Groups of 30 male and 30 female Fischer‐344 rats were fed dietary concentrations of 0. 30, 100, 300, 3000, or 10,000 ppm decarboxyfenvalerate (DC‐FEN) for up to 13 wk. An interim kill of 10 rats/sex · group was performed at 7 wk. Following 7 or 13 wk of dietary treatment, groups of rats were necropsied, which included evaluation of he‐mocellular, hemochemical, and uretic parameters, selected absolute and relative organ weights, and macroscopic and microscopic observations. DC‐FEN did not affect mortality. Body weight was decreased in male rats fed 10,000 ppm DC‐FEN. Statistically and toxicologically significant differences in clinicopathologic parameters were observed at either the highest or two highest exposure levels. Some statistically significant differences were noted in some hemocellular and/or hemochemical parameters at either 100 or 300 ppm. These subtle changes were either not dose‐related, inconsistent, or not of sufficient difference to be determined to have biological significance. Absolute and relative liver weights of male and female rats fed ≥300 ppm DC‐FEN were all higher than control values except for absolute weights in female rats (300 ppm) at the interim kill. Consistent significant increases in absolute or relative kidney weights were observed in male and female rats fed 3000 or 10,000 ppm DC‐FEN. Other statistically significant differences in absolute and/or relative organ weights were seen primarily where the higher doses had caused decreased carcass weight. Macroscopic treatment‐related liver enlargement (hepatomegaly) was observed in male and female rats fed 3000 or 10,000 ppm DC‐FEN. Only one female rat fed 300 ppm DC‐FEN had hepatomegaly at the terminal kill. Significant treatment‐related microscopic effects were limited to glomerulonephrosis in male and female rats fed 10,000 ppm and hepatocellular hypertrophy and other associated liver changes in male and female rats fed 3000 or 10,000 ppm DC‐FEN. Liver effects at doses <3000 ppm were indicative of a physiologic adaptive response and were not toxicologically significant. Therefore, the biologically significant no‐effect level was 300 ppm.