| Indication | For the treatment of the following systemic fungal infections: candidiasis, chronic mucocutaneous candidiasis, oral thrush, candiduria, blastomycosis, coccidioidomycosis, histoplasmosis, chromomycosis, and paracoccidioidomycosis. |
| Pharmacodynamics | Ketoconazole, like clotrimazole, fluconazole, itraconazole, and miconazole, is an imidazole antifungal agent. |
| Mechanism of action | Ketoconazole interacts with 14-α demethylase, a cytochrome P-450 enzyme necessary for the conversion of lanosterol to ergosterol. This results in inhibition of ergosterol synthesis and increased fungal cellular permeability. Other mechanisms may involve the inhibition of endogenous respiration, interaction with membrane phospholipids, inhibition of yeast transformation to mycelial forms, inhibition of purine uptake, and impairment of triglyceride and/or phospholipid biosynthesis. Ketoconazole can also inhibit the synthesis of thromboxane and sterols such as aldosterone, cortisol, and testosterone. |
| Absorption | Moderate |
| Volume of distribution | Not Available |
| Protein binding | 99% (in vitro, plasma protein binding) |
| Metabolism | Hepatic |
| Route of elimination | Not Available |
| Half life | 2 hours |
| Clearance | Not Available |
| Toxicity | Hepatotoxicity, LD50=86 mg/kg (orally in rat) |