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    Vorinostat (SAHA; MK0683)
    Vorinostat (SAHA; MK0683)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0255
    CAS #: 149647-78-9Purity ≥98%

    Description: Vorinostat (formerly known as suberanilohydroxamic acid, MK-0683; CCRIS-8456; HSDB 7930; SAHA; trade name: Zolinza) is a potent, orally bioavailable and non-selective pan-inhibitor of histone deacetylases (HDACs) with antitumor activity. It inhibits HDACs (pooled HDACs with all isoforms) with IC50 of ~10 nM in a cell-free assay. It inhibits HDAC1, HDAC2 and HDAC3 (Class I), HDAC7 (Class II) and HDAC11 (Class IV ) with ID50 values of 10 nM and 20 nM for HDAC1 and HDAC3, respectively. Vorinostat has been shown to bind to the active site of histone deacetylases and act as a chelator for Zinc ions also found in the active site of histone deacetylases. Vorinostat's inhibition of histone deacetylases results in the accumulation of acetylated histones and acetylated proteins that are crucial for cell differentiation. In October 2006, SAHA (Vorinostat) was approved by FDA as the first HDAC inhibitor for treating rare cutaneous T-cell lymphoma. 

    References: Proc Natl Acad Sci U S A. 1998;95(6):3003-7; Cancer Res. 2000;60(18):5165-70; Proc Natl Acad Sci U S A.2004;101(2):540-5. 

    Publications Citing Use of InvivoChem Vorinostat (SAHA; MK0683)Nature. 2021 Aug 25. doi: 10.1038/s41586-021-03850-3.  

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    Molecular Weight (MW)264.3
    CAS No.149647-78-9
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 53 mg/mL (200.5 mM)
    Water: <1 mg/mL
    Ethanol: 3 mg/mL (11.4 mM)
    Solubility (In vivo)2% DMSO+30% PEG 300+ddH2O: 5 mg/mL
    SynonymsMK0683; SAHA; M344; CCRIS 8456; CCRIS8456; CCRIS-8456; HSDB 7930; Vorinostat; suberoylanilide hydroxamic acid; MK-0683, MK 0683, MK0683, M344, HSDB 7930; Trade name: Zolinza

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    In Vitro

    In vitro activity: Vorinostat inhibits the activities of HDAC1 and HDAC3 with IC50 of 10 nM and 20 nM, respectively. Vorinostat also results in a marked hyperacetylation of histone H4. Vorinostat inhibits the growth of three prostate cancer cell lines LNCaP, PC-3 and TSU-Pr1 at micromolar concentrations (2.5-7.5 μM), and induces dose-dependent cell death in LNCaP cells. Vorinostat treatment in MCF-7 cells inhibits cell proliferation at an IC50 of 0.75 μM resulting in the accumulation of cells in the G1 and G2-M phase of the cell cycle. Vorinostat also induces differentiation in the estrogen receptor-negative cell line SKBr-3 and the retinoblastoma-negative cell line MDA-468. Vorinostat treatment at 1 μM for 8 hours or more is sufficient to irreversibly induce apoptosis of human multiple myeloma (MM) cells. The gene expression profiles of Vorinostat treated MM cells are not hallmarked by global transcriptional activation, but by coordinated transcriptional changes of specific functional groups of genes such as cytokine-induced proliferative/survival signaling cascades, oncogenes-tumor suppressor genes, regulators of apoptosis, DNA synthesis-repair and cell cycle, and proteasome-ubiquitin function.

    Kinase Assay: Immunoprecipitation-HDAC assays, the lysate of Jurkat cells is incubated for 1 hour on ice and cleared by centrifugation at 12,000 g for 10 minutes at 4 °C. Supernatants are precleared with 30 μL of 50% protein G-Sepharose slurry for 1 hour at 4 °C. Beads are pelleted by centrifugation and supernatants are incubated for 1 hour at 4 °C with 10 μg of IgG fraction from anti-HDAC1 or HDAC3 polyclonal antisera (preincubated 2 hours at room temperature with either the homologous or heterologous immunizing peptide). Both antisera are raised in rabbits against the carboxylterminal peptide of HDAC1 and HDAC3 by using synthetic peptides coupled to keyhole limpet hemocyanin. 30 μL of 50% protein G-Sepharose slurry is added for 1 hour at 4 °C. Immune complexes are pelleted by centrifugation and washed three times with 1 mL of lysis buffer. Beads are resuspended in 200 μL of HDAC buffer (20 mM Tris-HCl, pH 8.0/150 mM NaCl/10% glycerol), and the HDAC assay is performed with an 3H-acetylated peptide corresponding to amino acids 1-24 of histone H4. Released [3H]acetic acid is quantified by scintillation counting. For inhibitions studies, the immunoprecipitated complexes are preincubated with the different concentrations of Vorinostat for 30 minutes at 4 °C.

    Cell Assay: Cells (LNCaP, PC-3, and TSU-Pr1) are exposed to various concentrations of Vorinostat for 1, 2, 3 and 4 days. Cell viability is assessed by trypan blue dye exclusion.

    In VivoAdministration of Vorinostat (~100 mg/kg/day) significantly inhibits the growth of CWR22 human prostate xenografts in nude mice with tumor reductions of 78%, 97% and 97%, at doses of 25 mg/kg/day, 50 mg/kg/day and 100 mg/kg/day, respectively, compared with control. Vorinostat induces the accumulation of acetylated core histones and prostate-specific antigen mRNA expression in CWR22 cells, resulting in higher levels of serum prostate-specific antigen than predicted from tumor volume alone. Oral administration of Vorinostat (0.67g/L) crosses the blood-brain barrier, increases histone acetylation in the brain, and dramatically improves the motor impairment in the R6/2 mice model of Huntington's disease.
    Animal modelMale BALB/c nude (nu/nu) mice implanted with CWR22 tumor cells
    Formulation & DosageDissolved in DMSO; 100 mg/kg/day;  i.p. injection

    Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3003-7; Cancer Res. 2000 Sep 15;60(18):5165-70; Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):540-5. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Vorinostat (SAHA, MK0683)

    Vorinostat (SAHA, MK0683)

    Vorinostat (SAHA, MK0683)	 

    Effects of SAHA on regulators of apoptosis and sensitivity to caspase-dependent drug-induced apoptosis. Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):540-5. 

    Vorinostat (SAHA, MK0683)


    Vorinostat (SAHA, MK0683)

    Functional impact of SAHA on the ubiquitin/proteasome pathway. Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):540-5. 


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