Contains four deuterium atoms at the 3, 3′, 4, and 4′ positions. Intended for use as an internal standard for the quantification of 11β-PGF2α by GC- or LC-mass spectrometry. The primary plasma metabolite of PGD2 in vivo.1 Normal human urinary excretion of 11β-PGF2α is about 54 ng/mmol creatinine, which is increased nearly 3-fold during allergen-induced bronchoconstriction in asthmatics.2 It is equipotent to PGF2α in inducing human bronchial smooth muscle contractions and inhibition of adipose differentiation.3,4 11β-PGF2α inhibits ADP or thrombin-induced human platelet aggregation at concentrations of 0.14 to 2.8 µM.5
11β-Prostaglandin F2α-d4 (CAS 1240398-18-8) References
1 Liston, T.E., Roberts, L.J. Transformation of prostaglandin D2 to 9α,11β-(15S)-trihydroxy-prosta-(5Z,13E)-dien-1-oic acid (9α,11β-prostaglandin F2): A unique biologically active prostaglandin produced enzymatically in vivo in humans. Proc Natl Acad Sci USA 82 6030-6034 (1985). 2 O'Sullivan, S., Dahlén, B., Dahlén, S., et al. Increased urinary excretion of the prostaglandin D2 metabolite 9α,11β-prostaglandin F2 after aspirin challenge supports mast cell activation in aspirin-induced airway obstruction. J Allergy Clin Immunol 98 421-432 (1996). 3 Coleman, R.A., Sheldrick, R.L.G. Prostanoid-induced contraction of human bronchial smooth muscle is mediated by TP-receptors. Br J Pharmacol 96 688-692 (1989). 4 Lepak, N.M., Serrero, G. Inhibition of adipose differentiation by 9α, 11β-prostaglandins F2α Prostaglandins 46, 511-517 (1993). 5 Pugliese, G., Spokas, E.G., Marcinkiewicz, E., et al. Hepatic transformation of prostaglandin D2 to a new prostanoid, 9α,11β-prostaglandin F2, that inhibits platelet aggregation and constricts blood vessels. J Biol Chem 260 14621-14625 (1985)