A general model for analysis of linear and hyperbolic enzyme inhibition mechanisms

The mechanisms of reversible inhibitors with a single binding site on enzymes are usually divided into two basic groups: linear and hyperbolic (or partial). Each of these two groups is subdivided into three types: competitive, non-competitive and mixed. These six mechanisms are often considered separate identities. Here, prompted by the characterization of the inhibition of the wild-type and mutant β-glucosidase Sfβgly by imidazole and 2-amino-2-(hydroxymethyl)-1,3-propanediol (i.e. Tris), we developed a unifying enzyme kinetic model that integrates these six basic inhibition mechanisms into one. From this model, we deduced a general enzyme kinetic equation that, through modulation of simple parameters (i.e. the relative inhibitor affinity for two binding sites and the reactivity of the enzyme-substrate-inhibitor complex) is converted into the particular kinetic equation of each of those six inhibition mechanisms. In short, we conclude that the six fundamental inhibition mechanisms, linear and hyperbolic, are not separate behaviors but facets of the same general kinetic model presented here.

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Publication Details

Journal
FEBS Open Bio
Published
2025-09-24
DOI
https://doi.org/10.1002/2211-5463.70128
Primary Topic
Computational Drug Discovery Methods
Type
article
Field-Weighted Citation Impact
0.00

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article

A general model for analysis of linear and hyperbolic enzyme inhibition mechanisms

Sandro R. Marana, Rafael Siqueira Chagas
FEBS Open Bio
Computational Drug Discovery Methods
article

A general model for analysis of linear and hyperbolic enzyme inhibition mechanisms

Sandro R. Marana, Rafael Siqueira Chagas
article en

Abstract

The mechanisms of reversible inhibitors with a single binding site on enzymes are usually divided into two basic groups: linear and hyperbolic (or partial). Each of these two groups is subdivided into three types: competitive, non-competitive and mixed. These six mechanisms are often considered separate identities. Here, prompted by the characterization of the inhibition of the wild-type and mutant β-glucosidase Sfβgly by imidazole and 2-amino-2-(hydroxymethyl)-1,3-propanediol (i.e. Tris), we developed a unifying enzyme kinetic model that integrates these six basic inhibition mechanisms into one. From this model, we deduced a general enzyme kinetic equation that, through modulation of simple parameters (i.e. the relative inhibitor affinity for two binding sites and the reactivity of the enzyme-substrate-inhibitor complex) is converted into the particular kinetic equation of each of those six inhibition mechanisms. In short, we conclude that the six fundamental inhibition mechanisms, linear and hyperbolic, are not separate behaviors but facets of the same general kinetic model presented here.

FEBS Open BioVol. 16(2)
Universidade de São Paulo (BR)
Fundação de Amparo à Pesquisa do Estado de São Paulo, Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Conselho Nacional de Desenvolvimento Científico e Tecnológico
Openalex Percentile: Top 73%
Computational Drug Discovery Methods
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