Asked by Alcest
In 1991, aceclofenac was developed as an analog of a commonly prescribed NSAID, Diclofenac, via chemical modification in effort to improve the gastrointestinal tolerability of the drug.
All the nine studies included in this review indicate that aceclofenac is as effective diclofenac or even more effective than the latter. These studies performed also showed that aceclofenac was more tolerable compared to diclofenac with lower incidence of GI AEs including abdominal pain and dyspepsia. One study reported that diclofenac is cost-effective compared to aceclofenac; however, aceclofenac has a better efficacy and tolerability in the patients.
Reference: Vohra F, Raut A. Comparative efficacy, safety, and tolerability of diclofenac and aceclofenac in musculoskeletal pain management: A systematic review. Indian J Pain 2016;30:3-6
Both the gastric mucosal hexosamine content and gastroduodenal blood flow were significantly reduced by sodium diclofenac, while gastric mucosal hexosamine was significantly increased and gastroduodenal blood flow was unchanged with aceclofenac. Aceclofenac appears to have a low potential for causing gastroduodenal mucosal damage in humans.
Reference: Akira Yanagawa, Toru Endo, Koji Kusakari, Toshitaka Kudo, Jingoro Shimada, Yutaka Mizushima, Endoscopic evaluation of aceclofenac-induced gastroduodenal mucosal damage: a double-blind comparison with sodium diclofenac and placebo, Japanese Journal of Rheumatology, Volume 8, Issue 3, 1 September 1998, Pages 249–259, https://doi.org/10.3109/BF03041246
Aceclofenac is proposed to stimulate the synthesis of glycosaminoglycan in human osteoarthritic cartilage which may be mediated through its inhibitory action on IL-1 production and activity 1. The chrondroprotective effects are generated by 4'-hydroxyaceclofenac which suppresses IL-1 mediated production of promatrix metalloproteinase-1 and metalloproteinase-3 and interferes with the release of proteoglycan from chrondrocytes.
