prostaglandin a-2

PGA2 is a naturally occurring prostaglandin in gorgonian corals where it may function in self defense. It is generally not present in mammals. PGA2 has low biological potency in most bioassays, but it does show some antiviral/antitumor activity.[1] At a 25 uM concentration, PGA2 blocks the cell cycle progression of NIH 3T3 cells at the G1 and G2/M phase .[2] It has also been shown to act as a vasodilator with natriuretic properties.[3]

8-iso Prostaglandin A2 is an isoprostane produced by the nonenzymatic oxidation of arachidonic acid.

Prostaglandin A2-biotin (PGA2-biotin) is a biotin-labeled form of Prostaglandin A2. It retains the activity of inhibiting cell proliferation. Prostaglandin A2-biotin serves as an effective tool for studying the interaction between Prostaglandin A2 and cellular proteins and exploring its mechanism of inhibiting cell proliferation.

16,16-dimethyl PGA2 is a metabolism-resistant analog of PGA2 with a prolonged in vivo half-life. It inhibits the proliferation of Sendai virus in cultured African green monkey kidney cells by >90% at a concentration of 4 μg/ml. Daily infusion of 10 μg of 16,16-dimethyl PGA2 methyl ester into mice infected with influenza A virus increased survival by 40%. Similar treatment of mice inoculated with erythroleukemia cells delayed tumor growth and increased survival time.

Arbaprostil, a synthetic analog of prostaglandin E2 (PGE2) known as 15(R)-15-methyl prostaglandin E2, was developed for its cytoprotective activity. In the commercial production of bulk arbaprostil, one potential impurity is 15(R)-15-methyl Prostaglandin A2 (15(R)-15-methyl PGA2). The pharmacology and EP receptor binding affinity of 15(R)-15-methyl PGA2 have not been reported.

17-phenyl trinor-13,14-dihydro Prostaglandin A2 is a synthetic analog of prostaglandin with relatively unexplored biological activity. Similarly structured, particularly in its lower side chain, to the PGF2α analog latanoprost, which is an approved glaucoma treatment, this compound presents an interesting subject for further pharmaceutical research and potential therapeutic applications.

17-Phenyl trinor prostaglandin A2 is a synthetic analog of prostaglandin [1].

Aspirin is an orally active, selective, and irreversible inhibitor of COX-1 and COX-2 with IC₅₀ values of 5 and 210 μg/mL, respectively. It induces apoptosis, inhibits NF-κB activation and platelet prostaglandin synthesis, thereby preventing thrombosis. Additionally, it acts as a histone deacetylase inhibitor that upregulates p21, exhibiting anti-inflammatory, antipyretic, analgesic, and anti-platelet aggregation activities. Aspirin is commonly used to induce gastric ulcer models.

Ketoprofen (RP-19583) is a propionic acid derivative and nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic effects. It inhibits cyclo-oxygenase I and II, decreasing the formation of prostaglandin and thromboxane precursors. This reduction in prostaglandin synthesis, mediated by prostaglandin synthase, is responsible for its therapeutic effects. Additionally, Ketoprofen decreases thromboxane A2 formation via thromboxane synthase, inhibiting platelet aggregation.

Lornoxicam (Chlortenoxicam) (chlortenoxicam) is a new nonsteroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic, anti-inflammatory, and antipyretic properties. Lornoxicam differs from other oxicam compounds in its potent inhibition of prostaglandin biosynthesis, a property that explains the particularly pronounced efficacy of the drug. Lornoxicam is approved for use in Japan.

Rebamipide (OPC12759) is a quinolinone derivative with anti-ulcer and anti-inflammatory activities. Rebamipide induces cyclooxygenase 2 (COX2) synthesis which results in an increase in endogenous prostaglandin synthesis in the gastric mucosa. This agent also inhibits H. pylori-induced production of tumor necrosis factor (TNF) alpha and subsequent inflammation of the gastric mucosa. In addition, rebamipide scavenges oxygen-derived free radicals that potentially cause mucosal injury, and stimulates prostaglandin EP4 receptor gene expression followed by mucous secretion, thereby enhancing the gastric mucosal defense.

