SML2172
CLP290
≥98% (HPLC)
别名:
[5-Fluoro-2-[(Z)-(2-hexahydropyridazin-1-yl-4-oxo-thiazol-5-ylidene)methyl]phenyl] pyrrolidine-1-carboxylate
InChI key
DIXMMXNNKLCLOM-WJDWOHSUSA-N
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-
SMILES string
FC1=CC=C(/C=C2C(N=C(N3NCCCC3)S/2)=O)C(OC(N4CCCC4)=O)=C1
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Biochem/physiol Actions
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.
Enhancer of K+-Cl- cotransporter KCC2 activity, precursor of chloride extrusion enhancer CLP257
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
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
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
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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