| Identification | Back Directory | [Name]
P-(3-aMinopropyl)-P-butyl-Phosphinic acid | [CAS]
123690-78-8 | [Synonyms]
SGS 742
CGP36742
CGP36742 >=97% (NMR)
3-aminopropyl(butyl)phosphinic acid
P-(3-aMinopropyl)-P-butyl-Phosphinic acid
Phosphinic acid, P-(3-aminopropyl)-P-butyl- | [EINECS(EC#)]
802-883-5 | [Molecular Formula]
C7H18NO2P | [MDL Number]
MFCD00882735 | [MOL File]
123690-78-8.mol | [Molecular Weight]
179.2 |
| Chemical Properties | Back Directory | [Boiling point ]
383.9±25.0 °C(Predicted) | [density ]
1.057±0.06 g/cm3(Predicted) | [storage temp. ]
room temp | [solubility ]
H2O: soluble10mg/mL (clear solution, warmed) | [form ]
powder | [pka]
2.91±0.50(Predicted) | [color ]
white to beige | [Water Solubility ]
H2O: 10mg/mL (clear solution, warmed) |
| Hazard Information | Back Directory | [Uses]
CGP 36742 (SGS-742) is an orally active and selective antagonist of GABAB receptor (IC50 = 36 μM). CGP 36742 is a blood-brain barrier (BBB) penetrant compound and improves cognitive performances. CGP 36742 can be used for depression study[1][2][3][4]. | [Biological Activity]
CGP36742 was the first orally active GABAB-selective antagonist. The IC50 for blocking GABAergic transmission is 36 μM. Oral administration of CGP36742 in rats blocks baclofen-induced neuronal depressionand reduces learning deficit and passive avoidance in an olfactory bulbectomy depression model. | [in vivo]
CGP 36742 (10-30 mg/kg; i.p.; 30 min before test) exhibits antidepressant-like activity in the forced swim test in mice[1].
CGP 36742 (10 mg/kg; i.p.; once daily for 14 d) are effective in an olfactory bulbectomy (OB) model of depression in rats[1].
CGP 36742 (30-200 mg/kg; p.o.; administered in a cumulative manner at intervals of 2.5-3 h) blocks the neuronal depression induced by iontophoretically applied baclofen in anaesthetized rats[2].
CGP 36742 (1-10 mg/kg; i.v.; 25-30 min before test) dose dependently attenuates paired-pulse inhibition measured at latencies of > 100 ms[2].
CGP 36742 (50-1000 mg/kg; i.v. or p.o.; once or twice) can penetrate the blood-brain barrier in male Sprague-Dawley rats [3].
| Animal Model: | Male Albino Swiss mice (22-26 g)[1] | | Dosage: | 10, 30 mg/kg | | Administration: | Intraperitoneal injection (i.p.); 30 min before test | | Result: | Significantly reduced the immobility time in the forced swim test at both doses (10 mg/kg by 32% and 30 mg/kg by 40%).
Had no effect on the spontaneous locomotor activity in mice.
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| Animal Model: | Male Wistar rats (200-250 g), olfactory bulbectomy model[1] | | Dosage: | 10 mg/kg | | Administration: | Intraperitoneal injection (i.p.); once daily for 14 d | | Result: | Single administration did not alter the olfactory bulbectomy (OB)-induced learning deficit, induced following bulbectomy.
Restored the learning deficit in OB rats (five trials) without affecting performance in sham-operated animals.
Reduced the OB-related increase in the number of rearings + peepings.
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| Animal Model: | Male rats (weighing 280-320 g)[2] | | Dosage: | 30-200 mg/kg | | Administration: | Oral gavage (p.o.); administered in a cumulative manner at intervals of 2.5-3 h. | | Result: | Antagonized baclofen-induced inhibitory effects on spontaneously firing cortical neurons in a dose-dependent manner. |
| Animal Model: | Male Sprague-Dawley rats (200-325 g)[3] | | Dosage: | 50, 100, 200, 500, 1000 mg/kg | | Administration: | Intravenous injection (i.v.) via tail vein of 50, 100, 200 mg/kg, oral gavage (p.o.) of 500, 1000 mg.kg; in two rats given an i.v. injection of 100 mg/kg, a second i.v. injection of 100 mg/kg was given after 6 h and samples were collected for another 6 h. | | Result: | The appearance in the rat brain frontal cortex after i.v. injection was seen in the first 30 min dialyzate collected and peaked in the 1 h dialysate.
Removed or metabolized from brain in dialyzates collected 3 h post-injection.
The presence was again seen 30 min after the second 100 mg/kg i.v. injection administered 6 h after the first injection.
Showed the appearance in the third ventricle of the rat brain after two i.v. injections of 100 mg/kg with an interval of 6 h.
Showed that the highest concentrations were seen 1.5 or 2 h after the p.o..
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| [storage]
Store at -20°C | [References]
[1] Nowak G, et al. Antidepressant-like activity of CGP 36742 and CGP 51176, selective GABAB receptor antagonists, in rodents. Br J Pharmacol. 2006 Nov;149(5):581-90. DOI:10.1038/sj.bjp.0706845
[2] Olpe HR, et al. The actions of orally active GABAB receptor antagonists on GABAergic transmission in vivo and in vitro. Eur J Pharmacol. 1993 Mar 23;233(2-3):179-86. DOI:10.1016/0014-2999(93)90048-m
[3] Andrén PE, et al. Blood-brain barrier penetration of 3-aminopropyl-n-butylphosphinic acid (CGP 36742) in rat brain by microdialysis/mass spectrometry. J Mass Spectrom. 1998 Mar;33(3):281-7. DOI:10.1002/(SICI)1096-9888(199803)33:3<281::AID-JMS631>3.0.CO;2-W
[4] Pittaluga A, et al. Potentiation of NMDA receptor function through somatostatin release: a possible mechanism for the cognition-enhancing activity of GABA(B) receptor antagonists. Neuropharmacology. 2001 Sep;41(3):301-10. DOI:10.1016/s0028-3908(01)00066-1 |
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