Panobinostat

SKU: orb1305563

Description

Panobinostat

Research Area

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

Key Properties

• CAS Number: 404950-80-7
• MW: 349.43
• Purity: 99.75%
• Formula: C₂₁H₂₃N₃O₂
• SMILES: Cc1[nH]c2ccccc2c1CCNCc1ccc(\C=C\C(=O)NO)cc1
• Target: HDAC,HIV Protease,Apoptosis,Autophagy
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:6.4 mg/mL (18.32 mM);H2O:< 1 mg/mL (insoluble or slightly soluble);Ethanol:< 1 mg/mL (insoluble or slightly soluble);DMSO:247.5 mg/mL (708.3 mM)

Bioactivity

• Target IC50:
  HDAC (MOLT-4 cells):5 nM|HDAC (Reh cells):20 nM|HDAC1-9:3-61 nM|HDAC8:248 nM
• In Vivo:
  METHODS: To detect anti-tumor activity in vivo Panobinostat (20 mg/kg) was intraperitoneally injected five times per week for two weeks into SCID mice bearing human SCLC tumors H526, BKT, RG1, or H69. Results: Panobinostat significantly slowed dow the in vivo growth of tumors derived from SCLC cells and induced remission. METHODS: To investigat the potential for enhanced recovery of motor function after stroke, Panobinostat (3-10 mg/kg) was administered intraperitoneally to CD-1 mice with stroke every two days for ten days. Results: Neither physical exercise no the combination of Panobinostat substantially affected motor recovery in mice after stroke.Panobinostat treatment coupled with limited physical rehabilitation is unlikely to provide a therapeutic modality for stroke survivors with motor dysfunction.
• In Vitro:
  METHODS: Thirty-seven lung cancer cell lines were treated with Panobinostat (0-800 nMol/L) for 48-72 h, and cell viability was measured usin the MTT. Results: Panobinostat showed potent ant Proliferative activity and cytotoxicity against human and mouse lung cancer cell lines. METHODS: Human All cells MOLT-4 and Reh were treated with Panobinostat (10-100 nM) for 24-72 h. Apoptosis was detected by Flow Cytometry. Results: Panobinostat induced apoptosis in MOLT-4 and Reh cells in a time- and dose-dependent manner.
• Cell Research:
  Blasts from peripheral blood of 2 patients and from bone marrow of 4 patients were isolated with Ficoll-Hypaque, put in culture at a density of 500,000 cells mL with RPMI-1640 medium containing 10% fetal bovine serum and 50 units mL penicillin and streptomycin, and treated with different doses of LBH589 (0-100 μM) for up to 48 hours.
• Animal Research:
  AE17 and TC-1 cancer cells (1 × 10^6 cells) were injected int the flanks of adult f Male C57B-/- mice and severe combined immunodeficiency (SCID) mice. M30 (10 × 10^6 cells), A549 (5 × 10^6 cells), H69 (2.5 × 10^6 cells), BK-T (6.5 × 10^6), H526 (10 × 10^6), and RG1 (10 × 10^6) cells were also injected, but in the presence of matrigel (BD Biosciences), int the flanks of SCID mice. There were 5 to 10 mice in Each treatment group the experiments wit the A549 and H69 cell lines were repeated to ensur the statistical consistency o the results. Experiments were terminated whe the tumors in the control mice had grown to a size that threatene the quality of life o the mice. When tumors reached 100 to 500 mm3, panobinostat was administered via i.p. injections (10–20 mg/kg) on a daily schedule (5-days-on, 2-days-off regimen) fo the entire duration o the experiment. Control mice received i.p. injections with dextrose 5% in water ( Vehicle treatment"). Every tumor was measured with a caliper at least twice weekly. For evaluation o the effects of combination therapy on SCLC-derived tumors, SCID mice with H69 tumors were administered panobinostat as described above. Three days afte the initiation of panobinostat, and again 1 wk later, etoposide (40 mg/kg) was administered i.p.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Disclaimer: For research use only

Alternative Names

Apoptosis, Autophagy, Panobinostat, NVP-LBH 589, NVP-LBH589, NVP-LBH-589, inhibit, Inhibitor, Human immunodeficiency virus, HDAC, Histone deacetylases, HIVProtease, HIV, HIV Protease, LBH 589, LBH589, LBH-589

Compound Identifiers

PubChem CID

6918837