## Mechanism of Action of Antifungals **Key Point:** Griseofulvin does NOT inhibit DNA gyrase or cause DNA strand breaks. Its true mechanism is disruption of microtubule assembly by binding to tubulin, which impairs mitotic spindle formation and prevents cell division. ### Correct Mechanisms | Agent | Class | Mechanism | Target | |-------|-------|-----------|--------| | Amphotericin B | Polyene | Binds ergosterol → membrane pores → leakage | Cell membrane | | Fluconazole | Azole | Inhibits CYP51 (14α-demethylase) → ↓ ergosterol | Sterol synthesis | | Terbinafine | Allylamine | Inhibits squalene epoxidase → ↓ ergosterol | Early sterol pathway | | Griseofulvin | Antimitotic | Binds tubulin → disrupts microtubules | Cell division | **High-Yield:** The first three agents all target **ergosterol** (the fungal equivalent of cholesterol), either by disrupting the membrane itself or blocking its synthesis. Griseofulvin is fundamentally different — it is an **antimitotic** agent that prevents fungal cell division by disrupting the mitotic spindle. **Clinical Pearl:** Griseofulvin's mechanism explains why it is effective only against **dividing cells** and why it must be given for prolonged periods (weeks to months) — it works by preventing replication, not by killing existing fungal elements. This is why it is used for dermatophyte infections (which grow slowly) but NOT for systemic mycoses. **Mnemonic:** **GRIT** = Griseofulvin Restricts In Tubulin (microtubule disruption, not DNA damage). [cite:KD Tripathi 8e Ch 51]
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