Vorinostat [149647-78-9]

Biological Activity

Vorinostat (SAHA, Zolinza, MK-0683) is a selective and potent histone deacetylase (HDAC) inhibitor with the IC50 value of 10 nM for HDAC-1.The pan-HDAC inhibitor vorinostat (SAHA,Zolinza,MK-0683) potentiates the activity of the proteasome inhibitor carfilzomib in human DLBCL cells in vitro and in vivo.Vorinostat (SAHA, Zolinza, MK-0683),which also inhibits HDAC6,could enhance the activity of the novel proteasome inhibitor CFZ in DLBCL cells, including those resistant to bortezomib alone.

Product Citations

• 

  Cell Death Differ. 2026 Jan 31; .

  Targeting the USP7-PRMT6 epigenetic axis overcomes chemoresistance in breast cancer by coordinating H3R2me2a deposition and RNF168 methylation for DNA
  Vorinostat purchased from AbMole

• 

  FEBS J. 2024 Sep 09.

  MOF-mediated acetylation of CDK9 promotes global transcription by modulating P-TEFb complex formation
  Vorinostat purchased from AbMole

• 

  BMC Cancer. 2016 Nov 7;16(1):857.

  Vorinostat enhances the cisplatin-mediated anticancer effects in small cell lung cancer cells.
  Vorinostat purchased from AbMole

Customer Product Validations & Biological Datas

	Source	BMC Cancer (2016) . Figure 6. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	Antitumor activity in H209 xenografts
	Cell Lines	H209 cells line
	Concentrations	40mg/kg 4 times a week
	Incubation Time	5 weeks
	Results	As presented in Fig. 6, compared with vehicle and single-agent treatments, the combination treatment significantly inhibited tumor growth at day 5.

	Source	BMC Cancer (2016) . Figure 5. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	western blot
	Cell Lines	H209 and H146 cells line
	Concentrations	0.05, 0.1 and 0.2 μ M
	Incubation Time	24 h
	Results	As presented in Fig. 5a and b, vorinostat alone induced a dose-dependent reduction of TS protein levels in the H209 and H146 cells.

	Source	BMC Cancer (2016) . Figure 4. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	flow cytometry
	Cell Lines	H209 and H146 cells line
	Concentrations	0.1 μ M
	Incubation Time	24 h
	Results	The H146 cells treated with vorinostat demonstrated no distinct cell cycle arrest, whereas those treated with cisplatin exhibited cell cycle arrest in the S phase (Fig. 4b and d). Similarly, the combination treatment induced cell cycle arrest in the S phase in the H146 cells.

	Source	BMC Cancer (2016) . Figure 3. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	caspase-3 activity assay and Western blot
	Cell Lines	H209 and H146 cells line
	Concentrations	0, 0.05, 0.1 and 0.2 μ M
	Incubation Time	24 or 36 h
	Results	Therefore, our data indicated that the combination treatment dose dependently increased apoptosis in the proteolytic cleavage of PARP and activated caspase-3 in SCLC cells.

	Source	BMC Cancer (2016) . Figure 2. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	Cell viability assay and Western blot
	Cell Lines	H209 and H146 cells line
	Concentrations	0, 0.1 or 0.2 μ M
	Incubation Time	24 h
	Results	The combination treatments were more effective in inhibiting H209 cell viability in a dosedependent manner (Fig. 2a). Specifically, the cell viabilities observed when the cells were treated with combinations of cisplatin at 5 μM and vorinostat at 0.1 or 0.2 μM were 80.21 and 68.81 %, respectively (Fig. 2b).

	Source	BMC Cancer (2016) . Figure 1. Vorinostat (purity >99 %) was purchased from AbMole BioScience (Houston, TX, USA)
	Method	Cell viability assay and Western blot
	Cell Lines	H209 and H146 cells line
	Concentrations	0, 0.4 or 0.8 μ M
	Incubation Time	24 h
	Results	Overall, these results indicated that the triple combination treatment enhanced cytotoxic effects and promoted apoptosis in SCLC cells.

Protocol (for reference only)

Cell Experiment
Cell lines	HH, HuT78, MJ, MylA and SeAx cells
Preparation method	cell viability assay. The inhibitory effect of vorinostat on the viability of CTCL cell lines was examined through a CellTiter-Glo assay using various concentrations of vorinostat (0.01, 0.05, 0.15, 0.5, 1.25, 4, 10, 35, and 100 μM) for 72 h. All CTCL cell lines were sensitive to the investigated HDAC inhibitor. The inhibitory effect of vorinostat was reflected as a dose-dependent reduction in cell proliferation/viability. The IC50 of proliferation was determined at 0.146 μM in HH cells, at 2.062 μM in HuT78 cells, at 2.697 μM in MJ cells, at 1.375 μM in MylA and at 1.510 μM in SeAx cells.
Concentrations	0.01, 0.05, 0.15, 0.5, 1.25, 4, 10, 35, and 100 μM
Incubation time	72 h

Animal Experiment
Animal models	R6/2 mice motor impair
Formulation	solubilized in 5 molar equivalents of HOP-β-CD (ICN) in water
Dosages	0.67g/L
Administration	orally

Chemical Information

Molecular Weight	264.3
Formula	C14H20N2O3
CAS Number	149647-78-9
Solubility (25°C)	DMSO 55 mg/mL
Storage	Powder          -20°C   3 years ;  4°C   2 years In solvent       -80°C   6 months ;  -20°C   1 month

References

[1] Saelen MG, et al. Radiat Oncol. Radiosensitization by the histone deacetylase inhibitor vorinostat under hypoxia and with capecitabine in experimental colorectal carcinoma.

[2] Kakizaki A, et al. Australas J Dermatol. Successful treatment of syringotropic CD8+ mycosis fungoides accompanied by hypohidrosis with vorinostat and retinoids.

[3] Lautz TB, et al. PLoS One. The effect of vorinostat on the development of resistance to doxorubicin in neuroblastoma.