CGP55845
Based on 2 publication(s) in Google Scholar
CGP55845 is a selective GABAB receptor competitive antagonist (IC50 = 5 nM). CGP55845 prevents agonist binding (pKi = 8.35). CGP55845 blocks presynaptic GABAB receptors, relieves the inhibition of GABA release, and blocks GABAB-mediated inhibitory signaling. CGP55845 restores long-term potentiation and novel object recognition memory in knockout mice.
For research use only. We do not sell to patients.
- CAS No.: 150175-54-5
- Formula: C18H22Cl2NO3P
- Molecular Weight:402.25
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) CGP55845
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Biological Activity
Description
In Vitro
CGP55845 (1 µM) acts presynaptically to increase mIPSC frequency without altering quantal amplitude, mIPSC kinetics, or postsynaptic passive membrane properties in mouse Cajal-Retzius cells[1].
CGP55845 (1 µM) increases GABA release probability, reducing paired-pulse ratio and failure rate while attenuating paired-pulse correlation in mouse Cajal-Retzius cell GABAergic synapses[1].
CGP55845 (1 µM) reduces paired-pulse ratio across extracellular Ca2+ concentrations but does not change late eIPSC quantal amplitude in mouse Cajal-Retzius cells[1].
CGP 55845 (0.03-0.5 μM) is the most potent GABAB receptor antagonist tested in the hemisected rat spinal cord monosynaptic reflex assay, with an apparent Kd of 30.2 nM against (R)-Baclofen (HY-17354)-induced depression[3].
0.3 μM CGP55845 is as potent as 100 μM CGP35348 (HY-103530) in reversing the inhibitory effects of (R)-Baclofen[3].
CGP55845 (1 µM; 2-4 min) blocks IPSPB and increases NMDA EPSP duration and charge in dentate-hilus border interneurons, permitting a delayed polysynaptic burst[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
CGP55845 (0.5 mg/kg; i.p.; single injection; 2 h before NOR familiarization) impaired NOR memory and reduced PSD95-positive puncta in the perirhinal cortex of healthy wild-type mice without altering spine density or maturation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 2 months old; Cdkl5 KO strain backcrossed to C57BL/6J for three generations)[2]
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Dosage:0.5 mg/kg
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Administration:i.p.; single injection; 2 h before NOR familiarization
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Result:Restored NOR memory in Cdkl5 -/Y mice.
Increased dendritic spine number, shifted the immature/mature spine balance toward mature spines, and increased PSD95-positive puncta in the perirhinal cortex of Cdkl5 -/Y mice.
Decreased spontaneous locomotor activity in Cdkl5 -/Y mice.
Chemical Information
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CAS No. 150175-54-5
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Molecular Weight 402.25
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Formula C18H22Cl2NO3P
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SMILES
O=P(CC1=CC=CC=C1)(C[C@@H](O)CN[C@H](C2=CC=C(Cl)C(Cl)=C2)C)O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (2)
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Journal Impact Factor
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Most Recent
Purity & Documentation
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Data Sheet (275 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Kirmse K, et al. Ambient GABA constrains the strength of GABAergic synapses at Cajal-Retzius cells in the developing visual cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006 Apr 19;26(16):4216-27. [Content Brief]
[2]. Gennaccaro L, et al. A GABAB receptor antagonist rescues functional and structural impairments in the perirhinal cortex of a mouse model of CDKL5 deficiency disorder. Neurobiol Dis. 2021 Jun;153:105304. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)