Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disorder, with 1:500-1:200 prevalence worldwide. The recently discovered MYBPC3:c.772G>A variant is responsible for faster actin and myosin cycling and higher ATP consumption; to counterbalance the increased energy request, cardiomyocytes undergo a secondary functional remodeling, with the enhancement, among the others, of the late sodium current (INaL). Our aim is to investigate the anti-arrhythmic mechanisms of ranolazine, that mainly targets INaL, employing population of models and 3D biventricular electromechanical simulations by adopting the electromechanical model by Tomek and Land. We generated 10000 cells by randomizing maximal conductances, fluxes and transition rates of the cross-bridges using a Latin Hypercube Sampling within 50-200% of the basal value. We tested the effects of ranolazine at 3,6, and 10 µM extracting biomarkers relative to action potential, calcium transient and active tension 3D Simulations were performed with a human-based biventricular electromechanical framework calibrated and validated against experimental and clinical ventricular data. The framework was extended to incorporate MYBPC3:c.772G>A remodelling, confined to the hypertrophied septal region, together with a dose-dependent ranolazine block. c772G>A caused action potential duration prolongation (+80%), slower calcium decay (+22%), lower calcium amplitude (-16%) and reduced AT peak (-12%). The effect of ranolazine in HCM mildly shortened APD90 (-16%), reduced calcium amplitude and active tension (-11%, -20% respectively). At the organ scale, HCM showed preserved systolic function, (EF 63.5% vs 61.7%). Simulated ECGs showed marked QT prolongation, (350 vs 520 ms in lead V1), with altered T-wave morphology. Ranolazine produced dose-dependent shortening of repolarisation, with QT decreasing to 496, 476, and 459 ms in V1, at 3, 6, and 10 μM, respectively. EF decreased slightly to 62.9%, 62.5%, and 62.1% with minor changes in the pressure-volume loops. Overall, ranolazine acts mainly as an electrical modulator in this setting, improving repolarisation with limited negative inotropic effect.