Abafungin

Abafungin (BAY-W-6341) is a broad-spectrum fungicidal arylguanidine compound and a selective inhibitor of sterol-C-24-methyltransferase. Abafungin blocks the transmethylation reaction at the C-24 position of the sterol side chain during the ergosterol biosynthesis pathway. Abafungin directly disrupts fungal cell membrane integrity, and diminishes fungal viability independent of the fungal growth state. Abafungin can be applied to the research of fungal infections, particularly dermatomycoses^[1][2]. In Vitro:Abafungin (0.1-1 μg/mL; 24 h for Candida albicans, 3–5 days for other fungi) exhibits broad-spectrum in vitro antifungal activity against dermatophytes, Candida spp.,Aspergillus spp. and with species-specific MIC values ranging from ≤ 0.06 to 16 μg/mL^[1].
Abafungin (10 μg/mL; 48 h for C. albicans, 3-5 days for other fungi) completely inhibits C. albicans at 10 μg/mL after 48 h, with species-specific MFC values ranging from ≤ 0.06 to 32 μg/mL^[1].
Abafungin disrupts the cell membrane integrity of Candida albicans in a concentration-dependent manner and induces rapid ion release within 2 min at concentrations ≥ 10 μg/mL. For strain TIMM 0144, approximately 85% of total potassium is released within 2 min at 40 μg/mL^[1].
Abafungin (30 μg/mL; up to 30 min) triggers rapid ATP leakage, ATP degradation, and loss of viability in resting Candida albicans strain H12, whereas growing cells show transient ATP elevation, reduced ATP leakage, and delayed loss of viability^[1].
Abafungin (5×10^-5 M for phosphatidylserine, 1×10^-4 M for other substances; 1 min at 22°C) displays strong and specific interaction with purified phosphatidylserine, while showing no or only weak interaction with other tested phospholipids and sterols^[1].
Abafungin (0.01-10 μg/mL; 3 h) dose-dependently inhibits ergosterol biosynthesis in Candida albicans by reducing the incorporation of L-[methyl-¹⁴C]methionine into sterols^[1].
Abafungin (1 μg/mL; 24 h) inhibits sterol-C-24-methyltransferase in Candida albicans strain TIMM 0144, leading to the accumulation of lanosterol in the ergosterol biosynthesis pathway^[1].