FP receptor
Travoprost has affinity for the IP, TP, DP, EP1, EP3, and EP4 receptors that is sub-micromolar[1].
Travoprost is a potent and selective agonist of the prostaglandin FP receptor. The active form, travoprost acid, binds to the human FP receptor with a Ki of 52 ± 2 nM. [1]
Travoprost acid exhibits high selectivity over other prostanoid receptors, with Ki values >1,000 nM for DP, EP₁, EP₃, EP₄, IP, and TP receptors. [1]

Travoprost has affinity for the IP, TP, DP, EP1, EP3, and EP4 receptors that is sub-micromolar[1].

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In radioligand binding assays using bovine corpus luteum membranes, travoprost acid demonstrated high affinity for the FP receptor with a Ki of 52 ± 2 nM, which was superior to PGF₂α (Ki = 129 ± 12 nM) and latanoprost acid (Ki = 92 ± 14 nM). [1]
In functional assays measuring inositol phosphate synthesis in Swiss 3T3 fibroblasts (which express functional FP receptors), travoprost acid acted as a full agonist with an EC₅₀ of 2.7 ± 0.28 nM and an Emax of 100% (relative to natural ligand). This potency was greater than that of PGF₂α (EC₅₀ = 24.5 ± 9.2 nM) and latanoprost acid (EC₅₀ = 34.4 ± 5.2 nM). [1]
Travoprost acid showed no agonist activity (up to 10 µM) in stimulating adenylate cyclase via DP, EP₂, EP₄, or IP receptors, nor did it stimulate TP receptor-mediated phosphoinositide turnover. [1]
In a broad screening panel of over 32 non-prostanoid receptors (including muscarinic, α-adrenergic, β-adrenergic, and endothelin receptors), travoprost acid showed no affinity at concentrations up to 10 µM. [1]

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In radioligand binding assays using bovine corpus luteum membranes, travoprost acid demonstrated high affinity for the FP receptor with a Ki of 52 ± 2 nM, which was superior to PGF₂α (Ki = 129 ± 12 nM) and latanoprost acid (Ki = 92 ± 14 nM). [1]
In functional assays measuring inositol phosphate synthesis in Swiss 3T3 fibroblasts (which express functional FP receptors), travoprost acid acted as a full agonist with an EC₅₀ of 2.7 ± 0.28 nM and an Emax of 100% (relative to natural ligand). This potency was greater than that of PGF₂α (EC₅₀ = 24.5 ± 9.2 nM) and latanoprost acid (EC₅₀ = 34.4 ± 5.2 nM). [1]
Travoprost acid showed no agonist activity (up to 10 µM) in stimulating adenylate cyclase via DP, EP₂, EP₄, or IP receptors, nor did it stimulate TP receptor-mediated phosphoinositide turnover. [1]
In a broad screening panel of over 32 non-prostanoid receptors (including muscarinic, α-adrenergic, β-adrenergic, and endothelin receptors), travoprost acid showed no affinity at concentrations up to 10 µM. [1]

At a dose of 1 μg, travoprost causes less ocular irritation in the New Zealand albino (NZA) rabbit than PGF20 isopropyl ester. Travoprost applied topically to the eyes causes a noticeable miotic effect in cats after doses of 0.01, 0.03, and 0.1 μg. Applying 0.1 and 0.3 μg of travoprost orally every day resulted in a peak reduction of 22.7% and 28.6% in intraocular pressure (IOP) in the ocular hypertensive monkey. Travoprost applied topically to rabbits, cats, and monkeys did not result in ocular irritation or discomfort at doses up to 1 μg[1].

