SML2333
VU0463271
≥98% (HPLC), KCC2 inhibitor, powder
Synonym(s):
N-Cyclopropyl-N-(4-methyl-2-thiazolyl)-2-[(6-phenyl-3-pyridazinyl)thio]-acetamide, N-Cyclopropyl-N-(4-methyl-2-thiazolyl)-2-[(6-phenyl-3-pyridazinyl)thio]acetamide, N-Cyclopropyl-N-(4-methylthiazol-2-yl)-2-(6-phenylpyridazin-3-ylthio)acetamide
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About This Item
Empirical Formula (Hill Notation):
C19H18N4OS2
CAS Number:
Molecular Weight:
382.50
UNSPSC Code:
12352200
MDL number:
NACRES:
NA.21
Assay:
≥98% (HPLC)
Form:
powder
Product Name
VU0463271, ≥98% (HPLC)
assay
≥98% (HPLC)
form
powder
color
off-white to blue-gray
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
SMILES string
[s]1c(nc(c1)C)N(C4CC4)C(=O)CSc2nnc(cc2)c3ccccc3
InChI
1S/C19H18N4OS2/c1-13-11-26-19(20-13)23(15-7-8-15)18(24)12-25-17-10-9-16(21-22-17)14-5-3-2-4-6-14/h2-6,9-11,15H,7-8,12H2,1H3
InChI key
DPONSKCACOZTGN-UHFFFAOYSA-N
Biochem/physiol Actions
Potent and selective potassium-chloride cotransporter KCC2 inhibitor with greatly enhanced potency than its structural analogs VU0255011/ML077 & VU0240511.
VU0463271 is a potent and selective potassium-chloride cotransporter 2 (KCC2) inhibitor that displays greatly enhanced potency than its structural analogs VU0255011 (ML077) & VU0240511 (IC50 = 61, 537, and 568 nM, respectively). VU0463271 exhibits much reduced efficacy against the related Na-K-2Cl cotransporter 1 (NKCC1 inhibition max ~37% at 100 μM) and little affinity toward a panel of 68 GPCRs, ion channels, and transporters. Although VU0463271 is reported to exhibit affinity toward mitochondrial translocator protein TSPO (IC50 of 204 nM against PK11195 binding; rat heart) and inhibitory potency against α1B adrenergic receptor (IC50 of 364.7 nM; human α1B CHO transfectants), these proteins are not known to affect chloride homeostasis.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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D Subramanian et al.
Translational psychiatry, 8(1), 16-16 (2018-01-11)
Autism spectrum disorder (ASD) and temporal lobe epilepsy exhibit remarkable comorbidity, but for reasons not clearly understood. To reveal a common pathophysiological mechanism, we here describe and characterize an in vitro epileptiform activity in the rat hippocampus that exhibits common
Hannah Alfonsa et al.
Nature communications, 7, 13495-13495 (2016-11-18)
Chloride regulation affects brain function in many ways, for instance, by dictating the GABAergic reversal potential, and thereby influencing neuronal excitability and spike timing. Consistent with this, there is increasing evidence implicating chloride in a range of neurological conditions. Investigations
Matthew R Kelley et al.
Neuropharmacology, 108, 103-110 (2016-04-26)
Impaired neuronal inhibition has long been associated with the increased probability of seizure occurrence and heightened seizure severity. Fast synaptic inhibition in the brain is primarily mediated by the type A γ-aminobutyric acid receptors (GABAARs), ligand-gated ion channels that can