Quisinostat

Manufactured by Selleck Chemicals

Sourced in United States

Quisinostat is a laboratory equipment product manufactured by Selleck Chemicals. It is a histone deacetylase (HDAC) inhibitor used for research purposes in cell culture and biochemical assays.

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Lab products found in correlation

Romidepsin, by Selleck Chemicals (5 mentions) Panobinostat, by Selleck Chemicals (4 mentions) Cleaved caspase 3, by Cell Signaling Technology (2 mentions) Cleaved parp, by Cell Signaling Technology (2 mentions) Dimethyl sulfoxide (dmso), by Merck Group (2 mentions) Vorinostat, by Selleck Chemicals (2 mentions) Rpmi 1640 medium, by Thermo Fisher Scientific (1 mentions) Prestoblue cell viability reagent, by Thermo Fisher Scientific (1 mentions) Trichostatin a, by Selleck Chemicals (1 mentions) Peg400, by Merck Group (1 mentions) Tween 80, by Merck Group (1 mentions) Mannitol, by Merck Group (1 mentions) Peg300, by Merck Group (1 mentions) A 1331852, by Chemietek (1 mentions) Phosal 50 pg, by Lipoid (1 mentions) Napabucasin, by Selleck Chemicals (1 mentions) Panobinostat, by Merck Group (1 mentions) Navitoclax, by Chemietek (1 mentions) Hydroxypropyl β cyclodextrin, by Merck Group (1 mentions) Navitoclax, by Thermo Fisher Scientific (1 mentions)

15 protocols using quisinostat

Screening HDAC Inhibitors in Soft Tissue Sarcomas

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Cells were cultured in RPMI 1640 medium (Gibco) supplemented with 10% FBS. Cells were tested for mycoplasma and Short Tandem Repeats were characterized for authentication. One SS cell-line was used (SYO-1) [21 (link)]. Three LMS cell lines were included (JA192, LMS04 and LMS05). Quisinostat (Selleckchem) and trichostatin A (Selleckchem) were used for HDAC inhibition. Both compounds were dissolved in DMSO. Cells were seeded in triplicates on a 96-well plate and compounds were added after 24 hours. Cell viability was measured after 72 hours incubation with the compounds by adding PrestoBlue Cell Viability Reagent (Life Technologies) according to the manufacturers protocol. Fluorescence was measured reading the plate at 590 nm on a fluorometer (Victor3V, 1420 multi-label counter). Viability was determined in three independent experiments in triplicate.

van IJzendoorn D.G., Szuhai K., Briaire-de Bruijn I.H., Kostine M., Kuijjer M.L, & Bovée J.V. (2019). Machine learning analysis of gene expression data reveals novel diagnostic and prognostic biomarkers and identifies therapeutic targets for soft tissue sarcomas. PLoS Computational Biology, 15(2), e1006826.

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Drug Formulation and Preparation Protocol

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Napabucasin, panobinostat, and quisinostat were purchased from Selleckchem and A1331852 and Navitoclax from Chemietek, diluted in DMSO to make stock solutions, aliquoted and stored at −80C. Napabucasin was formulated by heating to 50C for 10 minutes and then sequentially adding 45% PEG300 (Sigma), 5% Tween80 (Sigma) and 45% sterile water, with vortexing after adding each component (Selleckchem). panobinostat was formulated by sequentially adding 48% PEG300 (Sigma), 2% Tween80 (Sigma) and 48% sterile water, with vortexing after adding each component (Selleckchem). quisinostat was formulated in 10% hydroxypropyl-b-cyclodextrin (Sigma), 25 mg/ml mannitol (Sigma), in sterile water(45 (link)). A1331852 was formulated by sequentially adding 10% Ethanol (Fisher), 60% Phosal 50 PG (Lipoid), and 30% PEG400 (Sigma), and vortexing (MedChemExpress). Navitoclax was formulated in 10% ethanol (Fisher), 30% PEG400 (Sigma), and 60% Phosal 50 PG (Lipoid), with vortexing after adding each component (MedChemExpress). Sorafenib was formulated in 90% corn oil (Selleckchem) with vortexing (MedChemExpress). Working solutions were made fresh prior to administration.

Lalazar G., Requena D., Ramos-Espiritu L., Ng D., Bhola P.D., de Jong Y.P., Wang R., Narayan N.J., Shebl B., Levin S., Michalidis E., Kabbani M., Vercauteren K.O., Hurley A.M., Farber B.A., Hammond W.J., Saltsman JA I.I.I., Weinberg E.M., Glickman J.F., Lyons B.A., Ellison J., Schadde E., Hertl M., Leiting J.L., Truty M.J., Smoot R.L., Tierney F., Kato T., Wendel H.G., LaQuaglia M.P., Rice C.M., Letai A., Coffino P., Torbenson M.S., Ortiz M.V, & Simon S.M. (2021). Identification of Novel Therapeutic Targets for Fibrolamellar Carcinoma Using Patient Derived Xenografts and Direct from Patient Screening. Cancer discovery, 11(10), 2544-2563.

