Pretreatment with erythromycin indu

Pretreatment with erythromycin induced an approximately 14–22-fold reduction in hERG affinity for pore-binding drugs atconcentrations of erythromycin, which by themselves only block hERG by 10% or less. These results suggest distinct,allosterically linked binding sites on opposite sides of the hERG channel. Occupancy of the external site by erythromycinreduces the affinity of the pore binding site. Furthermore, these results suggest that co-administration of erythromycin mayprovide some reduction in cardiac liability of potent hERG-blocking drugs.

Results (English) 1:

Pretreatment with an erythromycin induced Approximately 14-22-fold reduction in pore-hERG binding affinity for drugs atconcentrations of erythromycin, the which by Themselves only block hERG by 10% or less. Reviews These results suggest distinct, allosterically linked binding sites on opposite sides of the hERG channel. Occupancy of the external site by erythromycinreduces the affinity of the pore binding site. Furthermore, Reviews These results suggest that co-administration of erythromycin mayprovide some reduction in cardiac liability of potent hERG-blocking drugs.

Results (English) 2:

Pretreatment with interactions induced an approximately 14 – 22-fold reduction in hERG affinity for pore-binding drugs atconcentrations of interactions, which by themselves only block hERG by 10% or less. These results suggest distinct, allosterically linked binding sites on opposite sides of the hERG channel. Occupancy of the external site by erythromycinreduces the affinity of the pore binding site. Furthermore, these results suggest that co-administration of interactions mayprovide some reduction in cardiac liability of potent hERG-blocking drugs.