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VU 0240551 Sale

(Synonyms: N-(4-甲基-2-噻唑基)-2-[(6-苯基-3-哒嗪基)硫基]-乙酰胺) 目录号 : GC37927

A KCC2 cotransporter inhibitor

VU 0240551 Chemical Structure

Cas No.:893990-34-6

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥1,238.00
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5mg
¥1,125.00
现货
10mg
¥1,451.00
现货
50mg
¥6,131.00
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产品描述

VU0240551 is a K+/Cl- cotransporter 2 (KCC2) inhibitor (IC50 = 568 nM).1 It selectively inhibits KCC2 over Na+/K+/Cl- cotransporter 1 (NKCC1; IC50 = >50 ?M) but does inhibit the activity of adenosine A1 and A3 receptors, as well as inhibits activity of L-type calcium channels at the benzothiazepine site and human ether-a-go-go-related gene (hERG) potassium channels by greater than 50% in a panel of 68 receptors, ion channels, and transporters at 10 ?M. VU0240551 decreases potassium ion uptake by 70% in HEK293 cells expressing KCC2 when used at a concentration of 1 ?M.

1.Delpire, E., Days, E., Lewis, L.M., et al.Small-molecule screen identifies inhibitors of the neuronal K-Cl cotransporter KCC2Proc. Natl. Acad. Sci. USA106(13)5383-5388(2009)

Chemical Properties

Cas No. 893990-34-6 SDF
别名 N-(4-甲基-2-噻唑基)-2-[(6-苯基-3-哒嗪基)硫基]-乙酰胺
Canonical SMILES O=C(CSC1=NN=C(C2=CC=CC=C2)C=C1)NC3=NC(C)=CS3
分子式 C16H14N4OS2 分子量 342.44
溶解度 DMSO: ≥ 50 mg/mL (146.01 mM); Water: < 0.1 mg/mL (insoluble) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.9202 mL 14.6011 mL 29.2022 mL
5 mM 0.584 mL 2.9202 mL 5.8404 mL
10 mM 0.292 mL 1.4601 mL 2.9202 mL
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Research Update

Differential effects of GABA in modulating nociceptive vs. non-nociceptive synapses

Neuroscience 2015 Jul 9;298:397-409.PMID:25931332DOI:10.1016/j.neuroscience.2015.04.040

GABA (γ-amino-butyric acid) -mediated signaling is normally associated with synaptic inhibition due to ionotropic GABA receptors that gate an inward Cl(-) current, hyperpolarizing the membrane potential. However, there are also situations where ionotropic GABA receptors trigger a Cl(-) efflux that results in depolarization. The well-characterized central nervous system of the medicinal leech was used to study the functional significance of opposing effects of GABA at the synaptic circuit level. Specifically, we focused on synapses made by the nociceptive N cell and the non-nociceptive P (pressure) cell that converge onto a common postsynaptic target. It is already known that GABA hyperpolarizes the P cell, but depolarizes the N cell and that inhibition of ionotropic GABA receptors by bicuculline (BIC) has opposing effects on the synapses made by these two inputs; enhancing P cell synaptic transmission, but depressing N cell synapses. The goal of the present study was to determine whether the opposing effects of GABA were due to differences in Cl(-) homeostasis between the two presynaptic neurons. VU 0240551 (VU), an inhibitor of the Cl(-) exporter K-Cl co-transporter isoform 2 (KCC2), attenuated GABA-mediated hyperpolarization of the non-nociceptive afferent while bumetanide (BUM), an inhibitor of the Cl(-) importer Na-K-Cl co-transporter isoform 1 (NKCC1), reduced GABA-mediated depolarization of the nociceptive neuron. VU treatment also enhanced P cell synaptic signaling, similar to the previously observed effects of BIC and consistent with the idea that GABA inhibits synaptic signaling at the presynaptic level. BUM treatment depressed N cell synapses, again similar to what is observed following BIC treatment and suggests that GABA has an excitatory effect on these synapses. The opposing effects of GABA could also be observed at the behavioral level with BIC and VU increasing responsiveness to non-nociceptive stimulation while BIC and BUM decreased responsiveness to nociceptive stimulation. These findings demonstrate that distinct synaptic inputs within a shared neural circuit can be differentially modulated by GABA in a functionally relevant manner.