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Merck
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Key Documents

SML0593

Sigma-Aldrich

CGP52432

≥98% (HPLC)

Synonyme(s) :

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

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About This Item

Formule empirique (notation de Hill):
C15H24Cl2NO4P
Numéro CAS:
139667-74-6
Poids moléculaire :
384.24
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Pureté

≥98% (HPLC)

Forme

powder

Conditions de stockage

desiccated

Couleur

white to beige

Solubilité

H2O: 1 mg/mL, clear (warmed)

Température de stockage

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)

Clé InChI

GJZVQXWEIYRHBE-UHFFFAOYSA-N

Application

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

Actions biochimiques/physiologiques

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

Caractéristiques et avantages

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.

Autres remarques

Do not freeze.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

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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