Antifungal Membrane Attack Simulator

Antifungal Drug Class

Concentration (× MIC) 0.0×

Simulation speed 1.0×

Fungal Cell State

VIABLE

Membrane integrity

100%

Ergosterol content

100%

K⁺ ions leaked

Drug effect E(C)

How it works

Both drug classes target ergosterol, the sterol unique to fungal (not human) membranes, but through different mechanisms. Drug effect follows the standard pharmacodynamic Hill / E_max model used to describe real antifungal potency:

E(C) = Emax · C^γ / (EC50^γ + C^γ)

C    = drug concentration (× MIC)
EC50 = concentration at half-maximal effect
γ    = Hill coefficient (curve steepness)
Emax = maximum fractional effect

Polyenes (e.g. amphotericin B) bind ergosterol directly and self-assemble into transmembrane pores (barrel-stave/sponge model). Pore density scales with E(C) × ergosterol content, letting K⁺ leak out and killing the cell quickly — fungicidal, high Emax, low EC50.
Azoles (e.g. fluconazole) inhibit lanosterol 14α-demethylase (CYP51), blocking new ergosterol synthesis. Existing ergosterol is diluted out as the membrane turns over, so integrity falls slowly and rarely to zero — fungistatic, lower Emax, slower onset.
Membrane integrity is modeled as 0.25 + 0.75 × ergosterol for azoles (structural dependence) and as direct pore-driven decay for polyenes.
Below 15% integrity the cell is scored LYSING → DEAD; above ~60% it is VIABLE, between is STRESSED.

Clinical relevance: this Emax relationship, and the fungicidal-vs-fungistatic distinction it produces, is exactly why polyenes are reserved for severe systemic mycoses while azoles are first-line for milder or chronic infections such as oral/vaginal candidiasis.

Ergosterol Phospholipid K⁺ ion Membrane pore

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