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Topical ocular application of travoprost (0.01%, 0.001%) in New Zealand Albino (NZA) rabbits resulted in a significantly lower incidence and severity of conjunctival hyperemia, swelling, and ocular discharge compared to PGF₂α isopropyl ester (0.001%). [1]
In normotensive cats, travoprost (0.01, 0.03, and 0.1 µg) produced a dose-dependent miotic (pupil-constricting) response, characteristic of FP receptor agonists. The effect was more pronounced than that of equimolar doses of latanoprost or PGF₂α isopropyl ester, based on the area under the pupil diameter change curve (AUC). No ocular irritation was observed. [1]
In conscious cynomolgus monkeys with ocular hypertension (induced by laser trabeculoplasty), bilateral topical application of travoprost (0.1 and 0.3 µg, twice daily) produced a dose-dependent reduction in intraocular pressure (IOP). The 0.3 µg dose produced a peak IOP reduction of approximately 28.6%, sustained over 16 hours, without a preceding transient IOP increase. The 0.1 µg dose also showed sustained IOP reduction (18-22%) with repeated dosing. No miosis or ocular irritation was observed in monkeys. [1]

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Topical ocular application of travoprost (0.01%, 0.001%) in New Zealand Albino (NZA) rabbits resulted in a significantly lower incidence and severity of conjunctival hyperemia, swelling, and ocular discharge compared to PGF₂α isopropyl ester (0.001%). [1]
In normotensive cats, travoprost (0.01, 0.03, and 0.1 µg) produced a dose-dependent miotic (pupil-constricting) response, characteristic of FP receptor agonists. The effect was more pronounced than that of equimolar doses of latanoprost or PGF₂α isopropyl ester, based on the area under the pupil diameter change curve (AUC). No ocular irritation was observed. [1]
In conscious cynomolgus monkeys with ocular hypertension (induced by laser trabeculoplasty), bilateral topical application of travoprost (0.1 and 0.3 µg, twice daily) produced a dose-dependent reduction in intraocular pressure (IOP). The 0.3 µg dose produced a peak IOP reduction of approximately 28.6%, sustained over 16 hours, without a preceding transient IOP increase. The 0.1 µg dose also showed sustained IOP reduction (18-22%) with repeated dosing. No miosis or ocular irritation was observed in monkeys. [1]

Travoprost is the isopropyl ester prodrug of a high affinity, selective FP prostaglandin full receptor agonist. In contrast to travoprost acid's high affinity and efficacy at the FP receptor, there is only sub-micromolar affinity for the DP, EP1, EP3, EP4, IP, and TP receptors[1].

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FP Receptor Binding Assay: Washed total particulate membranes from bovine corpus luteum (final concentration 20 mg/ml) were incubated with [³H]PGF₂α (0.9–1.5 nM) in Krebs buffer (pH 7.4) for 2 hours at 23°C in a total volume of 500 µl. Non-specific binding was defined using 1–10 µM unlabeled PGF₂α or cloprostenol. The incubation was terminated by rapid vacuum filtration through glass fiber filters pre-soaked in 0.3% polyethyleneimine (PEI). Receptor-bound radioactivity was determined by scintillation spectrometry, and Ki values were calculated from competition curves using nonlinear curve-fitting software. [1]
DP, EP₁, EP₃, EP₄, IP, TP Receptor Binding Assays: Similar membrane-based radioligand binding assays were performed for other prostanoid receptors using specific cell membranes (e.g., human platelet membranes for DP, IP, TP; HEK-293 cell membranes expressing recombinant human EP₁/EP₄; bovine corpus luteum membranes for EP₃) and corresponding tritiated ligands ([³H]PGD₂, [³H]PGE₂, [³H]SQ29548, [³H]iloprost). Incubation conditions (time, temperature, buffer) varied by assay. Non-specific binding was defined with excess unlabeled corresponding ligand. Assays were terminated by vacuum filtration, and data were analyzed similarly. [1]

