Description
PGE1 is produced by the metabolism of dihomo-γ-linolenic acid (DGLA) by the cyclooxygenase pathway. PGE1 inhibits platelet aggregation (IC50 = 40 nM) and increases vasodilation.1,213,14-dihydro-16,16-difluoro PGE1 is a biologically active metabolite of PGE1, inhibiting platelet aggregation with comparable potency to the parent compound.3,2 The addition of two electron-withdrawing fluorine atoms, which should stabilize the molecule against hydrolytic cleavage, may be expected to delay degradation in vivo.4 13,14-dihydro-15(R,S)-hydroxy-16,16-difluoro PGE1-3,3’,4,4’-d4) contains four deuterium atoms at the 3, 3’, 4, and 4’ positions. It is intended for use as an internal standard for the quantification of 13,14-dihydro-15(R,S)-hydroxy-16,16-difluoro Prostaglandin E1 by GC- or LC-mass spectrometry (MS).WARNING This product is not for human or veterinary use.
References
[1] I. JÄRVING. ANTIAGGREGATING POTENCY OF E-TYPE PROSTAGLANDINS IN HUMAN AND RABBIT PLATELETS[J]. Proceedings of the Estonian Academy of Sciences. Chemistry, 1991, 32 1. DOI:
10.3176/chem.1991.3.09[2] WESTWICK J. The effect of pulmonary metabolites of prostaglandins E1, E2 and F2alpha on ADP-induced aggregation of human and rabbit platelets [proceedings].[J]. British Journal of Pharmacology, 1976, 58 2: 297P-298P.
[3] B A PESKAR. On the metabolism of prostaglandin E1 administered intravenously to human volunteers.[J]. Journal of Physiology and Pharmacology, 1991, 42 3: 327-331.
[4] Y HATANO. Vascular relaxing activity and stability studies of 10,10-difluoro-13,14-dehydroprostacyclin.[J]. Proceedings of the National Academy of Sciences of the United States of America, 1980, 77 11: 6846-6850. DOI:
10.1073/pnas.77.11.6846
