We use analytics and advertising cookies, which you can accept or reject; see our privacy policy.

Current choice:

Fig. 1 · Structure
Cat. No.
A10122
CAS No.
414864-00-9
Formula
C15H14N2O4S
Mol. Weight
318.4

Documents & Downloads

Belinostat (PXD101)

Cat. No. A10122 CAS 414864-00-9

HDAC inhibitor

Belinostat (PXD101) is a HDAC inhibitor that inhibits HDAC activity in HeLa cell extracts with an IC50 of 27 nM.

In Stock

Publications for Belinostat (PXD101)

1 publication citing this product

  1. Shariful Islam, .et al. , Blood Adv, 2020, 4(20): 5297-5310 PMID: 33108458
Notify me when the price drops

For laboratory research use only. We do not sell to patients.

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Bioactivity / Mechanism

Belinostat response is linked to class I HDAC biology: HDAC1 depletion increased its cellular viability IC50 1.9-fold in HeLa cells, while HDAC2 or HDAC3 depletion did not produce a significant shift. This supports HDAC1 involvement in that model without establishing exclusive target selectivity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
HDAC (Cell-free assay) 27 nM

In Vitro Studies

Belinostat inhibited WST-1 growth readouts in four human bladder carcinoma cell lines after 48 h, with substantial variation by model. At 5 μM, reported inhibition ranged from 23% in RT4 to 71% in 5637 cells. RT4 showed significant inhibition only at 5 μM among the displayed conditions. [2]

HDAC1 depletion reduces belinostat sensitivity in HeLa cells

Cell-based study · Human HeLa cervical cancer cells with individual HDAC1, HDAC2 or HDAC3 siRNA depletion and nondepleted control cells [1]

HDAC1 depletion increased the belinostat viability IC50 by 1.9-fold; HDAC2 or HDAC3 depletion did not show that significant shift. This functional result supports HDAC1 involvement, without demonstrating exclusive binding or isoform selectivity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Belinostat concentration producing half-maximal viability inhibition after HDAC depletionIC50 fold change 1.9-fold increase after HDAC1 knockdown; p < 0.01; n = 10; figure error bars are SEM of mean IC50[1]

Literature-Reported Treatment Conditions

Exposure duration
48 h drug exposure; cells plated 24 h after siRNA transfection
Method
Belinostat dose-response after individual class I HDAC depletion; HDAC protein reduction checked by immunoblot with actin loading control
Vehicle
Drugs dissolved in sterile water
Co-treatment
HDAC-targeting siRNA perturbation; not a pharmacological combination treatment
Reported limits
Exact belinostat concentration series is not specified in the read assay Methods. Methods describe scrambled-siRNA control; Figure 2 caption calls control mock-treated. No exact bar heights inferred.
Methods and source locations

Compound reported in the paper: Belinostat (PXD101); Compound label in the paper: Belinostat

Compound-level functional evidence in HeLa cells; no Adooq use or lot validation established.

Results: HDAC1 knockdown reduces sensitivity to the HDACi belinostat; Figure 2 and caption; Methods: Transfection of siRNA, CellTiter-Glo Assay; Figure 1A knockdown validation

Belinostat concentration producing half-maximal viability inhibition after HDAC depletion: ATP-dependent CellTiter-Glo viability; variable-slope sigmoidal dose-response fit; repeated-measures one-way ANOVA and Dunnett multiple comparisons — Results: HDAC1 knockdown reduces sensitivity to the HDACi belinostat; Figure 2 and caption; Methods: Transfection of siRNA, CellTiter-Glo Assay; Figure 1A knockdown validation

Variable growth inhibition across four bladder carcinoma cell lines

Cell-based study · Human urinary bladder carcinoma 5637, T24, J82 and RT4 cells [2]

At 5 μM for 48 h, reported growth inhibition ranged from 23% in RT4 to 71% in 5637. RT4 reached statistical significance only at 5 μM among the 1, 2 and 5 μM conditions shown. WST-1 is an indirect proliferation/metabolic endpoint.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Reduction in WST-1 signal relative to control after 5 μM belinostat for 48 hGrowth inhibition 5637: 71% (± 0.2, SEM); T24: 51% (± 1.0); J82: 41% (± 2.0); RT4: 23% (± 7.9). Figure 1 specifies SEM error bars.[2]
Growth inhibition compared with control at the displayed concentrationsReported significance 5637, T24, J82: p < 0.001 at 1, 2 and 5 μM; RT4: significant only at 5 μM (p = 0.01)[2]

Literature-Reported Treatment Conditions

Treatment concentration
1, 2 and 5 μM shown in Figure 1; the assay Methods describe exposure to 1–10 μM
Exposure duration
48 h
Method
Belinostat treatment of bladder carcinoma cultures followed by WST-1 readout
Vehicle
10 mM stock prepared in DMSO/PBS
Reported limits
Final vehicle concentration and whether control was explicitly vehicle-matched are not specified in the read cellular Methods/caption. Figure-specific exact independent-experiment count is stated only as at least 3.
Methods and source locations

Compound reported in the paper: Belinostat (PXD101); Compound label in the paper: Belinostat

Compound-level cellular observations; animal formulation and animal results are excluded.

Results: Belinostat inhibited bladder cancer cell growth; Figure 1 and caption; Methods: Cell culture, proliferation assay and belinostat; Statistical Analysis

Reduction in WST-1 signal relative to control after 5 μM belinostat for 48 h: WST-1 tetrazolium salt cleavage assay; Figure 1 representative of at least 3 independent experiments, mean of at least 8 wells per condition — Results: Belinostat inhibited bladder cancer cell growth; Figure 1 and caption; Methods: Cell culture, proliferation assay and belinostat; Statistical Analysis

Growth inhibition compared with control at the displayed concentrations: Student two-tailed t test as specified in Statistical Analysis; comparisons with control — Results: Belinostat inhibited bladder cancer cell growth; Figure 1 and caption; Methods: Cell culture, proliferation assay and belinostat; Statistical Analysis

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 414864-00-9
Applications HDAC inhibitor
Formula C15H14N2O4S
Molecular Weight 318.4
Synonyms PX105684
SMILES
C1=CC=C(C=C1)NS(=O)(=O)C2=CC=CC(=C2)/C=C/C(=O)NO

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 56 mg/mL (175.9 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
9 mg/mL
Vehicle
2% DMSO+30% PEG 300+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Dejligbjerg M, Grauslund M, Litman T, et al. Differential effects of class I isoform histone deacetylase depletion and enzymatic inhibition by belinostat or valproic acid in HeLa cells Molecular cancer (2008). PMID: 18789133 DOI: 10.1186/1476-4598-7-70 Source material
  2. [2] Buckley MT, Yoon J, Yee H, et al. The histone deacetylase inhibitor belinostat (PXD101) suppresses bladder cancer cell growth in vitro and in vivo Journal of translational medicine (2007). PMID: 17935615 DOI: 10.1186/1479-5876-5-49 Source material

Publications

1 publication citing this product

  1. Shariful Islam, .et al. , Blood Adv, 2020, 4(20): 5297-5310 PMID: 33108458

Added to your cart

View Cart Checkout
Loading...