pge 1

Limaprost (17α,20-dimethyl-δ2-PGE1) is an analog of PGE1 with structural modifications intended to give it a prolonged half-life and greater potency.It is a potent and orally active vasodilator. Limaprost increases blood flow and inhibits platelet aggregation. Limaprost (17α,20-dimethyl-δ2-PGE1) can be used for pain relief, has antianginal effects, and has potential for ischaemic symptoms treatment.

Prostaglandin E1 (Alprostadil) is the naturally occurring prostaglandin E1 (PGE1) which displays a variety of pharmacologic actions. Prostaglandin E1 is a potent vasodilator agent that increases peripheral blood flow, inhibits platelet aggregation, and induces bronchodilation. Used in the treatment of erectile dysfunction, this agent produces corporal smooth muscle relaxation by binding to PGE receptors, resulting in the activation of adenylate cyclase and the subsequent accumulation of 3'5'-cAMP.

Alprostadil sodium is a prostaglandin receptor ligand with Ki values of 36, 10, 1.1, 2.1, and 33 nM for EP1, EP2, EP3, EP4, and IP, respectively, in mice.It induces vasodilatation and inhibits platelet aggregation, and it can be used as a vasodilator for the study of peripheral vascular disease.

13,14-Dihydro-15(R)-Prostaglandin E1 (13,14-dihydro-15(R)-PGE1) is an analog of 13,14-dihydro-PGE1 characterized by its R-configured hydroxyl group at the C-15 position [1].

15-epi-PGE1 (15R-Prostaglandin E1; 15-Epiprostaglandin E1), a stereoisomer of PGE1, exhibits reduced biological activity [2]. This compound acts as a non-competitive inhibitor of human placental 15-Hydroxyprostaglandin dehydrogenase (15-PGDH), with an inhibitory concentration 50 (IC50) value of 170 μM [1].

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.

Bismuth Subsalicylate (Bismuth subsalicylat) is the active ingredient in the popular medication Pepto-Bismol that is used to treat nausea, heartburn, indigestion, upset stomach, diarrhea, and other temporary discomforts of the stomach and gastrointestinal tract.

6-Dehydrogingerdione sensitizes human hepatoblastoma Hep G2 cells to TRAIL-induced apoptosis via a reactive oxygen species-mediated mechanism that enhances DR5 expression, up-regulates Ser-15 phosphorylation, and triggers nuclear translocation of p53. Abrogation of p53 using small interfering RNA markedly reduces 6-Dehydrogingerdione-induced DR5 and diminishes TRAIL responsiveness. ROS generation accompanies DR5 activation, and pretreatment with N-acetyl-L-cysteine significantly attenuates these apoptotic responses, confirming 6-Dehydrogingerdione acts through p53-dependent and oxidative stress-mediated apoptotic pathways.

PGS-IN-1 (KME-4) is a potent inhibitor of prostaglandin synthetase (PGS, IC50: 0.28 μM) and 5-lipoxygenase (IC50: 1.05 μM).

Pelubiprofen is an orally active, non-steroidal anti-inflammatory agent, a selective cyclooxygenase-2 (COX-2) inhibitor, which effectively reduces PGE(2) production by inhibiting COX activity. Pelubiprofen inhibits LPS-induced phosphorylation of IKK-β and transforming growth factor-β activated kinase-1 (TAK1).

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

CAY10526 (BTH) is a selective mPGES-1 inhibitor that acts as an inhibitor of the NF-κB signaling pathway.

hPGDS-IN-1 is a hPGDS inhibitor. This compound specifically blocks the activity of human hematopoietic prostaglandin D synthase (hPGDS), an enzyme that catalyzes the conversion of PGH2 to PGD2. [Purity: 99.55% | Suppliers: MedChemExpress]

1,2,3-Trilinoelaidoyl-rac-glycerol is a triacylglycerol that contains linoelaidic acid at the sn-1, sn-2, and sn-3 positions. Dietary administration of 1,2,3-trilinoelaidoyl-rac-glycerol (0.6-6.3% w/w) lowers serum levels of thromboxane B2 , prostaglandin F2 (PGF2), and PGE in rats.1 |1. Bruckner, G., Goswami, S., and Kinsella, J.E. Dietary trilinoelaidate: Effects on organ fatty acid composition, prostanoid biosynthesis and platelet function in rats. J. Nutr. 114(1), 58-67 (1984).

