Ibuprofen arginine

Ibuprofen arginine (Ibu-AR) exerts antioxidant and anti-inflammatory effects in CFBE41o- bronchial epithelial cells and RAW 264.7 macrophages: it scavenges ROS, elevates NO, inhibits nitrite production, downregulates M1-related gene and protein levels such as TNF-α, IL-6, and iNOS, and suppresses p-STAT3/p-ERK1/2 signaling, without altering TLR4 expression^[1].

Ibuprofen arginate (24 h) inhibits COX-2-dependent PGE₂ production in RAW264.7 and A549 cells without reducing cell viability^[2].
Ibuprofen arginate (at increasing concentrations based on equimolar L-arginine; 24 h) can provide arginine substrate for iNOS in LPS-stimulated RAW264.7 macrophages cultured in arginine-free medium; it can restore iNOS activity in LPS-stimulated RAW264.7 macrophages in the presence of ADMA, L-NMMA (HY-18732), or L-NAME (HY-18729)^[2].
Ibuprofen arginate reverses L-NAME-induced contraction in isolated mouse thoracic aorta; it restores eNOS-dependent vasodilation in isolated rat thoracic aorta^[2].
Ibuprofen arginine (IBP-arginine) (4%; 5 min) is the most effective antibacterial solution against multispecies root canal biofilms, reducing RLU by 96%; it reduces the percentage of viable cells in multispecies endodontic biofilms to 19.84%^[4].
Ibuprofen arginine (4% diluted 1/100) maintains 62.14% and 60.18% 3T3-L1 fibroblast viability at 1 h and 24 h, respectively^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.