Ph CL 28A
Ph CL 28A is a prostaglandin 15-hydroxydehydrogenase (15-PGDH) inhibitor. Ph CL 28A increases the output of PGE2, PGF2α and endogenous arachidonic acid-derived PGI2 in isolated rat lungs, reduces the output of TxB2 and LTC4 in isolated rat hearts, and exhibits protective effects in rat models of inflammation and gastric mucosal injury. Ph CL 28A can be used in research related to acute inflammation and gastric ulcers.
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- CAS No.: 99435-38-8
- Formule: C18H16N2O7
- Masse moléculaire:372.33
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Ph CL 28A acts as a non-competitive inhibitor of purified human placental 15-PGDH, with Ki values of 18.7 nM and 57.6 nM against the substrate PGF2α and cofactor NAD+, respectively. It also inhibits 15-PGDH activity in rat colonic cytoplasmic supernatant, with an IC50 of 56 nM[1].
Ph CL 28A inhibits the inactivation of PGF2α in isolated perfused rat lungs, with an IC50 of 72 nM[1].
Ph CL 28A (0.3 μM) reduces the immunoreactive LTC4 output induced by A23187 (HY-N6687) from 5.7 ng to 4.0 ng in isolated rat hearts, and abolishes the delayed increase in coronary perfusion pressure[2].
Ph CL 28A (0.3 μM; pre-perfused for at least 20 min and continuously perfused) reduces the increase in coronary perfusion pressure and TxB2 output induced by exogenous arachidonic acid in isolated rat hearts, but does not affect myocardial contractile tension or 6-oxo-PGF1α output[2].
Ph CL 28A (0.3 μM; pre-perfused for 15 min and continuously perfused) increases the retention of PGE2 and PGF2α after single passage through the isolated rat pulmonary circulation, and prolongs the pulmonary outflow half-time of their radiotracers[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Ph CL 28A (30 mg/kg; i.p.; administered concurrently with carrageenan) inhibits leukocyte accumulation and reduces LTB4 levels in a carrageenan-induced rat pleurisy model, without affecting the levels of cyclooxygenase-derived eicosanoids[3].
Ph CL 28A (30 mg/kg; i.p.; single bolus injection) has no effect on systemic blood pressure in anesthetized normal rats, nor does it affect the hypotensive responses of these rats to acetylcholine or iloprost[3].
Ph CL 28A (3-30 mg/kg; i.p.; single administration) inhibits ethanol-induced gastric ulcers in female Wistar rats, with an ED50 of 13 mg/kg upon intraperitoneal injection, but shows no oral activity even at doses as high as 30 mg/kg[5].
Single administration of Ph CL 28A (30 mg/kg; i.p., p.o.) causes a slight but statistically significant decrease in ex vivo gastric PGF2α degradation levels in healthy female Wistar rats[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (male, 150-250 g, carrageenan-induced paw oedema)[3]
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Dosage:10 mg/kg (systemic i.p. simultaneous; local paw simultaneous); 30 mg/kg (systemic i.p. 90 min before, 60 min before, simultaneous, 60 min after; local paw simultaneous); 100 mg/kg (systemic i.p. simultaneous)
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Administration:i.p. (90 min before carrageenan, 60 min before carrageenan, simultaneous with carrageenan, 60 min after carrageenan); local paw injection (simultaneous with carrageenan)
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Result:Reduced paw oedema only at 1 hour post-carrageenan when given 30 mg/kg i.p. 90 min before carrageenan.
Achieved over 50% inhibition of oedema at 2 hours post-carrageenan when given 30 mg/kg i.p. simultaneously with carrageenan.
Produced marked reduction in early oedema (1 hour) with significant effects lasting up to 4 hours when given 10 mg/kg or 30 mg/kg i.p. simultaneously with carrageenan; these doses were equi-effective to indomethacin at 3 and 4 hours but less effective than 100 mg/kg of Ph CL 28A across all time points.
Reduced oedema at all measured time points (1-4 hours) to a greater extent than lower doses or indomethacin when given 100 mg/kg i.p. simultaneously with carrageenan.
Increased paw oedema by 70% at 1 hour (carrageenan alone: 0.61 mL; carrageenan + Ph CL 28A: 1.04 mL) and potentiated oedema for up to 4 hours when given 30 mg/kg via local paw injection simultaneously with carrageenan.
Increased paw oedema to ~200% of control levels for up to 4 hours when given 10 mg/kg via local paw injection simultaneously with carrageenan.
Did not alter 5-HT-induced paw oedema at systemic 30 mg/kg i.p. or local 10 mg/kg paw injection.
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Animal Model:Wistar rats (male, 300-400 g, carrageenan-induced pleurisy)[3]
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Dosage:30 mg/kg
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Administration:i.p.; simultaneous with carrageenan
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Result:Reduced total leukocyte numbers in pleural fluid to 42% of carrageenan-alone levels at 3 hours post-carrageenan, without altering the proportion of polymorphonuclear cells (70% vs. 77% in carrageenan-alone rats).
