Nvp bez235

Manufactured by Novartis

Sourced in Switzerland, United States

NVP-BEZ235 is a laboratory compound developed by Novartis. It is a dual inhibitor of phosphoinositide 3-kinase (PI3K) and the mammalian target of rapamycin (mTOR) signaling pathways. The core function of NVP-BEZ235 is to facilitate the study of these important cellular signaling mechanisms in research settings.

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Lab products found in correlation

Rad001, by Novartis (2 mentions) β actin, by Santa Cruz Biotechnology (2 mentions) Abt 263, by Active Motif (1 mentions) Abt 199, by Active Motif (1 mentions) Gdc 0941, by Chemietek (1 mentions) Sh sy5y, by American Type Culture Collection (1 mentions) Sk n sh, by American Type Culture Collection (1 mentions) Sk n as, by American Type Culture Collection (1 mentions) Sk n be 2 c, by American Type Culture Collection (1 mentions) Venor gem, by Minerva Biolabs (1 mentions) Rapamycin, by Selleck Chemicals (1 mentions) Staurosporine, by Alexis Biochemicals (1 mentions) Tgx 221, by Selleck Chemicals (1 mentions) Pik 90, by Selleck Chemicals (1 mentions) Doxorubicin, by Merck Group (1 mentions) Methotrexate, by Pfizer (1 mentions) Cisplatin, by Teva Pharmaceuticals (1 mentions) Cleaved parp, by Cell Signaling Technology (1 mentions) Wst reagent, by Takara Bio (1 mentions) Mouse monoclonal antibody for β actin, by Merck Group (1 mentions)

Close spelling variants of this product

BEZ235 (21 citations)

24 protocols using nvp bez235

Characterization of KRAS/EGFR Mutant NSCLC Cell Lines

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Human KRAS mutant and EGFR mutant NSLCLC cell lines were obtained from the Center for Molecular Therapeutics at the MGH Cancer Center which performs routine SNP and STR authentication (21 (link)); cell lines were passaged for less than 6 months following receipt. A427-R and DV-90-R resistant cell lines were generated by exposing parental cell lines to 1 μM AZD6244/GDC-0941 for three days followed by drug washout for 3 days. Cells were treated for 5-10 cycles, followed by maintenance in the continuous presence of drug. The N1, N2 (treatment naïve) and R1, R2, R3 (AZD6244/BEZ235 resistant) lines are tumor-derived cell lines from Kras p53^L/L mice. For cell culture studies, AZD6244 (Otava), GDC-0941 (Chemietek), ABT-263 (Active Biochem), ABT-199 (Active Biochem), NVP-BEZ235 (kindly provided by Novartis) were dissolved in DMSO to a final concentration of 10 mmol/l and stored at −20°C. Antibodies utilized for western blotting are listed in Supplementary Materials and Methods.

Hata A.N., Yeo A., Faber A.C., Lifshits E., Chen Z., Cheng K.A., Walton Z., Sarosiek K.A., Letai A., Heist R.S., Mino-Kenudson M., Wong K.K, & Engelman J.A. (2014). Failure to induce apoptosis via BCL-2 family proteins underlies lack of efficacy of combined MEK and PI3K inhibitors for KRAS mutant lung cancers. Cancer research, 74(11), 3146-3156.

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Neuroblastoma Cell Line Characterization

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Kelly, SH-SY5Y, SHEP, SK-N-SH, IMR32, SKN-Be2C, IMR5 and SK-N-AS human neuroblastoma cell lines were obtained from the University of California at San Francisco Cell Culture Facility (San Francisco, CA) and from the American Type Culture Collection (Manassas, VA). Cells were grown in DMEM or RPMI containing 10% fetal bovine serum (PAA “Gold”). In specified experiments, cells were serum starved in 0.2% FCS for 6 h before analysis and treated with recombinant human insulin-like growth factor-1 (IGF-1; Sigma) at 50ng/mL for 30 min before harvesting. NVP-BEZ235 (Novartis), Torin1 (Nathaniel Gray), staurosporine (Alexis Biochemicals), ZSTK474 (Alexis Biochemicals), GSK3β inhibitor (Calbiochem), TGX221 (Selleck chemicals), PIK90 (Selleck chemicals) and Rapamycin (Selleck chemicals) were all prepared as a 10mM stock solution in 100% DMSO. Working solutions were prepared freshly by dilution in 100% DMSO prior addition to the cell media at a final concentration of 0.1% DMSO. SHEP cells were stably transfected with constructs wild-type or mutant for MYCN and appropriate clones were screened and selected essentially as described previously [37 (link)]. Cells were regularly screened for Mycoplasma using a PCR-based assay (VenorGem, Minerva Biolabs).

Vaughan L., Clarke P.A., Barker K., Chanthery Y., Gustafson C.W., Tucker E., Renshaw J., Raynaud F., Li X., Burke R., Jamin Y., Robinson S.P., Pearson A., Maira M., Weiss W.A., Workman P, & Chesler L. (2016). Inhibition of mTOR-kinase destabilizes MYCN and is a potential therapy for MYCN-dependent tumors. Oncotarget, 7(36), 57525-57544.

