Product overview

Name SAHA
Alternative names Vorinostat; Suberoylanilide hydroxamic acid
Purity >98%
Description HDAC inhibitor
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Biological Data

Biological description

Class I and II histone deacetylase (HDAC) inhibitor (IC50 values are 10 and 20 nM for HDAC1 and HDAC3 respectively).

Induces accumulation of acetylated histones (H2A, H2B, H3 and H4 in transformed cultured cells).

Has a variety of actions - supresses cell growth in various cance cell lines, induces apoptoisis and activates autophagy. Also reduces pro-inflammatory cytokine production. Additionally shows anti-inflammatory, anti-retroviral, growth inhibitory and anti-cancer actions.

Solubility & Handling

Storage instructions -20°C
Solubility overview Soluble in DMSO (100mM)
Important This product is for RESEARCH USE ONLY and is not intended for therapeutic or diagnostic use. Not for human or veterinary use.

Calculators

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Dilution

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Chemical Data

Purity >98%
Chemical name N-Hydroxy-N'-phenyloctanediamide
Molecular Weight 264.32
Chemical structure SAHA  [149647-78-9] Chemical Structure
Molecular Formula C14H20N2O3
CAS Number 149647-78-9
PubChem identifier 5311
SMILES O=C(CCCCCCC(NO)=O)NC1=CC=CC=C1
InChiKey WAEXFXRVDQXREF-UHFFFAOYSA-N

References for SAHA

References are publications that support the biological activity of the product
  • The histone deacetylase inhibitor vorinostat (SAHA) increases the susceptibility of uninfected CD4+ T cells to HIV by increasing the kinetics and efficiency of postentry viral events.

    Lucera MB et al (2014) J Virol 88(18) : 10803-12.
  • Distinct pharmacological properties of second generation HDAC inhibitors with the benzamide or hydroxamate head group.

    Beckers T et al (2007) Int J Cancer 121(5) : 1138-48.
  • The antitumor histone deacetylase inhibitor suberoylanilide hydroxamic acid exhibits antiinflammatory properties via suppression of cytokines.

    Leoni F et al (2002) Proc Natl Acad Sci U S A 99(5) : 2995-3000.
  • Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses the growth of prostate cancer cells in vitro and in vivo.

    Butler LM et al (2000) Cancer Res 60(18) : 5165-70.

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