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Cell Culture and Epigenetic Inhibitor Protocols

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Cells were cultured in either DMEM/F-12 (BIN67, SCCOHT-1, COV434 and SVOG3e) or RPMI (all other lines) supplemented with 10% FBS and maintained at 37 °C in a humidified 5% CO₂-containing incubator. All cell lines have been certified by STR analysis, tested regularly for Mycoplasma and used for the study within six months of thawing. EPZ-6438 (23 (link)), quisinostat (24 (link)), SAHA, romidepsin and panobinostat were purchased from Selleckchem for in vitro studies. EPZ-6438 and quisinostat were purchased from Active Biochemku for in vivo studies.

Wang Y., Chen S.Y., Colborne S., Lambert G., Shin C.Y., Santos N.D., Orlando K.A., Lang J.D., Hendricks W.P., Bally M.B., Karnezis A.N., Hass R., Underhill T.M., Morin G.B., Trent J.M., Weissman B.E, & Huntsman D.G. (2018). Histone deacetylase inhibitors synergizes with catalytic inhibitors of EZH2 to exhibit anti-tumor activity in small cell carcinoma of the ovary, hypercalcemic type. Molecular cancer therapeutics, 17(12), 2767-2779.

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Drug Dissolution and Dilution Protocol

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Quisinostat and Tazemetostat were purchased from Selleckchem (Houston, TX, USA). Drugs were dissolved in dimethyl sulfoxide (DMSO) to reach a stock concentration of 5 mM and diluted in the indicated fresh medium for in vitro studies.

Souri Z., Jochemsen A.G., Versluis M., Wierenga A.P., Nemati F., van der Velden P.A., Kroes W.G., Verdijk R.M., Luyten G.P, & Jager M.J. (2020). HDAC Inhibition Increases HLA Class I Expression in Uveal Melanoma. Cancers, 12(12), 3690.

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Renal Fibrosis Induction Models

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All animal experiments were review and approved by the Intramural Committee on Ethical Conduct of Animal Experiments. To induce renal fibrosis, the unilateral ureteral obstruction (UUO) procedure was performed in the mice. Briefly, a flank incision was made and the left ureter was ligated with silk suture at two points and cut between the ligatures. After the surgery, the animals were injected peritoneally with quisinostat (100 mg/kg, Selleck, Cat# S1096) or vehicle twice a week until the day of sacrifice. The mice were sacrificed 14 days after the surgery. Alternatively, the mice were fed a high-fat diet (HFD, D12492, Research Diets) for 16 weeks as previously described (Xu et al., 2015 (link)). In the third model of renal fibrosis, the mice were implanted subcutaneously a minipump (Alzet 2004) that chronically released Ang II (1 μg/kg/min) for 4 weeks.

Mao L., Liu L., Zhang T., Qin H., Wu X, & Xu Y. (2020). Histone Deacetylase 11 Contributes to Renal Fibrosis by Repressing KLF15 Transcription. Frontiers in Cell and Developmental Biology, 8, 235.

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Synergistic Anti-cancer Combination Assay

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Cells were seeded in triplicate, in 96-well format and incubated for 72 hours. Cell survival was determined via the CellTitre-Blue Cell Viability assay (Promega, Fitchburg, WI, USA); the fluorescence was measured in a microplate reader (Victor, Perkin Elmer, San Jose, CA, USA). Synergism between Flavopiridol and Quisinostat was calculated using Compusyn software (Paramus, NJ, USA). Combination Index (CI) values below 0.9 were considered to be synergistic, between 0.9 and 1.1 additive effects and above 1.1 to be antagonistic. Flavopiridol was obtained from Selleck Chemicals (Houston, TX, USA) and Quisinostat was kindly provided by Johnson & Johnson.

Heijkants R., Willekens K., Schoonderwoerd M., Teunisse A., Nieveen M., Radaelli E., Hawinkels L., Marine J.C, & Jochemsen A. (2017). Combined inhibition of CDK and HDAC as a promising therapeutic strategy for both cutaneous and uveal metastatic melanoma. Oncotarget, 9(5), 6174-6187.

