Target intelligence / Profile preview

Enoyl-acyl carrier protein reductase InhA (InhA)

Target
InhA
Molecular classification
Enzyme, Reductase
01

Overview

Enoyl-acyl carrier protein reductase InhA is a key enzyme in the type II fatty acid biosynthesis (FAS-II) pathway of *Mycobacterium tuberculosis* (Mtb). It catalyzes the NADH-dependent reduction of enoyl-ACP to acyl-ACP, a critical step in the elongation cycle for mycolic acid synthesis. Mycolic acids are essential components of the mycobacterial cell wall, contributing to its impermeability and pathogenicity. InhA is a clinically validated drug target for tuberculosis, inhibited by drugs like Isoniazid and Ethionamide. Mutations in inhA or overexpression can lead to drug resistance.

02

Mechanism of action

Inhibition of mycolic acid synthesis via NADH-dependent reduction of enoyl-ACP intermediates.

03

Biological functions

Fatty acid biosynthesisMycolic acid synthesisReduction of enoyl-ACP
04

Disease associations

InfectionTuberculosis
05

Safety considerations

Drug resistance (mutations in inhA or overexpression)Cross-resistance to Isoniazid and Ethionamide
06

Interacting drugs

Isoniazid

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