Bromfenac sodium hydrate (Bromfenac monosodium salt sesquihydrate) is the sodium salt form of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and anti-inflammatory properties. Upon ophthalmic administration, bromfenac binds to and inhibits cyclooxygenase II (COX II), an enzyme that converts arachidonic acid to cyclic endoperoxides, which are prostaglandin (PG) precursors. By inhibiting PG formation, bromfenac prevents PG-induced inflammation, vasodilation, leukocytosis, disruption of the blood-aqueous humor barrier, increased vascular permeability, and elevated intraocular pressure (IOP).

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.

(2-{[2-(2-fluorophenoxy)ethyl]sulfanyl}-1H-benzimidazol-1-yl)acetic acid is a prostaglandin-like CRTH2 antagonist with an IC50 < 10 μM, which can be used in studies of rhinitis, COPD, rheumatoid arthritis, eczema and conjunctivitis.

HPGDS inhibitor 2 (GSK-2894631A) is a potent, selective hematopoietic prostaglandin D synthase (h-pgds) inhibitor, IC50 = 9.9 nm.

2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide inhibits stress-induced ulcers by maintaining phospholipase A2 and prostaglandin E2 levels in rats subjected to water immersion-restrained stress-induced ulceration.

HQL-79 is a selective and orally active human hematopoietic prostaglandin D synthase (H-PGDS) inhibitor. It inhibits the synthesis of PGD2 and acts as an anti-allergic agent (Kd: 0.8 μM and IC50: 6 μM). It also shows no obvious effect on COX-1, COX-2, m-P

Omidenepag (UR-7276) is a selective and potent prostaglandin E2 receptor 2 (EP2) agonist and a novel topical ocular hypotensive agent.Omidenepag is used in the study of glaucoma and hypertension.

HPGDS inhibitor 1 is a novel and selective inhibitor for Hematopoietic Prostaglandin D Synthase (HPGDS) with an IC50 Value of 0.7 nM.

AGU654 (Compound 44) is a selective mPGES-1 inhibitor with an IC50 value of 2.9 nM against mPGES-1. By inhibiting mPGES-1, AGU654 interrupts the pathway where COX-1/2 converts arachidonic acid to prostaglandin E2 (PGE2), effectively reducing inflammatory responses, pain, and fever symptoms. In models using activated human monocyte-derived macrophages and whole blood, AGU654 selectively inhibits PGE2 production induced by bacterial endotoxins, while preserving the production of other prostaglandins. In guinea pig models, AGU654 significantly alleviates fever, inflammation, and inflammatory pain, demonstrating excellent anti-inflammatory, analgesic, and antipyretic effects. AGU654 holds promise as a new approach for researching inflammatory diseases and pain.

4-Desmethyl-2-methyl celecoxib (Compound 1g) is an orally active and selective cyclooxygenase-2 (COX-2) inhibitor, with an IC50 value of 0.069 μM. It possesses anti-inflammatory, analgesic, and antipyretic properties and can reduce prostaglandin synthesis. This compound is a promising candidate for research into inflammatory diseases and pain-related conditions, such as rheumatoid arthritis and osteoarthritis.

Licarin A is a natural anti-inflammatory lignan that inhibiting PKCα/βII and p38 MAPK pathways, thereby decreasing TNF-α and prostaglandin D2 (PGD2) secretion as well as COX-2 expression.

2-MeSADP (2-Methylthioadenosine diphosphate; 2-Methylthio-ADP) is a potent agonist of purinergic (P2Y) receptors, displaying EC50 values of 19 nM for human P2Y13, 6.2 nM for mouse P2Y13, and 5 nM for human P2Y12. It also has pEC50 values of 8.29 for human P2Y1 and 5.75 for rat P2Y6. 2-MeSADP induces platelet aggregation and morphological changes, while inhibiting the accumulation of cyclic adenosine monophosphate in platelets in the presence of prostaglandin E1.

RJG-2036 is a potent covalent inhibitor of human prostaglandin reductase 2 (PTGR2) with an IC50 of 100 nM. It effectively inhibits NADPH-dependent reduction reactions, significantly reducing the secretion of inflammatory factors such as TNF-α and the release of various pro-inflammatory eicosanoids in LPS-stimulated THP-1 macrophages. RJG-2036 shows promise for research in inflammatory diseases.