Prostaglandin F1α

Prostaglandin F1α (PGF1α) is the putative metabolite of dihomo-γ-linolenic acid (DGLA) via the cyclooxygenase (COX) pathway. Both PGF1α and PGF2α have been shown to act as priming pheromones for male Atlantic salmon with a threshold concentration of 10-11 M. [1] PGF1α binds to the ovine corpus luteum FP receptor at only 8% of the relative potency of PGF2α. [2] It is only half as active as PGF2α in inducing human respiratory smooth muscle contractions in vitro. [3]

13,14-dihydro-15-keto Prostaglandin F1α (13,14-dihydro-15-keto PGF1α) is a metabolite of PGF1α that has been reported in the rat stomach. The measurement of 13,14-dihydro-15-keto PGF1α can be used as a marker of the in vivo production of PGF1α.

8-iso Prostaglandin F1α is an isoprostaglandin produced from arachidonic acid that induces concentration-dependent vasoconstrictor effects in pulmonary arteries (PA), pulmonary veins (PV) and mesenteric arteries (MA) through activation of TXA2R, tyrosine kinases and Rho kinases.

6,15-diketo-13,14-dihydro PGF1α is a metabolite of PGI2. It was shown to enhance intracellular cAMP and cholesterol catabolism in bovine arterial smooth muscle cells.

11-deoxy PGF1α is a synthetic analog of PGF1α. In whole animal studies, a dose of 32 mg/kg inhibited gastric acid secretion by 35%. 11-deoxy PGF1α is also known to cause rat uterine contractions at a dose 0.3 times that of PGF1α. It also exhibits vasopressor and bronchoconstrictor activities at about half the potency of PGF2α in guinea pigs.

15-keto PGF1α is the initial metabolite of PGF1α via 15-hydroxy PGDH. In mammals, oxidation of C-15 markedly attenuates receptor binding and activity. In fish, the 15-keto compounds serve as post-ovulatory pheromones and are more active than the parent prostaglandins.

2,3-Dinor-8-iso Prostaglandin F1α (2,3-dinor-8-iso PGF1α), an isoprostane and active metabolite of arachidonic acid deriving its formation from non-enzymatic free radical peroxidation, acts as an active metabolite of the platelet aggregation inhibitor 8-iso PGF2α. This compound exhibits vasoconstrictive properties in isolated porcine retinal and brain microvessels with EC50 values of 12.8 and 18.5 nM, respectively, yet it does not cause contraction in isolated rat aortic rings at a concentration of 31 µM. Further, at a concentration of 1 µM, it raises thromboxane B2 (TXB2) levels in isolated porcine brain slices, an effect reversible by thromboxane A synthase inhibitor CGS 12970, voltage-gated calcium channel inhibitor SKF 96365, or the nicotinic acetylcholine receptor (nAChR) antagonist α-conotoxin.

Δ17-6-keto Prostaglandin F1α (Δ17-6-keto PGF1α), a cyclooxygenase (COX) metabolite produced from eicosapentaenoic acid (EPA) in a variety of tissues including seminal vesicles, lungs, polymorphonuclear leukocytes, and ocular tissues, alongside other 3-series COX products from EPA such as PGF3α, PGE3, and thromboxane B3, is potentially linked to a lower occurrence of glaucoma in individuals consuming a marine-rich (EPA-rich) diet.

PGF1β, a biochemical compound, functions as a pivotal mediator in inflammatory processes and plays an integral role in uterine contractions. It exhibits significant regulatory effects on platelet aggregation and vasodilation, demonstrating its critical importance in cardiovascular health. Additionally, PGF1β contributes to the regulation of kidney function and electrolyte balance, illustrating its widespread impact across various physiological systems.

17-TFM-PGF1α (Compound 8) is a saturated prostaglandin analog. It exhibits a high affinity and receptor selectivity for the human prostaglandin F receptor (hFP receptor), with an EC50 of 85 nM.

Lornoxicam-d4 is intended for use as an internal standard for the quantification of lornoxicam by GC- or LC-MS. Lornoxicam is a COX inhibitor and non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory and analgesic properties. It inhibits production of thromboxane B2 from arachidonic acid in HEL human erythroleukemic cells, which endogenously express COX-1, as well as inhibits LPS-induced formation of prostaglandin F1α from arachidonic acid in Mono-Mac-6 cells, which endogenously express COX-2. Lornoxicam reduces LPS-induced production of nitric oxide and IL-6 in cell-based assays with IC50 values of 65 and 54 µM, respectively. It reduces carrageenan-induced paw edema in rats when administered intravenously at doses ranging from 0.1 to 9 mg kg. Formulations containing lornoxicam have been used in the management of postoperative pain.

5(6)-DiHET is a racemic compound synthesized through the action of epoxide hydrolases on 5(6)-EET, encompassing both enantiomeric forms. It serves as a quantitative marker for 5(6)-EET, facilitating its measurement by utilizing the compound's conversion to 5(6)-δ-lactone in solution. Additionally, 5(6)-DiHET activates large-conductance calcium-activated potassium (KCa1.1/BK) channels in rat small coronary artery smooth muscle cells, supporting its biological significance in vascular regulation. It also acts as a substrate for sheep seminal vesicle COX, leading to the in vitro production of 5,6-dihydroxy prostaglandin E1 and F1α metabolites. Notably, its levels diminish in the plasma of rats subjected to a high-fat diet, indicating a potential role in the pathophysiology of hyperlipidemia.

9-Keto Fluprostenol Isopropyl Ester, an ester derivative of the FP receptor agonist fluprostenol, undergoes oxidation at carbon 9. This compound serves as a potential prodrug for 9-keto fluprostenol, which may function as an agonist at EP receptors. Additionally, it is considered a possible metabolite of fluprostenol isopropyl ester (travoprost), drawing parallels to the metabolism of latanoprost by 15-hydroxyprostaglandin dehydrogenase observed in monkey cornea. Furthermore, certain F-series prostaglandins, such as 6-keto prostaglandin F1α (PGF1α), undergo conversion to their E-series counterparts in isolated human platelets, highlighting a metabolic pathway of relevance.