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Inhibitor Preparation and Storage

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The small-molecule inhibitor of IRS-1/2, NT157, was kindly provided by TyrNovo Ltd. (Israel) (27 (link)). Briefly, NT157 was dissolved in dimethyl sulfoxide (DMSO) to generate a 10-mM stock solution, which was stored at −80°C. Doxorubicin was purchased from Sigma (St. Louis, MO, USA), cisplatin was obtained from TEVA (Italy), and methotrexate was obtained from Pfizer (Italy). The signal transduction inhibitor that targets mTOR, Everolimus, was purchased from Sequoia Research Products (Pangbourne, UK). The PI-3K/mTOR dual inhibitor NVP-BEZ235 was kindly provided by Novartis (Basel, Switzerland). Working dilutions of all drugs were prepared immediately before use.

Garofalo C., Capristo M., Mancarella C., Reunevi H., Picci P, & Scotlandi K. (2015). Preclinical Effectiveness of Selective Inhibitor of IRS-1/2 NT157 in Osteosarcoma Cell Lines. Frontiers in Endocrinology, 6, 74.

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Biochemical Signaling Pathway Analysis

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Rabbit monoclonal antibody for phospho-Akt (Ser473), S6 ribosomal protein (S6), phospho-S6 ribosomal protein, phospho-4E-BP1, cleaved PARP and PKM2 were obtained from Cell Signaling Technology^®, Rabbit polyclonal antibody for cleaved caspase-3 was obtained from Cell Signaling Technology^®, mouse monoclonal antibody for HIF1-a was purchased from Santa Cruz Biotechnology^® and mouse monoclonal antibody for β-actin was purchased from Sigma^®. WST reagents were obtained from Takara Bio (Kyoto, Japan). NVP-BEZ235 and RAD001 were kindly provided by Novartis (Basel, Switzerland) without compensation.

Yasumizu Y., Hongo H., Kosaka T., Mikami S., Nishimoto K., Kikuchi E, & Oya M. (2018). PKM2 under hypoxic environment causes resistance to mTOR inhibitor in human castration resistant prostate cancer. Oncotarget, 9(45), 27698-27707.

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Immune Cell Profiling in Cellular Signaling

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Escherichia coli O55:B5 LPS and oleic acid were purchased from Sigma-Aldrich. Everolimus and NVP-BEZ235 were provided by Novartis. Phospho-S6 (Ser240/244) and phospho-Akt (Ser473) were purchased from Cell Signaling Technology. TER-119-APC, CD4-APC (RM4-5), CD8a-PerCP (53-6.7), CD19-FITC (6D5), I-Ab-PE (AF6-120.1), CD11c-FITC (N418), and F4/80-APC (BM8) antibodies for flow cytometry were purchased from BioLegend.

Üstün S., Lassnig C., Preitschopf A., Mikula M., Müller M., Hengstschläger M, & Weichhart T. (2015). Effects of the mTOR inhibitor everolimus and the PI3K/mTOR inhibitor NVP-BEZ235 in murine acute lung injury models. Transplant immunology, 33(1), 45-50.

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Rat kidney diabetes model for PI3K/mTOR inhibitor

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Rat kidney tissues and renal tumor specimens were obtained from previous short and long term experiments of 4 weeks and 24 months [7 (link), 21 (link), 42 (link)]. Briefly, diabetes was induced in adult inbred male Lewis rats (body weight 250–300 g) with a single subcutaneous dose of streptozotocin (80 mg/kg body weight) and was defined by a non-fasting blood-glucose level higher than 400 mg/dL. In short term experiments, groups of rats (n = 111) were subjected to daily oral administration of the PI3K/mTOR dual inhibitor, NVP/BEZ235 (kindly provided by Novartis, Basel, Switzerland), dissolved in 2% methylcellulose at a concentration of 40 mg/kg for one week or 10 mg/kg body weight for 4 weeks, respectively, or methylcellulose alone (control groups).

Ribback S., Cigliano A., Kroeger N., Pilo M.G., Terracciano L., Burchardt M., Bannasch P., Calvisi D.F, & Dombrowski F. (2015). PI3K/AKT/mTOR pathway plays a major pathogenetic role in glycogen accumulation and tumor development in renal distal tubules of rats and men. Oncotarget, 6(15), 13036-13048.

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NVP-BEZ235 Treatment for SACC-LM Tumors

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For in vitro experiments, cells were seeded in T75 flasks until becoming ~80% confluent. A final concentration of 500 nM NVP-BEZ235 (Novartis, Basel, Switzerland) dissolved in DMSO was then added for 4 hours. For in vivo experiments, we injected either 5 × 10⁶ SACC-LM cells subcutaneously or 2 × 10⁶ SACC-LM cells intravenously at day 0. Nine days after injection, mice were randomized into controls and treated groups, and received 35 mg/kg/day dissolved in 10%NMP/90%PEG300 (sigma-aldrich, St. Louis, MO, #328634, and #90878) daily for 21 days by oral gavage. The control group was orally treated with the vehicle only. Mice were sacrificed after 21 days of treatment and the tumor and lung tissues were harvested.

