HDAC (pan)

Every compound in the sci-wiki that affects hdac (pan); the ones you can source are floated to the front, then the reference-only entries. Tap any for the full entry, mechanism, and outlets.

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HDAC Inhibitor

Belinostat

Belinostat is an intravenous pan-HDAC inhibitor of the hydroxamic-acid type; "pan" means it blocks the HDAC family broadly rather than one class. It won accelerated approval for relapsed or refractory peripheral T-cell lymphoma (PTCL), an aggressive and hard-to-treat group of lymph-node cancers of T cells, on the strength of a single-arm registration trial. It sits alongside romidepsin and belinostat's oral cousins as part of the small group of HDAC inhibitors that carved out a niche specifically in T-cell lymphoma.

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HDAC Inhibitor

Panobinostat

Panobinostat is an oral pan-HDAC inhibitor, meaning it blocks the histone deacetylase family broadly rather than picking out one class; chemically it belongs to the potent hydroxamic-acid group. It was approved for multiple myeloma (a cancer of plasma cells in the bone marrow), used in combination with the proteasome inhibitor bortezomib and the steroid dexamethasone in patients whose disease had already relapsed. It is a genuinely active drug but a notably toxic one, and its story is a good illustration of how a real survival-adjacent benefit can be outweighed by side effects.

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HDAC Inhibitor

Trichostatin A

Trichostatin A, almost always shortened to TSA, is the classic laboratory HDAC inhibitor; it is a natural product first pulled from a Streptomyces bacterium (originally as an antifungal) that turned out to be an extremely potent, reversible blocker of the histone deacetylase family. It is not a medicine and is not used in people; instead it is one of the most heavily used tools in epigenetics research, the reference compound scientists reach for whenever they want to crank up histone acetylation in a dish and watch what happens to gene expression, cell behavior, or cell identity.

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