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Merck
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文件

SML2172

Sigma-Aldrich

CLP290

≥98% (HPLC)

别名:

[5-Fluoro-2-[(Z)-(2-hexahydropyridazin-1-yl-4-oxo-thiazol-5-ylidene)methyl]phenyl] pyrrolidine-1-carboxylate

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About This Item

经验公式（希尔记法）:
C19H21FN4O3S
CAS号:
1181083-81-7
分子量:
404.46
MDL號碼:
MFCD28166314
分類程式碼代碼:
12352200

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

FC1=CC=C(/C=C2C(N=C(N3NCCCC3)S/2)=O)C(OC(N4CCCC4)=O)=C1

InChI

1S/C19H21FN4O3S/c20-14-6-5-13(15(12-14)27-19(26)23-8-3-4-9-23)11-16-17(25)22-18(28-16)24-10-2-1-7-21-24/h5-6,11-12,21H,1-4,7-10H2/b16-11-

InChI 密鑰

DIXMMXNNKLCLOM-WJDWOHSUSA-N

生化／生理作用

CLP290 is a small molecule enhancer of KCC2 activity. It is an orally active and more bioavailable precursor of the selective K+-Cl- cotransporter KCC2 activator CLP257. CLP290 was recently shown to restore Cl- transport and rescue morphine-induced hyperalgesia (MIH) in morphine-treated rats.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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Martin Gagnon et al.
Nature medicine, 19(11), 1524-1528 (2013-10-08)
The K(+)-Cl(-) cotransporter KCC2 is responsible for maintaining low Cl(-) concentration in neurons of the central nervous system (CNS), which is essential for postsynaptic inhibition through GABA(A) and glycine receptors. Although no CNS disorders have been associated with KCC2 mutations
Francesco Ferrini et al.
Scientific reports, 7(1), 3870-3870 (2017-06-22)
Morphine-induced hyperalgesia (MIH) is a severe adverse effect accompanying repeated morphine treatment, causing a paradoxical decrease in nociceptive threshold. Previous reports associated MIH with a decreased expression of the Cl
Akiko Doi et al.
PloS one, 16(3), e0248113-e0248113 (2021-03-13)
Immature neurons dominantly express the Na+-K+-2Cl- cotransporter isoform 1 (NKCC1) rather than the K+-Cl- cotransporter isoform 2 (KCC2). The intracellular chloride ion concentration ([Cl-]i) is higher in immature neurons than in mature neurons; therefore, γ-aminobutyric acid type A (GABAA) receptor
Ming Chen et al.
eLife, 6 (2017-01-06)
Amyloid precursor protein (APP) is enriched at the synapse, but its synaptic function is still poorly understood. We previously showed that GABAergic short-term plasticity is impaired in App knock-out (App-/-) animals, but the precise mechanism by which APP regulates GABAergic

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