OVA-E1 peptide, a variant antagonist of SIINFEKL [OVA (257-264)], elicits comparable activation of the p38 and JNK cascades in both mutant and wild-type thymocytes.
Resolvin E1 is an effective endogenous pro-resolving mediator of inflammation. Resolvin E1 has unique counterregulatory actions that inhibit PMN transendothelial migration. Resolvin E1 also acts as an effective inhibitor of leukocyte infiltration, dendrit
13,14-dihydro Prostaglandin E1 (13,14-dihydro PGE1) is a biologically active metabolite of PGE1 with comparable potency to the parent compound. It is an inhibitor of ADP-induced platelet aggregation in human PRP and washed platelets with IC50 values of 31 and 21 nM, respectively. 13,14-dihydro PGE1 is a slightly more potent inhibitor of ADP-induced human platelet aggregation than PGE1 which has an IC50 value of 40 nM. Also, 13,14-dihydro PGE1 was shown to activate adenylate cyclase in NCB-20 hybrid cells with a Kact value of 668 nM.
Prostaglandin E1 (PGE1), though not predominantly found in nature, plays a significant role in clinical treatments, addressing conditions such as peripheral occlusive vascular disease, erectile dysfunction, and neonatal cardiology issues. The metabolism of PGE1 primarily begins with the oxidation at C-15, producing 13,14-dihydro-15-keto PGE1 as its major metabolite. Alternatively, inhibiting this pathway or overwhelming it with too much PGE1 could potentially enhance the production of 2,3-dinor metabolites, like 2,3-dinor PGE1, though their biological activities remain unreported. Cayman Chemical stands out as a prominent provider of prostaglandins and their metabolites, uniquely manufacturing 2,3-dinor PGE1.
Prostaglandin E1 (PGE1), synthesized through cyclooxygenase-mediated metabolism of dihomo-γ-linolenic acid (DGLA), functions by inhibiting platelet aggregation (IC50= 40 nM) and enhancing vasodilation. Its analog, 13,14-dihydro-16,16-difluoro PGE1, and the metabolite, 13,14-dihydro PGE1, both retain similar anti-aggregatory properties to the original compound. The inclusion of two electron-withdrawing fluorine atoms in 13,14-dihydro-16,16-difluoro PGE1 is believed to increase molecular stability and potentially extend bioavailability by resisting hydrolytic degradation.
13,14-Dihydro-19(R)-hydroxy Prostaglandin E1 (13,14-dihydro-19(R)-hydroxy PGE1) is posited as a theoretical metabolite resulting from the action of ω-1 hydroxylase on 13,14-dihydro PGE1. Its biosynthesis and biological activity remain unreported in scientific literature.