Cho, H. published the artcileInhibition of NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) by cyclooxygenase inhibitors and chemopreventive agents, Quality Control of 59973-80-7, the publication is Prostaglandins, Leukotrienes and Essential Fatty Acids (2002), 67(6), 461-465, database is CAplus and MEDLINE.
15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD+-dependent oxidation of 15(S)-hydroxyl group of prostaglandins and has been considered a key enzyme involved in biol. inactivation of prostaglandins. This enzyme is markedly induced by androgens in hormone-sensitive human prostate cancer cells and may be involved in tumorigenesis. Inhibition of this enzyme may be of value in anticancer therapy. Non-steroidal anti-inflammatory drugs (NSAIDs) which inhibit cyclooxygenases (COXs) have been shown to be chemopreventive in epidemiol. and animal-model studies. However, chemoprevention by these drugs may not be directly related to their inhibition of COXs. Other targets may be also involved in their chemopreventive activity. The authors have examined a variety of NSAIDs including COX-2 selective inhibitors, peroxisome proliferator-activated receptor (PPAR) γ agonists and phytophenolic compounds which have been shown to be chemopreventive for their effect on 15-PGDH. It was found that most of these compounds were potent inhibitors of 15-PGDH. Among these compounds, ciglitazone appeared to be the most powerful inhibitor (IC50=2.7 μM). Inhibition by ciglitazone was non-competitive with respect to NAD+ and uncompetitive with respect to PGE2.
Prostaglandins, Leukotrienes and Essential Fatty Acids published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Quality Control of 59973-80-7.
Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem