P-(3-aMinopropyl)-P-butyl-Phosphinic acid

Product NameP-(3-aMinopropyl)-P-butyl-Phosphinic acid
CAS123690-78-8
MFC7H18NO2P
MW179.2
EINECS802-883-5
MOL File123690-78-8.mol

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)
pka	2.91±0.50(Predicted)
form	powder
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

Safety Information

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

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.

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.

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..

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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