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    AR-42 (HDAC-42, NSC-736012, OSU-42)
    AR-42 (HDAC-42, NSC-736012, OSU-42)

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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 #: V0283
    CAS #: 935881-37-1Purity ≥98%

    Description: AR-42 (HDAC-42, NSC-736012, OSU-42 etc.) is a novel and potent histone deacetylase (HDAC) inhibitor with potential antitumor activity. It inhibits HDAC with an IC50 of 30 nM. It shows potent anti-proliferative activity in vitro against various cancer cell lines and high in vivo antitumor efficacy against different tumor types like human prostate and hepatic cancers.

    References: J Med Chem. 2005;48(17):5530-5; Clin Cancer Res. 2006;12(17):5199-206; Cancer Res. 2008;68(10):3999-4009.

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    Molecular Weight (MW)312.36
    CAS No.935881-37-1
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 63 mg/mL (201.7 mM)
    Water: <1 mg/mL
    Ethanol: 63 mg/mL (201.7 mM)
    Solubility (In vivo)0.5% methylcellulose+0.2% Tween 80: 30 mg/mL
    SynonymsHDAC-42;  AR42; AR 42; AR-42; (S)-HDAC-42; AR-42; NSC-736012; OSU-42; OSU 42; OSU42; OSU-HDAC-42; OSU HDAC-42; OSU HDAC 42; OSUHDAC-42

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    In Vitro

    In vitro activity: AR-42 treatment induces histone hyperacetylation and p21WAF/CIP1 overexpression, and inhibits the growth of DU-145 cells with IC50 of 0.11 μM. HDAC42 is potent in suppressing the proliferation of U87MG and PC-3 cells, in part, because of its ability to down-regulate Akt signaling. AR-42 inhibits the growth of PC-3 and LNCaP cells with IC50 of 0.48 μM and 0.3 μM, respectively. Compared to SAHA, AR-42 exhibits distinctly superior apoptogenic potency, and causes markedly greater decreases in phospho-Akt, Bcl-xL, and survivin in PC-3 cells. AR-42 treatment induces growth inhibition, cell- cycle arrest, apoptosis, and activation of caspases-3/7 in malignant mast cell lines. AR-42 treatment induces down-regulation of Kit via inhibition of Kit transcription, disassociation between Kit and heat shock protein 90 (HSP90), and up-regulation of HSP70. AR-42 treatment down-regulates the expression of p-Akt, total Akt, phosphorylated STAT3/5 (pSTAT3/5), and total STAT3/5. AR-42 potently inhibits the growth of JeKo-1, Raji, and 697 cells with IC50 of<0.61 μM. AR-42 also sensitizes CLL cells to TNF-Related Apoptosis Inducing Ligand (TRAIL), potentially through reduction of c-FLIP. AR-42 treatment also induces autophagy through downregulation of Akt/mTOR signaling and inducing ER stress in hepatocellular carcinoma (HCC) cells.

    Kinase Assay: HDAC activity is analyzed by using an HDAC assay kit. This assay is based on the ability of DU-145 nuclear extract, which is rich in HDAC activity, to mediate the deacetylation of the biotinylated [3H]-acetyl histone H4 peptide that is bound to streptavidin agarose beads. The release of [3H]-acetate into the supernatant is measured to calculate the HDAC activity. Sodium butyrate (0.25-1 mM) is used as a positive control.

    Cell Assay: Cells (DU-145) are exposed to varous concentrations of AR-42 for 96 hours. The medium is removed and replaced by 150 μL of 0.5 mg/mL of MTT in RPMI 1640 medium, and the cells are incubated in the CO2 incubator at 37 °C for 2 hours. Supernatants are removed from the wells, and the reduced MTT dye is solubilized with 200 μL/well of DMSO. Absorbance is determined on a plate reader at 570 nm.

    In VivoThe growth of PC-3 tumor xenografts is suppressed by 52% and 67% after treatment with AR-42 at 25 mg/kg and 50 mg/kg, respectively, whereas SAHA at 50 mg/kg suppresses growth by 31%. In contrast to mice treated with SAHA, intratumoral levels of phospho-Akt and Bcl-xL are markedly reduced in AR-42 treated mice. In the transgenic adenocarcinoma of the mouse prostate (TRAMP) model, administration of AR-42 not only decreases the severity of prostatic intraepithelial neoplasia (PIN) and completely prevents its progression to poorly differentiated carcinoma, but also shifts tumorigenesis to a more differentiated phenotype, suppressing absolute and relative urogenital tract weights by 86% and 85%, respectively. AR-42 significantly reduces leukocyte counts, and prolongs survival in three separate mouse models of B-cell malignancy without evidence of toxicity.
    Animal modelIntact male NCr athymic nude mice inoculated s.c. with PC-3 cells
    Formulation & DosageDissolved in methylcellulose/Tween 80; 50 mg/kg/day; Oral gavage

    J Med Chem. 2005 Aug 25;48(17):5530-5; Clin Cancer Res. 2006 Sep 1;12(17):5199-206; Cancer Res. 2008 May 15;68(10):3999-4009.

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




    OSU-HDAC42 suppressed the development of prostate lesions in 10-wk-old TRAMP mice. Cancer Res. 2008 May 15;68(10):3999-4009.


    OSU-HDAC42 prevented the progression of prostate lesions to poorly differentiated carcinoma in 24-wk-old TRAMP mice. Cancer Res. 2008 May 15;68(10):3999-4009.
    Characterization of OSU-HDAC42–associated testicular degeneration. Cancer Res. 2008 May 15;68(10):3999-4009.


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