Metal Preference Hierarchy in the HDAC8 Active Site: A DFT Study
Abstract
HDAC8 is a histone deacetylase enzyme that plays a key role in the development of various diseases in humans, including cancers, neurodegenerative diseases, and alcohol use disorder. Although HDAC8 is classified as a Zn2+-dependent metalloenzyme, available data regarding the affinity of other biologically relevant ions, such as Fe2+, Ni2+, Co2+, and Mg2+, for the HDAC8 enzyme active site remain unclear and contradictory. The mechanism by which these ions compete with Zn2+ for the HDAC8 active site is not well understood. In this study, we performed density functional theory (DFT) calculations at the B3LYP/6-31+G(d) level of theory, combined with polarizable continuum model computations (PCM) in water (ε = 78) and methanol (ε = 32). The results show that Zn2+ remains the thermodynamically preferred cofactor across all modeled reactions. Although Fe2+ and Co2+ gain partial stabilization upon increasing coordination number, the associated entropic and desolvation penalties prevent them from outcompeting Zn2+ under physiologically relevant conditions. Only a limited number of substitution reactions for Fe2+ and Co2+ yield ∆G values near thermodynamic neutrality, and only in specific coordination states. In contrast, all modeled Ni2+ substitution reactions are unfavorable, and Mg2+ is strongly excluded from the HDAC8 active site in all reactions. The resulting metal preference hierarchy—Zn2+ > Co2+ ≈ Fe2+ > Ni2+ > Mg2+—supports experimental observations and clarifies the intrinsic selectivity of the HDAC8 enzyme towards Zn2+. These insights provide a molecular basis for understanding HDAC8 metallo-regulation and may guide the rational design of novel, isoform-specific HDACi with improved binding properties.
Fields of Study & Subjects
Histone Deacetylase Inhibitors Research
Peptidase Inhibition and Analysis
Signaling Pathways in Disease
Publication details
- Journal / source
- Molecules
- Publisher
- MDPI AG
- Volume
- 31
- Issue
- 2
- Pages
- 306–306
- Publication date
- 15 January 2026
- Language
- EN