Uncovers selective HMG-CoA synthase 1 inhibitors in cancer, suggesting new therapeutic pathways.
Comprehensive target validation remains a significant bottleneck in chemical probe development, particularly for covalent inhibitors, where off-target reactivity can lead to toxicity. Using HMG-CoA synthase 1 (HMGCS1), an underexplored gatekeeper enzyme in the mevalonate pathway, we demonstrate how integrating orthogonal chemoproteomic methods can provide unbiased, comprehensive insights into the on- and off-target profiles of covalent inhibitors. Our study specifically highlights the limitations of traditional enrichment proteomics in distinguishing high-occupancy binders from low-occupancy binders, and it proposes a solution through a complementary scavenging proteomics approach that analyzes de-enriched fractions, providing target engagement ratios across the proteome. This framework facilitated the development of CNP7, a cyanopyrrolidine that covalently modifies HMGCS1's catalytic cysteine with remarkable selectivity, as assessed by comprehensive chemoproteomics. A 2.29 Å cryo-EM structure reveals how CNP7 engages the catalytic cysteine within HMGCS1's hydrophobic pocket. CNP7 treatment decreases HMG-CoA levels and induces global protein deprenylation within 4 h. Notably, CNP7 exhibits cell line-specific anticancer activity patterns that differ from those of statins, suggesting possible pathway node-specific vulnerabilities. Together, our study offers valuable chemical tools to modulate HMGCS1 activity and presents a framework for the rigorous characterization of covalent inhibitors in chemical biology and drug development.
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Sun et al. (2026) studied this question.
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