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Bez235

Manufactured by Novartis
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Sourced in Switzerland, United States

BEZ235 is a laboratory product developed by Novartis. It is a small molecule that inhibits the activity of the PI3K and mTOR enzymes. The core function of BEZ235 is to serve as a research tool for the study of cell signaling pathways involving PI3K and mTOR.

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Lab products found in correlation

Bkm120, by Novartis (7 mentions) Rad001, by Novartis (5 mentions) Bez235, by Merck Group (2 mentions) Polyethylene glycol 300, by Merck Group (2 mentions) Cgp57380, by Bio-Techne (2 mentions) Sb23580, by Selleck Chemicals (2 mentions) Ink128, by Selleck Chemicals (2 mentions) Casodex, by AstraZeneca (2 mentions) Pd98059, by Selleck Chemicals (2 mentions) Rapamycin, by LC Laboratories (2 mentions) Rapamycin, by Merck Group (2 mentions) Ruxolitinib, by Novartis (1 mentions) Pp242, by Merck Group (1 mentions) Rabbit anti cleaved caspase 3, by BD (1 mentions) Rabbit anti lc3b, by Cell Signaling Technology (1 mentions) Rabbit anti 4e bp1, by Cell Signaling Technology (1 mentions) Rabbit anti phospho 4ebp1, by Cell Signaling Technology (1 mentions) Rabbit anti mouse akt, by Cell Signaling Technology (1 mentions) Bgt226, by Novartis (1 mentions) Doxorubicin, by Pfizer (1 mentions)

21 protocols using bez235

1

Synergistic Targeting of PI3K and mTOR Pathways

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BKM120 (a selective pan class-I PI3-Kinase inhibitor), RAD001 (a mTOR specific allosteric inhibitor active against TORC1), BEZ235 (a double PI3K and mTOR inhibitor) and ruxolitinib (a JAK1/JAK2 kinase inhibitor) were kindly provided by Novartis (Basel, Switzerland); PP242 was purchased from Sigma-Aldrich (St Louis, MO, US). In-vitro and in-vivo formulations and administration schedules are detailed in Supplementary Methods.
Bartalucci N., Calabresi L., Balliu M., Martinelli S., Rossi M.C., Villeval J.L., Annunziato F., Guglielmelli P, & Vannucchi A.M. (2017). Inhibitors of the PI3K/mTOR pathway prevent STAT5 phosphorylation in JAK2V617F mutated cells through PP2A/CIP2A axis. Oncotarget, 8(57), 96710-96724.
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2

Multimodal Anti-Cancer Combination Therapy

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Everolimus, BGT226 AND BEZ235 were kindly provided by Novartis (Basel, Switzerland). Vincristine sulfate was purchased from Millennium Pharmaceuticals (Cambridge, MA), Doxorubicin from Pfizer (Melrose Park, NSW, Australia). Ionizing radiation was delivered using an X-ray irradiator (XRAD320, Precision X-Ray, Inc. East Haven, CT) at a dose rate of 0.91 Gy/minute. The following antibodies were purchased from Cell Signaling Technologies (Danvers, MA, USA): rabbit anti-phospho-4E-BP1, rabbit anti-4E-BP1, rabbit anti-phospho-S6RP, mouse anti-S6RP, rabbit anti-phospho-AKT (Ser475), rabbit anti-phospho-AKT (Thr308), rabbit anti-mouse AKT and rabbit anti-LC3B. Rabbit anti-cleaved caspase 3 was purchased from BD Pharmingen, (San Diego, CA, USA).
Wong J., Welschinger R., Hewson J., Bradstock K.F, & Bendall L.J. (2014). Efficacy of dual PI-3K and mTOR inhibitors in vitro and in vivo in acute lymphoblastic leukemia. Oncotarget, 5(21), 10460-10472.
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3

