arginase II Inhibitors

Arginase II inhibitors encompass a variety of compounds that directly or indirectly target the enzyme's activity, each acting through distinct mechanisms. Direct inhibitors such as Nω-Hydroxy-nor-L-arginine and Nor-NOHA effectively block arginase II by competing with its natural substrate, L-arginine, for the enzyme's active site. This mode of inhibition directly impairs the catalytic function of arginase II, highlighting the enzyme's substrate specificity and for targeted intervention. Similarly, L-lysine and L-ornithine serve as competitive inhibitors, binding to arginase II and hindering its ability to process L-arginine. These compounds demonstrate the efficacy of substrate competition as a strategy to inhibit arginase II activity.In contrast, compounds such as Bezafibrate, DFMO, Sildenafil, Simvastatin, Losartan, Dexamethasone, Aspirin, and Captopril modulate arginase II activity indirectly through various biological pathways. Bezafibrate, as a PPAR agonist, influences lipid metabolism, subsequently affecting arginase II expression. DFMO, targeting ornithine decarboxylase, impacts polyamine synthesis, indirectly altering arginase II function. Sildenafil, through enhancement of nitric oxide signaling, provides an alternative route to reduce arginase II activity. Statins like Simvastatin affect endothelial function, thereby modulating arginase II. Cardiovascular agents such as Losartan and Captopril alter the renin-angiotensin system, indirectly influencing arginase II activity. Anti-inflammatory compounds like Dexamethasone and Aspirin impact inflammatory pathways, which can in turn modulate arginase II activity. These diverse approaches to inhibiting arginase II underscore the complex regulation of the enzyme and the multiple pathways through which its activity can be modulated.