Cell lines

gastric mucosa

Preparation method

The solubility of this compound in DMSO is >11.1mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

40 or 400 μg/mL

Applications

In the gastric mucosa of dogs, carprofen increased in vitro conductance and permeability to mannitol. Carprofen (400 μg/mL) caused sloughing of epithelial cells. Carprofen appeared to compromise gastric mucosal integrity and barrier function in dogs.

Animal models

Dogs with chronic unilateral osteoarthritis of the stifle joint

Dosage form

10 days with a 30- to 60-day washout period

Application

Carprofen significantly suppressed PGE2 concentrations in blood at days 3 and 10. Carprofen significantly decreased gastric synthesis of PGE2 at day 3 but not day 10 of each treatment period. Carprofen decreased synovial fluid PGE2 concentrations in the affected and unaffected stifle joints at days 3 and 10.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

Carprofen is a nonsteroid anti-inflammatory agent, acts as a multi-target FAAH/COX inhibitor, with IC50s of 3.9 μM, 22.3 μM and 78.6 μM for COX-2, COX-1 and FAAH, respectively.

Carprofen (Compound 1) is a nonsteroid anti-inflammatory agent, acts as a multi-target FAAH/COX inhibitor, with IC50s of 3.9 μM, 22.3 μM and 78.6 μM for COX-2, COX-1 and FAAH, respectively[1]. Carprofen (10 μg/mL) shows cytoprotective effects in CCL and CaCL cells and decreases apoptosis of both cells. Carprofen (10 μg/mL) exhibits nonsignificant increase in PGE2 concentration, compared with that of the respective CCL or CaCL controls[2].

Carprofen (2.2 mg/kg, p.o.) significantly decreases PGE2 concentration in blood of dogs on days 3 and 10. Carprofen also decreases amounts of gastric PGE2 synthesis on day 3, but the inhibition is not obvious on day 10. In addition, Carprofen shows no activity against gastric PGE1 synthesis in dogs on day 3 and 10[3].

References:
[1]. Favia AD, et al. Identification and characterization of carprofen as a multitarget fatty acid amide hydrolase/cyclooxygenase inhibitor. J Med Chem. 2012 Oct 25;55(20):8807-26.
[2]. Waldherr K, et al. In vitro cytoprotective effects of acetylsalicylic acid, carprofen, meloxicam, or robenacoxib against apoptosis induced by sodium nitroprusside in canine cruciate ligament cells. Am J Vet Res. 2012 Nov;73(11):1752-8.
[3]. Sessions JK, et al. In vivo effects of carprofen, deracoxib, and etodolac on prostanoid production in blood, gastric mucosa, and synovial fluid in dogs with chronic osteoarthritis. Am J Vet Res. 2005 May;66(5):812-7.