Vorinostat

SKU: orb1308090

Description

Vorinostat

Research Area

Cell Biology, Epigenetics & Chromatin, Infectious Disease & Virology, Molecular Biology

Key Properties

• CAS Number: 149647-78-9
• MW: 264.32
• Purity: 99.93%
• Formula: C₁₄H₂₀N₂O₃
• SMILES: N(C(CCCCCCC(NO)=O)=O)C1=CC=CC=C1
• Target: HDAC,Virus Protease,Mitophagy,Apoptosis,Autophagy
• Solubility: DMSO:262.5 mg/mL (993.11 mM);Ethanol:2 mg/mL (7.57 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:12.5 mg/mL (47.29 mM)

Bioactivity

• Target IC50:
  Vorinostat cells:8.6 μM|ASPC1 cells:3.09 μM|4T1 cells:1.59 μM|ACHN cells:2.08 μM|A2780 cells:> 1000 nM|HDAC3:20 nM (ID50)|B16 cells:2.26 μM|518A2 cells:0.9 μM|A498 cells:25.08 μM|A375 cells:2.68 μM|AGS cells:4 μM|HDAC:~10 nM (cell free)|A431 cells:0.63 μM|B16 F10 cells:11.36 μM|HDAC1:10 nM (ID50)|SW1353 cells:2.0 μM
• In Vivo:
  METHODS: To detect anti-tumor activity in vivo, Vorinostat (50 mg/kg in HOP-β-CD) was administered intraperitoneally to Nude-Foxn1nu/nu mice bearing uterine sarcoma MES-SA five times per week for twenty-one days. RESULTS: A reduction in tumor growth of more than 50% was observed in the Vorinostat treatment group compared to the placebo group. METHODS: To study the effects in an animal model of true erythrocytosis (PV), Vorinostat (200 mg/kg in 50% PEG-400) was injected intraperitoneally into MxCre;Jak2V617F/+ mice five times per week for two weeks. RESULTS: Vorinostat treatment normalized peripheral blood counts and significantly reduced splenomegaly in Jak2V617F knockout mice.Vorinostat may have therapeutic potential for PV and other JAK2V617F-associated myeloproliferative tumors.
• In Vitro:
  METHODS: Synovial sarcoma cells SW-982 and chondrosarcoma cells SW-1353 were treated with Vorinostat (0.5-15 μM) for 48 h, and cell viability was measured by MST assay. RESULTS: Vorinostat inhibited the proliferation of SW-982 and SW-1353 cells in a dose-dependent manner with IC50s of 8.6 μM and 2.0 μM, respectively. METHODS: Uterine sarcoma cells MES-SA were treated with Vorinostat (3 μM) for 24-72 h. The expression levels of target proteins were detected using Western Blot. RESULTS: There was no difference in the expression of HDAC1 throughout the treatment period, and HDAC2, 3 and 7 showed significant inhibition of expression by Vorinostat.
• Cell Research:
  Cells were plated onto 100-mm tissue culture plates at a density of 2 × 10^6 for 48 h and then treated with SAHA or equal concentrations of the vehicle. For longer drug exposure times, medium with drug or vehicle were exchanged every 48 h. For wash-out experiments, cells were treated with SAHA daily for 60–72 h (drug and medium were exchanged at 48 h), then SAHA was washed out and replaced with 10% FCS containing DMEM .
• Animal Research:
  Athymic Nude-Foxn1nu/nu mice were used in the present study. They were housed at 22°C at a constant light-dark cycle (12-h light, 12-h dark) and had free access to water and rodent chow (4-5% fat, 21% protein). Twelve weeks old male mice (n = 14) were anesthetized with Isofluran and 5 × 10^6 MES-SA cells were injected subcutaneously into the right flank of the animal. Mice from a control group received placebo containing 300 μl of empty HOP-β-CD (2-hydroxypropyl-β-cyclodextrin) vesicles. Another group of mice received vorinostat dissolved in HOP-β-CD at a concentration of 50 mg/kg/day. Both, empty vesicles and vorinostat were administered intraperitoneally, starting on the day 4 after the injection of MES-SA tumor cells. Mice body weight and tumor size (w2 × l × 0.52; measured by caliper) were estimated twice a week. All mice were treated for 21 days and afterward sacrificed by cervical dislocation. Each tumor was isolated as a whole and different tumor parameters (weight, volume, size, and macroscopic appearance) were determined. Finally, tumor slices were cryopreserved and formalin fixed (4%) for further analyses .

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Autophagy, Apoptosis, inhibit, MK0683, MK-0683, MK 0683, Mitochondrial Autophagy, Mitophagy, Inhibitor, Human papillomavirus, HDAC8, HDAC, HDAC1, HDAC2, HDAC3, HDAC6, Histone deacetylases, HPV, Filovirus, suberoylanilide hydroxamic acid, SAHA, Vorinostat, Virus Protease, VirusProtease

Compound Identifiers

PubChem CID

5311