Voriconazole N-oxide

Voriconazole N-oxide (up to 640 μg/mL; 6 h) does not affect cell viability in HepG2 cells^[5].

Voriconazole N-oxide (UVA 2.0 J/cm²; 8 h) does not induce substantial apoptosis in HaCaT keratinocytes^[2].

Voriconazole N-oxide (400 μg/mL) increases basal respiration OCR in HepG2 cells, indicating uncoupling of the electron transport chain^[5].

Voriconazole N-oxide (UVA 0-3.0 J/cm²; 0-42 min) produces low-level ROS in HaCaT keratinocytes^[2].
Voriconazole N-oxide (400 μg/mL; 6 h) induces ROS accumulation and increases superoxide and H₂O₂ while decreasing CAT activity in HepG2 cells^[5].
Voriconazole N-oxide (200-800 μg/mL; 6 h) inhibits SOD1 protein levels in HepG2 cells^[5].
Voriconazole N-oxide (30 min; UVA 5 J cm⁻²) induces 8-oxoguanine oxidative DNA damage in normal human epidermal keratinocytes^[7].

Voriconazole N-oxide (135 μM; 14 days) regulates 36 genes in primary human keratinocytes, whereas no significant gene regulation is detected in SCCB12 cells^[1].
Voriconazole N-oxide (UVB 0-300 mJ/cm²) is converted to photo-modified Voriconazole N-oxide in a UVB dose-dependent manner^[2].
Voriconazole N-oxide (0.015-0.15 mM) is not glucuronidated by recombinant UGT2B10 or UGT1A6^[3].
Voriconazole N-oxide (0-100 μM; 5-40 min) inhibits CYP2C9 and CYP3A4 (probe substrate) in human liver microsomes with IC₅₀ values of 11.2 μM and 8.7 μM, respectively, while showing minimal inhibition of the other tested CYP isoforms^[4].
Voriconazole N-oxide (1 μM; 0-60 min) is metabolically stable in recombinant human CYP1A2, 2C9, 2C19, 2D6, and 3A4, with ≥95.8% remaining after 60 min^[4].
Voriconazole N-oxide inhibits BSEP-mediated taurocholic acid transport with an IC₅₀ of 237.65 μg/mL in the BSEP transport assay^[5].
Voriconazole N-oxide (30 μM; 24 h before irradiation; 5-7 days post-irradiation) sensitizes normal human epidermal keratinocytes to UVA, with a greater than three-fold reduction in survival at 10 J cm⁻², but does not sensitize them to UVB^[7].
Voriconazole N-oxide h(2 µM; 0-60 min) is formed from Voriconazole with CYP2C19 and CYP3A4 as major contributors in liver microsomes from healthy and CIA DBA/1J mice, while Voriconazole remained stable over 60 min^[8].