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Usage

Uses

Used in Pharmaceutical Applications:
PROSTAGLANDIN D2 is used as a therapeutic agent for the treatment of allergic asthma and anaphylaxis due to its role in the release from mast cells during these conditions.
Used in Sleep Regulation:
PROSTAGLANDIN D2 is used as a regulator of normal physiological sleep and body temperature in the brain, contributing to the maintenance of sleep-wake cycles and thermoregulation.
Used in Cardiovascular Applications:
PROSTAGLANDIN D2 is used as a vasodilator and inhibitor of platelet aggregation, which can help in the prevention of blood clot formation and the management of certain cardiovascular conditions.
Used in Oncology Research:
PROSTAGLANDIN D2 is used as an inhibitor of human ovarian tumor cell proliferation, with an IC50 of 6.8 μM, potentially contributing to the development of novel cancer treatments.
Used in Hair Growth Inhibition:
PROSTAGLANDIN D2 is used as a factor in hair loss and growth inhibition, as elevated levels of localized PGD2 have been linked to these conditions. This application could be relevant in the development of treatments for hair loss or as a tool in hair growth research.
Used in Allergy Research:
PROSTAGLANDIN D2 is used as a contributor to the activity of allergic asthma, making it a potential target for the development of new treatments or therapies for allergic reactions and asthma.

Biochem/physiol Actions

Primary prostaglandin in brain; induces inflammation; stimulates adenylyl cyclase.

InChI:InChI=1/C20H32O5/c1-2-3-6-9-15(21)12-13-17-16(18(22)14-19(17)23)10-7-4-5-8-11-20(24)25/h4,7,12-13,15-18,21-22H,2-3,5-6,8-11,14H2,1H3,(H,24,25)/b7-4-,13-12+/t15-,16+,17+,18-/m0/s1

Upstream product

• 506-32-1 all cis 5,8,11,14-eicosatetraenoic acid 
• 87789-19-3 (Z)-7-[(6R,7R,8S)-8-Hydroxy-6-((E)-(R)-3-hydroxy-oct-1-enyl)-1,4-dioxa-spiro[4.4]non-7-yl]-hept-5-enoic acid methyl ester 
• 87789-17-1 (Z)-7-[(6R,7R,8S)-8-Hydroxy-6-((E)-(R)-3-hydroxy-oct-1-enyl)-1,4-dioxa-spiro[4.4]non-7-yl]-hept-5-enoic acid 
• 87789-19-3 (Z)-7-[(6R,7R,8S)-8-Hydroxy-6-((E)-(S)-3-hydroxy-oct-1-enyl)-1,4-dioxa-spiro[4.4]non-7-yl]-hept-5-enoic acid methyl ester 
• 87789-17-1 (Z)-7-[(6R,7R,8S)-8-Hydroxy-6-((E)-(S)-3-hydroxy-oct-1-enyl)-1,4-dioxa-spiro[4.4]non-7-yl]-hept-5-enoic acid 

Downstream Products

• 62410-85-9 PGD₂ 9,15-bis(triphenylsilyl ether) 
• 64072-89-5 (12E)-Δ¹²-PGD₂ 
• 85235-10-5 (12Z)-Δ¹²-PGD₂ 
• 35850-13-6 15-Keto PGF₂a 
• 62410-86-0 PGF_2α 9,15-bis(triphenylsilyl ether) 
• 62410-87-1 (Z)-(1R,10R,11S,13R)-11-Triphenylsilanyloxy-13-((E)-(S)-3-triphenylsilanyloxy-oct-1-enyl)-2-oxa-bicyclo[8.2.1]tridec-7-en-3-one 
• 62410-84-8 prostaglandin F_2α 1,11-lactone 
• 67910-12-7 11-Dehydrothromboxane B₂ 

Relevant academic research and scientific papers

Selective induction of cyclo-oxygenase-2 activity in the permanent human endothelial cell line HUV-EC-C: Biochemical and pharmacological characterization

1. Cyclo-oxygenase (COX), the enzyme responsible for the conversion of arachidonic acid (AA) to prostaglandin H2 (PGH2), exists in two forms, termed COX-1 and COX-2 which are encoded by different genes. COX-1 is expressed constitutively and is known to be the site of action of aspirin and other nonsteroidal anti-inflammatory drugs. COX-2 may be induced by a series of pro-inflammatory stimuli and its role in the development of inflammation has been claimed. 2. Endothelial cells are an important physiological source of prostanoids and the selective induction of COX-2 activity has been described for finite cultures of endothelial cells, but not for permanent endothelial cell lines. 3. The HUV-EC-C line is a permanent endothelial cell line of human origin. We have determined the COX activity of these cells under basal conditions and after its exposure to two different stimuli, phorbol 12-myristate 13-acetate (PMA) and interleukin-1β (IL-1β). 4. Both PMA and IL-1β produced dose- and time-dependent increases of the synthesis of the COX-derived eicosanoids. These increases were maximal after the treatment with 10 nM PMA for 6 to 9 h. Under these conditions, the main eicosanoid produced by the cells was PGE2. 5. The increase of COX activity by PMA or IL-1β correlated with an increase of the enzyme's apparent V(max), whilst the affinity for the substrate, measured as apparent K(m), remained unaffected. 6. Treatment of the cells with PMA induced a time-dependent increase in the expression of both COX-1 and COX-2 mRNAs. Nevertheless, this increase was reflected only as an increase of the COX-2 isoenzyme at the protein level. 7. The enzymatic activity of the PMA-induced COX was measured in the presence of a panel of enzyme inhibitors, and the IC50 values obtained were compared with those obtained for the inhibition of human platelet COX activity, a COX-1 selective assay. Classical non-steroidal anti-inflammatory drugs (NSAIDs) inhibited both enzymes with varying potencies but only the three compounds previously shown to be selective COX-2 inhibitors (SC-58125, NS-398 and nimesulide) showed higher potency towards the COX of PMA-treated HUV-EC-C. 8. Overall, it appears that the stimulation of the HUV-EC-C line with PMA selectively induces the COX-2 isoenzyme. This appears to be a suitable model for the study of the physiology and pharmacology of this important isoenzyme, with a permanent endothelial cell line of human origin.

Studies on the Properties of Prostaglandin Synthetase of Caprine Seminal Vesicles

The prostaglandin (PG) synthetase complex in the microsomal fraction of caprine (goat) seminal vesicles was found to have the highest PGE2 synthetase activity in comparison to that in similar other animal sources. The results of the investigations on the kinetics of PGE2 synthesis, factors influencing product formation, cofactor requirement and stability of the enzyme system show that the PG-synthetase complex from goat vesicular gland was very unstable, and its properties were generally comparable to that from the highly active ovine seminal vesicular multienzyme complex.