antimycotics

Antimycotics, or antifungal agents, are drugs used to treat fungal infections in humans. They range from topical preparations for superficial infections to systemic medications for invasive mycoses. The choice of agent depends on the organism, site of infection, patient factors, and drug tolerability.

The main drug classes include polyenes, azoles, allylamines, echinocandins, and antimetabolites. Polyenes such as amphotericin B and nystatin bind ergosterol in fungal membranes, increasing membrane permeability. Azoles (for example fluconazole, itraconazole, voriconazole, posaconazole, isavuconazole) inhibit ergosterol synthesis by blocking lanosterol 14‑α-demethylase. Allylamines, notably terbinafine, inhibit squalene epoxidase, blocking ergosterol production. Echinocandins (caspofungin, micafungin, anidulafungin) inhibit β-1,3-glucan synthesis, weakening the fungal cell wall. The antimetabolite flucytosine is converted within fungal cells to metabolites that disrupt DNA and RNA synthesis.

Indications vary by agent and organism. Azoles cover many Candida species and some molds; amphotericin B remains a broad-spectrum option for severe systemic infections; echinocandins are first-line for invasive candidiasis and some aspergillosis cases; terbinafine is common for dermatophyte infections; topical formulations address cutaneous and mucosal infections. Resistance is an emerging concern, especially among Candida and Aspergillus species, and antifungal stewardship guides appropriate use and de‑escalation.

Safety and monitoring require attention to organ function and drug interactions. Amphotericin B can cause nephrotoxicity; azoles may cause hepatotoxicity and strong drug interactions via cytochrome P450 enzymes; flu cytosine can cause bone marrow suppression. Therapy duration depends on infection site, organism, and clinical response.