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Seizure-Convulsion Ion Channel Portfolio

Introduction

Ion channels expressed in the central nervous system (CNS) are closely linked to hereditary epilepsy. Gain-of-function mutations in excitatory ion channels—such as voltage-gated sodium channels (Nav1.1, Nav1.2, Nav1.3 and Nav1.6), the voltage-gated calcium channel Cav3.2, and hyperpolarization-activated HCN1 and HCN2 channels—have been shown to cause sustained depolarizing currents, leading to excessive neuronal excitability. This hyperexcitability serves as a key driver of epileptic seizures and convulsions.

Similarly, loss-of-function mutations in inhibitory channels, including the voltage-gated potassium channel KCNQ, calcium-activated potassium channel BK, and the ligand-gated chloride channel GABAA, can also result in hyperexcitability. Drug-induced side effects that mimic these mutation-related alterations in ion channel function can exacerbate neurological complications.

Other Relevant Channels: Chloride Channel (CLC-2): Helps maintain chloride homeostasis and neuronal stability; Ligand-Gated NMDA Receptors: Modulate excitatory neurotransmission, often implicated in seizure activity.

On the other hand, antiepileptic drugs often counteract these effects by inhibiting excitatory channels or activating inhibitory channels. Therefore, the ion channels included in our seizure-convulsion panel represent promising therapeutic targets for managing hyperexcitability-related conditions, including seizures, pain, neurodegeneration, anxiety, migraines, and psychosis, as well as for reducing the risk of adverse neurological events.


Seizure-Convulsion ion channel Portfolio

Our seizure-Convulsion Ion Channel Portfolio targets ion channels associated with the central nervous system (CNS), which play a critical role in the hyperexcitability underlying seizures and convulsions. This panel includes key excitatory and inhibitory ion channels linked to inherited forms of epilepsy and offers a platform for evaluating potential. this Seizure-Convulsion Ion Channel Portfolio provides a comprehensive framework for understanding and targeting the mechanisms of neuronal hyperexcitability in epilepsy and related conditions. By integrating key excitatory and inhibitory ion channels, this panel facilitates the development of targeted therapies to manage seizures with greater precision.


Protein Assay Table

Ion channel FamilyTargetMethodSpeciesMode
Voltage-gated sodium channelNav1.1Manual patch clamphumanAgonist or Antagonist
Nav1.2Manual patch clamphumanAgonist or Antagonist
Nav1.3Manual patch clamphumanAgonist or Antagonist
Nav1.6Manual patch clamphumanAgonist or Antagonist
Nav1.7Manual patch clamphumanAgonist or Antagonist
Voltage-gated calcium channelCav2.1Manual patch clamphumanAgonist or Antagonist
Cav3.2Manual patch clamphumanAgonist or Antagonist
Voltage-gated potassium channelKv1.2Manual patch clamphumanAgonist or Antagonist
Kv2.1Manual patch clamphumanAgonist or Antagonist
Kv4.2Manual patch clamphumanAgonist or Antagonist
Kv4.3Manual patch clamphumanAgonist or Antagonist
KCNQ2/3Manual patch clamphumanAgonist or Antagonist
Potassium channel, calcium activatedBKManual patch clamphumanAgonist or Antagonist
IKManual patch clamphumanAgonist or Antagonist
SK2Manual patch clamphumanAgonist or Antagonist
SK3Manual patch clamphumanAgonist or Antagonist
Ligand-gated ion channelGABAα1β2γ2Manual patch clamphumanAgonist or Antagonist
GABAα2β2γ2Manual patch clamphumanAgonist or Antagonist
GABAα6β3γ2Manual patch clamphumanAgonist or Antagonist
nAChRα4β2Manual patch clamphumanAgonist or Antagonist
NR1/NR2AManual patch clamphumanAgonist or Antagonist
NR1/NR2BManual patch clamphumanAgonist or Antagonist
Hyperpolarization-activated channelHCN1Manual patch clamphumanAgonist or Antagonist
HCN2Manual patch clamphumanAgonist or Antagonist
Transient receptor potential channelTRPV1Manual patch clamphumanAgonist or Antagonist
TRPV4Manual patch clamphumanAgonist or Antagonist
TRPC6Manual patch clamphumanAgonist or Antagonist
TRPM8Manual patch clamphumanAgonist or Antagonist

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