Isavuconazole(BAL-4815; RO-0094815) is the active component of the new azole antifungal agent BAL8557, exhibits MIC(50)s/MIC(90)s ranged from 0.002/0.004 mg/liter for C. albicans to 0.25/0.5 mg/liter for C. glabrata.

＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

艾沙康唑; BAL-4815; RO-0094815

DMSO : ≥ 50 mg/mL (114.29 mM)

Fungal

Isavuconazole inhibits cytochrome P450 (CYP)–dependent 14α-lanosterol demethylation, which is essential for fungal cell membrane ergosterol synthesis. This blockade produces methylated sterols in the fungal membrane, altering its function and allowing the accumulation of ergosterol toxic precursors in the cytoplasm, which leads to cell death.

Isavuconazonium sulfate, the prodrug of isavuconazole, is available in both intravenous and oral formulations. After intravenous infusion, the prodrug is broken down quickly to the active component, isavuconazole, and an inactive cleavage product. Following oral administration, plasma concentrations of the active compound reach maximum concentrations (Cmax) by 2–3 hours; the prodrug and cleavage product are not measurable in plasma after oral administration. In healthy adult volunteers, isavuconazole exhibits linear and dose-proportional pharmacokinetics. The oral bioavailability of isavuconazole is 98%. Absorption of isavuconazole is not affected by food intake. In addition to excellent bioavailability, isavuconazole serum concentrations show low intersubject variability. In healthy volunteers, the Cmax at steady state was 2.5 ± 1.0 µg/mL. Isavuconazole has a large volume of distribution, is >99% protein bound, and has a long terminal half-life of 100-130 hours. Metabolism of isavuconazole takes place in the liver via the CYP enzyme family, specifically CYP3A4 and CYP3A5 isoenzymes.