| Indication | For the treatment of candidiasis (a yeast-like fungal infection) of the vulva and vagina. |
| Pharmacodynamics | Terconazole is a triazole antifungal agent available for intravaginal use. It is structurally related to imidazole-derivative antifungal agents, although terconazole and other triazoles have 3 nitrogens in the azole ring. By inhibiting the 14-alpha-demethylase (lanosterol 14-alpha-demethylase), Terconazole inhibits ergosterol synthesis. Depletion of ergosterol in fungal membrane disrupts the structure and many functions of fungal membrane leading to inhibition of fungal growth. |
| Mechanism of action | Terconazole may exert its antifungal activity by disrupting normal fungal cell membrane permeability. Terconazole and other triazole antifungal agents inhibit cytochrome P450 14-alpha-demethylase in susceptible fungi, which leads to the accumulation of lanosterol and other methylated sterols and a decrease in ergosterol concentration. Depletion of ergosterol in the membrane disrupts the structure and function of the fungal cell leading to a decrease or inhibition of fungal growth. |
| Absorption | Following intravaginal administration of terconazole in humans, absorption ranged from 5-8% in three hysterectomized subjects and 12-16% in two non-hysterectomized subjects with tubal ligations |
| Volume of distribution | Not Available |
| Protein binding | 94.9% |
| Metabolism | Systemically absorbed drug appears to be rapidly and extensively metabolized. Terconazole primarily undergoes oxidatative N- and O-dealkylation, dioxolane ring cleavage, and conjugation. |
| Route of elimination | Following oral (30 mg) administration of 14C-labelled terconazole, excretion of radioactivity was both by renal (32-56%) and fecal (47-52%) routes. |
| Half life | 6.9 hours (range 4.0-11.3) |
| Clearance | Not Available |
| Toxicity | The oral LD50 values were found to be 1741 and 849 mg/kg for the male and female in rat. |