To restore native biodiversity on island ecosystems containing invasive rodents, partial- and whole-island eradications generally rely on broadcast baiting with anticoagulant rodenticides (ARs). This approach can result in bait pellets entering aquatic environments, raising concerns about effects to non-target fish. Salmonids are a dominant group of fishes on many temperate islands targeted for rodent eradication, and AR toxicity data for salmonids are limited. Our goal was to determine if coho salmon (Oncorhynchus kisutch) are susceptible to coagulopathy and death via exposure to commonly used ARs. We assessed risk of ARs to coho using dose-response curves generated through intraperitoneal injections after determining that coho would not directly ingest the AR baits. Median lethal doses (96-h LD₅₀) estimated using 100 % corn oil carrier were 85.7 µg/g for brodifacoum and 54.0 µg/g for diphacinone. Acetone (30–41 %), used to dissolve ARs in corn oil, reduced the toxicity of diphacinone (LD₅₀ = 102.3 µg/g, p < 0.001) but not brodifacoum (LD₅₀ = 73.3 µg/g, p = 0.126) indicating that solvent choice can influence toxicity outcomes. Behavioral changes and onset of mortality differed between the two ARs, with diphacinone acting more rapidly. Tissue analysis supported a difference in toxicokinetics between the two ARs, with significant decreases in liver and muscle residues for diphacinone but not brodifacoum. Sublethal brodifacoum exposure (53.9 µg/g; LD₁₃) impaired blood clotting at 72- and 96- h but returned to baseline by 120 h. No clotting impairment was observed up to 144 h after diphacinone exposure (45.5 µg/g; LD₄), suggesting a non-coagulopathy mode of action. These findings will inform risk assessments when considering use of these ARs for rodent management near streams and shorelines and clearly demonstrate that brodifacoum causes coagulopathy in coho.