What is the mechanism of action (MOA) of Terbinafine?

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From the Guidelines

Terbinafine works by inhibiting the enzyme squalene epoxidase, thus blocking the conversion of squalene to squalene epoxide in the biosynthetic pathway of ergosterol, an integral component of the fungal cell wall. This mechanism of action results in both a depletion of ergosterol, which has a fungistatic effect, together with an accumulation of squalene, which appears to be directly fungicidal 1. The minimum inhibitory concentration (MIC) of terbinafine is very low, approximately 0.004 µg mL–1, which is equivalent to the minimal fungicidal concentration (MFC), demonstrating that this drug is truly fungicidal in vitro 1.

Some key points about terbinafine's mechanism of action include:

  • It is fungicidal against many dermatophytes, unlike azole antifungals that only inhibit fungal growth (fungistatic) 1
  • The medication specifically targets fungi while having minimal effect on human cells because mammalian cells use cholesterol rather than ergosterol in their cell membranes
  • Terbinafine is particularly effective against dermatophytes (causing tinea infections), but also works against some yeasts and molds
  • The drug concentrates well in skin, nails, and hair follicles, making it especially useful for treating onychomycosis (nail fungus) and other dermatophyte infections 1
  • Its lipophilic nature allows it to persist in these tissues for weeks to months after discontinuation, contributing to its effectiveness in treating stubborn fungal infections.

From the FDA Drug Label

Terbinafine, an allylamine antifungal, inhibits biosynthesis of ergosterol, an essential component of fungal cell membrane, via inhibition of squalene epoxidase enzyme. The mechanism of action (MOA) of Terbinafine is the inhibition of squalene epoxidase, an enzyme necessary for the biosynthesis of ergosterol, a key component of fungal cell membranes. This results in fungal cell death due to increased membrane permeability caused by the accumulation of squalene. 2

From the Research

Mechanism of Action of Terbinafine

  • Terbinafine inhibits the biosynthesis of ergosterol, a principal sterol in fungi, at the level of squalene epoxidase 3, 4.
  • This inhibition results in ergosterol-depleted fungal cell membranes, leading to a fungistatic effect, and the toxic accumulation of intracellular squalene, leading to a fungicidal effect 3, 4.
  • The cidal action of terbinafine is closely associated with the development of high intracellular squalene concentrations, which interfere with fungal membrane function and cell wall synthesis 4.

Effects on Fungal Cell Membranes

  • Terbinafine-treated fungi accumulate squalene while becoming deficient in ergosterol, an essential component of fungal cell membranes 4.
  • The accumulation of squalene and deficiency of ergosterol lead to interference with fungal membrane function and cell wall synthesis, ultimately resulting in the death of the fungal cells 4.

Specificity and Potency of Terbinafine

  • Terbinafine is a potent non-competitive inhibitor of squalene epoxidase from Candida, with a Ki value of 30 nM 4.
  • In contrast, inhibition of rat liver squalene epoxidase only occurs at higher drug concentrations, and is competitive with squalene, indicating that terbinafine has no effect on cholesterol biosynthesis in vivo 4.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Terbinafine: a review of its use in onychomycosis in adults.

American journal of clinical dermatology, 2003

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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