Product Categories

BEZ235 (NVP-BEZ235)

BEZ235 (NVP-BEZ235) is a dual ATP-competitive PI3K and mTOR inhibitor of p110α, p110γ, p110δ and p110β with IC50 of 4 nM, 5 nM, 7 nM and 75 nM, respectively, and also inhibits ATR with IC50 of 21 nM.

Catalog No.S1009

7 Reviews 25 Product Citations

: Tel: +1-832-582-8158[email protected]

BEZ235 (NVP-BEZ235) Chemical Structure
Molecular Weight: 469.55

Validation & Quality Control

Product Citations(25)

Nature, 2012, 487(7408):505-9

Blood, 2011, 118(14), 3911-3921

Cancer Res, 2011, 71(15), 5067-5074

Cancer Res, 2010, 70(11), 4709-4718

Cancer Res, 2010, 70(12), 4982-4994
Clin Cancer Res, 2012, 18(9):2515-25

Sci Signal, 2012, 5(224):rs4

Clin Cancer Res, 2010, 16(24), 6029-6039

J Neurosci, 2012, 32(1):264-74

Oncogene, 2012, ahead of print
Oncogene, 2012, ahead of print

J Invest Dermatol, 2012, 132(7):1850-9

Breast Cancer Res, 2011, 13(3), R52

Neoplasia, 2012, 14(1), 34-43

J Virol, 2012, 86(8):4578-85
Breast Cancer Res, 2013, ahead of print

Int J Proteomics, 2011, 2011, 215496

Cancer Cell, 2012, 21(2), 155-167

Eur J Cancer, 2010, 46(6), 1111-1121

Eur J Cancer, 2012, 48(6), 936-943
Mol Pharmacol, 2012, 81(5):748-58

Cancer Lett, 2013, 329(2), 236-242

PLoS One, 2012, 7(9):e46518

Hum Pathol, 2012, 43(12):2197-206

J Surg Oncol, 2012, 106(8):972-80

Customer Reviews(7) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

BEZ235 (NVP-BEZ235) is available in the following compound libraries:

Inhibitor Library (96-well) Kinase Inhibitor Library (96-well) Chemical Library (96-well) Cambridge Cancer Compound Library(96-well)

Product Information

Compare PI3K Inhibitors

Cat.No.	Product Name	Solubility (25°C)
Cat.No.	Product Name	Water	DMSO	Ethanol
S1009	BEZ235 (NVP-BEZ235)	<1 mg/mL	1 mg/mL	<1 mg/mL
S1105	LY294002	<1 mg/mL	36 mg/mL	21 mg/mL
S1065	GDC-0941	<1 mg/mL	44 mg/mL	<1 mg/mL
S2226	CAL-101 (GS-1101)	<1 mg/mL	83 mg/mL	35 mg/mL
S2247	BKM120 (NVP-BKM120)	<1 mg/mL	82 mg/mL	2 mg/mL
S2638	NU7441 (KU-57788)	<1 mg/mL	3 mg/mL	<1 mg/mL
S2814	BYL719	<1 mg/mL	88 mg/mL	5 mg/mL
S1038	PI-103	<1 mg/mL	24 mg/mL	<1 mg/mL
S1169	TGX-221	<1 mg/mL	12 mg/mL	<1 mg/mL
S2758	Wortmannin	<1 mg/mL	86 mg/mL	<1 mg/mL
S2636	A66	<1 mg/mL	79 mg/mL	1 mg/mL
S1072	ZSTK474	<1 mg/mL	21 mg/mL	<1 mg/mL
S1118	XL147	<1 mg/mL	3 mg/mL	<1 mg/mL
S2767	3-Methyladenine	<1 mg/mL	4 mg/mL	4 mg/mL
S1268	IC-87114	<1 mg/mL	0.66 mg/mL	<1 mg/mL
S1410	AS-605240	<1 mg/mL	0.4 mg/mL	<1 mg/mL
S2671	AS-252424	<1 mg/mL	61 mg/mL	<1 mg/mL
S1523	XL765 (SAR245409)	<1 mg/mL	15 mg/mL	<1 mg/mL
S2658	GSK2126458	<1 mg/mL	101 mg/mL	<1 mg/mL
S1205	PIK-75	<1 mg/mL	3 mg/mL	<1 mg/mL
S2743	PF-04691502	<1 mg/mL	14 mg/mL	<1 mg/mL
S1462	AZD6482	<1 mg/mL	82 mg/mL	28 mg/mL
S2628	PF-05212384 (PKI-587)	<1 mg/mL	2 mg/mL	<1 mg/mL
S2696	GDC-0980 (RG7422)	<1 mg/mL	20 mg/mL	<1 mg/mL
S1489	PIK-93	<1 mg/mL	78 mg/mL	<1 mg/mL
S1187	PIK-90	<1 mg/mL	0.28 mg/mL	<1 mg/mL
S2802	BAY80-6946	0.002 mg/mL	0.002 mg/mL	0.01 mg/mL
S1352	TG100-115	<1 mg/mL	9 mg/mL	<1 mg/mL
S1219	YM201636	<1 mg/mL	35 mg/mL	<1 mg/mL
S1360	GSK1059615	<1 mg/mL	2 mg/mL	<1 mg/mL
S2227	PIK-294	<1 mg/mL	98 mg/mL	<1 mg/mL
S2681	AS-604850	<1 mg/mL	57 mg/mL	5 mg/mL
S2699	CH5132799	<1 mg/mL	12 mg/mL	<1 mg/mL
S2682	CAY10505	<1 mg/mL	58 mg/mL	<1 mg/mL
S2749	NVP-BGT226	<1 mg/mL	30 mg/mL	<1 mg/mL
S2759	PI3K/HDAC InhibitorⅠ	<1 mg/mL	102 mg/mL	<1 mg/mL
S2207	PIK-293	<1 mg/mL	80 mg/mL	<1 mg/mL
S2739	PKI-402	<1 mg/mL	0.4 mg/mL	<1 mg/mL
S2870	TG 100713	<1 mg/mL	2 mg/mL	<1 mg/mL
S8002	GSK2636771	<1 mg/mL	87 mg/mL	19 mg/mL
S7028	IPI-145 (INK1197)	<1 mg/mL	84 mg/mL	<1 mg/mL

