iNOS/PGE2-IN-1 is an iNOS/PGE2 inhibitor and a potent anti-inflammatory agent. iNOS/PGE2-IN-1 exhibits an inhibitory effect on LPS-induced NO production and has a low ulcerogenic potential.

11-Deoxy-16,16-dimethyl Prostaglandin E2 (11-deoxy-16,16-dimethyl PGE2) is a stable synthetic analog of Prostaglandin E2 (PGE2), acting as an agonist for both EP2 and EP3 receptors. It effectively inhibits gastric acid secretion and ulcer formation in rats, with ED50 values of 1 mg/kg and 0.021 mg/kg, respectively. This compound is also 900 times more potent than Prostaglandin F2α (PGF2α) in inducing contraction of human respiratory tract smooth muscle in vitro.

16,16-Dimethyl prostaglandin E2 is an orally active vertebrate Hematopoietic stem cells homeostasis critical regulator. It can act through EP2/EP4 and has an interaction with the Wnt pathway.

EP4 antagonist 14 is a prostaglandin E2 receptor subtype EP4 antagonist, demonstrating an IC50 of 1.1 nM in a HEK293 human receptor reporter assay and blocking β-arrestin recruitment due to PGE2 with an IC50 of 0.9 nM. At 10 µM, it reduces PGE2-stimulated mRNA levels of Il-4, macrophage mannose receptor 1 (Mrc1), chitinase-like protein 3 (Chil3), chemokine (C-X-C) motif ligand 1 (Cxcl1), triggering receptor expressed on myeloid cells 2 (Trem2), and arginase-1 (Arg1) in RAW 264.7 macrophages. When used at 30 mg/kg per day alongside anti-PD-1 antibodies, it curbs tumor growth and enhances CD8+ T cell infiltration in tumors using a CT26 murine colon cancer model.

Prostaglandin E2 (PGE2) inhibitor 3 is a selective inhibitor targeting microsomal prostaglandin E synthase-1 (mPGES-1; IC50 = 0.2 µM), demonstrating greater selectivity for mPGES-1 over COX-1, COX-2, 5-lipoxygenase (5-LO), and soluble epoxide hydrolase (sEH) in assays at 10 µM. This compound effectively reduces IL-1β-induced PGE2 production in A549 cells and decreases LPS-induced IL-6 and PGE2 in J774A.1 macrophages at concentrations of 10 and 1 µM, respectively. Additionally, it blocks the production of 5-LO-derived products, including leukotriene B4 (LTB4) and 5-H(p)ETE, in response to calcium ionophore A23187 alone or combined with arachidonic acid, with IC50 values of 4.9 and 5.2 µM, respectively. When administered in vivo at doses of 10 mg/kg, PGE2 inhibitor 3 effectively prevents leukocyte infiltration in a mouse model of zymosan-induced peritonitis.

19(R)-hydroxy Prostaglandin E2 (19(R)-hydroxy PGE2), present in the semen of primates, including humans, acts as a potent smooth muscle relaxant and is a selective agonist for the EP2 receptor. It exhibits an EC50 value of 200 nM for relaxing cat tracheal rings that express EP2 receptors.

20-Ethyl Prostaglandin E2 (20-ethyl PGE2) is an analog of Prostaglandin E2 (PGE2) characterized by an extended ω-chain due to two additional methylene carbon atoms. Compared to unoprostone, a clinically approved glaucoma medication and the only extensively studied prostaglandin analog sharing this structural modification, 20-ethyl PGE2 maintains the natural 15(S) allylic hydroxyl in its lower side chain, potentially enhancing its effectiveness. Unoprostone, despite being an F-series prostaglandin, exhibits reduced affinity for FP receptors because of its lower side chain modifications (13,14-dihydro-15-keto), which diminishes its medicinal potency. Notably, 20-ethyl PGE2's efficacy relative to unoprostone and its interaction with EP or other prostanoid receptors remains unconfirmed due to the lack of published ligand binding assays. E-type prostaglandins, including 20-ethyl PGE2, are broadly acknowledged for their inflammatory, cytoprotective, and diverse biological activities.

