Daunomycin inhibits the B leads to Z transition in poly d(G-C).

The cancer drug daunomycin is an effective inhibitor of the B leads to Z transition in poly d(G-C) in 4 M NaCl. Both the rate and extent of the B leads to Z transition are decreased by the drug, as judged by equilibrium and kinetic studies. Daunomycin can, under some conditions, convert Z form DNA back to B form. Drug binding to poly d(G-C) in 4 M NaCl is slow and highly cooperative, consistent with a role for daunomycin as an allosteric effector on the B leads to Z equilibrium. Since daunomycin binds preferentially to alternating purine-pyrimidine sequences, which are the very sequences capable of undergoing the B leads to Z transition, these effects may be an important part of the mechanism by which the drug inhibits transcription and replication.