Research Area
Research Area

Combination Therapy

Combination Therapy

BEZ235 (NVP-BEZ235) + Rapamycin	NVP-BEZ235 in vitro results in the nuclear translocation of p27, greater reduction in tumor cell proliferation, and more complete suppression of Akt, Mnk-1, eIF4E, and 4EBP-1 phosphorylation and cyclin D1 and hypoxia-inducible factor 2α (HIF2α) expression than that achieved with Rapamycin in RCC cell lines. NVP-BEZ235 induces growth arrest in both the 786-O and A498 xenografts that is associated with inhibition of Akt and S6 phosphorylation as well as the induction of apoptosis and reduction in markers of tumor cell proliferation. In contrast, Rapamycin induces only minimal growth retardation. ^[4]
BEZ235 (NVP-BEZ235) + PD-98059	BEZ235 (1 µM) and PD98059 (10 µM) significantly inhibits EGF-induced IL-8 production in SPC-A1 cells. PD98059 (10 µM) only has about 10% inhibitory effects, while BEZ235 (1 µM) shows about 30% inhibitory effects in SPC-A1 cells. BEZ235(1 µM) down-regulats EGF-increased phosphorylation of AKT, while PD98059 (10 µM) inhibits EGF-increased phosphorylation of ERK in SPC-A1 cells. ^[5]
BEZ235 (NVP-BEZ235) + PI-103	PI-103 (< 2.5 μM) is less effective than NVP-BEZ235 (< 2.5 μM) in inhibiting T-ALL cell line growth at all the concentrations tested. ^[7]
BEZ235 (NVP-BEZ235) + U0126	U0126 (10 µM) combined with NVP-BEZ235 (250 nM) synergistically suppresses cell proliferation with a 45–70% reduction, and combined therapy markedly induces G1 arrest in in cells with alterations in K-Ras. ^[6]
BEZ235 (NVP-BEZ235) + LY294002	The IC50 values for NVP-BEZ235 and LY294002 toward PI3Kα inhibition increase in a linear manner, in agreement with an inhibition by ATP competition, when test in presence of increasing ATP concentrations (26 nM to 400 μM). NVP-BEZ235 is able to reduce IGF-I-induced S473P-Akt levels below the limit of detection, whereas the phosphorylation of the p85 binding site on IGF-IR (Y1316) is not altered. Similar results are obtained with the PI3K inhibitors LY294002. NVP-BEZ235 leads to its complete nuclear relocalization as shown by the time-dependent increased in the fluorescent signal obtained in the nuclei in U2OS cells stably expressing a GFP-FKHRL1 chimeric protein. A similar effect is observed when cells are treated with LY294002. ^[3]

Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description	BEZ235 (NVP-BEZ235) is a dual ATP-competitive PI3K and mTOR inhibitor of p110α, p110γ, p110δ and p110β with IC50 of 4 nM, 5 nM, 7 nM and 75 nM, respectively, and also inhibits ATR with IC50 of 21 nM.
Targets	p110α	p110γ	p110δ	p110β	ATR
IC50	4 nM	5 nM	7 nM	75 nM ^[1]	21 nM ^[9]
In vitro	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 BEZ23 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]
In vivo	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]
Clinical Trials
Features

Protocol(Only for Reference)

Kinase Assay:
^[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.

