Lbh589

Manufactured by Novartis

Sourced in United States, Switzerland

LBH589 is a laboratory equipment product offered by Novartis. It is designed for use in scientific research and analysis. The core function of LBH589 is to provide a reliable and consistent platform for various laboratory procedures and experiments. The detailed specifications and intended use of this product are not available for this response.

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Lab products found in correlation

10 protocols using lbh589

HDAC Inhibitor and Curcumin Treatment

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The HDAC inhibitor LBH589 (diluted in saline solution) (Novartis Pharmaceuticals, East Hanover, NJ, USA) and Curcumin (diluted in DMSO solution) (Sigma Aldrich Steinheim, Germany) were used. REH and MOLT-4 cell lines were treated with LBH589 and Curcumin at the half maximal inhibitory concentration (IC₅₀) and maintained in culture for 2 days. Then cells were washed in PBS and used for different assays. The IC₅₀ value was determined using GraphPad Prism log (inhibitor) vs response (variable slope) software (version 5, La Jolla, CA, USA).

Garitano-Trojaola A., José-Enériz E.S., Ezponda T., Unfried J.P., Carrasco-León A., Razquin N., Barriocanal M., Vilas-Zornoza A., Sangro B., Segura V., Prósper F., Fortes P, & Agirre X. (2018). Deregulation of linc-PINT in acute lymphoblastic leukemia is implicated in abnormal proliferation of leukemic cells. Oncotarget, 9(16), 12842-12852.

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Evaluation of Epigenetic Modifiers

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LBH589 was from Novartis (Basel, Switzerland). MS-275 was from Selleck Chemicals (Houston, TX, USA). Valproic acid (VPA), ATRA, and propidium iodide (PI) were from Sigma-Aldrich (St Louis, MO, USA).

Hennig D., Müller S., Wichmann C., Drube S., Pietschmann K., Pelzl L., Grez M., Bug G., Heinzel T, & Krämer O.H. (2014). Antagonism between granulocytic maturation and deacetylase inhibitor-induced apoptosis in acute promyelocytic leukaemia cells. British Journal of Cancer, 112(2), 329-337.

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Chemical Compounds in Cancer Research

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Romidepsin (Celgene, Summit, NJ, USA), LBH589 (Novartis, East Hanover, NJ, USA) and PXD101 (Onxeo former Topotarget, Cambridge, MA, USA) were resuspended in DMSO. Carfilzomib (PR-171), Ponatinib (AP24534), Dronedarone HCl, Paroxetine HCl, Bazedoxifene HCl, Benzethonium chloride, CUDC-907, AR-42, SGI-1027, UNC0642, Roxadustat FG-4592, Ruxolitinib, UNC1215, RG2833, Camptothecin, Teniposide, Duloxetine HCl, and Lapatinib were purchased from Selleck Chem (Houston, TX, USA). Alexidine hydrochloride was purchased from Cayman (Ann Arbor, MI, USA). Antibodies against PRA/B (#3153), PRB (#3157), FOXO1 (#2880), p21 (#2947), cyclin D1 (#2926), and Myc (#13987) were from Cell Signaling (Danvers, MA, USA), and mCherry (EPR20579) was from Abcam (Waltham, MA, USA). PAEP (PA5-54152) were from Fisher scientific (Waltham, MA, USA). β-actin antibody (#A1978) was obtained from Sigma Aldrich (St. Louis, MO, USA).

Li Y., Zhou W., Meng X., Murray S.D., Li L., Fronk A., Lazaro-Camp V.J., Wen K.K., Wu M., Dupuy A., Leslie K.K, & Yang S. (2022). Utilizing an Endogenous Progesterone Receptor Reporter Gene for Drug Screening and Mechanistic Study in Endometrial Cancer. Cancers, 14(19), 4883.

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Assessing Neurodevelopmental Effects of LBH589

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Pups were genotyped 3 d after birth, divided into groups of 10 according to genotype, and marked daily throughout the experiment. The animals were treated with LBH589 (Novartis) using the following doses: 0.001 mg salt/kg body weight, 0.01 mg salt/kg body weight, 0.1 mg salt/kg body weight, and 1 mg salt/kg body weight. Control animals were treated with vehicle: 0.03 M lactic acid/5% dextrose in water buffered to pH 4.2–4.5 with 0.1 M NaOH. LBH589 was administered i.p. every 48 h from P8 to P20. The behavioral tests were performed at P11 (USV), P17 (startle response and PPI), and P21 (NCT). Pups were killed at day 21 for histology.

Siebzehnrübl F.A., Raber K.A., Urbach Y.K., Schulze-Krebs A., Canneva F., Moceri S., Habermeyer J., Achoui D., Gupta B., Steindler D.A., Stephan M., Nguyen H.P., Bonin M., Riess O., Bauer A., Aigner L., Couillard-Despres S., Paucar M.A., Svenningsson P., Osmand A., Andreew A., Zabel C., Weiss A., Kuhn R., Moussaoui S., Blockx I., Van der Linden A., Cheong R.Y., Roybon L., Petersén Å, & von Hörsten S. (2018). Early postnatal behavioral, cellular, and molecular changes in models of Huntington disease are reversible by HDAC inhibition. Proceedings of the National Academy of Sciences of the United States of America, 115(37), E8765-E8774.

