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Vorinostat

Cat. No. M1780
Vorinostat Structure
Synonym:

SAHA; Zolinza; MK-0683; Suberoylanilide hydroxamic acid

Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 40  USD40 In stock
50mg USD 24  USD24 In stock
100mg USD 46  USD46 In stock
250mg USD 60  USD60 In stock
500mg USD 90  USD90 In stock
1g USD 120  USD120 In stock
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Quality Control & Documentation
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
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
Conversion of different model animals based on BSA (PMID: 27057123)
Species Mouse Rat Rabbit Guinea pig Hamster Dog
Weight (kg) 0.02 0.15 1.8 0.4 0.08 10
Body Surface Area (m2) 0.007 0.025 0.15 0.05 0.02 0.5
Km factor 3 6 12 8 5 20
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

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] Lee EQ, et al. Clin Cancer Res. Phase I Study of Vorinostat in Combination with Temozolomide in Patients with High-Grade Gliomas: North American Brain Tumor Consortium Study 04-03.

[4] Witt O, et al. Klin Padiatr. Phase I/II Intra-patient Dose Escalation Study of Vorinostat in Children with Relapsed Solid Tumor, Lymphoma or Leukemia.

[5] Archin NM, et al. Nature. Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy.

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

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Keywords: Vorinostat, SAHA; Zolinza; MK-0683; Suberoylanilide hydroxamic acid supplier, HDAC, inhibitors, activators


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