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FP Receptor Binding Assay: Washed total particulate membranes from bovine corpus luteum (final concentration 20 mg/ml) were incubated with [³H]PGF₂α (0.9–1.5 nM) in Krebs buffer (pH 7.4) for 2 hours at 23°C in a total volume of 500 µl. Non-specific binding was defined using 1–10 µM unlabeled PGF₂α or cloprostenol. The incubation was terminated by rapid vacuum filtration through glass fiber filters pre-soaked in 0.3% polyethyleneimine (PEI). Receptor-bound radioactivity was determined by scintillation spectrometry, and Ki values were calculated from competition curves using nonlinear curve-fitting software. [1]
DP, EP₁, EP₃, EP₄, IP, TP Receptor Binding Assays: Similar membrane-based radioligand binding assays were performed for other prostanoid receptors using specific cell membranes (e.g., human platelet membranes for DP, IP, TP; HEK-293 cell membranes expressing recombinant human EP₁/EP₄; bovine corpus luteum membranes for EP₃) and corresponding tritiated ligands ([³H]PGD₂, [³H]PGE₂, [³H]SQ29548, [³H]iloprost). Incubation conditions (time, temperature, buffer) varied by assay. Non-specific binding was defined with excess unlabeled corresponding ligand. Assays were terminated by vacuum filtration, and data were analyzed similarly. [1]

The ability of a number of prostaglandin F 2 alpha (PGF 2 alpha) analogs to mobilize intracellular Ca2+[Ca2+]iand to compete for [3H]PGF 2 alpha binding to prostaglandin F 2 alpha receptors (FP) was evaluated. Radioligand binding studies measuring displacement of [3H]PGF 2 alpha by a variety of FP prostaglandin analogs yielded the following rank order of affinities: travoprost acid [(+)-16-m-trifluorophenoxy tetranor PGF 2 alpha; (+)-fluprostenol] > bimatoprost acid (17-phenyl-trinor PGF 2 alpha) >> unoprostone (13,14-dihydro-15-keto-20-ethyl PGF 2 alpha) = bimatoprost (17-phenyl-trinor PGF 2 alpha ethyl amide) > or = Lumigan (bimatoprost ophthalmic solution). In FP functional studies, travoprost acid (EC50= 17.5-37 nM, n = 13), bimatoprost acid (EC50= 23.3-49.0 nM, n = 6-12), unoprostone (EC50= 306-1270 nM, n = 4-8), bimatoprost (EC50= 3070- 3940 nM, n = 4-9), and Lumigan (EC50= 1470-3190 nM, n = 5-9) concentration dependently stimulated [Ca2+]imobilization via the rat (A7r5 cells), mouse (3T3 cells), and cloned human ocular FP prostanoid receptors. The rank order of potency of these compounds at the FP receptor of the three species was similar and in good agreement with the determined binding affinities. The agonist effects of these compounds were concentration dependently blocked by the FP receptor-selective antagonist, AL-8810 (11beta-fluoro-15-epi-15-indanyl-tetranor PGF 2 alpha) (Ki= 0.6-1.3 microM). These studies have demonstrated that bimatoprost, unoprostone, and bimatoprost acid possess direct agonist activities at the rat, mouse, and human FP prostanoid receptor and that travoprost acid is the most potent of the synthetic FP prostaglandin analogs tested[2].

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FP Receptor Functional Assay (Phosphoinositide Turnover): Confluent Swiss 3T3 fibroblasts were loaded with [³H]-myo-inositol (1.0–1.5 µCi in 0.5 ml DMEM) for 24–30 hours at 37°C. Cells were then rinsed and pre-incubated with DMEM/F-12 medium containing 10 mM LiCl. They were subsequently exposed to the test agonist or vehicle in the same LiCl-containing medium for 60 minutes at 37°C. The reaction was stopped by adding ice-cold 0.1 M formic acid. Total [³H]-inositol phosphates ([³H]-IPs) were extracted from cell lysates using anion exchange chromatography (AG 1-X8 resin columns), eluted with ammonium formate solutions, and quantified by scintillation counting. [1]
DP, EP₂, EP₄, IP Receptor Functional Assay (Adenylyl Cyclase Stimulation): Cells expressing specific receptors (e.g., embryonic bovine tracheal fibroblasts for DP, human non-pigmented ciliary epithelial cells for EP₂, CHO cells for EP₄, NCB-20 cells for IP) were grown to confluence. Cells were rinsed and pre-incubated for 20 minutes with DMEM/F-12 medium containing 1 mM isobutyl methylxanthine (IBMX) and 0.8 mM ascorbate. They were then exposed to agonists for 15 minutes at 23°C. The reaction was terminated with ice-cold acetic acid, neutralized, and intracellular cAMP levels were quantified using a standard radioimmunoassay (RIA) kit. [1]

