What is the MOA for the antifungal Griseofulvin?

• A. Inhibits ergosterol synthesis
• B. Inhibits fungal cell wall synthesis
• C. Inhibits fungal mitosis by interfering with microtubule formation
• D. Binds to DNA

Answer: (C)

Griseofulvin works by disrupting fungal cell division. It binds to tubulin and prevents proper microtubule formation, which is essential for assembling the mitotic spindle during mitosis. Without a functional spindle, chromosomes can’t separate, so fungal cell division is halted and growth slows or stops. This is why the drug is considered fungistatic rather than rapidly fungicidal. It accumulates in keratin-containing tissues, so it’s especially effective against dermatophytes infecting skin, hair, and nails as new tissue forms.

Other MOAs described don’t fit griseofulvin: blocking ergosterol synthesis affects fungal membrane formation (as with many azoles and allylamines), inhibiting cell wall synthesis targets echinocandins, and binding to DNA describes other DNA-targeting agents rather than mitotic interference.