The voltage-gated human-Ether-à-go-go-Related Gene (hERG) potassium channel is the molecular correlate of the rapid delayed rectifier potassium current, IKr, which is an important determinant of repolarisation of the action potential in cardiac myocytes. Loss of function in hERG due to inherited mutations results in Long QT Syndrome Type 2 (LQT2), which can result in the potentially fatal arrhythmia, Torsades de Pointes. However, our ability to predict how such mutations influence cellular electrophysiology and thus behaviour at larger scales depends critically on a faithful characterisation of ion channel kinetics. In this study, we tested the ability of a previously-developed sinusoidal voltage clamp protocol to characterise kinetics of the LQT2-related R56Q hERG mutation. Membrane currents were recorded in Xenopus laevis oocytes injected with cRNA encoding wild type (WT) or R56Q mutant hERG channels at room temperature using the two-electrode voltage clamp technique. We optimised a mathematical model to whole-cell current traces evoked by the sinusoidal voltage clamp protocol, as well as traditional activation and inactivation square step voltage clamp protocols. The models were then used to predict the response to a premature stimulation protocol, where R56Q hERG showed smaller protective currents in response to premature stimuli than WT due to accelerated channel deactivation. Furthermore, the models were able to predict the response to a complex series of physiologically-relevant action potential waveforms with quantitative accuracy. Our study demonstrates the broader applicability of sinusoidal voltage protocols for rapid characterisation of ion channel kinetics, extending the approach to mutations in hERG which underlie congenital rhythm disorders. The resulting predictive models can be used for improved assessment of clinical phenotypes arising from abnormalities in hERG, due to genetic mutation or pharmacological modulation.