Comparative Pharmacology
Head-to-head clinical analysis: BIMATOPROST versus TRAVATAN Z.
Peer-Reviewed Evidence
Head-to-head clinical analysis: BIMATOPROST versus TRAVATAN Z.
BIMATOPROST vs TRAVATAN Z
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Bimatoprost is a synthetic prostamide analog that selectively mimics the effects of prostamide F2α. It binds to prostaglandin F (FP) receptors on ciliary muscle cells and trabecular meshwork cells, increasing uveoscleral outflow and possibly trabecular outflow of aqueous humor, thereby reducing intraocular pressure. It also directly stimulates the prostaglandin FP receptor, leading to increased matrix metalloproteinase activity and remodeling of the extracellular matrix in the ciliary body.
Selective FP prostanoid receptor agonist; increases uveoscleral outflow of aqueous humor by binding to FP receptors in the ciliary muscle and trabecular meshwork, leading to matrix metalloproteinase activation and remodeling of extracellular matrix.
One drop of 0.01% or 0.03% ophthalmic solution instilled into the affected eye(s) once daily in the evening.
One drop in the affected eye(s) once daily in the evening. Ophthalmic solution 0.004% (travoprost 0.04 mg/mL).
None Documented
None Documented
Clinical Note
moderateBimatoprost + Unoprostone
"Bimatoprost may increase the hypotensive activities of Unoprostone."
Clinical Note
moderateBimatoprost + Hydrochlorothiazide
"Bimatoprost may increase the hypotensive activities of Hydrochlorothiazide."
Clinical Note
moderateBimatoprost + Epoprostenol
"Bimatoprost may increase the hypotensive activities of Epoprostenol."
Clinical Note
moderateVardenafil + Bimatoprost
"Vardenafil may increase the antihypertensive activities of Bimatoprost."
Terminal half-life: ~45 minutes (intravenous); after topical ocular administration, systemic half-life is similar due to rapid systemic clearance, with clinical effect lasting 24 hours due to ocular tissue binding
Terminal elimination half-life is 45 minutes; due to rapid hydrolysis to active acid, the clinical effect duration is longer than the half-life suggests.
Renal: <67% (unchanged and metabolites), Biliary/fecal: ~25%
Primarily eliminated via hepatic metabolism; renal excretion of metabolites accounts for approximately 20% of the dose; fecal excretion is minimal.
Category C
Category C
Prostaglandin Analog
Prostaglandin Analog