Prostaglandin E-1

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.

Dihomo-γ-Linolenic acid methyl ester is the methyl ester form of Dihomo-γ-Linolenic acid which has anti-inflammatory and anti-proliferative effects.

13,14-dihydro-15-keto Prostaglandin E1 inhibits ADP-induced platelet aggregation in human isolated platelet-rich plasma (IC50=14.8 μg/mL) and is a PGE1 metabolite.

19(R)-hydroxy Prostaglandin E1 is an agonist of EP1 and EP3 receptor subtypes and exhibits contractile activity on smooth muscle and is the major prostaglandin in primate semen.

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.

8-iso Prostaglandin E1 causes spasm in the pulmonary veins of dogs and also acts as a vasodilator.

16,16-dimethyl Prostaglandin E1 is a PGE1 (T1626) analog that induces bronchoconstriction and vascular smooth muscle contraction and inhibits indomethacin-induced cell elongation.

1a,1b-dihomo Prostaglandin E1 is a class of prostaglandin compounds.

6-keto Prostaglandin E1 is a bioactive derivative of PGE1 that plays a role in antiplatelet aggregation and depolymerization.

11-deoxy Prostaglandin E1 is a prostaglandin E1 analogue that has bronchodilator activity and can inhibit histamine-induced bronchoconstriction and cause relaxation of tracheal strips in isolated guinea pigs.

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), 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-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].

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.

Prostaglandin E1 ethanolamide, an analog of Prostaglandin E1 (PGE1), can potentially inhibit the GLI2-induced expression of target genes such as Gli1 and Ptch1, thereby reducing tumor growth [1].

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.

Tetranor-Prostaglandin E1 (tetranor-PGE1), a metabolite of PGE1 and PGE2, undergoes formation through β-oxidation.

Prostaglandin E1-d4 is the deuterated form of Prostaglandin E1. Prostaglandin E1 (Alprostadil) is a prostaglandin receptor ligand with Ki values of 1.1 nM, 2.1 nM, 10 nM, 33 nM, and 36 nM for mouse EP3, EP4, EP2, IP, and EP1, respectively. It induces vasodilation and inhibits platelet aggregation, and serves as a vasodilator in research on peripheral vascular diseases.

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

mPGES-1 Inhibitor-1 is a novel selective inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1) with anti-inflammatory and analgesic activity for the study of acute liver injury.

Vedaprofen (PM 150) inhibits COX-1 and reduces prostaglandin H2 synthesis with anti-inflammatory activities. Vedaprofen is an inhibitor of Escherichia coli sliding clamp with the IC50 of 222 μM and Ki of 131 μM.

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.

Zaloglanstat (ISC-27864) is a selective, orally active mPGES-1 inhibitor with an IC50 of 5 nM against human mPGES-1, demonstrating analgesic effects in osteoarthritis and inflammatory arthritis.

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