Decreased pleural fluid LTB4 levels to 77% of carrageenan-alone levels at 3 hours post-carrageenan.
Did not affect pleural fluid TxB2 (125% of control) or 6-oxo-PGF1α (102% of control) levels.
Did not alter circulating leukocyte counts when administered alone.
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Animal Model:Wistar (female, 180-250 g, fasted for 22 h, 6 per group, ethanol-induced gastric ulcers)[5]
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Dosage:3 mg/kg (i.p.); 10 mg/kg (i.p.); 30 mg/kg (i.p.); 30 mg/kg (p.o.)
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Administration:i.p.; p.o.; single dose (30 minutes before ethanol exposure)
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Result:Reduced mean ulcer score to 2.8 (ulcer index 283) at 3 mg/kg i.p..
Reduced mean ulcer score to 2.5 (ulcer index 252) at 10 mg/kg i.p..
Reduced mean ulcer score to 0.3 (ulcer index 6) at 30 mg/kg i.p..
Achieved an ED50 of 13 mg/kg for i.p. administration against ethanol-induced ulcers.
Showed no protective effect against ethanol-induced gastric ulcers at 30 mg/kg p.o..
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Animal Model:Wistar (female, 180-250 g, fasted for 22 h, 6 per group, phenylbutazone-induced gastric ulcers)[5]
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Dosage:3 mg/kg (i.p.); 10 mg/kg (i.p.); 30 mg/kg (i.p.); 30 mg/kg (p.o.)
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Administration:i.p.; p.o.; single dose (30 minutes before phenylbutazone exposure)
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Result:Reduced mean ulcer score to 1.6 (ulcer index 135) at 3 mg/kg i.p..
Reduced mean ulcer score to 1.3 (ulcer index 83) at 10 mg/kg i.p..
Reduced mean ulcer score to 0.7 (ulcer index 44) at 30 mg/kg i.p..
Achieved an ED50 of 3 mg/kg for i.p. administration against phenylbutazone-induced ulcers.
Showed no protective effect against phenylbutazone-induced gastric ulcers at 30 mg/kg p.o..
Increased gastric prostaglandin E2 (PGE2) levels by 88% (from 180 ng/g to 340 ng/g) in non-ulcerogen-treated control rats at 30 mg/kg p.o..
Had no effect on 6-keto-PGF1α or thromboxane B2 (TXB2) levels in non-ulcerogen-treated control rats at 30 mg/kg p.o..
Had no effect on prostaglandin synthesis in control or phenylbutazone-treated rats at 30 mg/kg i.p..
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Animal Model:Wistar (female, 180-250 g, 6 per group, healthy non-ulcerized)[5]
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Dosage:30 mg/kg (i.p.); 30 mg/kg (p.o.)
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Administration:i.p.; p.o.; single dose
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Result:Reduced ex vivo gastric PGF2α breakdown from 1153 ng h-1 g-1 tissue to 937 ng h-1 g-1 tissue at 30 mg/kg p.o..
Reduced ex vivo gastric PGF2α breakdown from 977 ng h-1 g-1 tissue to 798 ng h-1 g-1 tissue at 30 mg/kg i.p..
Chemical Information
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CAS No. 99435-38-8
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Masse moléculaire 372.33
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Formule C18H16N2O7
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SMILES
O=C(CC1=CC(/N=N/C2=CC(C(OC)=O)=CC(C(OC)=O)=C2)=CC=C1O)O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Berry CN, et al. Highly potent inhibition of prostaglandin 15-hydroxydehydrogenase in-vitro and of prostaglandin inactivation in perfused lung by the new azobenzene analogue, Ph CL 28A. The Journal of pharmacy and pharmacology. 1985 Sep;37(9):622-8. [Content Brief]
[2]. Nakamura M, et al. Effects of Ph CL 28A on eicosanoid synthesis in rat isolated hearts. Prostaglandins. 1991 Oct;42(4):303-12. [Content Brief]
[3]. Santana AC, et al. Anti-inflammatory activities of Ph CL28A in rats in vivo. European journal of pharmacology. 1993 Feb 09;231(2):237-42. [Content Brief]
[4]. Bakhle YS, et al. Inhibitors of prostaglandin dehydrogenase (Ph CL 28A and Ph CK 61A) increase output of prostaglandins from rat isolated lung. British journal of pharmacology. 1987 Sep;92(1):189-96. [Content Brief]
[5]. Berry CN, et al. Sulphasalazine and PhCL28A inhibit the formation of ethanol- and phenylbutazone-induced rat gastric ulcers: lack of involvement of endogenous prostaglandins?. British journal of pharmacology. 1988 Mar;93(3):465-72. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Ph CL 28A Related Classifications
HY-183433 Related Classifications
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