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Panobinostat (LBH589)HDAC inhibitor

Panobinostat (LBH589)

Catalog No. A8178
Size Price Stock Qty
10mM (in 1mL DMSO) $60.00 In stock
Evaluation Sample $28.00 In stock
10mg $60.00 In stock
50mg $120.00 In stock
200mg $270.00 In stock
500mg $440.00 In stock

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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Ballante F, Reddy DR, et al. "Structural insights of SmKDAC8 inhibitors: Targeting Schistosoma epigenetics through a combined structure-based 3D QSAR, in vitro and synthesis strategy." Bioorg Med Chem. 2017 Apr 1;25(7):2105-2132. PMID:28259528
2.Bagnall NH, Hines BM, et al. "Insecticidal activities of histone deacetylase inhibitors against a dipteran parasite of sheep, Lucilia cuprina." Int J Parasitol Drugs Drug Resist. 2017 Apr;7(1):51-60. PMID:28110187
3. Chatterjee N, Tian M, et al. "Keap1-Independent Regulation of Nrf2 Activity by Protein Acetylation and a BET Bromodomain Protein." PLoS Genet. 2016 May 27;12(5):e1006072. PMID:27233051

Quality Control

Chemical structure

Panobinostat (LBH589)

Related Biological Data

Panobinostat (LBH589)

Related Biological Data

Panobinostat (LBH589)

Related Biological Data

Panobinostat (LBH589)

Related Biological Data

Panobinostat (LBH589)

Related Biological Data

Panobinostat (LBH589)

Biological Activity

Description Panobinostat (LBH589) is a novel broad-spectrum inhibitor of HDAC with IC50 of 5 nM.
Targets HDAC (MOLT-4 cells) HDAC (Reh cells)        
IC50 5 nM 20 nM        


Cell experiment [1]:

Cell lines

MCF-7aro, LTEDaro, Exe-R, Let-R, Ana-R cell lins

Preparation method

The solubility of this compound in DMSO is <10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reaction Conditions

6d; 20 nM


To study cellular response to AIs and the mechanisms of acquired AI resistance, we used the previously generated AI-responsive cell line MCF-7aro and AI-resistant variants of MCF-7aro created following in vitro selection against each AI (i.e., Exe-R, Let-R, and Ana-R) or long-term culture in the absence of estrogen (i.e., LTEDaro). MCF-7aro, LTEDaro and three AI-resistant cell lines were exposed to increasing concentrations of LBH589. This drug-inhibited proliferation of all cell lines in a dose-dependent manner.

Animal experiment [1]:

Animal models

Female, 6- to 7-week-old ovariectomized, BALB/c Nu–Nu athymic mice

Dosage form

20 mg/kg, three times per week, intraperitoneal injection


To evaluate the inhibitory effects of LBH589 on AI resistance in vivo, we used the exemestane-resistant MCF7aro xenograft model. LBH589 treatment significantly inhibited the growth of exemestane-resistant tumors; tumor weight at the end of experiment was significantly lesser in mice treated with LBH589 than in control mice. No mice in the LBH589 treat-ment groups showed significant body weight loss indicating that the LBH589 treatment was well tolerated. Consistent with the effect of LBH589 on gross character-istics of the tumors, proliferation (assessed by Ki-67 staining) of tumor cells was significantly decreased in LBH589-treated mice and apoptosis (assessed by staining for cleaved PARP) of tumor cells was significantly increased.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Kubo M, Kanaya N, Petrossian K, et al. Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat)[J]. Breast cancer research and treatment, 2013, 137(1): 93-107.

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Chemical Properties

Cas No. 404950-80-7 SDF Download SDF
Synonyms Panobinostat,LBH589,LBH-589, Faridak, NVP-LBH589,
Chemical Name (E)-N-hydroxy-3-[4-[[2-(2-methyl-1H-indol-3-yl)ethylamino]methyl]phenyl]prop-2-enamide
Formula C21H23N3O2 M.Wt 349.43
Solubility >17.5mg/mL in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request


Panobinostat, as known as LBH589, is a novel and potent hydroxamic acid-based deacetylase inhibitor (DACis)that inhibits a broad spectrum of histone deacetylases (HDACs), including all Classes 1, 2 and 4 HDAC enzymes, at low nanomolar concentrations. According to previous studies, it not only induces apoptosis in multiple myeloma (MM) cells via caspase activation and poly(ADP-ribose) polymerase (PARP) cleavage, but also induces potent cell growth inhibition, cell-cycle arrest, and apoptosis in a time- and dose-dependent manner in both Philadelphia chromosome-negative (Ph-) actue lymphoblastic leukemia (ALL) cells lines (T-cell MOLT-4 and pre-B-cell Reh), which are correlated with induction of histone (H3K9 and H4K8) hyperacetylation, activation of p21 and p27, and suppression of c-Myc.


Wenlin Shao, Joseph D. Growney, Yun Feng, Gregory O’Connor, Minying Pu, Wenjing Zhu, Yung-Mae Yao, Paul Kwon, Stephen Fawell and Peter Atadja. Activity of deacetylase inhibitor panobinostat (LBH589) in cutaneous T-cell lymphoma models: defining molecular mechanisms of resistance. Int. J. Cancer: 127, 2199-2208 (2010)

Laurence Catley, Ellen Weisberg, Tanyel Kiziltepe, Yu-Tzu Tai, Teru Hideshima, Paola Neri, Pierfrancesco Tassone, Peter Atadja, Dharminder Chauhan, Nikhil C. Munshi and Keneth C. Anderson. Aggresome induction by proteasome inhibitor bortezomib and α-tubulin hyperacetylation by tubulin deacetylase (TDAC) inhibitor LBH589 are synergistic in myeloma cells. Blood (2006); 108(10): 3441-3449

Anna Scuto, Mark Kirschbaum, Claudia Kowolik, Leo Kretzner, Agnes Juhasz, Peter Atadja, Vinod Pullarkat, Ravi Bhatia, Stephen Forman, Yun Yen, and Richard Jove. The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells. Blood (2008); 111(10):5093-5100