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Measuring Sphere Formation and Clonogenicity

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Measurement of sphere formation and clonogenicity [30 (link), 56 (link)] was performed by plating single cells in type I collagen coated (1 μg/cm², BD Biosciences) 6-well or 96-well cell culture dishes, respectively. After a 24 hours settling time, cells were treated with AIIB2 (10 μg/ml), SP600125 (2.5–200 μM, Santa Cruz Biotechnology), LBH589 (0.625–80 nM, Novartis AG, [39 (link)]) and combinations thereof for 24 hours and then washed. Cells were irradiated 1 h after addition of inhibitors with 2, 4 or 6 Gy single X-ray doses. Non-specific IgG isotype antibodies (10 μg/ml) or DMSO (equal amount as inhibitors, < 0.1 % v/v) (AppliChem) were used as control. After a cell line-dependent growth period, cell colonies were fixed with 80% EtOH, stained with Coomassie blue (Merck Millipore) and colonies containing > 50 cells were counted. After a 6 d growth period, spheres containing > 25 cells were microscopically counted [56 (link)].

Vehlow A., Klapproth E., Storch K., Dickreuter E., Seifert M., Dietrich A., Bütof R., Temme A, & Cordes N. (2017). Adhesion- and stress-related adaptation of glioma radiochemoresistance is circumvented by β1 integrin/JNK co-targeting. Oncotarget, 8(30), 49224-49237.

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HDAC Inhibitor Preparation and Use

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LBH589 was kindly provided by Novartis (Basel, Switzerland). MGCD0103, MS275, PXD101, PCI34051, and ACY1215 were purchased from Selleck Chemicals (Houston, TX). DMSO-reconstituted HDACi aliquots were stored at −80°C. For in vitro studies, stocks were diluted to final concentration immediately prior to use. For in vivo use, LBH589 was dissolved and sonicated in 5% dextrose.

Woods D.M., Sodré A.L., Villagra A., Sarnaik A., Sotomayor E.M, & Weber J. (2015). HDAC Inhibition Upregulates PD-1 Ligands in Melanoma and Augments Immunotherapy with PD-1 Blockade. Cancer immunology research, 3(12), 1375-1385.

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Reagent Preparation for Cell Assays

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Reagents were purchased from Sigma (St. Louis, MO) unless otherwise mentioned. Drugs were made in stock and diluted in cell culture medium. Doxycycline was dissolved in water. Stock solutions of LBH589 (Novartis, Basel, Switzerland) was dissolved in DMSO and added to the media at the indicated concentrations. Pan-caspase inhibitor Z-VAD-FMK was dissolved in DMSO at 50 mM.

Tung B., Ma D., Wang S., Oyinlade O., Laterra J., Ying M., Lv S.Q., Wei S, & Xia S. (2018). Krüppel-like factor 9 and histone deacetylase inhibitors synergistically induce cell death in glioblastoma stem-like cells. BMC Cancer, 18, 1025.

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SAHA and LBH589 effects on EGFR

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LBH589 was provided by Novartis (Basel, Switzerland). Suberoylanilide hydroxamic acid (SAHA; also called vorinostat or zolinza) was purchased from Selleck Chemicals (Houston, TX). EGFR antibody (sc-71034) was purchased from Santa Cruz Biotechnology (Santa Cruz, CA). p-EGFR (Y1065) and p-EGFR (Y1173) antibodies were purchased from Cell Signaling Technology, Inc (#2234; Beverly, MA) and AbboMax (#600–290; San Jose, CA), respectively. The sources for other agents and antibodies were the same as described previously^{21 (link)}.

Zang H., Qian G., Zong D., Fan S., Owonikoko T.K., Ramalingam S.S, & Sun S.Y. (2020). Overcoming acquired resistance of EGFR-mutant NSCLC cells to osimertinib by combining osimertinib with the HDAC inhibitor, panobinostat (LBH589). Cancer, 126(9), 2024-2033.

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Combination Therapy with LBH589 and RAD001

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LBH589 and RAD001 were synthesized and provided by Novartis (Basel, Switzerland) under a Material Transfer Agreement (MTA).

Ramakrishnan V., Kimlinger T., Timm M., Haug J., Rajkumar S.V, & Kumar S. (2014). Multiple mechanisms contribute to the synergistic anti-myeloma activity of the pan-histone deacetylase inhibitor LBH589 and the rapalog RAD001. Leukemia research, 38(11), 1358-1366.

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Apoptosis Induction Reagents Protocol

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Sigma-Aldrich: Butyrate, valproic acid, cycloheximide, staurosporine; Axxora: Caspase-1, -4 und -9, Z-VAD-FMK, Ac-DEVD-pNA, Ac-VEID-pna and Z-LLL-al (MG132); MERCK: Z-DEVD-FMK; Santa Cruz Biotechnology: Ac-VEID-FMK; Novartis: LBH589.

Licht V., Noack K., Schlott B., Förster M., Schlenker Y., Licht A., Krämer O.H, & Heinzel T. (2014). Caspase-3 and Caspase-6 cleave STAT1 in leukemic cells. Oncotarget, 5(8), 2305-2317.

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