Synonyms 15-hydroxyprostaglandin dehydrogenase, 15-hydroxyprostaglandin dehydrogenase (NAD(+)), 15-hydroxyprostaglandin dehydrogenase [NAD(+)] + [9] |
Introduction Catalyzes the NAD-dependent dehydrogenation (oxidation) of a broad array of hydroxylated polyunsaturated fatty acids (mainly eicosanoids and docosanoids, including prostaglandins, lipoxins and resolvins), yielding their corresponding keto (oxo) metabolites (PubMed:10837478, PubMed:16757471, PubMed:16828555, PubMed:21916491, PubMed:25586183, PubMed:8086429). Decreases the levels of the pro-proliferative prostaglandins such as prostaglandin E2 (whose activity is increased in cancer because of an increase in the expression of cyclooxygenase 2) and generates oxo-fatty acid products that can profoundly influence cell function by abrogating pro-inflammatory cytokine expression (PubMed:15574495, PubMed:25586183). Converts resolvins E1, D1 and D2 to their oxo products, which represents a mode of resolvin inactivation. Resolvin E1 plays important roles during the resolution phase of acute inflammation, while resolvins D1 and D2 have a unique role in obesity-induced adipose inflammation (PubMed:16757471, PubMed:22844113). |
Target |
Mechanism 15-PGDH inhibitors |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication |
Drug Highest PhasePhase 1 |
First Approval Ctry. / Loc.- |
First Approval Date20 Jan 1800 |
Target |
Mechanism 15-PGDH inhibitors |
Active Org. |
Originator Org. |
Active Indication |
Inactive Indication- |
Drug Highest PhasePreclinical |
First Approval Ctry. / Loc.- |
First Approval Date20 Jan 1800 |
Target |
Mechanism 15-PGDH inhibitors |
Active Org. |
Originator Org. |
Active Indication- |
Inactive Indication- |
Drug Highest PhasePreclinical |
First Approval Ctry. / Loc.- |
First Approval Date20 Jan 1800 |