• SyncroPatch 384/768i

    世界最速のオートパッチ
  • SyncroPatch 384/768i

    384ch同時測定 => 768chへアップグレード可能
  • SyncroPatch 384/768i

    ギガシールによるHTS
  • SyncroPatch 384/768i

    Analysis Software even more powerful than before
  • SyncroPatch 384/768i

    最先端技術によるアッセイ柔軟性

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.

Summary:

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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