Home>>Lipids>> Cyclooxygenase>>15-keto Latanoprost (free acid)

15-keto Latanoprost (free acid) Sale

(Synonyms: 15-酮基拉坦前列素酸) 目录号 : GC40989

An analytical standard

15-keto Latanoprost (free acid) Chemical Structure

Cas No.:369585-22-8

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Sample solution is provided at 25 µL, 10mM.

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Quality Control & SDS

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产品描述

15-keto Latanoprost is a potential metabolite of latanoprost when administered to animals. 15-keto Latanoprost is also one of the common minor impurities found in commercial preparations of the bulk drug compound. Although much less potent that the parent compound latanoprost, 15-keto latanoprost still retains the ability to produce a small but measurable decrease (1 mm Hg) in the intraocular pressure of normal cynomolgus monkeys when administered at a dose of 1 µg/eye. 15-keto Latanoprost is also a miotic in the normal cat eye, causing an 8 mm Hg reduction in pupillary diameter at 5 µg/eye. Again, this is not as potent as many other F-type prostaglandins; for example, prostaglandin F2α will produce this degree of miosis at a dose of less than 1 µg/eye.

Chemical Properties

Cas No. 369585-22-8 SDF
别名 15-酮基拉坦前列素酸
Canonical SMILES O[C@@H]1[C@H](C/C=C\CCCC(O)=O)[C@@H](CCC(CCC2=CC=CC=C2)=O)[C@H](O)C1
分子式 C23H32O5 分子量 388.5
溶解度 DMF: 50 mg/ml,DMSO: 33 mg/ml,DMSO:PBS (1:1): 500 µ g/ml,Ethanol: 50 mg/ml 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.574 mL 12.87 mL 25.74 mL
5 mM 0.5148 mL 2.574 mL 5.148 mL
10 mM 0.2574 mL 1.287 mL 2.574 mL
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Research Update

Corneal permeability to and ocular metabolism of phenyl substituted prostaglandin esters in vitro

Prostaglandins Leukot Essent Fatty Acids 1994 Apr;50(4):161-8.PMID:8022849DOI:10.1016/0952-3278(94)90139-2

The corneal permeability to and metabolism of four phenyl substituted prostaglandin analogues have been studied in vitro. Porcine corneas were mounted in incubation chambers dividing each chamber into an epithelial and endothelial side compartment. The analogues were added to incubation medium on the epithelial side. The permeability coefficients of 17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhDH100A), 15-keto-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA12), 13,14-dihydro-15-hydroxy (R, S)-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA34) and 13,14-dihydro-17-phenyl-18,19,20-trinor-PGF2 alpha-1-isopropyl ester (PhXA41) were determined to be in the range of 5.1-11.0 x 10(-6) cm x s-1. All analogues in the endothelial compartment had been hydrolysed to corresponding acids but any other metabolism of PhDH100A, PhXA34 and PhXA41 after 4 h of incubation was minimal. In contrast, PhXA12 free acid was extensively metabolised to the 13,14-dihydro metabolite. To investigate whether the porcine ocular tissues contain 15-hyroxyprostaglandin dehydrogenase (15-PGDH) activity, prostaglandin F2 alpha (PGF2 alpha) and PhDH100A were used as substrates. PGF2 alpha and the phenyl-substituted analogues were also tested for their capacity as substrate to 15-PGDH in general. The 15-PGDH activity was low in all ocular tissues. The capacity of various ocular tissues or purified 15-PGDH to metabolise PhDH100A was lower than with PGF2 alpha as substrate. PhXA34 and PhXA41 were found not to be metabolised by 15-PGDH. Thus, the phenyl substituted PG esters penetrated the cornea and in the process were hydrolysed to their corresponding acids. No appreciable further metabolism occurred except for PhXA12 which was reduced by delta 13-reductase.