NOS1 and ischemia reperfusion injury: To investigate the structural basis of this resistance, we constructed three molecular models representing distinct redox states of NADP(H), FAD, and FMN, and derived new parameters for these cofactors (oxidized and reduced forms) using the def2-TZVP basis set.<h4>Results</h4>While those inhibitors showed some therapeutic benefit in ischemia-reperfusion injury, they failed to suppress nNOS activity to physiological levels.