| Identification | Back Directory | [Name]
PXD-101 | [CAS]
866323-14-0 | [Synonyms]
Belista
Belinostat（E）
PXD101;PX105684;PXD-101;PXD 101;PX-105684
(2E)-N-Hydroxy-3-[3-[(phenylamino)sulfonyl]phenyl]-2-propenamide
2-PropenaMide, N-hydroxy-3-[3-[(phenylaMino)sulfonyl]phenyl]-, (2E)- | [Molecular Formula]
C15H14N2O4S | [MOL File]
866323-14-0.mol | [Molecular Weight]
318.348 |
| Chemical Properties | Back Directory | [Melting point ]
172 °C(Solv: ethyl acetate (141-78-6)) | [density ]
1.427±0.06 g/cm3(Predicted) | [storage temp. ]
Sealed in dry,Room Temperature | [solubility ]
DMSO:64.0(Max Conc. mg/mL);201.4(Max Conc. mM) | [form ]
powder to crystal | [pka]
8.27±0.10(Predicted) | [color ]
White to Light yellow to Light orange |
| Hazard Information | Back Directory | [Definition]
ChEBI: Belinostat is a hydroxamic acid-type histone deacetylase (HDAC) inhibitor with antineoplastic activity. It has a role as an antineoplastic agent and an EC 3.5.1.98 (histone deacetylase) inhibitor. It is a hydroxamic acid, a sulfonamide and an olefinic compound. | [Enzyme inhibitor]
This synthetic epigenetic modulator (FW = 318.35 g/mol; CAS 866323-14-
0), also known as PXD101 and the IUPAC name, (2E) -N-hydroxy-3-[3-
(phenylsulfamoyl) phenyl]prop-2-enamide, inhibits histone deacetylase (IC50
= 27 nM) and induces a concentration-dependent increase (over the 0.2–5
μM range) in histone H4 acetylation and alters expression of genes located
on DNA associated with its parent histone octamer. A simple and
sensitive high-performance liquid chromatography ultraviolet method has
been developed for the quantification of PXD101 in human plasma. In
Rhesus monkeys, belinostat is cleared rapidly from plasma with a half-life
of 1.0 h, a mean residence time of 0.47 h, and a clearance of 425 mL/min/m2
. CSF drug exposure is <1% of plasma drug exposure and <10% of free
(non-protein bound) plasma drug exposure. The DNA-methylation inhibitor
decitabine and histone-deacetylase inhibitor belinostat increases the efficacy
of chemotherapeutic agents in tumors that acquired drug resistance due to
DNA methylation and gene silencing. |
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