Kinase Inhibitor Effects on Cellular PpIX

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Effects of small molecule inhibitors on PpIX in cell lysates and medium were examined in Caki-2 cells. The inhibitors evaluated include lapatinib, gefitinib, sunitinib, vismodegib, vemurafenib, sorafenib, everolimus, Alpelisib, palbociclib, BEZ-235, BKM-120, and PD-325901, which are all kinase inhibitors except vismodegib. Alpelisib, BKM-120 and BEZ-235 are gifts from Novartis and all other inhibitors were purchased from LC Laboratories (Woburn, MA). All inhibitors were dissolved in DMSO and sterilized using 0.22-μm pore size filters. Cells were incubated with ALA (1 mM) alone, inhibitors (all at 1 μM) alone, or ALA (1 mM) in combined with inhibitors (1 μM) in complete RPMI 1640 medium for 4 h. Ko143 (1 μM) was used as a positive control in the screening. The level of PpIX in cell lysates and medium after treatment was measured with spectrofluorometry as described above.
Howley R., Mansi M., Shinde J., Restrepo J, & Chen B. (2020). Evaluation of aminolevulinic acid-mediated protoporphyrin IX fluorescence and enhancement by ABCG2 inhibitors in renal cell carcinoma cells. Journal of photochemistry and photobiology. B, Biology, 211, 112017.
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4

Combinatorial Compound Screening Protocol

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BEZ235, RAD001, and BKM120 were provided by Novartis Pharmaceuticals Corporation (East Hanover, NJ, USA). AZD2014 was obtained from AstraZeneca (London, United Kingdom). Cisplatin was obtained from Fresenius-Kabi (Bad Homburg, Germany). Stock solution were prepared in DMSO, stored at −20°C, and diluted in fresh medium for each experiment.
Yu C.C., Hung S.K., Lin H.Y., Chiou W.Y., Lee M.S., Liao H.F., Huang H.B., Ho H.C, & Su Y.C. (2017). Targeting the PI3K/AKT/mTOR signaling pathway as an effectively radiosensitizing strategy for treating human oral squamous cell carcinoma in vitro and in vivo. Oncotarget, 8(40), 68641-68653.
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5

Cell Line Drug Combination Optimization

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LNCaP, C4-2 and C4-2B cells were treated with AZD-1208 (PIM inhibitor; Astrazeneca), BEZ235 (also known as Dactolisib, PI3K/mTOR inhibitor; Novartis), AUM302 (previously known as IBL-302, PIM/PI3K/mTOR inhibitor; AUM Biosciences. AUM-302 was previously IBL-302 compound licensed by Inflection Biosciences from The Spanish National Cancer Centre CNIO), or a combination of AZD-1208 and BEZ235. The vehicle for all drugs was the RPMI 1640 media with 10% FBS. Drug concentrations were previously optimised for the purpose of these experiments and are as follows: AZD-1208—6.25 μM; BEZ235—0.293 µM; AUM302—0.16 nM. Treatment duration was 4 h, as optimized using quantitative PCR (Supplementary Fig. S3).
Luszczak S., Simpson B.S., Stopka-Farooqui U., Sathyadevan V.K., Echeverria L.M., Kumar C., Costa H., Haider A., Freeman A., Jameson C., Ratynska M., Ben-Salha I., Sridhar A., Shaw G., Kelly J.D., Pye H., Gately K.A., Whitaker H.C, & Heavey S. (2020). Co-targeting PIM and PI3K/mTOR using multikinase inhibitor AUM302 and a combination of AZD-1208 and BEZ235 in prostate cancer. Scientific Reports, 10, 14380.
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6

Cytotoxicity Assay of Chemotherapeutics

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A volume of 100 μL per well of cells in supplemented media were incubated at 37°C and 5% CO2 with doxorubicin (Sigma-Aldrich, Milwaukee, WI, USA), idarubicin (Sigma-Aldrich), BEZ-235 (provided by Novartis, Inc.), or selumetinib (ChemieTek, Indianapolis, IN, USA). Each compound was plated using a nine-point logarithmic concentration scale ranging from 15 nM to 100 μM. Stock solutions of doxorubicin and idarubicin (10 mM) were prepared in water while stock solutions of BEZ-235 and selumetinib (25 mM and 75 mM, respectively) were prepared in 100% dimethyl sulfoxide (DMSO) (Sigma-Aldrich). Subsequent dilutions and controls were prepared to account for the inclusion of water or DMSO in the stock solution.
Frick A., Fedoriw Y., Richards K., Damania B., Parks B., Suzuki O., Benton C.S., Chan E., Thomas R.S, & Wiltshire T. (2015). Immune cell-based screening assay for response to anticancer agents: applications in pharmacogenomics. Pharmacogenomics and Personalized Medicine, 8, 81-98.
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7

