Ferroptosis is a kind of controlled cell dying that may be caused by inhibition from the cystine-glutamate antiporter, system xc-. One of the existing system xc- inhibitors, imidazole ketone erastin (IKE) is really a potent, metabolically stable inhibitor of system xc- and inducer of ferroptosis potentially appropriate for in vivo applications. We investigated the pharmacokinetic and pharmacodynamic options that come with IKE inside a diffuse large B cell lymphoma (DLBCL) xenograft model and shown that IKE exerted an antitumor effect by inhibiting system xc-, resulting in glutathione depletion, fat peroxidation, and also the induction of ferroptosis biomarkers in vitro as well as in vivo. Using untargeted lipidomics and qPCR, we identified distinct options that come with fat metabolic process in IKE-caused ferroptosis. Additionally, biodegradable polyethylene glycol-poly(lactic-co-glycolic acidity) nanoparticles were employed to assist in IKE delivery and exhibited reduced toxicity in contrast to free IKE inside a DLBCL xenograft model.