Anticoagulant rodenticides (ARs) are the most widely used means of rodent pest control worldwide. These poisons cause death due to uncontrolled hemorrhage by interfering with vitamin K metabolism, a critical cofactor in the production of blood coagulation proteins. Predatory birds are at high risk of cumulative AR toxicosis from consumption of AR-poisoned rodents. Moreover, highly potent second-generation AR compounds have prolonged residual effects on coagulation protein synthesis after a single exposure. Wildlife AR exposure is typically measured by chemical analyses of postmortem liver tissue to detect individual compounds. Although sensitive and specific, chemical quantitation of ARs is limited by expense, slow turnaround time, and invasive sampling unsuitable for clinical practice. Importantly, defined thresholds of liver AR residues associated with clinical signs of toxicosis that impact survival are unknown for predatory birds. Variable potencies among AR compounds and interspecies differences in vitamin K metabolism further complicate differentiation of toxic from non-toxic liver AR residue concentrations by chemical analysis alone. Surveys of birds of prey from around the world reveal that AR exposure is highly prevalent. Liver residues are typically found in more than 50% of tested birds, with some surveys documenting 100% exposure. Our project fills a gap in surveillance and clinical care of raptors by developing a biomarker of AR toxicosis that defines clinically relevant AR exposure thresholds in living birds. We aim to optimize a novel biomarker assay that detects a dysfunctional coagulation protein indicative of vitamin K deficiency and relate results to liver AR concentrations. Long-term, we aim to use this assay as a rapid antemortem screening test for AR toxicosis applicable to any predatory bird species and any AR compound. Ultimately, these results will improve treatment of exposed wildlife and inform policy decisions surrounding AR use.