The hERG gene (KCNH2) encodes a potassium ion channel responsible for the repolarizing IKr current in the cardiac action potential.
Abnormalities in this channel may lead to either Long QT syndrome (LQT2) (with loss-of-function mutations) or Short QT syndrome (with gain-of-function mutations). Both cause potentially fatal cardiac arrhythmia, due to repolarization disturbances of the cardiac action potential.

Stable recordings. A series of drug concentrations can be applied to one cell. The top figures show the original traces and the corresponding IC₅₀. Five concentrations of Quinidine (0.1, 0.3, 1, 3 and 10 μM) have been applied.
The lower figure shows the corresponding Imax (-40 mV) including a wash out step and an additional application of the blocker to demonstrate the stability of whole cell recordings.
Cells were kindly provided by Cytomyx/Millipore, UK.

Pharmacology. The NPC-16 chips enable precise drug testing even with sticky compounds like some hERG blockers. Terfenadine showed a concentration dependent block of hERG with an IC₅₀ = 11.0 ± 3 nM,  Flunarizine showed an IC₅₀ of 163.7 ± 19 nM and Cisapride 8.9 ± 3 nM. hERG expressing HEK293 cells were kindly provided by Cytomyx/Millipore, UK.