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| | P-(3-aMinopropyl)-P-butyl-Phosphinic acid Basic information |
| Product Name: | P-(3-aMinopropyl)-P-butyl-Phosphinic acid | | Synonyms: | P-(3-aMinopropyl)-P-butyl-Phosphinic acid;CGP36742;SGS 742;3-aminopropyl(butyl)phosphinic acid;Phosphinic acid, P-(3-aminopropyl)-P-butyl-;CGP36742 >=97% (NMR);CGP 36742(SGS-742);DVD-742 | | CAS: | 123690-78-8 | | MF: | C7H18NO2P | | MW: | 179.2 | | EINECS: | 802-883-5 | | Product Categories: | | | Mol File: | 123690-78-8.mol |  |
| | P-(3-aMinopropyl)-P-butyl-Phosphinic acid Chemical Properties |
| 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) | | InChI | 1S/C7H18NO2P/c1-2-3-6-11(9,10)7-4-5-8/h2-8H2,1H3,(H,9,10) | | InChIKey | ONNMDRQRSGKZCN-UHFFFAOYSA-N | | SMILES | CCCCP(O)(=O)CCCN |
| Hazard Codes | Xn | | Risk Statements | 22-36 | | Safety Statements | 26 | | WGK Germany | 3 | | RTECS | SZ4113300 | | Storage Class | 11 - Combustible Solids | | Hazard Classifications | Acute Tox. 4 Oral
Eye Irrit. 2 |
| | P-(3-aMinopropyl)-P-butyl-Phosphinic acid Usage And Synthesis |
| 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 depression, and 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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| | 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 |
| | P-(3-aMinopropyl)-P-butyl-Phosphinic acid Preparation Products And Raw materials |
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