echinokandins

Echinokandins are a class of antifungal agents derived from the fermentation products of certain soil-dwelling fungi, primarily *Aspergillus nidulans* and related species. These compounds are notable for their unique mechanism of action, which distinguishes them from other antifungal drugs. Echinokandins inhibit the synthesis of β-(1,3)-D-glucan, a critical component of the fungal cell wall. By disrupting this structural element, they weaken the cell wall, leading to osmotic instability and eventual cell lysis, particularly in dividing fungal cells.

The first echinokandin to be developed for clinical use was caspofungin, approved by regulatory agencies in the late 1990s. It was followed by micafungin and anidulafungin, which share similar chemical structures and pharmacological properties. These drugs are primarily used to treat invasive fungal infections caused by yeasts such as *Candida* species, including resistant strains. They are particularly valuable in cases where other antifungal treatments, such as azoles or polyenes, have failed or are contraindicated.

Echinokandins are administered intravenously due to their poor oral bioavailability. They exhibit a favorable safety profile, with the most common side effects being mild to moderate infusion-related reactions, such as fever or chills, and mild gastrointestinal disturbances. Unlike some other antifungals, echinokandins have a low potential for drug interactions, as they are metabolized primarily by the liver without relying on cytochrome P450 enzymes.

Resistance to echinokandins remains relatively rare but has been documented in some clinical isolates, particularly among *Candida* species like *Candida auris* and certain non-*Candida* molds. Monitoring and stewardship programs are essential to mitigate the emergence of resistance. Echinokandins are considered first-line or alternative treatments for serious fungal infections, particularly in immunocompromised patients, such as those undergoing chemotherapy or organ transplantation.