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.

Cell Assay:
^[2]

Cell lines	HCT116, DLD-1 and SW480 cells
Concentrations	0-1 μM
Incubation Time	48 hours
Method	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.

Animal Study:
^[1]

Animal Models	Female Harlan athymic nude mice
Formulation	NMP/polyethylene glycol 300 (10/90, v/v)
Dosages	45 mg/kg
Administration	p.o.

References

Chemical Information

Download BEZ235 (NVP-BEZ235) SDF

Molecular Weight (MW)	469.55
Formula	C₃₀H₂₃N₅O
CAS No.	915019-65-7
Synonyms	N/A

Solubility (25°C) DMSO 1 mg/mL Water <1 mg/mL Ethanol <1 mg/mL
Storage	2 years -20°CPowder
	2 weeks4°Cin DMSO
	6 months-80°Cin DMSO

Chemical Name	2-methyl-2-(4-(3-methyl-2-oxo-8-(quinolin-3-yl)-2,3-dihydroimidazo[4,5-c]quinolin-1-yl)phenyl)propanenitrile

Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (7)

Click to enlarge

Rating

Source

Breast Cancer Res , 2011, 13, R52. BEZ235 (NVP-BEZ235) 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).

Click to enlarge

Rating

Source

Eur J Cancer, 2010, 46, 1111-1121. BEZ235 (NVP-BEZ235) 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

Click to enlarge

Rating

Source

Dr Zhang of Tianjin Medical University. BEZ235 (NVP-BEZ235) purchased from Selleck

Method

Western blot

Cell Lines

breast cancer cells

Concentrations

0-10 nM

Incubation Time

3 h

Results

Click to enlarge

Rating

Source

Dr Zhang of Tianjin Medical University. BEZ235 (NVP-BEZ235) purchased from Selleck

Method

Western blot

Cell Lines

breast cancer cells

Concentrations

0-50 nM

Incubation Time

3 h

Results

Click to enlarge

Rating

Source

Cancer Res, 2010, 70, 4982-4994. BEZ235 (NVP-BEZ235) 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).

Click to enlarge

Rating

Source

Clin Cancer Res, 2010, 16, 6029-6039. BEZ235 (NVP-BEZ235) 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.

Click to enlarge

Rating

Source

Breast Cancer Res, 2011, 13, R52. BEZ235 (NVP-BEZ235) 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)

Product Citations (25)

Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors. [Wilson TR, et al. Nature 2012;487(7408):505-9]
PubMed: 22763448
FERM domain mutations induce gain of function in JAK3 in adult T-cell leukemia/lymphoma. [Elliott NE, et al. Blood 2011;118(14), 3911-3921]
PubMed: 21821710
Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition. [Shi H, et al. Cancer Res 2011;71(15), 5067-5074]
PubMed: 21803746