Esflurbiprofen is an inhibitor of COX-1 and COX-2.

Povafonidine (PGE-6201204) is a potent alpha-2 adrenoreceptor agonist that constricts blood vessels and reduces mucosal congestion, making it useful for nasal congestion research [1].

Suprofen (Suprol) is an IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.

AS1940477 is p38 MAPK inhibitor. AS1940477 inhibited the enzymatic activity of recombinant p38α and β isoforms but showed no effect against other 100 protein kinases including p38γ and δ isoforms. In human peripheral blood mononuclear cells, AS1940477 inhibited lipopolysaccharide (LPS)- or phytohemagglutinin A (PHA)-induced production of proinflammatory cytokines, including TNFα, IL-1β, and IL-6 at low concentrations (LPS/TNFα, IC(50)=0.45n M; PHA/TNFα, IC(50)=0.40 nM). In addition, equivalent concentrations of AS1940477 that inhibited cytokine production also inhibited TNFα- and IL-1 β-induced production of IL-6, PGE(2), and MMP-3 in human synovial stromal cells. AS1940477 was also found to potently inhibit TNF production in whole blood (IC(50)=12 nM) and effectively inhibited TNFα production induced by systemically administered LPS in rats at less than 0.1mg/kg (ED(50)=0.053 mg/kg) with an anti-inflammatory effect lasting for 20h after oral administration. Overall, this stu......

AF3442 is a potent and selective mPGES-1 inhibitor (microsomal prostaglandin (PG) E synthase-1). AF3442 caused a concentration-dependent inhibition of PGE(2) in human recombinant mPGES-1 with an IC(50) of 0.06microM. AF3442 is a selective mPGES-1 inhibitor which reduced monocyte PGE(2) generation also in the presence of plasma proteins. Pharmacological inhibition of mPGES-1 did not translate into redirection of PGH(2) metabolism towards other terminal PG synthases in monocytes. The functional relevance of this observation deserves to be investigated in vivo.

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].

19(R)-Hydroxylated prostaglandins (PGs) are present at µg/ml concentrations in the semen of some mammalian species, notably primates, with the majority being from the PGE series and featuring a 15(S),19(R) hydroxyl stereochemistry. These compounds are also observed in marsupials' seminal plasma, where F-type 1 and 2-series compounds are predominant. The 15(R)-hydroxy epimer represents the inverse or "unnatural" isomer at C-15 for these 19-hydroxylated PGs. Although the biological function of 19(R)-hydroxylated PGs remains unclear, 19(R)-hydroxylation in the F-series leads to a notable reduction in receptor-mediated biological activity in certain assays.

Dehydroglyasperin D exhibits anticancer, anti-inflammatory, anti-obesity, antioxidant and anti-aldose reductase effects, it inhibits the proliferation of HT-29 human colorectal cancer cells through direct interaction with phosphatidylinositol 3-kinase; it also mediates suppression of both COX-2 expression and the MLK3 signalling pathway through direct binding and inhibition of MLK3. Dehydroglyasperin D shows strong ferric reducing activities and effectively scavenged DPPH, ABTS(+), and singlet oxygen radicals.

Sappanone A is a high isoflavanone that exhibits anti-inflammatory effects by modulating Nrf2.Sappanone A attenuates allergic airway inflammation in ovalbumin-induced asthma.

Skullcapflavone I (Standard) is a reference standard for research and analysis in studies involving Skullcapflavone I. Skullcapflavone I has anti-inflammatory and anti-allergic potential, it can significantly inhibit LPS stimulated NO and PGE(2) release in J774A.1 macrophages and inhibit LPS induced IL-6 production in a concentration dependent manner. Skullcapflavone I selectively induces apoptosis in T-HSC/Cl-6 cells via caspase-3 and caspase-9 activation.