Liu H., Du L., Wang R., Wei C., Liu B., Zhu L., Liu P., Liu Q., Li J., Lu S.L, & Xiao J. (2015). High frequency of loss of PTEN expression in human solid salivary adenoid cystic carcinoma and its implication for targeted therapy. Oncotarget, 6(13), 11477-11491.

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Combination Therapy for Pancreatic Cancer

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NVP-AUY922 and NVP-BEZ235 were provided by Novartis (Basel, Switzerland). Gemcitabine and oxaliplatin were purchased from TTY Biopharm (Taipei, Taiwan). For the in vitro experiments, 10 mM stock solutions of NVP-AUY922 and NVP-BEZ235 were prepared in 100% DMSO and stored at −20°C (NVP-AUY922) and 4°C (NVP-BEZ235). For administration, optimized NVP-AUY922 and NVP-BEZ235 salts with high solubility in aqueous solution were formulated in D5W. NVP-AUY922 was delivered by intraperitoneal (ip) injection in a volume of 6.25 mg/kg. NVP-BEZ235 was delivered orally (po) in a volume of 15 mg/kg. Gemcitabine (50 mg/kg) and oxaliplatin (2 mg/kg) were delivered by ip injection.

Chen M.H., Chiang K.C., Cheng C.T., Huang S.C., Chen Y.Y., Chen T.W., Yeh T.S., Jan Y.Y., Wang H.M., Weng J.J., Chang P.M., Liu C.Y., Li C.P., Chao Y., Chen M.H., Huang C.Y, & Yeh C.N. (2014). Antitumor activity of the combination of an HSP90 inhibitor and a PI3K/mTOR dual inhibitor against cholangiocarcinoma. Oncotarget, 5(9), 2372-2389.

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Cell Viability Assay for Cancer Drugs

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RP-R07, UOK-109 and UOK-146 cells (3000 cells/well) were seeded in 96-well plates and incubated for 24 h at 37 °C and 5% CO₂. The following day, cells were treated with drugs with defined concentrations. All drugs for in-vitro study sunitinib (LC laboratories), USA), gemcitabine (LC laboratories), USA), doxorubicin (LC laboratories), USA), crizotinib (LC laboratories), USA), BKM-120 (Novartis, USA), MLN0128 (Millenium, USA) and NVP-BEZ235 (Novartis, USA) were dissolved in DMSO for the preparation of stock solutions (10mM). Cell viability was determined by measuring dehydrogenase activity. We changed the medium and applied 100 μL of serum-free medium with 25 μL of MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (5 mg/mL) to each well and incubated the cells for 4 h at 37 °C and 5% CO₂ to allow the formation of a purple formazan salt. The medium was replaced with 100 μL of methanol to dissolve the formazan crystals and the plates were incubated for a further 15 min at room temperature before the absorbance was measured at λ = 570 nm using a Micro Plate Reader (BioTek Synergy HTX, USA).

Damayanti N.P., Budka J.A., Khella H.W., Ferris M.W., Ku S.Y., Kauffman E., Wood A.C., Ahmed K., Chintala V.N., Adelaiye-Ogala R., Elbanna M., Orillion A., Chintala S., Kao C., Linehan W.M., Yousef G.M., Hollenhorst P.C, & Pili R. (2018). Therapeutic targeting of TFE3/IRS-1/PI3K/mTOR axis in translocation renal cell carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 24(23), 5977-5989.

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Apoptosis Induction in Cell Cultures

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Dulbecco's Modified Eagle's Medium/Nutrient Mixture F-12 Ham (DMEM–F12), propidium iodide and Penicillin/Streptomycin 100 × stock solution were purchased from Sigma-Aldrich Chemie GmbH (Buchs, Switzerland). Trypsin solution 0.25% was purchased from GIBCO (Life Technologies Europe, Zug, Switzerland). Fetal calf serum (FCS, CVFSVF00-01) was purchased from Eurobio (Ulis (Les), France). Puromycin was purchased from AppliChem (Darmstadt, Germany). Z-Val-Ala-DL-Asp-fluoromethylketone (Z-VAD-FMK) was purchased from BACHEM (Bubendorf, CH, Switzerland). Nec-1 was purchased Enzo LifeSciences AG (Lausen, Switzerland). NVP-BEZ235 was obtained from Novartis (Basel, Switzerland) and GDC-0980 was obtained from Genentech (Roche, Basel, Switzerland). U0126 was purchased from Cell Signaling Technology (Allschwil, Switzerland). Nivaquine (chloroquine sulfate) was purchased from Sanofi Aventis (Paris, France). Recombinant His₆-GFP-Annexin V was kindly provided by T Kaufmann (Bern, CH, Switzerland).

Echeverry N., Ziltener G., Barbone D., Weder W., Stahel R.A., Broaddus V.C, & Felley-Bosco E. (2015). Inhibition of autophagy sensitizes malignant pleural mesothelioma cells to dual PI3K/mTOR inhibitors. Cell Death & Disease, 6(5), e1757-.

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