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.