ArticleACS medicinal chemistry letters2026
Toward Tumor-Conditional Release of Histone Deacetylase Inhibitors from Nongenotoxic Drug Conjugates.
Article in ACS medicinal chemistry letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Inhibition of histone deacetylase (HDAC) metalloenzymes with hydroxamic acid-based inhibitors is compromised by generally poor metalloenzyme selectivity and the potential for genotoxicity arising from isocyanate metabolites. Here, we applied our previously described platform for iron-(II)-activatable drug delivery to the pan-HDAC inhibitor panobinostat and its study in multiple myeloma cell line models. We demonstrate successful caging of HDAC activity in conjugate form, as well as mitigation of genotoxicity in a bioisosteric control. Finally, we identify the carboxy esterase CES1 as being responsible for unexpected proteolytic instability of the panobinostat conjugate in vitro and in vivo, identifying a focus for future work toward the ultimate goal of mitigating hydroxamate toxicity and mutagenicity through tumor-conditional activation.
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