S166
Saclofen
solid
Synonym(s):
β-(Aminomethyl)-4-chlorobenzeneethanesulfonic acid
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About This Item
Empirical Formula (Hill Notation):
C9H12ClNO3S
CAS Number:
Molecular Weight:
249.71
NACRES:
NA.32
PubChem Substance ID:
UNSPSC Code:
51111800
MDL number:
Form:
solid
Quality level:
form
solid
Quality Level
color
white
solubility
0.1 M NaOH: 20 mg/mL
SMILES string
NCC(CS(O)(=O)=O)c1ccc(Cl)cc1
InChI
1S/C9H12ClNO3S/c10-9-3-1-7(2-4-9)8(5-11)6-15(12,13)14/h1-4,8H,5-6,11H2,(H,12,13,14)
InChI key
JYLNVJYYQQXNEK-UHFFFAOYSA-N
Gene Information
human ... GABBR1(2550), GABBR2(9568)
mouse ... GABBR1(54393), GABBR2(242425)
rat ... GABBR1(81657), GABBR2(83633)
Application
Saclofen has been used to prevent the inhibitory action of oxytocin on capsaicin-induced glutamatergic spontaneous excitatory transmission in rat neurons.
Saclofen has been used as a GABAB receptor antagonist to study the analgesic effect of repeated injections of oxycodone in rats.
Biochem/physiol Actions
Saclofen might possess sympathetic nervous system-dependent anti-inflammatory action.
Saclofen is the sulphonic analog of baclofen and is a selective GABAB receptor antagonist.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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Eisuke Koya et al.
Neuropharmacology, 56 Suppl 1, 177-185 (2008-06-21)
Cue-induced drug-seeking in rodents progressively increases after withdrawal from cocaine, suggesting that cue-induced cocaine craving incubates over time. Here, we explored the role of the medial prefrontal cortex (mPFC, a brain area previously implicated in cue-induced cocaine seeking) in this
Molecular Mechanisms Underlying the Enhanced Analgesic Effect of Oxycodone Compared to Morphine in Chemotherapy-Induced Neuropathic Pain
Karine T
PLoS ONE (2014)
David P Archer et al.
Anesthesia and analgesia, 104(4), 840-846 (2007-03-23)
Synaptic plasticity is thought to provide a molecular mechanism for learning and memory. N-methyl-d-aspartate receptor-mediated plasticity requires that N-methyl-d-aspartate receptor activation coincides with postsynaptic depolarizing potentials (DPSP(A)'s). Pentobarbital, in high concentrations, enhances DPSP(A)'s, but high concentrations suppress synaptic plasticity, probably