Prostaglandin E2 Serinol Amide acts as a weak inhibitor against the hydrolysis of [3H]2-oleoylglycerol, but it is non-hydrolyzable and cannot produce PGE2. Consequently, it is unable to inhibit leukotriene B4 biosynthesis, superoxide production, migration, and the release of antimicrobial peptides [1].

16-phenoxy tetranor PGE2, the free acid form of sulprostone, results from the hydrolysis of the methylsulfonamide bond. It is identified as a minor metabolite in human plasma following the parenteral administration of sulprostone.

15-keto-Prostaglandin E2, an endogenous metabolite, inhibits STAT3 activation through binding to Cys259 and regulates breast cancer cell growth and progression. Additionally, it binds and stabilizes the EP2 and EP4 receptors, activates PPAR-γ, and promotes fungal growth [1] [2] [3].

13,14-dihydro-15-keto Prostaglandin E2 (13,14-dihydro-15-keto PGE2) serves as the predominant metabolite of PGE2 in plasma, created through a 15-keto PGE2 intermediate by the action of 15-oxo-PG Δ13 reductase. Unlike its precursor PGE2, this compound exhibits poor binding affinity towards EP2 and EP4 PGE2 receptors (Ki values of 12 and 57 µM, respectively) in CHO cells and fails to stimulate adenylate cyclase activity therein (EC50s >18 and >38 µM, respectively). Concentrations of 13,14-dihydro-15-keto PGE2 are notably higher in the plasma of pregnant women during their third trimester and at labor and delivery stages, whereas its levels are found to be reduced in the tumor tissues of patients with non-small cell lung cancer (NSCLC) compared to adjacent healthy tissue.

17-Phenyl trinor Prostaglandin E2 (17-phenyl trinor PGE2) is a synthetic analog of PGE2, functioning as an agonist at the EP1 and EP3 receptors. It induces contraction of the guinea pig ileum at a 11 µM concentration and displays slightly less potency than PGE2 in stimulating the gerbil colon and rat uterus. Notably, with an ED50 value of 350 µg/kg, 17-phenyl trinor PGE2 exhibits 4.4 times greater antifertility efficacy in hamsters compared to PGE2.

Prostaglandin E2 (PGE2) is a naturally occurring hormone involved in a variety of physiological processes in the body, including smooth muscle contraction and relaxation, regulation of vasodilatation and constriction, regulation of blood pressure, and inflammatory regulation.

Prostaglandin E2 Ethanolamide (PGE 2 -EA), an analog of PGE2, is enzymatically synthesized through COX-2 oxygenation of endocannabinoids. It has the potential to modulate the production of the proinflammatory cytokine TNF-α in human blood and monocytic cells [1] [2].

15(R)-Prostaglandin E2, the C-15 epimer of the more physiologically abundant 15(S)-PGE2 (sc-201225) isomer, is produced mainly from arachidonic acid (sc-200770) via the action of COX and PGES enzymes. Present in nearly all cell types, PGE2 interacts with four distinct receptors, EP1 to EP4, leading to a wide range of biological effects. However, 15(R)-Prostaglandin E2 exhibits significantly lower efficacy in most biological assays compared to its 15(S) counterpart. Notably, acid catalyzed epimerization can transform 15(R)-Prostaglandin E2 into the more active 15(S)-Prostaglandin E2 form.

Prostaglandin E2-1-glyceryl ester, a member of the Prostaglandin Glycerol Ester family, serves as an endocannabinoid ligand targeting the CB1 receptor. This compound triggers a swift and transient surge in intracellular free calcium levels [1] [2].

11β-PGE2 is the C-11 epimer of PGE2. It is a moderate inhibitor of PGE2 binding to rat hypothalamic membranes with a Ki value of 53 nM.[1] 11β-PGE2 also stimulates bone resorption in rats at concentrations of 10-8 to 10-6 M which is similar to PGE2.2 11β-PGE2 inhibits PGE2 binding to the prostaglandin transporter protein with a Ki of 56 nM.[3] .

Prostaglandin E2-biotin, an analog of prostaglandin, is utilized in the research of Nurr1-related diseases, including cancer and autoimmune diseases [1].

