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Description: Potent pan-HDAC inhibitor
Chemical Name: (2E)-N-Hydroxy-3-[3-[(phenylamino)sulfonyl]phenyl]-2-propenamide
Purity: ≥98% (HPLC)
Literature (2)

Biological Activity for Belinostat

Belinostat is a potent pan-HDAC inhibitor (IC50 = 28 nM). Dose-dependently reduces tumor volume in a rat model of glioblastoma and induces 70% and 28% apoptosis in LN-229 and LN-18 glioma cell lines (IC50 values are 210 nM and 300 nM respectively). In H358 cells, Belinostat dose-dependently reduces cell viability and upregulates amino acids and metabolites of the TCA and urea cycle. Also potently inhibits C4 release from stem cell-derived astrocytes and shows antidepressant activity. Belinostat is brain penetrant.

Technical Data for Belinostat

M. Wt 318.35
Formula C15H14N2O4S
Storage Store at -20°C
Purity ≥98% (HPLC)
CAS Number 866323-14-0
PubChem ID 6918638
Smiles S(NC1=CC=CC=C1)(=O)(=O)C2=CC(/C=C/C(NO)=O)=CC=C2

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

Tocris products are intended for laboratory research use only, unless stated otherwise.

Solubility Data for Belinostat

Solvent Max Conc. mg/mL Max Conc. mM
DMSO 31.84 100
ethanol 31.84 100

Preparing Stock Solutions for Belinostat

The following data is based on the product molecular weight 318.35. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Select a batch to recalculate based on the batch molecular weight:
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 3.14 mL 15.71 mL 31.41 mL
5 mM 0.63 mL 3.14 mL 6.28 mL
10 mM 0.31 mL 1.57 mL 3.14 mL
50 mM 0.06 mL 0.31 mL 0.63 mL

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References for Belinostat

References are publications that support the biological activity of the product.

Finn et al (2005) Novel sulfonamide derivatives as inhibitors of histone deacetylase. Helv.Chim.Acta 88 1630

Kusaczuk et al (2016) Molecular and cellular effects of a novel hydroxamate-based HDAC inhibitor - belinostat - in glioblastoma cell lines: a preliminary report. Invest.New Drugs 34 552 PMID: 27468826

Peter et al (2022) Histone deacetylase inhibitor belinostat regulates metabolic reprogramming in killing KRAS-mutant human lung cancer cells. Mol.Carcinog. 62 1136 PMID: 37144836

Rapino et al (2023) Small-molecule screen reveals pathways that regulate C4 secretion in stem cell-derived astrocytes. Stem Cell Reports 18 237 PMID: 36563689

Gurbani et al (2019) Assessing treatment response of glioblastoma to an HDAC inhibitor using whole-brain spectroscopic MRI. Tomography 5 53 PMID: 30854442

If you know of a relevant reference for Belinostat, please let us know.

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Keywords: Belinostat, Belinostat supplier, pan, HDAC, inhibitor, inhibits, inhibitors, glioblastoma, glia, H358, cells, NSCLC, lung, cancer, Non-selective, HDACs, Other, Apoptosis, 7981, Tocris Bioscience

Citations for Belinostat

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Currently there are no citations for Belinostat. Do you know of a great paper that uses Belinostat from Tocris? Please let us know.

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Literature in this Area

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!

*Please note that Tocris will only send literature to established scientific business / institute addresses.

Epigenetics Scientific Review

Epigenetics Scientific Review

Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.

Rheumatoid Arthritis Poster

Rheumatoid Arthritis Poster

Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.