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Merck

SML0593

Sigma-Aldrich

CGP52432

≥98% (HPLC)

Synonym(e):

[3-[[(3,4-Dichlorophenyl)methyl]amino]propyl](diethoxymethyl)-phosphinic acid

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About This Item

Empirische Formel (Hill-System):
C15H24Cl2NO4P
CAS-Nummer:
Molekulargewicht:
384.24
UNSPSC-Code:
12352200
NACRES:
NA.77

Qualitätsniveau

Assay

≥98% (HPLC)

Form

powder

Lagerbedingungen

desiccated

Farbe

white to beige

Löslichkeit

H2O: 1 mg/mL, clear (warmed)

Lagertemp.

2-8°C

InChI

1S/C15H24Cl2NO4P/c1-3-21-15(22-4-2)23(19,20)9-5-8-18-11-12-6-7-13(16)14(17)10-12/h6-7,10,15,18H,3-5,8-9,11H2,1-2H3,(H,19,20)

InChIKey

GJZVQXWEIYRHBE-UHFFFAOYSA-N

Anwendung

CGP52432 has been used as a γ-aminobutyric acid B (GABAB) antagonist:
  • to study its effects on the simulation of the onset of status epilepticus (SE) in mice
  • for voltage-clamp recording in mice neurons
  • to study its effects on the GABAB receptor-mediated neurotransmission in guinea pig hippocampus

Biochem./physiol. Wirkung

CGP52432 is a very potent antagonist of GABAB receptors. (IC50 = 85 nM).
CGP52432 participates in inhibiting the glycine overflow in the hippocampus.

Leistungsmerkmale und Vorteile

This compound is featured on the GABAB Receptors page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Sonstige Hinweise

Do not freeze.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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K Yang et al.
Neuroscience, 193, 411-420 (2011-08-03)
Metabotropic GABA type B (GABA(B)) receptors are abundantly expressed in the rat spinal dorsal horn. Activation of GABA(B) receptors by exogenous agonists inhibits synaptic transmission, which is believed to underlie the GABA(B) receptor-mediated analgesia. However, little effort has been made
M Katherine Kelm et al.
Journal of neurophysiology, 100(6), 3417-3428 (2008-10-24)
Ethanol increases miniature inhibitory postsynaptic current frequency and decreases the paired-pulse ratio, which suggests that ethanol increases both spontaneous and evoked GABA release, respectively. We have shown previously that ethanol increases GABA release at the rat interneuron-Purkinje cell synapse and
Shuhei Kobuchi et al.
European journal of pharmacology, 623(1-3), 113-118 (2009-09-22)
Enhanced renal sympathetic nerve activity during ischemic period and the renal venous norepinephrine overflow after reperfusion play important roles in the development of ischemic acute kidney injury. We investigated the effect of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter mainly in
A E Matukhno et al.
Zhurnal vysshei nervnoi deiatelnosti imeni I P Pavlova, 62(3), 372-382 (2012-08-16)
By means of local microapplication of GABA, picrotoxin and CGP 52432, different roles of GABAA and GABAB receptors in the geneses of primary and secondary components of evoked potentials in the somatosensory barrel cortex of rats were shown. The authors
Chunguang Zhang et al.
Endocrinology, 150(5), 2388-2394 (2009-01-24)
Gamma-aminobutyric acid (GABA) is one of the most important neurotransmitters that regulate the excitability of GnRH neurons. Numerous studies have shown that GABA activates Cl(-) currents in GnRH neurons, and these effects are antagonized by GABA(A) receptor antagonists. The GABA(B)

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