A common metabolic pathway for several prostaglandins (PGs), including PGD2, involves the reduction of the double bond between C-13 and C-14 and oxidation of the hydroxyl group at C-15, producing 13,14-dihydro-15-keto PGs. The removal of four carbons at the α-terminus and oxidation of the terminal ω-carbon produces the abundant urinary metabolites, including tetranor-PGDM.{15162} 13,14-dihydro-15-keto-tetranor PGD2 is a potential metabolite of PGD2. It would be produced from the known metabolite 13,14-dihydro-15-keto PGD2 (Item No. 12610), which is a known agonist for the CRTH2/DP2 receptor.{5248}
A potential metabolite of PGD2, presumably produced from the known metabolite 13,14-dihydro-15-keto PGD2
Formal name: 9α-hydroxy-11,15-dioxo-2,3,4,5-tetranor-prostanoic acid
Synonyms:
Molecular weight: 298.4
CAS: 1204116-69-7
Purity: ≥95%
Formulation: A solution in ethanol
Product Type|Biochemicals|Lipids|Prostaglandins||Research Area|Lipid Biochemistry|Cyclooxygenase Pathway
The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
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The nuclear factor-κB (NF-κB) regulates the expression of numerous genes involved in immunity and inflammation, cellular stress responses, growth, and apoptosis. Resveratrol, a polyphenolic trans-stilbene, is a known inhibitor of the activation of NF-κB and exhibits activity against a wide variety of cancer cells. CAY10512 is a substituted trans-stilbene analog of resveratrol that is 100-fold more potent as measured by antioxidant activity. The IC50 value for inhibition of TNFα-induced activation of NF-κB by CAY10512 is 0.15 µM compared to 20 µM by resveratrol.{14545}
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