Date published: 2025-12-21

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KQT2 Inhibitors

KQT2 inhibitors are chemical compounds that target the Kv7.2/Kv7.3 potassium channels, also referred to as the KQT2 channels. These channels are part of a broader family of voltage-gated potassium channels that play a critical role in regulating the electrical excitability of neurons and other excitable cells. KQT2 channels specifically help control the flow of potassium ions across cell membranes, influencing the cell's membrane potential and the ability to generate action potentials. Inhibitors of KQT2 act by blocking or reducing the activity of these channels, altering the flow of potassium ions and affecting the overall electrical properties of the cells in which these channels are expressed. This modulation can lead to changes in cellular excitability, influencing the way that cells respond to stimuli.

Structurally, KQT2 inhibitors are often designed to interact with specific sites within the Kv7.2/Kv7.3 channels, typically through mechanisms that involve binding to the channel's pore or voltage-sensing domains. These interactions can stabilize specific conformations of the channel, preventing it from opening or promoting its closed state. The precise molecular architecture of KQT2 inhibitors can vary widely, and these compounds may feature diverse chemical backbones and functional groups that provide selective affinity for the KQT2 channel subtypes. Modulation of KQT2 channels by these inhibitors is of significant interest in research focused on understanding cellular electrophysiology, as these channels are key contributors to maintaining the balance of ion flows in excitable tissues such as the brain and heart.

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Retinoic Acid, all trans

302-79-4sc-200898
sc-200898A
sc-200898B
sc-200898C
500 mg
5 g
10 g
100 g
$65.00
$319.00
$575.00
$998.00
28
(1)

Retinoic Acid could bind to retinoic acid receptors which then act as transcription factors to repress or activate gene expression, potentially leading to the downregulation of KCNQ2 transcription.