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Histone deacetylase (HDAC) inhibitors are a class of compounds that interfere with the way HDAC proteins function. HDACs themselves work by changing the way proteins called histones bind to the DNA within cells and in doing so cause certain genes to be “switched off”.

Myeloma and many other cancer cells contain an excess of HDACs, the consequences of which are that pivotal genes involved in cell growth are switched off allowing the myeloma cells to grow and multiply out of control.

HDAC inhibitors block the actions of HDACs; several are currently being investigated as potential treatments for myeloma.

In the following video, Dr Charlotte Pawlyn explains how histone deacetylase inhibitors work in treating myeloma.


Vorinostat is an oral drug that is taken once a day. It is approved for use as a treatment for cutaneous T-cell lymphoma (CTCL).

As a single agent, vorinostat appears to only have modest activity against myeloma cells but appears to be more effective when combined with other anti-myeloma drugs.

In a Phase III trial known as Vantage 088, the combination of vorinostat and Velcade produced higher response rates (56%) in relapsed and/or refractory patients compared to Velcade alone (41%) although there was no significant improvement in disease progression or survival.

The most common side-effects associated with vorinostat included low blood and platelet counts, diarrhoea and fatigue.

Vorinostat is currently being tested in combination with Revlimid as maintenance treatment for newly diagnosed patients in the Myeloma XI trial.

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