The biochemistry and genetics of kdr-type resistance in the Ectiban-R strain of German cockroach were studied to provide information on the molecular basis of this resistance and to allow for more detailed comparison to the well-studied kdr mechanism in house files. The kdr-type resistance in Ectiban-R is autosomal, incompletely recessive, probably monofactorial, and may be different from the mechanism responsible for resistance to pyrethrins in other cockroach strains. Ectiban-R was cross-resistant to bioallethrin (48-fold), deltamethrin (17-fold), fenvalerate (59-fold), aconitine (16-fold), batrachotoxin (8.7-fold), and verapamil (5.4-fold), but not to other sodium channel drugs. Using [3H]saxitoxin as a probe of the sodium channel we found no difference in binding affinity or number of binding sites per head (or per mg protein) between resistant and susceptible strains. Our results suggest that the sodium channels of kdr-type-resistant German cockroaches are qualitatively different than those of the susceptible strain. © 1991.