Terbinafine clinical pharmacology: Difference between revisions
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==Clinical Pharmacology== | |||
<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = TERBINAFINE (TERBINAFINE HYDROCHLORIDE) TABLET [AUROBINDO PHARMA LIMITED] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=6600e2b3-65df-4fc3-8081-d574537d27e3 | publisher = | date = | accessdate = }}</ref> | ===Mechanism of Action=== | ||
Terbinafine is an allylamine antifungal. | |||
===Pharmacodynamics=== | |||
The pharmacodynamics of terbinafine tablets is unknown. | |||
===Pharmacokinetics=== | |||
Following oral administration, terbinafine is well absorbed (>70%) and the bioavailability of terbinafine tablets as a result of first-pass metabolism is approximately 40%. Peak plasma concentrations of 1 mcg/mL appear within 2 hours after a single 250 mg dose; the AUC is approximately 4.56 mcg•h/mL. An increase in the AUC of terbinafine of less than 20% is observed when terbinafine tablets are administered with food. | |||
In plasma, terbinafine is >99% bound to plasma proteins and there are no specific binding sites. At steady-state, in comparison to a single dose, the peak concentration of terbinafine is 25% higher and plasma AUC increases by a factor of 2.5; the increase in plasma AUC is consistent with an effective half-life of ~36 hours. Terbinafine is distributed to the sebum and skin. A terminal half-life of 200 to 400 hours may represent the slow elimination of terbinafine from tissues such as skin and adipose. Prior to excretion, terbinafine is extensively metabolized by at least 7 CYP isoenzymes with major contributions from CYP2C9, CYP1A2, CYP3A4, CYP2C8, and CYP2C19. No metabolites have been identified that have antifungal activity similar to terbinafine. Approximately 70% of the administered dose is eliminated in the urine. In patients with renal impairment (creatinine clearance ≤50 mL/min) or hepatic cirrhosis, the clearance of terbinafine is decreased by approximately 50% compared to normal volunteers. No effect of gender on the blood levels of terbinafine was detected in clinical trials. No clinically relevant age-dependent changes in steady-state plasma concentrations of terbinafine have been reported.<ref name="dailymed.nlm.nih.gov">{{Cite web | last = | first = | title = TERBINAFINE (TERBINAFINE HYDROCHLORIDE) TABLET [AUROBINDO PHARMA LIMITED] | url = http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=6600e2b3-65df-4fc3-8081-d574537d27e3 | publisher = | date = | accessdate = }}</ref> | |||
==References== | ==References== | ||
Latest revision as of 23:49, 7 January 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, M.D. [2]
Clinical Pharmacology
Mechanism of Action
Terbinafine is an allylamine antifungal.
Pharmacodynamics
The pharmacodynamics of terbinafine tablets is unknown.
Pharmacokinetics
Following oral administration, terbinafine is well absorbed (>70%) and the bioavailability of terbinafine tablets as a result of first-pass metabolism is approximately 40%. Peak plasma concentrations of 1 mcg/mL appear within 2 hours after a single 250 mg dose; the AUC is approximately 4.56 mcg•h/mL. An increase in the AUC of terbinafine of less than 20% is observed when terbinafine tablets are administered with food. In plasma, terbinafine is >99% bound to plasma proteins and there are no specific binding sites. At steady-state, in comparison to a single dose, the peak concentration of terbinafine is 25% higher and plasma AUC increases by a factor of 2.5; the increase in plasma AUC is consistent with an effective half-life of ~36 hours. Terbinafine is distributed to the sebum and skin. A terminal half-life of 200 to 400 hours may represent the slow elimination of terbinafine from tissues such as skin and adipose. Prior to excretion, terbinafine is extensively metabolized by at least 7 CYP isoenzymes with major contributions from CYP2C9, CYP1A2, CYP3A4, CYP2C8, and CYP2C19. No metabolites have been identified that have antifungal activity similar to terbinafine. Approximately 70% of the administered dose is eliminated in the urine. In patients with renal impairment (creatinine clearance ≤50 mL/min) or hepatic cirrhosis, the clearance of terbinafine is decreased by approximately 50% compared to normal volunteers. No effect of gender on the blood levels of terbinafine was detected in clinical trials. No clinically relevant age-dependent changes in steady-state plasma concentrations of terbinafine have been reported.[1]
References
Adapted from the FDA Package Insert.