Numerous Cu(II) complexes of NSAIDs with improved anti-inflammatory activity and decreased Gastrointestinal (GI) toxicity have been developed as a result of the suggested curative qualities of Cu-based Non-Steroidal Anti-Inflammatory Medicines (NSAIDs). Since many of today's anti-inflammatory medication regimens, especially those based on NSAIDs, remain either woefully ineffective or linked to significant renal, GI, and cardiovascular side effects, it is important that these low toxicity Cu medicines eventually find their way to a wider human market. However, it is still unclear where Cu-NSAIDs' anti-inflammatory and gastric-sparing effects come from. Apart from their commonly reported Superoxide Dismutase (SOD)-like activity in vitro, their potential to affect copper metabolism has been a subject of contention. Relatively little is known, however, regarding how they eventually control the inflammatory process and/or immune system.
