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V3890

Sigma-Aldrich

VU0240551

≥98% (HPLC)

Sinônimo(s):

CID 7211972, N-(4-Methyl-2-thiazolyl)-2-[(6-phenyl-3-pyridazinyl)thio]-acetamide, SID 56405457, VU0240551-1, VU0240551-2-D4

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About This Item

Fórmula empírica (Notação de Hill):
C16H14N4OS2
Número CAS:
893990-34-6
Peso molecular:
342.44
Número MDL:
MFCD05957363
Código UNSPSC:
12352200
ID de substância PubChem:
329829046
NACRES:
NA.77

Ensaio

≥98% (HPLC)

Formulário

powder

solubilidade

DMSO: >20 mg/mL

temperatura de armazenamento

2-8°C

cadeia de caracteres SMILES

Cc1csc(NC(=O)CSc2ccc(nn2)-c3ccccc3)n1

InChI

1S/C16H14N4OS2/c1-11-9-23-16(17-11)18-14(21)10-22-15-8-7-13(19-20-15)12-5-3-2-4-6-12/h2-9H,10H2,1H3,(H,17,18,21)

chave InChI

WJRWSLORVIHRNX-UHFFFAOYSA-N

Ações bioquímicas/fisiológicas

VU0240551 is a potent, selective KCC2 inhibitor.
VU0240551 is a potent, selective KCC2 inhibitor. KCC2 is a potassium-chloride exchanger expressed specifically in neurons. KCC2 functions to lower intracellular chloride concentrations below the electrochemical potential of the cells, thereby increasing the hyperexcitability of the neurons. KCC2 activity enhances GABA and other inhibitory neurotransmission and is implicated in pain processing. VU0240551 was discovered in a high-throughput screen, followed by directed medicinal chemistry. VU0240551 is selective for KCC2 over NKCC1. VU0240551 binds competitively to the K+ site and binds noncompetitively to the Cl- site. VU0240551 is the only small molecule with specificity for a KCC family member.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Escolha uma das versões mais recentes:

Certificados de análise (COA)

Lot/Batch Number
035M4779V
044M4775V
099K4605

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Mogens Andreasen et al.
Journal of neurophysiology, 117(4), 1512-1523 (2017-01-20)
The loop diuretic furosemide is known to have anticonvulsant effects, believed to be exerted through blockade of glial Na
Josiane C S Mapplebeck et al.
Cell reports, 28(3), 590-596 (2019-07-18)
The behavioral features of neuropathic pain are not sexually dimorphic despite sex differences in the underlying neuroimmune signaling. This raises questions about whether neural processing is comparably altered. Here, we test whether the K+-Cl- co-transporter KCC2, which regulates synaptic inhibition
Martin Heubl et al.
Nature communications, 8(1), 1776-1776 (2017-11-28)
The K+-Cl- co-transporter KCC2 (SLC12A5) tunes the efficacy of GABAA receptor-mediated transmission by regulating the intraneuronal chloride concentration [Cl-]i. KCC2 undergoes activity-dependent regulation in both physiological and pathological conditions. The regulation of KCC2 by synaptic excitation is well documented; however
Nicolas Doyon et al.
PLoS computational biology, 7(9), e1002149-e1002149 (2011-09-21)
Chloride homeostasis is a critical determinant of the strength and robustness of inhibition mediated by GABA(A) receptors (GABA(A)Rs). The impact of changes in steady state Cl(-) gradient is relatively straightforward to understand, but how dynamic interplay between Cl(-) influx, diffusion
Kwan Yeop Lee et al.
Pain, 156(12), 2431-2437 (2015-07-18)
Synaptic inhibition plays a key role in processing somatosensory information. Blocking inhibition at the spinal level is sufficient to produce mechanical allodynia, and many neuropathic pain conditions are associated with reduced inhibition. Disinhibition of spinal neurons can arise through decreased

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