Activation of FOXO3a is sufficient to reverse mitogen-activated protein/extracellular signal-regulated kinase kinase inhibitor chemoresistance in human cancer. [Yang JY, et al. Cancer Res 2010;70(11), 4709-4718]
PubMed: 20484037
Correlating phosphatidylinositol 3-Kinase inhibitor efficacy with signaling pathway status: in silico and biological evaluations. [Dan S, et al. Cancer Res 2010;70(12), 4982-4994]
PubMed: 20530683
Inhibition of MEK and PI3K/mTOR suppresses tumor growth but does not cause tumor regression in patient-derived xenografts of RAS-mutant colorectal carcinomas. [Migliardi G, et al. Clin Cancer Res 2012;18(9):2515-25]
PubMed: 22392911
MicroSCALE screening reveals genetic modifiers of therapeutic response in melanoma. [Wood KC, et al. Sci Signal 2012;5(224):rs4]
PubMed: 22589389
Vertical targeting of the phosphatidylinositol-3 kinase pathway as a strategy for treating melanoma. [Aziz SA, et al. Clin Cancer Res 2010;16(24), 6029-6039]
PubMed: 21169255
Dock3 stimulates axonal outgrowth via GSK-3β-mediated microtubule assembly. [Namekata K, et al. J Neurosci 2012;32(1):264-74]
PubMed: 22219288
Targeting the eIF4A RNA helicase blocks translation of the MUC1-C oncoprotein. [Jin C, et al. Oncogene 2012;ahead of print]
PubMed: 22689062
The MAPK pathway functions as a redundant survival signal that reinforces the PI3K cascade in c-Kit mutant melanoma. [Todd JR, et al. Oncogene 2012;ahead of print]
PubMed: 23246970
Acquired Resistance to BRAF Inhibition Can Confer Cross-Resistance to Combined BRAF/MEK Inhibition. [Gowrishankar K, et al. J Invest Dermatol 2012;132(7):1850-9]
PubMed: 22437314
Elevated insulin-like growth factor 1 receptor signaling induces antiestrogen resistance through the MAPK/ERK and PI3K/Akt signaling routes. [Zhang Y, et al. Breast Cancer Res 2011;13(3), R52]
PubMed: 21595894
The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses. [Mukherjee B, et al. Neoplasia 2012;14(1), 34-43]
PubMed: 22355272
The PI3K/Akt pathway contributes to arenavirus budding. [Urata S, et al. J Virol 2012;86(8):4578-85]
PubMed: 22345463
Metabolic biomarkers for response to PI3K inhibition in basal-like breast cancer. [Moestue SA, et al. Breast Cancer Res 2013;ahead of print]
PubMed: 23448424
Signatures of drug sensitivity in nonsmall cell lung cancer. [Gong HC, et al. Int J Proteomics 2011;2011, 215496]
PubMed: 22091388
An animal model of MYC-driven medulloblastoma. [Pei Y, et al. Cancer Cell 2012;21(2), 155-167]
PubMed: 22340590
Inhibition profiles of phosphatidylinositol 3-kinase inhibitors against PI3K superfamily and human cancer cell line panel JFCR39. [Kong D, et al. Eur J Cancer 2010;46(6), 1111-1121]
PubMed: 20129775
ZSTK474, a specific phosphatidylinositol 3-kinase inhibitor, induces G1 arrest of the cell cycle in vivo. [Dan S, et al. Eur J Cancer 2012;48(6), 936-943]
PubMed: 22088482
Lapatinib and Obatoclax kill tumor cells through blockade of ERBB1/3/4 and through inhibition of BCL-XL and MCL-1. [Cruickshanks N, et al. Mol Pharmacol 2012;81(5):748-58]
PubMed: 22357666
Activation of the unfolded protein response bypasses trastuzumab-mediated inhibition of the PI-3K pathway. [Kumandan S, et al. Cancer Lett 2013;329(2), 236-242]
PubMed: 23200669
Modulators of Sensitivity and Resistance to Inhibition of PI3K Identified in a Pharmacogenomic Screen of the NCI-60 Human Tumor Cell Line Collection. [Kwei KA, et al. PLoS One 2012;7(9):e46518]
PubMed: 23029544
Clinicopathologic and biological analysis of PIK3CA mutation in ovarian clear cell carcinoma. [Rahman M, et al. Hum Pathol 2012;43(12):2197-206]
PubMed: 22705003
Activated mTOR/P70S6K signaling pathway is involved in insulinoma tumorigenesis. [Zhan HX, et al. J Surg Oncol 2012;106(8):972-80]
PubMed: 22711648

Tech Support & FAQs

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

Tel: +1-832-582-8158 Ext:3Monday–Friday 9:00 AM–5:00 PM (Central Time)

If you have any other enquiries, please leave a message.

* Indicates a Required Field

Related PI3K Inhibitors

Deforolimus (Ridaforolimus)

Deforolimus (Ridaforolimus, AP23573, MK-8669) is a selective mTOR inhibitor with IC50 of 0.2 nM.
PI-103

PI-103 is a potent, ATP-competitive PI3K inhibitor of DNA-PK, p110α, mTORC1, PI3KC2β, p110δ, mTORC2, p110β, and p110γ with IC50 of 2 nM, 8 nM, 20 nM, 26 nM, 48 nM, 83 nM, 88 nM and 150 nM, respectively.
GDC-0941

GDC-0941 is a potent inhibitor of PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ with IC50 of 3 nM, 33 nM, 3 nM and 75 nM, respectively.
ZSTK474

ZSTK474 is a potent pan-class I PI3K inhibitor with IC50 of 37 nM.
KU-55933

KU-55933 is a potent and specific ATM inhibitor with IC50 and K_i of 13 nM and 2.2 nM, respectively.
LY294002

LY294002 is a PI3K inhibitor for p110α, p110δ and p110β with IC50 of 0.5 μM, 0.57 μM and 0.97 μM, respectively.
XL147

XL147 (SAR245408) is a selective and reversible class I PI3K inhibitor for wild type and mutant p110α with IC50 of 40 nM and 40 nM, respectively.
TGX-221

TGX-221 is a potent, selective PI3K inhibitor for p110β with IC50 of 8.5 nM.
PIK-90

PIK-90 is a potent and cell permeable inhibitor of p110α, p110β, p110γ and p110δ with IC50 of 11 nM, 350 nM, 18 nM and 58 nM, respectively.
PIK-75

PIK-75 is a selective and competitive inhibitor of p110α with IC50 of 5.8 nM and also potently inhibits DNA-PK with IC50 of 2 nM.

PI3K/Akt/mTOR Pathway Products

> Download

Choose Your Country or Region

Product Categories

BEZ235 (NVP-BEZ235)