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Vorinostat

Catalog No. T1583 CAS 149647-78-9

Synonyms: MK0683, suberoylanilide hydroxamic acid, SAHA

Vorinostat (SAHA) is a pan-histone deacetylase (HDAC) inhibitor (IC50=10 nM) with inhibitory activity against HDAC1/2/3/6/7/11. Vorinostat has antitumor activity, induces cell differentiation, blocks the cell cycle and induces apoptosis.

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Vorinostat, CAS 149647-78-9

Pack Size	Availability	Price/USD
200 mg	In stock	$ 44.00
500 mg	In stock	$ 86.00
1 g	In stock	$ 101.00
1 mL * 10 mM (in DMSO)	In stock	$ 50.00

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Purity: 99.93%

Purity: 99.47%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	Vorinostat (SAHA) is a pan-histone deacetylase (HDAC) inhibitor (IC50=10 nM) with inhibitory activity against HDAC1/2/3/6/7/11. Vorinostat has antitumor activity, induces cell differentiation, blocks the cell cycle and induces apoptosis.
Targets&IC50	HDAC:~10 nM (cell free)
In vitro	METHODS: Synovial sarcoma cells SW-982 and chondrosarcoma cells SW-1353 were treated with Vorinostat (0.5-15 μM) for 48 h, and cell viability was measured by MST assay. RESULTS: Vorinostat inhibited the proliferation of SW-982 and SW-1353 cells in a dose-dependent manner with IC50s of 8.6 μM and 2.0 μM, respectively. [1] METHODS: Uterine sarcoma cells MES-SA were treated with Vorinostat (3 μM) for 24-72 h. The expression levels of target proteins were detected using Western Blot. RESULTS: There was no difference in the expression of HDAC1 throughout the treatment period, and HDAC2, 3 and 7 showed significant inhibition of expression by Vorinostat. [2]
In vivo	METHODS: To detect anti-tumor activity in vivo, Vorinostat (50 mg/kg in HOP-β-CD) was administered intraperitoneally to Nude-Foxn1nu/nu mice bearing uterine sarcoma MES-SA five times per week for twenty-one days. RESULTS: A reduction in tumor growth of more than 50% was observed in the Vorinostat treatment group compared to the placebo group. [1] METHODS: To study the effects in an animal model of true erythrocytosis (PV), Vorinostat (200 mg/kg in 50% PEG-400) was injected intraperitoneally into MxCre;Jak2V617F/+ mice five times per week for two weeks. RESULTS: Vorinostat treatment normalized peripheral blood counts and significantly reduced splenomegaly in Jak2V617F knockout mice.Vorinostat may have therapeutic potential for PV and other JAK2V617F-associated myeloproliferative tumors. [3]
Cell Research	Cells were plated onto 100-mm tissue culture plates at a density of 2 × 10^6 for 48 h and then treated with SAHA or equal concentrations of the vehicle. For longer drug exposure times, medium with drug or vehicle were exchanged every 48 h. For wash-out experiments, cells were treated with SAHA daily for 60–72 h (drug and medium were exchanged at 48 h), then SAHA was washed out and replaced with 10% FCS containing DMEM [3].
Animal Research	Athymic Nude-Foxn1nu/nu mice were used in the present study. They were housed at 22°C at a constant light-dark cycle (12-h light, 12-h dark) and had free access to water and rodent chow (4-5% fat, 21% protein). Twelve weeks old male mice (n = 14) were anesthetized with Isofluran and 5 × 10^6 MES-SA cells were injected subcutaneously into the right flank of the animal. Mice from a control group received placebo containing 300 μl of empty HOP-β-CD (2-hydroxypropyl-β-cyclodextrin) vesicles. Another group of mice received vorinostat dissolved in HOP-β-CD at a concentration of 50 mg/kg/day. Both, empty vesicles and vorinostat were administered intraperitoneally, starting on the day 4 after the injection of MES-SA tumor cells. Mice body weight and tumor size (w2 × l × 0.52; measured by caliper) were estimated twice a week. All mice were treated for 21 days and afterward sacrificed by cervical dislocation. Each tumor was isolated as a whole and different tumor parameters (weight, volume, size, and macroscopic appearance) were determined. Finally, tumor slices were cryopreserved and formalin fixed (4%) for further analyses [1].

