Introduction
Depression is driven by imbalances in neurotransmission and neuronal plasticity, impacting key brain regions like the prefrontal cortex and hippocampus. Ion channels are pivotal in regulating these processes. Voltage-gated sodium channels (e.g., Nav1.3, Nav1.7) and potassium channels (e.g., Kv1.1, KCNQ2/3) control neuronal excitability, while calcium channels (e.g., Cav2.2) support synaptic plasticity. GABA receptors and NMDA receptors fine-tune the brain's excitatory-inhibitory balance, which is often disrupted in depression.
Targeting ion channels in depression offers a promising avenue for developing more effective and selective treatments. By modulating ion channels involved in synaptic plasticity, neuronal excitability, and neurotransmitter release, new therapies could restore the balance of excitatory and inhibitory signaling that is disrupted in depression.
Depression Ion Channel Portfolio
Our Depression Ion Channel Portfolio offers a targeted approach to understanding and treating depression by profiling the ion channels and receptors that regulate mood and cognitive function. By focusing on channels that influence mood-related brain regions, this portfolio helps uncover the underlying mechanisms of depression and accelerates the development of innovative therapies.
Targeting ion channels such as sodium, potassium, calcium, GABA, and NMDA receptors allows us to develop selective, potent, and safe treatments that restore balance in mood regulation and promote neuroplasticity—key to overcoming depression
Ion channel Family | Target | Method | Species | Mode |
---|---|---|---|---|
Voltage-gated potassium channel | KCNQ2/3 | Manual patch clamp | human | Agonist or Antagonist |
KCNQ3/5 | Manual patch clamp | human | Agonist or Antagonist | |
KV1.1 | Manual patch clamp | human | Agonist or Antagonist | |
Two-pore domain potassium channel | TREK-1 | Manual patch clamp | human | Agonist or Antagonist |
Voltage-gated calcium channel | L type calcium channel | Manual patch clamp | human | Agonist or Antagonist |
N type calcium channel | Manual patch clamp | human | Agonist or Antagonist | |
Voltage-gated sodium channel | Nav1.3 | Manual patch clamp | human | Agonist or Antagonist |
Nav1.7 | Manual patch clamp | human | Agonist or Antagonist | |
Ligand-gated ion channel | NR1/NR2A | Manual patch clamp | human | Agonist or Antagonist |
NR1/NR2B | Manual patch clamp | human | Agonist or Antagonist | |
nAChR α7/RIC3 | Manual patch clamp | human | Agonist or Antagonist | |
nAChR α4β2 | Manual patch clamp | human | Agonist or Antagonist | |
AMPA receptor | Manual patch clamp | human | Agonist or Antagonist | |
GABAA(α2β3γ2) | Manual patch clamp | human | Agonist or Antagonist | |
GABAA(α3β3γ2) | Manual patch clamp | human | Agonist or Antagonist | |
GABAA(α4β3γ2) | Manual patch clamp | human | Agonist or Antagonist | |
GABAA(α4β3δ) | Manual patch clamp | human | Agonist or Antagonist | |
GABAA(α5β3γ2) | Manual patch clamp | human | Agonist or Antagonist |
We value your inquiries and are here to provide you with tailored solutions for your drug discovery and development needs. Whether you have questions, require more information, or are interested in discussing potential collaborations, our team of experts is just a message away.
Feel free to reach out to us.