PCI 34051

  • CAT Number: I005646
  • CAS Number: 950762-95-5
  • Molecular Formula: C₁₇H₁₆N₂O₃
  • Molecular Weight: 296.32
  • Purity: ≥95%
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PCI-34051 (CAT: I005646) is a selective inhibitor of histone deacetylase 8 (HDAC8). It belongs to the class of compounds known as hydroxamic acids and is specifically designed to target HDAC8. HDAC enzymes play a role in the regulation of gene expression by removing acetyl groups from histone proteins, thereby affecting chromatin structure and gene transcription. By inhibiting HDAC8, PCI-34051 can lead to an accumulation of acetylated histones and modulation of gene expression. This compound has been studied for its potential therapeutic applications in various diseases, including cancer and neurological disorders.

Catalog Number I005646
CAS Number 950762-95-5
Molecular Formula


Purity 95%
Target HDAC
Solubility DMSO: ≥ 30 mg/mL
Storage 3 years -20C powder
IC50 10nM
InChI InChI=1S/C17H16N2O3/c1-22-15-6-2-12(3-7-15)11-19-9-8-13-4-5-14(10-16(13)19)17(20)18-21/h2-10,21H,11H2,1H3,(H,18,20)

1:Leukemia. 2008 May;22(5):1026-34. doi: 10.1038/leu.2008.9. Epub 2008 Feb 7. A novel histone deacetylase 8 (HDAC8)-specific inhibitor PCI-34051 induces apoptosis in T-cell lymphomas.Balasubramanian S,Ramos J,Luo W,Sirisawad M,Verner E,Buggy JJ, PMID: 18256683 DOI: 10.1038/leu.2008.9 </br><span>Abstract:</span> We have developed a potent, histone deacetylase 8 (HDAC8)-specific inhibitor PCI-34051 with >200-fold selectivity over the other HDAC isoforms. PCI-34051 induces caspase-dependent apoptosis in cell lines derived from T-cell lymphomas or leukemias, but not in other hematopoietic or solid tumor lines. Unlike broad-spectrum HDAC inhibitors, PCI-34051 does not cause detectable histone or tubulin acetylation. Cells defective in T-cell receptor signaling were still sensitive to PCI-34051-induced apoptosis, whereas a phospholipase C-gamma1 (PLCgamma1)-defective line was resistant. Jurkat cells showed a dose-dependent decrease in PCI-34051-induced apoptosis upon treatment with a PLC inhibitor U73122, but not with an inactive analog. We found that rapid intracellular calcium mobilization from endoplasmic reticulum (ER) and later cytochrome c release from mitochondria are essential for the apoptotic mechanism. The rapid Ca(2+) flux was dependent on PCI-34051 concentration, and was blocked by the PLC inhibitor U73122. Further, apoptosis was blocked by Ca(2+) chelators (BAPTA) and enhanced by Ca(2+) effectors (thapsigargin), supporting this model. These studies show that HDAC8-selective inhibitors have a unique mechanism of action involving PLCgamma1 activation and calcium-induced apoptosis, and could offer benefits including a greater therapeutic index for treating T-cell malignancies.

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