American Society of Hirudotherapy

The High-Affinity Chymotrypsin Inhibitor Eglin C Poorly Inhibits Human Chymotrypsin-Like Protease: Gln192 and Lys218 Are Key Determinants

Structural biology article published in Proteins (2024)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportSalivary PharmacologyDrug DevelopmentNémeth BZ, Kiss B, Sahin-Tóth M, Magyar C, Pál G · Proteins, 2024

Abstract

Eglin C, a small protein from the medicinal leech, has been long considered a general high-affinity inhibitor of chymotrypsins and elastases. Here, we demonstrate that eglin C inhibits human chymotrypsin-like protease (CTRL) weaker by several orders of magnitude than other chymotrypsins. In order to identify the underlying structural aspects of this unique deviation, we performed comparative molecular dynamics simulations on experimental and AlphaFold model structures of bovine CTRA and human CTRL. Our results indicate that in CTRL, the primary determinants of the observed weak inhibition are amino-acid positions 192 and 218 (using conventional chymotrypsin numbering), which participate in shaping the S1 substrate-binding pocket and thereby affect the stability of the protease-inhibitor complexes.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsHumansMolecular Dynamics SimulationAnimalsChymotrypsinCattleBinding SitesAmino Acid SequenceProtein Binding

Summary

Molecular dynamics simulations identify Gln192 and Lys218 as key determinants causing weak inhibition of human chymotrypsin-like protease (CTRL) by leech-derived eglin C, refining understanding of substrate specificity in serine proteases.

Why This Matters for Hirudotherapy

This study examined why eglin C—a small protein from the medicinal leech long regarded as a general high-affinity inhibitor of chymotrypsins and elastases—weakly inhibits human chymotrypsin-like protease (CTRL) by several orders of magnitude compared with other chymotrypsins. Using comparative molecular dynamics simulations on bovine CTRA and human CTRL structures, the authors identified amino-acid positions 192 and 218 as key determinants shaping the S1 substrate-binding pocket and affecting protease-inhibitor complex stability. This is relevant to ASH's domain insofar as eglin C is a characterized leech-secretome inhibitor, and the work refines understanding of its target selectivity. Caveat: the study is computational/in silico (molecular dynamics), provides structural-mechanistic insight only, and offers no therapeutic or in-vivo data.

Citation

The High-Affinity Chymotrypsin Inhibitor Eglin C Poorly Inhibits Human Chymotrypsin-Like Protease: Gln192 and Lys218 Are Key Determinants.

Németh BZ, Kiss B, Sahin-Tóth M, Magyar C, Pál G · Proteins, 2024

Added to ASH library: May 26, 2026 · Site last updated: June 18, 2026

This website provides educational information and does not constitute medical advice, diagnosis, or treatment recommendations. Medicinal leech therapy carries clinically meaningful risks and should be performed only by qualified clinicians under institutionally approved protocols. FDA 510(k) clearance for medicinal leeches is limited to specific indications; investigational and off-label discussions are labeled accordingly. For patient-specific guidance, consult a qualified healthcare provider.