CA wild-type: 9 × 103 cells/well) to account for differential growth kinetics. After 16 hours, cells are incubated with increasing concentrations of BEZ235, and the drug-containing growth medium is changed every 24 hours. Cell viability is assessed 16 hours after the initial plating and 48 hours after initiation of drug treatment using the colorimetric MTS assay CellTiter 96® AQueous One Solution Cell Proliferation Assay, as per the manufacturer's instructions. Cell viability after drug treatment is normalized to that of untreated cells also grown for 48 hours. For western blot analysis, cells are plated with zero or maximum inhibitory dose (500 nM) BEZ235 for 2, 6, 24, or 48 hours.

動物実験:

[1]

動物モデル Female Harlan athymic nude mice
製剤 NMP/polyethylene glycol 300 (10/90, v/v)
投薬量 45 mg/kg
投与方法 p.o.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

SpeciesMouseRatRabbitGuinea pigHamsterDogMonkeyBaboon
Weight (kg)0.020.151.80.40.0810312
Body Surface Area (m2)0.0070.0250.150.050.020.50.240.6
Km factor361285201220
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×  mouse Km(3)  = 11.2 mg/kg
rat Km(6)
1

参考

化学情報

Download BEZ235 (NVP-BEZ235, Dactolisib) SDF
分子量 469.55
化学式

C30H23N5O

CAS No. 915019-65-7
保管 2年-20℃
6月-80℃in solvent
別名 N/A
溶解度 (25°C) * In vitro DMF 18 mg/mL warmed (38.33 mM)
DMSO 0.01 mg/mL (0.02 mM)
<1 mg/mL (<1 mM)
In vivo NMP/polyethylene glycol 300 (10/90, v/v) 30 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* 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.
化学名 2-methyl-2-(4-(3-methyl-2-oxo-8-(quinolin-3-yl)-2,3-dihydroimidazo[4,5-c]quinolin-1-yl)phenyl)propanenitrile

カスタマーフィードバック (8)


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Source Cancer Res, 2010, 70, 4982-4994. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Detection of lipid kinase activities of PI3K p110α mutants
Cell Lines HEK293T cells
Concentrations
Incubation Time
Results "Evaluation of relative kinase activity of these mutants revealed that mutant P449T exhibited gain of function (>2-fold) compared with wild-type PI3K α (Fig. A). With regard to two hotspot mutants (E545K and H1047R), we examined the effect of NVP-BEZ235 and other PI3K inhibitors on their enzymatic activity and found no striking difference in their efficacies compared with wild-type p110α (Fig. B).

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Source Clin Cancer Res, 2010, 16, 6029-6039. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Synergism studies, Immunoblot assays, Clonogenic assays
Cell Lines Melanoma cell
Concentrations 0.1-100 μM
Incubation Time 1-24 h
Results One of the proposed mechanisms of resistance to PI3KIs is mutation in the Ras-Raf pathway, which are found in more than half of melanomas. By ANOVA, no association was found between the IC50 values of NVP-BEZ235 and the presence or absence of B-Raf mutations (Fig. A). The targets of NVP-BEZ235, pAkt and pP70S6K, were both decreased with exposure to the drug in a time- and dose-dependent fashion, as shown in Figure B for YUVON and YUSIK cell lines. Clonogenicity was studied in YUVON and YUSIK cells with exposure to the dual PI3K/mTOR inhibitor. As shown in Figure C, NVP-BEZ235 effectively inhibits clonogenicity at low nanomolar concentrations.

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Source Breast Cancer Res , 2011, 13, R52. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Immunofluorescence staining
Cell Lines MCF7 cells, IGF1R cells
Concentrations
Incubation Time
Results We investigated the effect of IGF-1 stimulation on MCF7/IGF-1R 4-OH-TAM resistance in a structurally and physiologically relevant context by use of a modified 3D culture. Both parental MCF7 (Figure a) and MCF7/IGF-1R cells (Figure b) were responsive to E2 or IGF-1 by forming acini on Matrigel, but the response was significantly larger in MCF7/IGF-1R cells with altered a cinar morphogenesis. inhibition of IGF -1R/ERK/Akt signaling by respective kinase inhibitors restored 4-OH-TAM sensitivity of MCF7/IGF-1R cells in 3D culture (Figure c).

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Source Breast Cancer Res, 2011, 13:R52. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Western blot, A sulforhodamine B ( SRB) colorimetric assay
Cell Lines MCF7 cells, GF-1R cells
Concentrations 0.01-10 μM
Incubation Time
Results IGF-1-stimulated proliferation was drastically restrained by BEZ235 at either 1 or 10 μM (Figure a).While IGF-1R and ERK signaling remained unaffected in response to IGF-1, the phosphorylation level of Akt was diminished with an increase in the dose of BEZ235, largely at 0.1 μM and entirely at 0.5 μM (Figure b). Likewise, the cell proliferation rate decreased correspondingly to Akt phosphorylation levels, significantly dropping at 0.1μM BEZ235 (Figure c)

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Source Eur J Cancer, 2010, 46, 1111-1121. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method LanthaScreen assay
Cell Lines JFCR39 cell lines
Concentrations 0.016 μM
Incubation Time
Results As shown in Fig. A, NVP-BEZ235 and other inhibitors all inhibited mTOR in a dose-dependent manner. The IC50 values were calculated and are shown in Fig. B. NVP-BEZ235 inhibited mTOR potently, with IC50 value of 0.002 μM. In contrast, ZSTK474, GDC-0941 and LY294002 weakly inhibited mTOR, with IC50 values of 0.377, 0.413 and 3.86μM, respectively. To further demonstrate their selectivity for class I PI3K, the IC50 values of these inhibitors for mTOR were divided by their corresponding IC50s for class I PI3Ka, and the resulting ratios were plotted in Fig. C. Clearly, ZSTK474 and GDC-0941 revealed much higher selectivity for inhibiting class I PI3K than the other two inhibitors. In contrast, NVP-BEZ235 more potently inhibited the activity of mTOR than that of class I PI3K

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Source Dr. Zhang of Tianjin Medical University. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Western blot
Cell Lines breast cancer cells
Concentrations 0-10 nM
Incubation Time 3 h
Results

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Rating
Source Dr. Zhang of Tianjin Medical University. BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Western blot
Cell Lines breast cancer cells
Concentrations 0-50 nM
Incubation Time 3 h
Results

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Source BEZ235 (NVP-BEZ235, Dactolisib) purchased from Selleck
Method Western Blotting
Cell Lines xenografts
Concentrations
Incubation Time
Results Phospholipase A2 group 4A (PLA2G4A) expression was increased after BEZ235 treatment in basal-like xenografts.

文献中の引用 (81)

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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