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FP Receptor Functional Assay (Phosphoinositide Turnover): Confluent Swiss 3T3 fibroblasts were loaded with [³H]-myo-inositol (1.0–1.5 µCi in 0.5 ml DMEM) for 24–30 hours at 37°C. Cells were then rinsed and pre-incubated with DMEM/F-12 medium containing 10 mM LiCl. They were subsequently exposed to the test agonist or vehicle in the same LiCl-containing medium for 60 minutes at 37°C. The reaction was stopped by adding ice-cold 0.1 M formic acid. Total [³H]-inositol phosphates ([³H]-IPs) were extracted from cell lysates using anion exchange chromatography (AG 1-X8 resin columns), eluted with ammonium formate solutions, and quantified by scintillation counting. [1]
DP, EP₂, EP₄, IP Receptor Functional Assay (Adenylyl Cyclase Stimulation): Cells expressing specific receptors (e.g., embryonic bovine tracheal fibroblasts for DP, human non-pigmented ciliary epithelial cells for EP₂, CHO cells for EP₄, NCB-20 cells for IP) were grown to confluence. Cells were rinsed and pre-incubated for 20 minutes with DMEM/F-12 medium containing 1 mM isobutyl methylxanthine (IBMX) and 0.8 mM ascorbate. They were then exposed to agonists for 15 minutes at 23°C. The reaction was terminated with ice-cold acetic acid, neutralized, and intracellular cAMP levels were quantified using a standard radioimmunoassay (RIA) kit. [1]

Travoprost produced a lower incidence of ocular irritation than PGF20 isopropyl ester at a dose of 1 microg in the New Zealand albino (NZA) rabbit. Topical ocular application of travoprost produced a marked miotic effect in cats following doses of 0.01, 0.03 and 0.1 microg. In the ocular hypertensive monkey, b.i.d. application of 0.1 and 0.3 microg of travoprost afforded peak reduction in intraocular pressure (IOP) of 22.7% and 28.6%, respectively. Topical application of travoprost was well tolerated in rabbits, cats and monkeys, causing no ocular irritation or discomfort at doses up to 1 microg. Travoprost is a promising ocular hypotensive prostaglandin FP derivative that has the ocular hypotensive efficacy of PGF2alpha isopropyl ester but with less severe ocular side effects.[1]

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\n
\nAcute Ocular Irritation in NZA Rabbits: Travoprost was formulated in phosphate-buffered saline containing 0.01% polysorbate 80. A single 30 µL aliquot of the test formulation was instilled into both eyes of each rabbit (n=5 per group). Ocular irritation (conjunctival hyperemia, swelling, discharge) was evaluated biomicroscopically at 1, 2, 3, and 5 hours post-dose using the Hackett and McDonald scoring system. Data are reported qualitatively as the percent incidence of eyes with a score of +2 or greater. [1]
\nAcute Miotic Response in Normotensive Cats: Animals were restrained. Baseline horizontal pupil diameter (PD) was measured. A single 30 µL aliquot of travoprost formulation was instilled into one eye of each cat (n=6 per dose); the contralateral eye received vehicle. PD was measured at 0.5, 1, 1.5, 2, 2.5, 3, 4, and 5 hours post-dose. The area under the curve (AUC) for PD change from 1 to 5 hours was calculated. [1]
\nAcute IOP Response in Ocular Hypertensive Monkeys: Conscious cynomolgus monkeys with laser-induced ocular hypertension in the right eye were used. Travoprost (formulated as above) was administered topically as a single 30 µL aliquot to the lasered eye. A twice-daily (b.i.d.) dosing regimen was used over three days (0900 hr on Days 1, 2, 3; 1630 hr on Days 1, 2). IOP was measured using an applanation pneumatonometer under light corneal anesthesia at baseline and at selected time points post-dose (up to 7 hours after morning doses, and 16 hours after the last afternoon dose). Percent change from baseline IOP was calculated for statistical analysis. [1]
\n