Echinatin (Retrochalcone) disturb the mitochondrial energy transfer reactions and membrane permeability, at a low concentration cause deterioration of respiratory control and oxidative phosphorylation of isolated rat liver mitochondria, inhibits DNP-ATPase activity while stimulating range latent ATPase activity. Echinatin has significant antioxidant activities, it shows strong scavenging activity toward the ABTS + radical, it also dose-dependently inhibits LPS induced reactive oxygen species (ROS) production in RAW 264.7 cells and inhibits the production of nitric oxide (NO), interleukin-6 (IL-6) and prostaglandin E2 (PGE2) in LPS-induced macrophage cells.

L-161982 is a selective antagonist of EP4 receptor. L-161982 could inhibit PGE2-induced ERK phosphorylation and cell proliferation of HCA-7 cells. L-161982 could alleviate collagen-induced arthritis in mice.

Amentoflavone (3',8''-Biapigenin), as a potent inhibitor of CYP3A4 and CYP2C9, can interact with many other medications. CYP3A4 and CYP2C9 are proteins used for drug metabolism in the body. Amentoflavone also is an inhibitor of human cathepsin B. It has antimalarial activity in trials significant affinities towards the Delta-1, kappa opioid receptors (as an antagonist) and binds to benzodiazepine receptors. Amentoflavone may be a potential lead for a new type of anti-inflammatory agents having the dual inhibitory activity of group II phospholipase A2 and cyclooxygenase. Amentoflavone and quercetin differentially exerted suppression of PGE2 biosynthesis via downregulation of COX-2/iNOS expression.

Aligeron is a non-selective prostaglandin (PG) antagonist that inhibits PGF2α- and PGE2-induced decreases in blood pressure in cats, and can be used to inhibit PGF2α-induced diarrhea in mice and PGE2-induced paw edema in rats.Aligeron is known to have an antioxidant-protective effect against vascular complications.

COX-2-IN-6 is a potent, selective, and orally available cyclooxygenase-2 (COX-2) inhibitor with an IC50 of 0.84 μM and a Ki of 69 nM.COX-2-IN-6 inhibits COX-2-driven PGE2 synthesis with an IC50 of 0.60 μM.COX-2-IN-6 is used to prevent colorectal cancer. COX-2-IN-6 can be used to prevent colorectal cancer.

AS2717638 is an orally active and selective lysophosphatidic acid receptor 5 (LPA5) antagonist (IC50: 38 nM for hLPA5). It also significantly improves PGF2α-, PGE2-, and AMPA-induced allodynia.

Polygalacin D shows anti- proliferation, anti-inflammary, and hepatoprotective activities, it can inhibit the expression of lipopolysaccharide (LPS)-induced iNOS and COX-2 protein and mRNA without an appreciable cytotoxic effect on RAW 264.7 macrophages, and can suppress induction by LPS of pro-inflammatory cytokines such as prostaglandin E2 (PGE2).

MR-L2 is a reversible and noncompetitive allosteric activator of long-isoform phosphodiesterase-4 (PDE4).

Prostaglandin E2 (PGE2), one of the most widely investigated PGs, can be used as a biomarker of inflammation, disease state, or therapeutic effectiveness. However due to its rapid metabolism, direct measurement of PGE2 in biological samples is difficult. The major urinary metabolite of PGE2, tetranor-PGEM, serves as an indirect marker of PGE2 biosynthesis. Though like PGE2, tetranor-PGEM is also chemically unstable. tetranor-PGAM is a dehydration product of tetranor-PGEM and can be measured as a surrogate for tetranor-PGEM levels in urine.

Ligustroside shows little antioxidant, and anti-inflammatory properties, it shows a significant inhibition effect on prostaglandin E2 (PGE2)-release. Ligustroside shows moderate antiviral activities against parainfluenza type 3 virus.

