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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.
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
 . figure 6..jpg) |
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. |
 . figure 5..jpg) |
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. |
 . figure 4..jpg) |
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. |
 . figure 3..jpg) |
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. |
 . figure 2..jpg) |
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). |
 . figure 1..jpg) |
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. |
| 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 |
| 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 |
| Related HDAC Products |
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CM-444 is an inhibitor for HDAC and DNA methyltransferases (DNMT) with IC50 values of 6 nM-0.6 μM and 1.8-2.3 μM, respectively. CM-444 is an inducer for the differentiation of acute myeloid leukemia cells. CM-444 exhibits anti-leukemic activity and improves the survival rate in mouse models. |
| CM-1758
CM-1758 is a histone deacetylase (HDAC) inhibitor. CM-1758 inhibits tumor growth in vivo. CM-1758 induces acetylation of non-histone proteins in acute myeloid leukemia cells. |
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T-518 is an orally active, selective, and blood-brain barrier permeable HDAC6 inhibitor with an IC50 value of 36 nM for human HDAC6. |
| SE-7552
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| BRD9757
BRD9757 is a potent, capless and selective HDAC6 inhibitor with an IC50 of 30 nM. |
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