Tafluprost is a prostaglandin analog with a high affinity for the fluoroprostaglandin (FP) receptor. It is indicated for reducing elevated intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension. In clinical studies, administration of tafluprost 0.0015% once daily to patients with open-angle glaucoma or ocular hypertension and a baseline IOP of 23 to 26 mmHg resulted in an IOP decrease of approximately 6 to 8 mmHg after 3 months and 5 to 8 mmHg after 6 months. A prospective, randomized, double-masked, parallel-group study compared the safety and efficacy of tafluprost to that of latanoprost over 24 months in patients with open-angle glaucoma or ocular hypertension. Both drugs caused a significant reduction in IOP that was maintained throughout the study period (-7.1 mmHg for tafluprost and -7.7 mmHg for latanoprost at 24 months). As with other prostaglandin analogs, tafluprost has been associated with changes to pigmented tissues including increased pigmentation of eyelashes, the iris, and periorbital tissue. Changes in iridal pigmentation may be permanent. Tafluprost was approved by the FDA in February 2012.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Ophthalmic Administration
-Tafluprost is for ophthalmic use only.
-Tilt the head back slightly and pull the lower eyelid down with the index finger to form a pouch. Squeeze one drop into the pouch and gently close the eyes for 1 to 2 minutes. Do not blink.
-To avoid contamination, do not touch the tip of the dropper to the eye, fingertips, or other surface. Tafluprost does not contain a preservative. Instruct patients to use immediately after opening and discard remaining contents from individual unit immediately after administration.
-The solution may be used concomitantly with other topical ophthalmic drug products to lower intraocular pressure. If more than one topical ophthalmic drug is being used, the drugs should be administered at least 5 minutes apart.
Macular edema (including cystoid macular edema) has been reported during therapy with ophthalmic prostaglandin analogs. The most common adverse effect associated with tafluprost use is conjunctival hyperemia (4% to 20%) in clinical trials. Other ocular adverse events reported during controlled clinical studies of tafluprost include ocular irritation/stinging (7%), ocular pruritus including allergic conjunctivitis (5%), cataracts (3%), xerophthalmia (3%), ocular pain (3%), and blurred vision (2%). In clinical trials, approximately 1% of patients discontinued tafluprost due to ocular adverse events. During post-marketing use of tafluprost and other ophthalmic prostaglandins, iritis, uveitis, and periorbital and lid changes including deepening of the eyelid sulcus have been observed.
Tafluprost ophthalmic solution may cause skin hyperpigmentation of the periorbital tissue (eyelid), iridal discoloration (manifested as increased pigmentation of the iris), and increased pigmentation of the eyelashes. Eyelash darkening and growth of eyelashes were reported at an incidence of 2%. Pigmentation changes are caused by an increase in the amount of melanosomes in melanocytes. The brown pigmentation around the pupil typically spreads concentrically towards the periphery of the iris and the entire iris or parts of the iris become more brownish. The change in iris color occurs slowly and may not be noticeable for several months to years. The pigmentation of the iris is expected to be permanent, while pigmentation of the periorbital tissue and eyelash changes have been reported to be reversible in some patients. The long-term effects of this hyperpigmentation are unknown; however, patients who develop noticeably increased iris pigmentation should receive regular ophthalmic exams. Nevi and freckles of the iris have not been reported to be affected by tafluprost therapy.
Common cold (4%) and urinary tract infection (2%) were reported during controlled clinical studies of tafluprost.
Headache was reported in 6% of patients during controlled clinical trials of tafluprost.
Cough was reported in 3% of patients during tafluprost clinical trials. Exacerbations of asthma and dyspnea were noted in post-marketing reports.
Use tafluprost with caution in the presence of active ocular inflammation (e.g., iritis, uveitis) because the inflammation may be exacerbated.
Use tafluprost with caution in patients with aphakia, pseudophakic patients with a torn posterior lens capsule, and patients with known risk factors for macular edema. Macular edema, including cystoid macular edema, has been reported during treatment with ophthalmic prostaglandin analogs.
The safety and efficacy of tafluprost have not been established in neonates, infants, children, or adolescents. According to the manufacturer, there are potential safety concerns related to increased pigmentation after long-term use.
There are no adequate and well-controlled studies of tafluprost in pregnant women, limited experience with latanoprost, another ophthalmic prostaglandin analog, in human pregnancy has not resulted in clinically significant risk to the fetus. In addition, the mean plasma concentrations of tafluprost after ophthalmic administration were below the limit of quantification, suggesting exposure to the fetus is low. According to the manufacturer, tafluprost should not be administered during pregnancy unless the potential benefit justifies the potential risk to the fetus; the manufacturer also recommends that females of childbearing age or potential have adequate contraceptive measures in place.
It is not known whether tafluprost is excreted in human milk. There is minimal systemic absorption of tafluprost after ophthalmic administration; therefore, clinically significant amounts of the drug are not expected to be bioavailable to a nursing infant via breast-milk. To further minimize the amount of drug that reaches the systemic circulation and breast milk, apply pressure over the tear duct by the corner of the eye for 1 minute after ophthalmic administration. According to the manufacturer, caution should be exercised when it is administered to a breast-feeding woman. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition.
For the reduction of increased intraocular pressure in patients with open-angle glaucoma or ocular hypertension.:
Ophthalmic dosage:
Adults: Instill 1 drop in the conjunctival sac of the affected eye(s) once daily in the evening. More frequent administration may decrease the IOP-lowering effect.
Maximum Dosage Limits:
-Adults
1 drop/day in each affected eye.
-Geriatric
1 drop/day in each affected eye.
-Adolescents
Safety and efficacy have not been established.
-Children
Safety and efficacy have not been established.
-Infants
Safety and efficacy have not been established.
-Neonates
Safety and efficacy have not been established.
Patients with Hepatic Impairment Dosing
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
*non-FDA-approved indication
There are no drug interactions associated with Tafluprost products.
Tafluprost acid, a prostaglandin analog that acts as a selective agonist at the fluoroprostaglandin (FP) prostanoid receptor, is believed to reduce intraocular pressure by increasing uveoscleral outflow. The exact mechanism of action of tafluprost is unknown.
Tafluprost is administered topically to the eye. It is an ester prodrug and is hydrolyzed to its biologically active acid metabolite, tafluprost acid, in the eye. The acid metabolite is further metabolized via fatty acid beta-oxidation and phase II conjugation.
Affected cytochrome P450 (CYP450) isoenzymes and drug transporters: none
-Route-Specific Pharmacokinetics
Other Route(s)
Ophthalmic Route
After ocular administration, tafluprost is absorbed through the cornea. After administration of one drop of tafluprost 0.0015%, peak plasma concentrations of tafluprost acid are achieved within 10 minutes. In healthy volunteers, the mean plasma Cmax of tafluprost acid were 26 pg/mL on day 1 and 27 pg/mL on day 8. Reduction of intraocular pressure begins approximately 2 to 4 hours after the first dose with the maximum effect occurring in about 12 hours. Tafluprost concentrations were undetectable in plasma 30 minutes after ocular administration (limit of quantification, 10 pg/mL).