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\nAcute Ocular Irritation in NZA Rabbits: Travoprost was formulated in phosphate-buffered saline containing 0.01% polysorbate 80. A single 30 µL aliquot of the test formulation was instilled into both eyes of each rabbit (n=5 per group). Ocular irritation (conjunctival hyperemia, swelling, discharge) was evaluated biomicroscopically at 1, 2, 3, and 5 hours post-dose using the Hackett and McDonald scoring system. Data are reported qualitatively as the percent incidence of eyes with a score of +2 or greater. [1]
\nAcute Miotic Response in Normotensive Cats: Animals were restrained. Baseline horizontal pupil diameter (PD) was measured. A single 30 µL aliquot of travoprost formulation was instilled into one eye of each cat (n=6 per dose); the contralateral eye received vehicle. PD was measured at 0.5, 1, 1.5, 2, 2.5, 3, 4, and 5 hours post-dose. The area under the curve (AUC) for PD change from 1 to 5 hours was calculated. [1]
\nAcute IOP Response in Ocular Hypertensive Monkeys: Conscious cynomolgus monkeys with laser-induced ocular hypertension in the right eye were used. Travoprost (formulated as above) was administered topically as a single 30 µL aliquot to the lasered eye. A twice-daily (b.i.d.) dosing regimen was used over three days (0900 hr on Days 1, 2, 3; 1630 hr on Days 1, 2). IOP was measured using an applanation pneumatonometer under light corneal anesthesia at baseline and at selected time points post-dose (up to 7 hours after morning doses, and 16 hours after the last afternoon dose). Percent change from baseline IOP was calculated for statistical analysis. [1]

Absorption, Distribution and Excretion
Following ophthalmic application, travoprost is absorbed via the cornea. In multiple-dose pharmacokinetic studies, many patients had plasma free acid concentrations below 0.01 ng/mL, which is the limit of quantitation for this assay. In these studies, the mean peak plasma concentration (Cmax) of travoprost free acid was 0.018 ± 0.007 ng/mL (range 0.01 to 0.052 ng/mL), with a time to peak concentration (Tmax) of approximately 30 minutes. Travoprost free acid is rapidly cleared from plasma. Within one hour of administration, the concentration of travoprost free acid is typically below the limit of quantitation. Less than 2% of the topical ophthalmic travoprost dose is excreted in the urine as travoprost free acid within 4 hours. [No further information available.]

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Metabolism/Metabolites
Travoprost is an isopropyl ester prodrug that is hydrolyzed by esterases in the cornea to its biologically active free acid. In vivo, travoprost free acid is metabolized to inactive metabolites via the following pathways: β-oxidation of the α-(carboxylic acid) chain to produce 1,2-dinomethyl and 1,2,3,4-tetranormethyl analogs; partial oxidation of the 15-hydroxyl group; and reduction of the 13,14 double bond.

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Biological Half-Life
The terminal elimination half-life of travoprost free acid was estimated in 14 subjects, ranging from 17 minutes to 86 minutes, with a mean half-life of 45 minutes.

Effects During Pregnancy and Lactation
◉ Overview of Medication Use During Lactation
There is currently no information regarding the use of travoprost during lactation. Due to its short half-life, it is unlikely to enter the infant's bloodstream and will not cause any adverse effects on breastfed infants. Professional guidelines consider the use of prostaglandin eye drops during lactation to be acceptable. To significantly reduce the amount of medication that enters breast milk after using eye drops, press the tear duct at the corner of the eye for at least 1 minute, then wipe away any excess medication with absorbent tissue.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
As of the revision date, no relevant published information was found.

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Protein Binding
No relevant information.

