This strategy of using a competing agonist with a longer half-life has been successfully used to treat addiction to opiates such as heroin by substituting with methadone.

[4] Vanoxerine has been through human trials up to Phase II,[5][6][7] but development was stopped due to observed QTc effects in the context of cocaine use.

It was found that piperidine analogs are still fully active DRIs, although they do not have any affinity for the "piperazine binding site" unlike the GBR compounds.

Further SAR revealed that while there are 4 atoms connecting the two fluorophenyl rings to the piperazine, the ether in the chain could be omitted in exchange for a tertiary nitrogen.

[14] Experiments have successfully been performed on cell cultures,[citation needed] canine hosts and testing has moved towards human trials.

[15] Vanoxerine is a multichannel blocker, acting on IKr (potassium), L-type calcium and sodium ion channels.

[15] By blocking these specific channels, there is a prolongation of the action potential of the cell, preventing reactivation by a reentrant circuit.

[15] Vanoxerine is a drug that was in the midst of recruiting participants for a phase III human clinical trial for its use as a cardiac antiarrhythmic when safety concerns arose.