Inhibitor Combination Protocol

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RAD001 and the PI3K inhibitors (BEZ235, BKM120 and BYL719) were generously provided by Novartis Oncology (Basel, Swiss). Inhibitors were dissolved in dymethil sulfoxide (DMSO, Sigma- Aldrich), and the stock solutions were diluted to final concentrations in medium.
Passacantilli I., Capurso G., Archibugi L., Calabretta S., Caldarola S., Loreni F., Fave G.D, & Sette C. (2014). Combined therapy with RAD001 e BEZ235 overcomes resistance of PET immortalized cell lines to mTOR inhibition. Oncotarget, 5(14), 5381-5391.
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8

Phase I Study of BEZ235 for Advanced Cancers

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For this IRB-approved study, BEZ235 was supplied by Novartis Oncology (East Hanover, NJ, USA). Patients ≥18 years with cytologically or histologically confirmed advanced or metastatic solid cancers that had exhausted standard therapies were eligible for enrollment. At least one measurable lesion defined by RECIST 1.1 was required [18 (link)]. Key inclusion criteria were Eastern Cooperative Oncology Group performance status (ECOG PS) ≤2, ability to understand and sign informed consent, and adequate bone marrow and organ function [19 (link)]. Key exclusion criteria included prior anticancer therapy within 4 weeks prior to enrollment, poorly controlled diabetes, chronic immunosuppression, other serious disease that may impact survival, abnormal gastrointestinal function resulting in poor BEZ235 absorption, or required treatment with other drugs that are known to modulate isoenzyme CYP3A4.
Wise-Draper T.M., Moorthy G., Salkeni M.A., Karim N.A., Thomas H.E., Mercer C.A., Beg M.S., O’Gara S., Olowokure O., Fathallah H., Kozma S.C., Thomas G., Rixe O., Desai P, & Morris J.C. (2017). A Phase Ib Study of the Dual PI3K/mTOR Inhibitor Dactolisib (BEZ235) Combined with Everolimus in Patients with Advanced Solid Malignancies. Targeted Oncology, 12(3), 323-332.
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9

Inhibiting PI3K, mTOR Signaling Pathways

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BEZ235 and BKM120 (Novartis Pharmaceuticals) and AZD8055 (#CT-A8055, ChemieTek) were dissolved in 0.1% DMSO. Control groups were treated with equal amounts of DMSO.
Cell transfections were performed by reverse transfection with Interferin (PolyPlus) using 5 nM short Interfering RNA (siRNA) oligonucleotides for PI3K110α (#L-003018), p85β (#L-003021), mTOR (#L-003008) and non-targeting (#D-001810) from Dharmacon RNAi Technologies. Doses in tissue culture were chosen based on the lowest concentration to reduce pAKT repeatably and by at least approximately 3-fold.
Kelly C.J., Hussien K., Fokas E., Kannan P., Shipley R.J., Ashton T.M., Stratford M., Pearson N, & Muschel R.J. (2014). Regulation of O2 consumption by the PI3K and mTOR pathways contributes to tumor hypoxia. Radiotherapy and Oncology, 111(1), 72-80.
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10

In-vivo Evaluation of mTOR Inhibitors

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The Institute Animal Care and Use Committee at Indiana University approved all mouse protocols used in this study. Mice were housed in a BSL-2 level animal facility maintained on a 12-h light/dark cycle, at a constant temperature (22±2°C) and relative humidity (55±15%). NSG mice for in-vivo study were purchased from an in-house colony maintained at Indiana University. Approximately six-week old NSG mice were implanted subcutaneously with ~ 3 mm3 pieces of RP-R07 tumor and allowed to grow until tumors reached 200 mm3 in volume prior to treatment with either vehicle, Rapamycin (EMD chemicals, USA), MLN0128 (kindly provided by Millenium Pharmaceuticals, USA) or BEZ-235 (kindly provided by Novartis Pharmaceuticals, USA). Tumor bearing mice received therapy with Rapamycin (2 mg/kg daily; i.p. injection). MLN0128, (3 mg/kg, three times a week; i.p. injection), BEZ-235 (25 mg/kg daily-five days per week; oral gavage) or vehicle (daily-five days per week; oral gavage). Throughout the study all mice receiving therapy were weighed twice weekly to monitor for toxicities. Tumor growth was assessed by serial caliper measurements twice weekly.
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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