CGP 52432

Potent, selective GABAB antagonist CAS# 139667-74-6

CGP 52432

Catalog No. BCC6989----Order now to get a substantial discount!

Product Name & Size Price Stock
CGP 52432:10mg $215.00 In stock
CGP 52432:20mg $366.00 In stock
CGP 52432:50mg $860.00 In stock
CGP 52432:100mg $1505.00 In stock
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Quality Control of CGP 52432

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Chemical structure

CGP 52432

3D structure

Chemical Properties of CGP 52432

Cas No. 139667-74-6 SDF Download SDF
PubChem ID 132252 Appearance Powder
Formula C15H24Cl2NO4P M.Wt 384.24
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 5 mg/mL (13.01 mM; Need ultrasonic and warming)
Chemical Name 3-[(3,4-dichlorophenyl)methylamino]propyl-(diethoxymethyl)phosphinic acid
SMILES CCOC(OCC)P(=O)(CCCNCC1=CC(=C(C=C1)Cl)Cl)O
Standard InChIKey GJZVQXWEIYRHBE-UHFFFAOYSA-N
Standard InChI 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)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of CGP 52432

DescriptionPotent, selective GABAB receptor antagonist (IC50 = 85 nM).

CGP 52432 Dilution Calculator

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CGP 52432 Molarity Calculator

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Preparing Stock Solutions of CGP 52432

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.6025 mL 13.0127 mL 26.0254 mL 52.0508 mL 65.0635 mL
5 mM 0.5205 mL 2.6025 mL 5.2051 mL 10.4102 mL 13.0127 mL
10 mM 0.2603 mL 1.3013 mL 2.6025 mL 5.2051 mL 6.5064 mL
50 mM 0.0521 mL 0.2603 mL 0.5205 mL 1.041 mL 1.3013 mL
100 mM 0.026 mL 0.1301 mL 0.2603 mL 0.5205 mL 0.6506 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on CGP 52432

CGP 52432: a novel potent and selective GABAB autoreceptor antagonist in rat cerebral cortex.[Pubmed:8103461]

Eur J Pharmacol. 1993 Jun 24;237(2-3):191-5.

As previously reported GABAB receptors are heterogeneous. Three pharmacologically distinct receptor subtypes mediating inhibition of gamma-aminobutyric acid (GABA), glutamate or somatostatin release, respectively, exist on axon terminals of rat cerebral cortex. We investigated the novel GABAB receptor antagonist, [3-[[(3,4-dichlorophenyl)methyl]amino]propyl](diethoxy-methyl) phosphinic acid (CGP 52432), on the above receptor subtypes. The effects of (-)-baclofen on the K(+)-evoked release of GABA, glutamate or somatostatin from rat cortical synaptosomes were antagonized by CGP 52432. The IC50 of the drug at GABA autoreceptors (0.085 microM) was 35- and 100-fold lower than at the receptors regulating somatostatin and glutamate overflow, respectively. At the autoreceptor the calculated pA2 for CGP 52432 amounted to 7.70, which makes the drug about 1000-fold more potent than phaclofen at this receptor. The potency and selectivity characteristics of CGP 52432 indicate that the drug is by far the most appropriate tool to investigate the terminal GABAB autoreceptors of the rat cerebral cortex.

The GABA(B) antagonist CGP 52432 attenuates the stimulatory effect of the GABA(B) agonist SKF 97541 on luteinizing hormone secretion in the male sheep.[Pubmed:11976401]

Exp Biol Med (Maywood). 2002 May;227(5):315-20.

The objectives of this study were to determine if the gamma-aminobutyric acid (GABA)(B) agonist, 3-aminopropyl (methyl) phosphinic acid (SKF97541), would increase luteinizing hormone (LH) secretion when infused by microdialysis into the medial basal hypothalamus (MBH) of the castrated ram, and to determine if the action of SKF97541 would be attenuated by co-infusion of the GABA(B) antagonist CGP52432. Initial experiments established that infusion of SKF alone, at concentrations as low as 5 microM, increased mean LH, LH pulse amplitude, and in some cases, pulse interval. In the last experiment, animals were treated with artificial cerebrospinal fluid (CSF) alone, SKF alone (30 microM), 3-[[(3, 4-dichlorophenol) methyl] amino] propyl] diethoxymethyl) phosphinic acid (CGP) alone (500 microM), or SKF plus CGP. SKF increased both mean LH and LH pulse amplitude as compared with CSF. CGP alone had no significant effect on LH, but it attenuated the effect of SKF on mean LH. These observations indicate that the stimulatory effects of GABA(B) agonists on LH pulse patterns are mediated through GABA(B) receptors and provide further evidence that GABA(B) receptors located in the MBH can regulate pulsatile GnRH-LH release.

