CGP 36742
(Synonyms: SGS-742) 目录号 : GC35669
A GABAB receptor antagonist
Cas No.:123690-78-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
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- Datasheet
CGP 36742 is an antagonist of GABAB receptors (IC50 = 36 ?M).1 It is selective for GABAB over a panel of 11 receptors, including GABAA, at 1 mM. CGP 36742 (3 mg/kg) reduces paired-pulse inhibition of the late inhibitory postsynaptic potential (IPSP) in CA1 pyramidal neurons in rats. It increases latency to step-down in a passive avoidance test in mice in a dose-dependent manner.2 CGP 36742 (10 and 30 mg/kg) decreases immobility time in the forced swim test in mice.3
1.Olpe, H.R., Steinmann, M.W., Ferrat, T., et al.The actions of orally active GABAB receptor antagonists on GABAergic transmission in vivo and in vitroEur. J. Pharmacol.233(2-3)179-186(1993) 2.Mondadori, C., Jaekel, J., and Preiswerk, G.CGP 36742: The first orally active GABAB blocker improves the cognitive performance of mice, rats, and rhesus monkeysBehav. Neural Biol.60(1)62-68(1993) 3.Nowak, G., Partyka, A., Palucha, A., et al.Antidepressant-like activity of CGP 36742 and CGP 51176, selective GABAB receptor antagonists, in rodentsBr. J. Pharmacol.149(5)581-590(2006)
| Cas No. | 123690-78-8 | SDF | |
| 别名 | SGS-742 | ||
| Canonical SMILES | O=P(CCCN)(O)CCCC | ||
| 分子式 | C7H18NO2P | 分子量 | 179.2 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.5804 mL | 27.9018 mL | 55.8036 mL |
| 5 mM | 1.1161 mL | 5.5804 mL | 11.1607 mL |
| 10 mM | 0.558 mL | 2.7902 mL | 5.5804 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
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Antidepressant-like activity of CGP 36742 and CGP 51176, selective GABAB receptor antagonists, in rodents
Br J Pharmacol 2006 Nov;149(5):581-90.PMID:16921399DOI:10.1038/sj.bjp.0706845.
Background and purpose: A crucial role for the GABAB receptor in depression was proposed several years ago, but there are limited data to support this proposition. Therefore we decided to investigate the antidepressant-like activity of the selective GABAB receptor antagonists CGP 36742 and CGP 51176, and a selective agonist CGP 44532 in models of depression in rats and mice. Experimental approach: Effects of CGP 36742 and CGP 51176 as well as the agonist CGP 44532 were assessed in the forced swim test in mice. Both antagonists were also investigated in an olfactory bulbectomy (OB) model of depression in rats, while CGP 51176 was also investigated in the chronic mild stress (CMS) rat model of depression. The density of GABAB receptors in the mouse hippocampus after chronic administration of CGP 51176 was also investigated. Key results: The GABAB receptor antagonists CGP 36742 and CGP 51176 exhibited antidepressant-like activity in the forced swim test in mice. The GABAB receptor agonist CGP 44532 was not effective in this test, however, it counteracted the antidepressant-like effects of CGP 51176. The antagonists CGP 36742 and CGP 51176 were effective in an OB model of depression in rats. CGP 51176 was also effective in the CMS rat model of depression. Administration of CGP 51176 increased the density of GABAB receptors in the mouse hippocampus. Conclusions and implications: These data suggest that selective GABAB receptor antagonists may be useful in treatment of depression, and support an important role for GABA-ergic transmission in this disorder.
CGP 36742: the first orally active GABAB blocker improves the cognitive performance of mice, rats, and rhesus monkeys
Behav Neural Biol 1993 Jul;60(1):62-8.PMID:8216160DOI:10.1016/0163-1047(93)90729-2.
The learning capacity of experimental animals in cognitive tests can be improved by blockade of the GABAB receptors. After treatment with the GABAB antagonist CGP 36742, mice performed better in a passive-avoidance test; rats did likewise in a partner-recognition test, and rhesus monkeys also in a "conditional spatial color" task. The effects demonstrated in these three different species and covering diverse manifestations of learning and memory give reason to hope that this new active principle may prove therapeutically useful.
Effect of CGP 36742 on the extracellular level of neurotransmitter amino acids in the thalamus
Neurochem Int 1999 May;34(5):391-8.PMID:10397367DOI:10.1016/s0197-0186(99)00042-x.