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In the described animal models (rabbit, cat, monkey), topical ocular doses up to 1 µg of travoprost were well tolerated without causing ocular irritation or discomfort. [1]
This study reported that travoprost had a lower incidence of ocular side effects (congestion, swelling) compared to PGF₂α isopropyl ester, which is attributed to its higher selectivity for FP receptors. [1]
In the described animal models (rabbit, cat, monkey), topical ocular doses up to 1 µg of travoprost were well tolerated without causing ocular irritation or discomfort. [1]
This study reported that travoprost had a lower incidence of ocular side effects (congestion, swelling) compared to PGF₂α isopropyl ester, which is attributed to its higher selectivity for FP receptors. [1]

[1]. Preclinical efficacy of travoprost, a potent and selective FP prostaglandin receptor agonist. J Ocul Pharmacol Ther. 2001 Oct;17(5):421-32.

[2]. Real-time intracellular Ca2+ mobilization by travoprost acid, bimatoprost, unoprostone, and other analogs via endogenous mouse, rat, and cloned human FP prostaglandin receptors. J Pharmacol Exp Ther . 2003 Jan;304(1):238-45.

Travoprost is an isopropyl ester of prostaglandin F2α, in which the pentyl group is replaced by 3-(trifluoromethyl)phenoxymethyl. As a synthetic analog of prostaglandin F2α, travoprost eye drops can be used topically to control the progression of open-angle glaucoma and ocular hypertension by lowering intraocular pressure. It is a prodrug; its isopropyl ester group is hydrolyzed in the cornea by esterases to the biologically active free acid, fluprostol. It has multiple functions, including antiglaucoma medication, antihypertensive drug, prodrug, ophthalmic drug, and prostaglandin receptor agonist. It belongs to the prostaglandin Fα, (trifluoromethyl)benzene, and isopropyl ester compounds. Functionally, it is related to fluprostol. Travoprost is a synthetic isopropyl ester prodrug, a prostaglandin F2α (F2α) analog, and a selective FP prostaglandin receptor agonist. It is used to lower intraocular pressure in patients with open-angle glaucoma and ocular hypertension. Unlike other prostaglandin analogs, travoprost exhibits complete agonistic activity and high selectivity towards prostaglandin receptors, resulting in greater efficacy in lowering intraocular pressure and a lower risk of off-target side effects. Travoprost is a prostaglandin analog. Travoprost is a synthetic lipophilic isopropyl ester prodrug of the active compound travoprost free acid, a prostaglandin F2α analog with anti-glaucoma properties. After administration, travoprost is hydrolyzed to free acid by corneal esterase, which then selectively stimulates prostaglandin F (FP prostaglandin) receptors, thereby increasing uveal-scleral outflow and leading to a decrease in intraocular pressure. Travoprost is a cloprostanol derivative used as an antihypertensive drug to treat open-angle glaucoma and ocular hypertension. Indications: Travoprost is indicated for lowering intraocular pressure in patients with open-angle glaucoma or ocular hypertension. It can also be used in children aged 2 months to 18 years.
Lowers intraocular pressure in adults with ocular hypertension or open-angle glaucoma (see Section 5.1). Used to lower intraocular pressure in children aged 2 months to <18 years with ocular hypertension or pediatric glaucoma (see Section 5.1).
Lowers intraocular pressure in adults with ocular hypertension or open-angle glaucoma (see Section 5.1). Used to lower intraocular pressure in children aged 3 years to <18 years with ocular hypertension or pediatric glaucoma.
Glaucomatosis Treatment

