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Panobinostat

Farydak

Pan-HDAC inhibitor

Evidence Score

30

theoretical
Mechanism of Action

Non-selective histone deacetylase inhibitor that increases histone acetylation, opposing the epigenetic silencing in SDH-deficient tumors. May work synergistically with DNMT inhibitors to reverse the multi-layered epigenetic dysregulation.

Pathway Connections
Epigenetic Dysregulation

Succinate inhibits TET family DNA demethylases and Jumonji-domain histone demethylases, causing global DNA and histone hypermethylation. This silences tumor suppressors and blocks differentiation.

Upstream event:

Succinate inhibits TET1/2/3 and KDM histone demethylases

Downstream effects:

DNA hypermethylation (CIMP phenotype)5-hydroxymethylcytosine lossTumor suppressor silencingHistone hypermethylationDifferentiation block
Molecular Targets

DNMT1

DNA methyltransferase 1

downstream

Maintenance DNA methyltransferase. Contributes to hypermethylation phenotype. Target of azacitidine and decitabine.

UniProt: P26358

Quick Facts
FDA Approved

Approved Indications

  • Multiple myeloma (in combination)
ChEMBL IDCHEMBL500113
PubChem CID6918837
Evidence

Evidence from PubMed, OpenTargets, and ChEMBL will appear here once external data integration is enabled.

Coming in Phase 3

AI Analysis

Have Claude analyze this drug's repurposing potential for SDH-deficient diseases.