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Evaluating Base Editing Efficiency

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To measure the base editing efficiency at endogenous sites, 1.6 × 10⁵ HEK293T/17 cells or 8 × 10⁴ HeLa cells were seeded in wells of 24-well plates one day before transfection. When confluency was 70%–80%, the cells were transfected with plasmids encoding BEs (ABE7.10, BE3, ABEmax and BE4max; 1.5 μg) or Cas9 (0.5 μg) and a plasmid encoding gRNA (500 ng) using Lipofectamine 2000 (3 μl for BEs and 2 μl for Cas9) as previously described (19 (link)). For the delivery of ribonucleoprotein (RNP), 10 μg of Cas9 or ABE7.10 proteins and 6 μg of synthetic gRNA (Integrated DNA Technologies) were incubated at 25°C to form the RNP complex. The RNP complex and HEK293T/17 cells (1.5 × 10⁶) were resuspended in Neon electroporation R buffer and delivered using the Neon transfection system (Thermo Fisher Scientific) in two 20-ms pulses of 1300 V according to the manufacturer's protocol. Then, 5–10 nM of romidepsin (Selleckchem), abexinostat (Selleckchem), quisinostat (Selleckchem), 100 nM of trichostatin A (TSA, Sigma-Aldrich) and 0.5 μM of vorinostat (Sigma-Aldrich) were applied 6 h after plasmid DNA transfection or 1 h after RNP delivery at designated concentrations. gDNA was extracted 72 h after transfection using the DNeasy Blood and Tissue kit (Qiagen) according to the manufacturer's protocol. The base editing efficiency was determined as described in the next subsection.

Shin H.R., See J.E., Kweon J., Kim H.S., Sung G.J., Park S., Jang A.H., Jang G., Choi K., Kim I., Kim J.S, & Kim Y. (2021). Small-molecule inhibitors of histone deacetylase improve CRISPR-based adenine base editing. Nucleic Acids Research, 49(4), 2390-2399.

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Epigenetics Compound Library Composition

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A detailed list of all compounds (n = 128) included in the epigenetics compound library (L1900, Selleckchem, Houston, TX, USA) is presented in the supplementary files (Table S3). The histone deacetylase (HDAC) inhibitors romidepsin (S3020, Selleckchem), panobinostat (S1030, Selleckchem), dacinostat (S1095, Selleckchem), quisinostat (S1096, Selleckchem), and fimepinostat (S2759, Selleckchem) were dissolved in DMSO.

Venneker S., van Eenige R., Kruisselbrink A.B., Palubeckaitė I., Taliento A.E., Briaire-de Bruijn I.H., Hogendoorn P.C., van de Sande M.A., Gelderblom H., Mei H., Bovée J.V, & Szuhai K. (2022). Histone Deacetylase Inhibitors as a Therapeutic Strategy to Eliminate Neoplastic “Stromal” Cells from Giant Cell Tumors of Bone. Cancers, 14(19), 4708.

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Combinatorial Anti-Cancer Drug Screening

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Sorafenib, quisinostat (JNJ-26481585), JNK inhibitor SP600125, AKT inhibitor MK2206 2HCL and Caspase inhibitor Z-VAD-FMK were from Selleckchem (Houston, Texas, USA). Dimethylsulfoxide was purchased from Sigma-Aldrich (St. Louis, MO, USA). Minimum Essential Medium Eagle (MEM), fetal bovine serum (FBS) were from Gibco Life Technologies (Grand Island, NY, USA). The Cell Counting Kit-8 was purchased from Dojindo (Kumamoto, Japan). The cell cycle staining kit was from MultiSciences (Hangzhou, China). The Annexin V-FITC apoptosis detection kit was obtained from KeyGen Biotech (Nanjing, China). The EdU Apollo567 In Vitro Imaging Kit was from Ribobio (Guangzhou, China). The BCA protein assay kit was from Thermo Fisher Scientific Inc (Waltham, Massachusetts, USA). The following antibodies were used: HDAC1, HDAC2, HDAC4 (Proteintech), p21Cip1, CyclinD1, CyclinE1, CyclinA2, cdk2, cdk4, cdk6, Cleaved-Caspase-3, Cleaved-Caspase-9, Caspase-3, Caspase-9, Cleaved-PARP, PARP, phospho-JNK, JNK, PI3K-p110, PI3K- p85, phospho-AKT⁴⁷³, phospho-c-jun, Bcl-xl, Bcl2, Bax, Survivin, Ki67, GAPDH (Cell Signaling Technology).

He B., Dai L., Zhang X., Chen D., Wu J., Feng X., Zhang Y., Xie H., Zhou L., Wu J, & Zheng S. (2018). The HDAC Inhibitor Quisinostat (JNJ-26481585) Supresses Hepatocellular Carcinoma alone and Synergistically in Combination with Sorafenib by G0/G1 phase arrest and Apoptosis induction. International Journal of Biological Sciences, 14(13), 1845-1858.

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Combination Therapy Evaluation

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Decitabine (DAC), Quisinostat (Quis), Mitoxanthrone (Mtx) and Bortezomib (Bz) were purchased at Selleckchem (Munich, Germany). Melphalan (Mel) was obtained from Sigma-Aldrich. For in vivo experiments, DAC and Quis were used as a filter sterilized 10% hydroxypropyl-cyclodextran suspension.

De Beck L., Melhaoui S., De Veirman K., Menu E., De Bruyne E., Vanderkerken K., Breckpot K, & Maes K. (2018). Epigenetic treatment of multiple myeloma mediates tumor intrinsic and extrinsic immunomodulatory effects. Oncoimmunology, 7(10), e1484981.

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