• Our CiPA Instruments

    Patchliner & SyncroPatch 384PE (CiPA ion channel working group); CardioExcyte 96 (CiPA myocyte working group)

  • CiPA hERG Protocol

    This protocol was used for hERG studies on the Patchliner and SyncroPatch 384PE.

  • HTS CiPA hERG Assay

    Effects of Cisapride using the CiPA hERG protocol on the SyncroPatch 384PE

  • Myocyte & Ion Channel Effects

    Arrhythmic Field potentials in iPSC-derived Cardiomyocytes (CardioExcyte 96) and hERG current inhibition (SyncroPatch 384PE)

  • Gigaseal HTS patch clamp

    CiPA-specified cardiac ion channels recorded at high throughput

  • Gigaseal HTS patch clamp

    High throughput recordings of cardiac ion channels at physiological temperature

  • CardioExcyte 96 screening tool

    CardioExcyte 96 with integrated liquid handling for cardiac safety screening

NaV1.5 - "High Throughput Pharmacology of NaV1.5 Channels on Nanion's SyncroPatch 384PE"

icon sp96   SyncroPatch 384PE (a predecessor model of SyncroPatch 384i) application note   logo pdf   (1.6 MB)
Cells were kindly provided by Millipore.


The NaV1.5 channel, encoded by the SCN5A gene, is a voltage-gated sodium (NaV) channel found in skeletal muscle and heart. It is TTX insensitive with an IC50 in the micromolar range. NaV1.5 is responsible for the upstroke of the cardiac action potential in both ventricular and atrial myocytes and is therefore critical for generation and propagation of the cardiac action potential in human heart. Block of this channel can lead to prolongation of the QRS interval of the electrocardiogram (ECG) and can have profound effects on the rate of cardiac deploarization and conduction velocity, thus causing potentially dangerous cardiac arrythmias. Furthermore, effects of NaV1.5 inactivation can modify cardiac repolarization. Given the importance of this channel in maintaining cardiac function, it has become an important target in compound safety screening. Local anaesthetics, such as lidocaine, have been shown to exhibit state- and use-dependence when acting on the cardiac sodium channel. The IC50 was shown to be approximately 30 times lower at depolarized holding potentials where inactivation was almost complete. For this reason, it is important to test potency of compounds at different holding potentials. Here we present high quality data with reliable pharmacology on hNaV1.5 expressing HEK293 cells at a high throughput collected on the SyncroPatch 384PE. Current-voltage plots and concentration response curves for four NaV channel blockers are shown, including lidocaine at different holding potentials.

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