We have evaluated the effect of the brain penetrating GABAb antagonist, CGP 36742 on GABAb receptors using in vivo microdialysis in the ventrobasal thalamus of freely moving rat. When a solution of 1 mM CGP 36742 in ACSF was dialyzed into the ventrobasal thalamus, 2-3-fold increases of extracellular Glu, Asp and Gly running parallel with significant decreases of contralateral extracellular Asp and Gly were observed. Unilateral applications of Glu receptor antagonists (0.5 mM MK801, 0.1 mM CNQX) evoked 2-3-fold decreases of CGP 36742-specific elevations of extracellular Asp, Glu and Gly. Administration of CNQX and MK801 in the absence of CGP 36742 did not alter the extracellular Glu and Gly concentrations whereas extracellular Asp concentrations diminished by 42-45% at both sides. By contrast, no changes of extracellular Gly accompanied the 5-10-fold enhancements of extracellular Asp and Glu, observed during application of the Glu uptake inhibitor, tPDC (1mM). Suspensions of resealed plasmalemma fragments from the rat thalamus were mixed rapidly with the membrane impermeant form of the fluorescence indicator, bis-fura-2 and the changes in fluorescence intensity in response to CGP 36742 (0.5 mM), and the GABAb agonist, baclofen (0.1 mM), were monitored on the time scale of 0.04 ms(-10)s. Progress of CGP 36742-mediated influx, and baclofen-mediated efflux of Ca++ ion, antagonized by CGP 36742, was observed in the 1 ms(-10s) period of time. These data support the hypothesis that background ventrobasal activities and thalamocortical signaling are under the control of inhibitory GABAb receptors in the ventrobasal thalamus.
Repeated administration of desipramine and a GABAB receptor antagonist, CGP 36742, discretely up-regulates GABAB receptor binding sites in rat frontal cortex
Br J Pharmacol 1993 Oct;110(2):724-35.PMID:8242244DOI:10.1111/j.1476-5381.1993.tb13872.x.
1. GABAB receptor binding site densities within laminar regions of the rat frontal cortex were examined autoradiographically following repeated administration (21 days) of the antidepressants desipramine, paroxetine and amitriptyline in addition to the GABAB receptor antagonists, CGP 35348 and CGP 36742. beta 1-Adrenoceptor autoradiography was studied in parallel with that for GABAB receptor sites. 2. The effects of these compounds were examined concomitantly on the GABAB receptor-mediated inhibition of forskolin- and enhancement of noradrenaline-stimulated cyclic AMP production. 3. GABAB receptor binding was increased by both desipramine (20 mg kg-1, p.o. and 10 mg kg-1, i.p.) and CGP 36742 (100 mg kg-1, i.p.) in the outer laminar region of the frontal cortex by around 50% above control levels. Conversely, no significant changes were mediated by paroxetine, amitriptyline, CGP 35348 or the GABAB receptor agonist, baclofen. 4. With the exception of paroxetine, all compounds down-regulated the total beta-adrenoceptor population throughout frontal cortical laminae which was attributable to the beta 1-adrenoceptor subtype. In contrast, the reduction in beta-adrenoceptors mediated by CGP 35348 and CGP 36742 did not occur as a consequence of reduced beta 1-adrenoceptor numbers. 5. Protracted treatment with CGP 35348, failed to influence forskolin-stimulated cyclic AMP production; however, a significant increase in the accumulation of cyclic AMP produced in response to forskolin was seen after treatment with CGP 36742. 6. Such discretely localized changes in GABAB receptor densities induced by desipramine and CGP 36742 may provide an explanation for the discrepancies reported in membrane binding studies and possibly implicate a role for GABAB receptor antagonists in antidepressant therapy.
Chronic (-)baclofen or CGP 36742 alters GABAB receptor sensitivity in rat brain and spinal cord
Neuroreport 1995 Jan 26;6(2):399-403.PMID:7538812DOI:10.1097/00001756-199501000-00042.
Administration of the GABAB receptor agonist, (-)-baclofen 10 mg kg-1, i.p. daily for 21 days to rats prevented (-)-baclofen-induced hyperpolarizing responses and synaptically-evoked late inhibitory potentials (IPSPs) in olfactory cortical neurones recorded intracellularly from 450 microns brain slices. In contrast, pre-treatment with CGP 36742 induced a significant increase in (-)-baclofen-mediated post-synaptic responses and late IPSP amplitude. In the spinal cord, the potency of (-)-baclofen in inhibiting electrically-evoked substance P-like immunoreactivity or amino acid release was significantly reduced or increased in slices from rats pre-treated with the GABAB agonist or antagonist, respectively. These data suggest that functional responses to GABAB receptor activation in the mammalian central nervous system can be up- or down-regulated.