GABA(B) receptors as potential targets for drugs able to prevent excessive excitatory amino acid transmission in the spinal cord.[Pubmed:9874164]

Eur J Pharmacol. 1998 Dec 4;362(2-3):143-8.

The effects of GABA(B) receptor activation on the Ca2+-dependent depolarization-induced overflow of endogenous glutamic acid and gamma-aminobutyric acid (GABA) was studied in rat spinal cord nerve terminals exposed in superfusion to 15 mM KCl. The GABA(B) receptor agonist (-)-baclofen inhibited the K+-evoked overflow of glutamate (EC50=0.098 microM) but was almost inactive against that of GABA. The overflow of both transmitters could be quite similarly inhibited by two other GABA(B) receptor agonists, 3-APPA (3-aminopropylphosphonous acid; EC50=0.087 and 0.050 microM in the case of GABA and glutamate, respectively) and CGP 44532 (3-amino-2(S)-hydroxypropyl)methylphosphinic acid; EC50=0.81 and 0.50 microM). The GABA(B) receptor antagonist CGP 35348 [3-amino-propyl(diethoxymethyl)phosphinic acid] blocked the effect of 3-APPA (1 microM) at the autoreceptors (IC50 approximately = 1 microM), but not at the heteroreceptors. In contrast, the effects of 3-APPA at both autoreceptors and heteroreceptors could be similarly prevented by another GABA(B) receptor antagonist, CGP 52432 [3-[[(3,4-dichlorophenyl)methyl]amino]propyl](diethoxymethyl) phosphinic acid (IC50 approximately = 10 microM). The data suggest that, in the spinal cord, GABA(B) autoreceptors on GABA-releasing terminals differ pharmacologically from GABA(B) heteroreceptors on glutamatergic terminals. Selective GABA(B) receptor ligands may be helpful for conditions characterized by excessive glutamatergic transmission in the spinal cord.

Blockade of GABA(B) receptors facilitates muscarinic agonist-induced epileptiform activity in immature rat piriform cortex in vitro.[Pubmed:9750001]

Naunyn Schmiedebergs Arch Pharmacol. 1998 Aug;358(2):168-74.

The effects of the selective GABA(B) receptor antagonist [3-[[(3,4-dichlorophenyl)methyl]aminolpropyl] (diethoxymethyl) phosphinic acid (CGP 52432) on muscarinic (mAChR) and metabotropic glutamate (mGluR) responsiveness were studied in slices of piriform cortex from both immature (P16-P22) and adult (> or =P40) rats, using a conventional intracellular recording technique. In both adult and immature slices, CGP 52432 (1 microM) had no effect on neuronal membrane properties, whereas it selectively abolished the late inhibitory postsynaptic potential (IPSP) evoked by local electrical stimulation of association fibre terminals. Age-related changes in mAChR (but not mGluR) responsiveness were also detected. In adult neurones, bath-application of the mAChR agonist oxotremorine-M (OXO-M; 10 microM), or the selective mGluR agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD; 10 microM) evoked similar membrane depolarization and inhibition of evoked excitatory postsynaptic potentials (EPSPs). However, while 1S,3R-ACPD and OXO-M produced indistinguishable slow excitatory effects in immature slices, during superfusion with OXO-M, neurones exhibited spontaneous paroxysmal depolarizing shifts (PDSs) that were suppressed in the presence of atropine (1 microM) or the selective GABA(B) receptor agonist beta-parachlorophenyl-gamma-aminobutyric acid [(-)baclofen; 10 microM]. Also, application of OXO-M resulted in a pronounced prolongation (rather than a decrease) of electrically evoked postsynaptic potentials (PSPs) which now exhibited recurrent superimposed spike discharges. In adult slices, in the continuous presence of CGP 52432 (1 microM; 20 min pre-incubation), a subsequent exposure to 10 microM OXO-M or 1S,3R-ACPD failed to induce any spontaneous epileptiform activity, and evoked PSPs were consistently suppressed. In contrast, in immature slices, after incubation in CGP 52432 (1 microM; 20 min), a subsequent application of a low dose of OXO-M (2.5 microM), which was inactive per se, was able to produce spontaneous PDSs and a prolongation of evoked PSPs. We conclude that a reduction in GABA(B)-mediated synaptic inhibition in immature slices (in co-operation with other factors) may contribute to the facilitation of excitatory neurotransmission and therefore play a role in the generation of mAChR-induced epileptiform activity.

Description

CGP52432 is a GABAB receptor antagonist, with an IC50 of 85 nM.

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