Pan-HDAC inhibitor targeting class I/II/IV HDACs (principally HDAC1 and HDAC2), restoring histone acetylation that is lost as a downstream consequence of succinate-driven epigenetic silencing in SDH-deficient tumors. SDH loss causes succinate accumulation → α-KG-dependent dioxygenase inhibition → CIMP hypermethylation + H3K9me3/H3K27me3 histone hypermethylation; HDAC inhibition partially reverses the histone compaction arm of this dual epigenetic silencing even though it does not directly target DNA methylation. In pheochromocytoma/paraganglioma specifically, panobinostat has been shown to upregulate the norepinephrine transporter (NET/SLC6A2) and MIBG uptake at nanomolar concentrations, providing a mechanistic rationale for combining it with 131I-MIBG radioiodine therapy (Martiniova et al., Endocr Relat Cancer 2011, PMID 21098082). A Phase 2 trial of panobinostat in neuroendocrine tumors (NCT00985946) enrolled 15 patients before termination, providing early tolerability data in this tumor class. Synergy with DNMT inhibitors (e.g., decitabine) to reverse both DNA methylation and histone deacetylation simultaneously is mechanistically plausible but unproven in SDH-deficient models.