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Vorinostat (SAHA, MK0683) HDAC inhibitor

Catalog No.A4084
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10mM (in 1mL DMSO)
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Sample solution is provided at 25 µL, 10mM.

Product Citations

1.Hari Prasad, Rajini Rao. "The Amyloid Clearance Defect in ApoE4 Astrocytes is Corrected by Epigenetic Restoration of NHE6." bioRxiv. 2018.January. 4
2.Mirza AN, Fry MA, et al. "Combined inhibition of atypical PKC and histone deacetylase 1 is cooperative in basal cell carcinoma treatment." JCI Insight. 2017 Nov 2;2(21). pii: 97071. PMID:29093271
3.Hai Y, Shinsky SA, et al. "Histone deacetylase 10 structure and molecular function as a polyamine deacetylase." Nat Commun. 2017 May 18;8:15368. PMID:28516954
4.Bagnall NH, Hines BM, et al. "Insecticidal activities of histone deacetylase inhibitors against a dipteran parasite of sheep, Lucilia cuprina." Int J Parasitol Drugs Drug Resist. 2017 Apr;7(1):51-60. PMID:28110187
5.Sun, Yuefeng, et al. "Fe65 Suppresses Breast Cancer Cell Migration and Invasion through Tip60 Mediated Cortactin Acetylation." Scientific reports 5 (2015). PMID:26166158

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Chemical structure

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Related Biological Data

Vorinostat (SAHA, MK0683)

Biological Activity

Description Vorinostat (suberoylanilide hydroxamic acid, SAHA) is an inhibitor of HDAC with IC50 of ~10 nM.
Targets HDAC          
IC50 ~10 nM          


Cell experiment: [1]

Cell lines

Human cutaneous T-cell lymphomas (CTCL) cell lines

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reaction Conditions

IC50: 0.146 μM HH 2.062 μM HuT78 2.697 μM MJ 1.375 μM MylA 1.510 μM SeAx 72h


Vorinostat dose-dependently reduced cell proliferation with IC50 values of 0.146 μM, 2.062 μM, 2.697 μM, 1.375 μM and 1.510 μM in HH, HuT78, MJ, MylA and SeAx cells, respectively.

Animal experiment : [2]

Animal models

C57BL/6 mice bearing Eμ-myc lymphomas

Dosage form

C57BL/6 mice bearing Eμ-myc lymphomas were injected with vorinostat (200 mg/kg i.p.) and lymphoma cells were harvested after the indicated time points. The percentage of tumor cells in the lymph node of C57BL/6mice bearing Eμ-myc lymphomas treated with vorinostat was determined by FACS analysis.


Vorinostat induced a marked accumulation of Eμ-myc lymphomas displaying DNA fragmentation in vivo.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Wozniak M B, Villuendas R, Bischoff J R, et al. Vorinostat interferes with the signaling transduction pathway of T cell receptor and synergizes with PI3K inhibitors in cutaneous T-cell lymphoma. haematologica, 2010: haematol. 2009.013870.

[2] Lindemann R K, Newbold A, Whitecross K F, et al. Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma. Proceedings of the National Academy of Sciences, 2007, 104(19): 8071-8076.

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Chemical Properties

Cas No. 149647-78-9 SDF Download SDF
Synonyms SAHA, suberoylanilide hydroxamic acid, Suberanilohydroxamic acid, SAHA cpd
Chemical Name N'-hydroxy-N-phenyloctanediamide
Formula C14H20N2O3 M.Wt 264.3
Solubility >4.4mg/mL in DMSO Storage Store at -20°C
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.

Research Update

1. A pediatric phase 1 trial of vorinostat and temozolomide in relapsed or refractory primary brain or spinal cord tumors: a Children's Oncology Group phase 1 consortium study. Pediatr Blood Cancer. 2013 Sep;60(9):1452-7. doi: 10.1002/pbc.24541. Epub 2013 Mar 28.
The MTD, DLT and PK properties of vorinostat, an HDAC inhibitor, were determined in a study utilizing vorinostat plus temozolomide to treat children with refractory or recurrent CNS malignancies.
4. Clinical pharmacology profile of vorinostat, a histone deacetylase inhibitor. Cancer Chemother Pharmacol. 2013 Sep;72(3):493-508. doi: 10.1007/s00280-013-2220-z. Epub 2013 Jul 3.
Although it’s been used to treat advanced CTCL patients, vorinostat, a HDACi with anti-cancer activity, is currently being evaluated to treat other solid tumors and hematological malignancies.
5. Biomarker modulation following short-term vorinostat in women with newly diagnosed primary breast cancer. Clin Cancer Res. 2013 Jul 15;19(14):4008-16. doi: 10.1158/1078-0432.CCR-13-0033. Epub 2013 May 29.
The effect of vorinostat, which is a HDACi capable of inducing cell-cycle arrest, apoptosis and differentiation, on biomarker modulation in women with breast cancer was evaluated.


Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor (HDACi), that plays key roles in epigenetic or non-epigenetic regulation, inducing growth arrest, differentiation and apoptosis of tumor cells.[1] Vorinostat is a small molecular with the formular of C14H20N2O3 and molecular weight of 264.3. The major mechanism of HDACi-induced apoptosis is the activation of the intrinsic apoptotic pathway. HDACi can activate the intrinsic apoptotic pathway by releasing of cytochrome c from mitochondria and regulating of Bcl-2 family expression.[2]


[1] Hui-ming Z, Qian-hai D, Wei-ping C, Ru-bin L. Vorinostat, a HDAC inhibitor, showed anti-osteoarthritic activities through inhibition of iNOS and MMP expression, p38 and ERK phosphorylation and blocking NF-kB nuclear translocation. International Immunopharmacology. 2013, 17. 329-335.

[2] Norihisa U, Sayaka K, Hisanori M, Katsuhiko Y, Airo T. Requirement of p38 MAPK for a cell-death pathway triggered by vorinostat in MDA-MB-231 human breast cancer cells. Cancer Letters. 2012, 315. 112-121.