L-NIL is a selective nitric oxide synthase (iNOS) inhibitor that reverses burn-induced activation of glycogen synthase kinase-3β in rat skeletal muscle and may slow the progression of squamous cell carcinoma lung.

mouse inducible NO synthase:3.3 μM, rat brain constitutive NO synthase:92 μM

The IC50 values of L-NIL for miNOS and rcNOS were 3.3 and 92 pM, respectively, indicating that L-NIL was 28-fold more selective for miNOS. In addition, the potency of L-NIL on miNOS was approximately 6 times higher than that of L-NMA or L-NNA, and L-NIL produced concentration-dependent inhibition of both inducible NOS (miNOS) in mice and constitutive NOS (rcNOS) in the rat brain, with a higher potency on miNOS [1].

L-NIL protects the integrity of the tarsal, talus and calcaneus bones as well as the soft tissue surrounding the joint, while adjuvant controls exhibit severe deterioration of these bones and dramatic soft tissue swelling. L-NIL limits progression of preexisting atherosclerosis in hypercholesterolemic rabbits. Increased intimal collagen accumulation may participate in iNOS-induced atherosclerosis progression.L-NIL may prove particularly useful in determining the role of nitric oxide production by inducible NOS in models of chronic inflammation (e.g., adjuvant arthritis). L-NIL suppresses the increase in plasma nitrite levels and joint inflammation associated with adjuvant-induced arthritis in a dose-dependent manner. L-NIL attenuates the inducible nitric oxide synthase immunoreactivity in adjuvant-treated rats[2];L-NIL (10 and 30 mg/kg, IP) prevents inflammation, oxidative stress and autophagy induced by renal IR in mice.[4]