The group IVA phospholipase A2 (PLA2), known as calcium-dependent cytosolic PLA2 (cPLA2), selectively releases arachidonic acid (AA) from membrane phospholipids, playing a central role in initiating the synthesis of prostaglandins (PGs) and leukotrienes (LTs). Pyrrophenone inhibits cPLA2α with an IC50 of 4.2 nM in enzyme assays and potently blocks the release of AA and the production of PGE2 and LTC4 in cells (IC50 = 24, 25, and 14 nM, respectively). Its action is reversible and selective, as pyrrophenone inhibits the secretory type IB and IIA PLA2s with more than a hundred-fold less potency. Pyrrophenone has also been shown to inhibit calcium ionophore (A23187)-stimulated AA release from monocytic cells, interleukin-1-induced PGE2 synthesis in mesangial cells, and the production of PGE2, LTs, and platelet-activating factor by human neutrophils, always with maximal inhibition at concentrations below 1 μM.

Luvangetin may have anti-inflammatory activity, it can inhibit NO and PGE2 production in LPS-stimulated BV2 cells. Luvangetin shows significant protection against pylorus-ligated and aspirin-induced gastric ulcers in rats and cold restraint stress-induced

Questinol exhibits significant anti-obesity activity. It shows anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, it can inhibit the production of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6 and inhibit NO an

(R)-Butaprost (free acid) is a prostaglandin E2 (PGE2) analog exhibiting high EP2 receptor subtype selectivity, commonly used to delineate EP receptor expression in human and animal tissues and cells. In 1986, Gardiner induced significant confusion regarding its structure by incorrectly identifying the selective C-16 epimer as (R)-butaprost (refer to the British Journal of Pharmacology, page 46, as TR 4979, and notes). By removing the methyl ester and restoring the native carboxylic acid at C-1, the binding affinity for prostaglandin receptors was enhanced, given such free acids typically display 10 to 100 times greater affinity than their ester counterparts. Although not extensively studied pharmacologically, (R)-butaprost is generally viewed as the less active C-16 epimer, with careful studies conducted later in the United States and Japan ultimately establishing the correct active structure as the 16(S) epimer.

11-deoxy Prostaglandin E2 (11-deoxy PGE2) is a stable, synthetic analog of PGE2 . In contrast to PGE2 which has bronchodilation effects, 11-deoxy PGE2 is a powerful bronchoconstrictor and contracts human respiratory tract smooth muscle with potencies ranging from 5 to 30 times higher than PGF2α .

HHS-0701 is a sulfur-triazole exchange (SuTEx) ligand. HHS-0701 is a potent inhibitor of tyrosine-reactive prostaglandin reductase 2 (PTGR2). HHS-0701 can block PTGR2 metabolism of the lipid substrate 15-Keto-PGE2.

Thielavin A is a fungal metabolite originally isolated from T. terricola that is related to thielavin B . Thielavin A inhibits COX, blocking both the conversion of arachidonic acid to prostaglandin H2 and the conversion of PGH2 to PGE2 . Thielavin A also inhibits glucose-6-phosphatase in rat liver microsomes (IC50 = 4.6 μM). It is a non-competitive inhibitor of α-glucosidase from S. cerevisiae (IC50 = 23.8 μM; Ki = 27.8 μM).

Evatanepag (CP-533536 free acid) is an EP2 receptor selective prostaglandin E2 (PGE2) agonist that induces local bone formation with EC50 of 0.3 nM.CP-533536 demonstrated the ability to heal fractures when administered locally as a single dose in rat models of fracture healing.

tetranor-PGEM is the major urinary metabolite of PGE1 and PGE2, and is used as a marker of PGE2 biosynthesis.[1],[2] About 15% of an infused dose of PGE2 appears as this metabolite in the urine of humans. Normal healthy males excrete 7-40 μg of tetranor-PGEM over a 24-hour period.[1]

Epibetulinic acid has anti-inflammatory activity, it exhibits potent inhibitory effects on NO and prostaglandin E(2) production in mouse macrophages (RAW 264.7) stimulated with bacterial endotoxin.

Prostaglandin E2 (PGE2) isopropyl ester is a more lipophilic form of the free acid, PGE2. PG esters have enhanced lipid solubility compared to their parent compounds. They are generally hydrolyzed to the free acid by endogenous esterases upon in vivo administration, making the esters useful prodrugs. In general, the C-1 esters of PGs show greatly diminished receptor activity in vitro compared to the parent free acids.