Synonyms	MK0683, suberoylanilide hydroxamic acid, SAHA
Molecular Weight	264.32
Formula	C14H20N2O3
CAS No.	149647-78-9

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

Ethanol: 2 mg/mL(7.6 mM)

DMSO: 125 mg/mL (472.90 mM), Sonification is recommended

References and Literature

1. Bernhart E, et al. Histone deacetylase inhibitors vorinostat and panobinostat induce G1 cell cycle arrest and apoptosis in multidrug resistant sarcoma cell lines. Oncotarget. 2017 Aug 24;8(44):77254-77267. 2. Hrzenjak A, et al. Histone deacetylase inhibitor vorinostat suppresses the growth of uterine sarcomas in vitro and in vivo. Mol Cancer. 2010 Mar 4;9:49. 3. Akada H, et al. Efficacy of vorinostat in a murine model of polycythemia vera. Blood. 2012 Apr 19;119(16):3779-89. 4. Hockly E, et al. Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease. Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):2041-6. 6. Wang J, et al. Snail determines the therapeutic response to mTOR kinase inhibitors by transcriptional repression of 4E-BP1. Nat Commun. 2017 Dec 20;8(1):2207. 7. Wellinger L C, Hogg S J, Newman D M, et al. BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity[J]. bioRxiv. 2021

Citations

1. Wellinger L C, Hogg S J, Newman D M, et al. BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity. Cancer Immunology Research. 2022, 10(1): 87-107. 2. Wellinger L C, Hogg S J, Newman D M, et al. Bet inhibition enhances TNF-mediated antitumor immunity. Cancer Immunology Research. 2022, 10(1): 87-107 3. Yuting Meng,Xixi Qian,Li Zhao,Nan Li,Shengjie Wu,Baoan Chen,Tong Sun,Xuerong Wang Trichostatin A downregulates bromodomain and extra-terminal proteins to suppress osimertinib resistant non-small cell lung carcinoma. Cancer Cell International. 2021, 21(1): 1-12. 4. Wang C, Huang M, Lin Y, et al.ENO2-derived phosphoenolpyruvate functions as an endogenous inhibitor of HDAC1 and confers resistance to antiangiogenic therapy.Nature Metabolism.2023: 1-22. 5. Liang X L, Ouyang L, Yu N N, et al.Histone deacetylase inhibitor pracinostat suppresses colorectal cancer by inducing CDK5-Drp1 signaling-mediated peripheral mitofission.Journal of Pharmaceutical Analysis.2023 6. Du T, Hu X, Hou Z, et al.Re-expression of epigenetically silenced PTPRR by histone acetylation sensitizes RAS-mutant lung adenocarcinoma to SHP2 inhibition.Cellular and Molecular Life Sciences.2024, 81(1): 1-14.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Cancer Drug Library Anti-Cancer Clinical Compound Library Anti-Cancer Approved Drug Library Drug Repurposing Compound Library Anti-Cancer Active Compound Library Inhibitor Library DNA Damage & Repair Compound Library Approved Drug Library FDA-Approved Drug Library Drug-Fragment Library

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Keywords

Vorinostat 149647-78-9 Apoptosis Autophagy Chromatin/Epigenetic DNA Damage/DNA Repair Microbiology/Virology Virus Protease Mitophagy HDAC MK0683 Filovirus Histone deacetylases suberoylanilide hydroxamic acid Human papillomavirus inhibit Inhibitor MK 0683 SAHA Mitochondrial Autophagy HPV MK-0683 inhibitor

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