Molecular Models
a3c4b5d6 by Katewinslet
Generally all the HDAc inhibitors are made up of three primary parts. They are (A) a chelating group which chelates with zinc ion; (B) a hydrophobic spacer group; (C) an aromatic enzyme binding group which is very specific in its action. It was discovered that low molecular weight molecules containing hydroxamic acid moiety are highly potent in inhibiting histone deacetylases. Belinostat or PXD101 was obtained from this series of molecules and has both the chelating group which chelates with zinc and hydroxamic acid. The chelating group is the main cause behind the high potency of Belinostat. It was very efficient under both in vitro and in vivo conditions and was tested in both, tumor cell lines and xenografts models from human beings [2].
Belinostat had shown an increased acetylation of Histone H4 and H3 in a dose dependent manner. At a concentration of 0.2-3.4 μm this inhibitor induced apoptosis by causing the cleavage of PARP. Research also has shown that the cell death was only due to apoptosis and not due to cytotoxicity [2]. Belinostat stimulates the expression of p21(Cip1/WAF1) which is a kinase inhibitor and is cyclin dependent. This induction was observed even at a lower concentration.
During MCL known as mantle cell lymphoma a tranlocation of the gene takes place. This translocation is also represented as t(11;14)(q13;q32) and this leads to the increased expression of cyclin D1. Bortezomib is a potent proteasome inhibitor in MCL. Belinostat was very effective in causing cytotoxicity of the MCL cells, under in vitro conditions. When this HDACinhibitor was clubbed with bortezomib it leads to depolarization of the mitochondrial membrane. This further leads to apoptosis of the MCL cells. However this combination of inhibitors had no effect on normal cells hence showing their specificity in action. The concentration of cyclin D1 and Bcl-XL was found to be decreased and the acetylated α-tubulin and histone H3 were found to be increased [3].
Three HCC cell lines were studied under the action of Belinostat. This inhibitor was effective in inhibiting the growth within these cell lines (Hep3B, HepG2, PLC/PRF/5). It stimulated the process of apoptosis and had no effect on the expression of the viral gene. It also showed varying effects on the tumor suppressor genes [4].
In summary Belinostat is an efficient inhibitor of HDACs which acts efficiently along with other inhibitors. It induces apoptosis and arrests the growth of various tumor cells.
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January 17, 2012 10:22 pm
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