Enzymatically-derived prostaglandin E2 (PGE2) is an optically pure compound whereas PGE2 derived from the free radical-catalyzed peroxidation of arachidonate is a racemic mixture. Ent-PGE2 is the opposite enantiomer of PGE2. Significant amounts of racemic PGE2 (rac-PGE2) are generated in vitro and in vivo in settings of oxidative stress via the isoprostane pathway. A proposed mechanism for the formation of rac-PGE2 involves the base catalyzed equilibration from 15-E2t-isoprostane (8-iso-PGE2), generated from the 15-H2t-isoprostane endoperoxide.

PF-9184 is a potent and selective inhibitor of human microsomal prostaglandin E synthase-1 (mPGES-1), IC50 =16.5 nM. PF-9184 inhibits IL-1β-induced PGE2 synthesis in vitro.

9-deoxy-9-methylene Prostaglandin E2 (9-deoxy-9-methylene PGE2) is a stable, isosteric analog of PGE2 . 9-deoxy-9-methylene PGE2 retains the biological profile of PGE2 with fewer side effects. In the rat 9-deoxy-9-methylene PGE2 is equipotent to PGE2 in decreasing blood pressure. It also stimulates the gerbil colon and primate uterus at the same potency as PGE2.

U-51605, a stable analog of the endoperoxide prostaglandin H2 (PGH2), functions as an inhibitor with greater selectivity towards prostacyclin (PGI) synthase over thromboxane (TX) synthase. It also acts as a partial agonist at TP receptors. Studies show that at a concentration of 2.8 µM, U-51605 effectively inhibits PGI synthase in human foreskin fibroblasts, while a concentration of 5.6 µM is required to inhibit human platelet TX synthase. Furthermore, U-51605, at up to 1 µM, decreases the release of prostacyclin in SHR aorta triggered by the calcium ionophore A-23187 without impacting TXA2 production, and notably enhances the release of PGE2 and PGF2α.

IKKβ-IN-1 is a potent, orally active inhibitor of IkappaB (IKK-β) (IC50: 0.20 μM). IKKβ-IN-1 reduces the inhibition of PGE2 and TNF-α production in murine macrophages. IKKβ-IN-1 protects mice from infection shock-induced death.

EP2 receptor antagonist-2 (CID891729) is a compound that not only serves as an antagonist to the EP2 receptor, blocking its activation by PGE2, but also reduces lactate dehydrogenase (LDH) release triggered by N-methyl-D-aspartate (NMDA).

ExcisaninA may be a potent inhibitor of AKT signaling pathway in tumor cells, it can inhibit invasion by suppressing MMP-2 and MMP-9 expression, it may be a potential anti-metastatic chemotherapeutic agent for the treatment of breast cancer. Excisanin A shows comparable inhibitory effects on the LPS-induced production of NO and PGE2, and activation of NF-kappaB without affecting cell viability.Excisanin A induces apoptosis in colon cancer cell line SW620 as determined by Annexin V staining, the cleavage of caspase-3 and the proteolytic degradation of poly (ADP-ribose) polymerase (PARP).

9-deoxy-9-methylene-16,16-dimethyl Prostaglandin E2 (Meteneprost) is a potent analog of prostaglandin E2 with an extended half-life in vivo. In combination with various other prostaglandin derivatives, it results in the termination of first trimester pregnancy in monkeys. A single intramuscular injection containing 0.5 mg of meteneprost and 7.5 mg of 17-phenyl trinor PGF1α is very effective in terminating early pregnancy. This prostaglandin mixture is ineffective on monkeys in their third trimester of pregnancy. Meteneprost, when compared to PGE2 and PGF1α, in monkey and rat, does not result in unwanted side effects such as fever or gastrointestinal problems.

KW-8232, an orally active anti-osteoporotic agent, reduces the biosynthesis of PGE2[1].

1a,1b-dihomo Prostaglandin E2 (PGE2) is a rare polyunsaturated fatty acid first identified in extracts of sheep vesicular gland microsomes, known to contain COX, incubated with adrenic acid . 1a,1b-dihomo PGE2 has also been identified in conditioned media of RAW 264.7 macrophages stimulated with endotoxin and arachidonic acid . This product is thought to be produced by elongation of AA to adrenic acid, which is then metabolized sequentially by COX and PGE synthase.