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Merck
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Key Documents

SML0593

Sigma-Aldrich

CGP52432

≥98% (HPLC)

Sinônimo(s):

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

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About This Item

Fórmula empírica (Notação de Hill):
C15H24Cl2NO4P
Número CAS:
139667-74-6
Peso molecular:
384.24
Código UNSPSC:
12352200
NACRES:
NA.77

Ensaio

≥98% (HPLC)

forma

powder

condição de armazenamento

desiccated

cor

white to beige

solubilidade

H2O: 1 mg/mL, clear (warmed)

temperatura de armazenamento

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)

chave InChI

GJZVQXWEIYRHBE-UHFFFAOYSA-N

Aplicação

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

Ações bioquímicas/fisiológicas

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

Características e benefícios

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.

Outras notas

Do not freeze.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Encontre a documentação dos produtos que você adquiriu recentemente na biblioteca de documentos.

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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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