KCC2 Inhibitors
The class of KCC2 inhibitors comprises a diverse array of chemical compounds strategically designed to modulate cellular processes and signaling pathways, leading to the effective inhibition of KCC2. VU0240551 inhibits KCC2 by specifically targeting the protein and impeding its transport activity, resulting in reduced chloride extrusion from neurons. This disruption of chloride homeostasis affects GABAergic signaling, contributing to altered neuronal excitability. DIOA (Dioctylazacrown) inhibits KCC2 by blocking its transport activity, leading to decreased chloride extrusion from neurons. This disruption of chloride homeostasis has implications for GABAergic signaling and may contribute to altered inhibitory neurotransmission and neuronal hyperexcitability. VU0463271 inhibits KCC2 by directly interacting with the protein, causing a reduction in its transport activity. This inhibition disrupts chloride homeostasis, leading to altered GABAergic signaling and potential effects on neuronal excitability and synaptic transmission. ML077 inhibits KCC2 by specifically targeting the protein and impeding its transport activity. This inhibition results in reduced chloride extrusion from neurons, disrupting normal neuronal chloride homeostasis. The altered chloride levels have implications for GABAergic signaling and neuronal excitability.
Niflumic Acid inhibits KCC2 by blocking its transport activity, resulting in decreased chloride extrusion from neurons. This disruption of chloride homeostasis has implications for GABAergic signaling and may contribute to altered inhibitory neurotransmission and neuronal hyperexcitability. CFTRinh-172 inhibits KCC2 by modulating the activity of the cystic fibrosis transmembrane conductance regulator (CFTR). By affecting CFTR, it indirectly influences chloride homeostasis in neurons, potentially altering GABAergic signaling and neuronal excitability. VU0359595 inhibits KCC2 by specifically targeting the protein and impeding its transport activity, resulting in reduced chloride extrusion from neurons. This inhibition disrupts normal neuronal chloride homeostasis, contributing to altered GABAergic signaling and neuronal excitability. Collectively, these inhibitors showcase the intricate strategies employed to modulate KCC2 activity, offering a foundation for the development of targeted interventions aimed at inhibiting KCC2 function in diverse cellular contexts.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
VU0240551 | 893990-34-6 | sc-253834 | 5 mg | $150.00 | ||
VU0240551 inhibits KCC2 by specifically targeting the protein and impeding its transport activity, leading to reduced chloride extrusion from neurons. This inhibition disrupts normal neuronal chloride homeostasis, contributing to altered GABAergic signaling and neuronal excitability. | ||||||
Difluoromethylornithine | 70052-12-9 | sc-204723 sc-204723A sc-204723B sc-204723C sc-204723D sc-204723E | 10 mg 25 mg 100 mg 250 mg 1 g 5 g | $58.00 $130.00 $158.00 $311.00 $964.00 $4726.00 | 2 | |
Difluoromethylornithine inhibits KCC2 indirectly by influencing the polyamine pathway. By inhibiting ornithine decarboxylase, it modulates polyamine levels, which can lead to altered KCC2 expression and function. This indirect modulation affects chloride homeostasis and GABAergic signaling in neurons. | ||||||
Niflumic acid | 4394-00-7 | sc-204820 | 5 g | $31.00 | 3 | |
Niflumic Acid inhibits KCC2 by blocking its transport activity, resulting in decreased chloride extrusion from neurons. This disruption of chloride homeostasis affects GABAergic signaling, leading to altered inhibitory neurotransmission and potentially contributing to neuronal hyperexcitability. | ||||||
CFTR Inhibitor-172 | 307510-92-5 | sc-204680 sc-204680A | 10 mg 50 mg | $165.00 $510.00 | 10 | |
CFTRinh-172 inhibits KCC2 by modulating the activity of the cystic fibrosis transmembrane conductance regulator (CFTR). By affecting CFTR, it indirectly influences chloride homeostasis in neurons, potentially altering GABAergic signaling and neuronal excitability. | ||||||
A-967079 | 1170613-55-4 | sc-363348 sc-363348A sc-363348B | 5 mg 25 mg 100 mg | $86.00 $365.00 $924.00 | 5 | |
A-967079 inhibits KCC2 by modulating its transport activity. This inhibition leads to decreased chloride extrusion from neurons, disrupting normal chloride homeostasis. The altered chloride levels have implications for GABAergic signaling, contributing to changes in neuronal excitability and synaptic transmission. | ||||||
Tolvaptan | 150683-30-0 | sc-364638 sc-364638A | 10 mg 50 mg | $122.00 $612.00 | ||
Tolvaptan inhibits KCC2 by influencing the vasopressin V2 receptor, leading to downstream effects on intracellular signaling pathways. This indirect modulation can affect KCC2 expression and function, disrupting chloride homeostasis in neurons and influencing GABAergic signaling and neuronal excitability. | ||||||
Flufenamic acid | 530-78-9 | sc-205699 sc-205699A sc-205699B sc-205699C | 10 g 50 g 100 g 250 g | $26.00 $77.00 $151.00 $303.00 | 1 | |
Flufenamic Acid inhibits KCC2 by blocking its transport activity, resulting in decreased chloride extrusion from neurons. This disruption of chloride homeostasis affects GABAergic signaling, leading to altered inhibitory neurotransmission and potentially contributing to neuronal hyperexcitability. | ||||||
VU0359595 | 1246303-14-9 | sc-475843 | 5 mg | $190.00 | 1 | |
VU0359595 inhibits KCC2 by specifically targeting the protein and impeding its transport activity, leading to reduced chloride extrusion from neurons. This inhibition disrupts normal neuronal chloride homeostasis, contributing to altered GABAergic signaling and neuronal excitability. | ||||||