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Mechanism of Action
Travoprost is a prodrug. After administration, travoprost is absorbed through the cornea and hydrolyzed to its active metabolite—travoprost free acid. The ester group of the free acid allows it to penetrate more effectively into the aqueous humor. The exact mechanism of action of travoprost is not fully understood, but it is generally believed to be related to its complete agonistic activity against prostaglandin FP receptors. Travoprost free acid reduces intraocular pressure by binding to prostaglandin FP receptors, increasing aqueous humor outflow via the trabecular meshwork and uveal-scleral pathways. Pharmacodynamics: Travoprost has a preferential affinity for prostaglandin FP receptors and exhibits complete agonistic activity across the nanomolar concentration range. Travoprost has no significant affinity for other prostaglandin receptors or non-prostaglandin receptors. The reduction in intraocular pressure induced by travoprost is observed approximately two hours after administration, reaching its maximum effect after 12 hours. A single dose significantly reduces intraocular pressure, and the effect lasts for more than 24 hours. Travoprost (AL-6221) is an isopropyl ester prodrug of the selective FP prostaglandin agonist fluprostol, a single enantiomer. It is an analogue of PGF₂α isopropyl ester, in which carbon atoms 17-20 are substituted with m-trifluoromethylphenoxy groups. [1]
The research and development goal is to reduce related side effects, such as congestion, foreign body sensation, pain and photophobia, while maintaining the intraocular pressure-lowering efficacy of PGF₂α isopropyl ester. [1]
The miotic effect observed in cats confirms that the topically applied travoprost can penetrate into the anterior segment of the eye and hydrolyze into an active acid form. [1]
This study concludes that travoprost is a promising intraocular pressure-lowering drug with efficacy comparable to PGF₂α isopropyl ester, but with fewer ocular side effects due to its high selectivity for FP receptors. [1]

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Travoprost (AL-6221) is an isopropyl ester prodrug of the single enantiomer of the selective FP prostaglandin agonist fluoroprostol. It is an analog of PGF₂α isopropyl ester in which carbon atoms at positions 17-20 are replaced by m-trifluoromethylphenoxy. [1]
The research and development goal is to reduce related side effects, such as congestion, foreign body sensation, pain, and photophobia, while maintaining the intraocular pressure-lowering efficacy of PGF₂α isopropyl ester. [1] The miotic effect observed in cats confirms that topically applied travoprost can penetrate into the anterior segment of the eye and hydrolyze into its active acid form. [1] This study concludes that travoprost is a promising intraocular pressure-lowering drug with efficacy comparable to PGF₂α isopropyl ester, but with fewer ocular side effects due to its higher selectivity for FP receptors. [1]

C26H35F3O6

500.5477

500.24

C, 62.39; H, 7.05; F, 11.39; O, 19.18

157283-68-6

5,6-trans-Travoprost; 1563176-59-9

5282226

Colorless to light yellow liquid (Oil like)

1.0±0.1 g/cm3

237.5±9.0 °C at 760 mmHg

90.6±0.0 °C

0.1±0.5 mmHg at 25°C

1.545

3.17

3

9

13

35

693

5

FC(C1C([H])=C([H])C([H])=C(C=1[H])OC([H])([H])[C@@]([H])(/C(/[H])=C(\[H])/[C@@]1([H])[C@@]([H])(C([H])([H])[C@@]([H])([C@]1([H])C([H])([H])C([H])=C([H])C([H])([H])C([H])([H])C([H])([H])C(=O)OC([H])(C([H])([H])[H])C([H])([H])[H])O[H])O[H])O[H])(F)F

MKPLKVHSHYCHOC-AHTXBMBWSA-N

InChI=1S/C26H35F3O6/c1-17(2)35-25(33)11-6-4-3-5-10-21-22(24(32)15-23(21)31)13-12-19(30)16-34-20-9-7-8-18(14-20)26(27,28)29/h3,5,7-9,12-14,17,19,21-24,30-32H,4,6,10-11,15-16H2,1-2H3/b5-3-,13-12+/t19-,21-,22-,23+,24-/m1/s1

propan-2-yl (Z)-7-[(1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3R)-3-hydroxy-4-[3-(trifluoromethyl)phenoxy]but-1-enyl]cyclopentyl]hept-5-enoate

Fluprostenol isopropyl ester; AL6221; Flu-Ipr; Travatan; Travatan Z; Travoprost; Izba; AL-6221; Travaprost; Otx-tp;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Ethanol: ~60 mg/mL (~119.9 mM)
DMSO: ≥ 41.67 mg/mL (~83.3 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (4.16 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (4.16 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (4.16 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)