Polyene antifungal

Nystatin

Binds ergosterol in fungal membranes, forming pores that leak ions and kill susceptible yeasts. Negligible systemic absorption from typical oral use.

AntimicrobialAntimicrobial action

Primary Mechanism of Action

Clinical / Scientific

Nystatin associates with membrane ergosterol, creating channels that dissipate ion gradients. Mammalian cholesterol-rich membranes are less affected at therapeutic local concentrations, supporting selective fungal toxicity.

Pathway Targets

Ergosterol-containing membranes

Scientific explanation

Pore formation and ion leakage.

Pathway Convergence

Clinical / Scientific

Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.

Membrane pore injury

Target to downstream effect: Ergosterol binding → Ion-channel-like pores → Loss of electrochemical gradients

Ergosterol binding
↓
Ion-channel-like pores
↓
Loss of electrochemical gradients

Mechanistically Relevant Repurposed & Adjunctive Applications

Mucosal candidiasis

Established

Mechanistic rationale

Established topical/oral non-absorbed polyene for labelled Candida infections.

Mechanistic Application Matrix

Biological TargetMechanismPotential RelevanceEvidence Level
ErgosterolMembrane pore formationFungal ion homeostasisEstablished mechanism

In Plain Language

Nystatin punches tiny holes in yeast membranes by grabbing ergosterol, so the cell’s salts leak out.

Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.