ChemicalBook CAS DataBase List 75645-24-8

75645-24-8

Name	Asiaol-Gm1-tetrasaccharide
CAS	75645-24-8
Molecular Formula	C26H45NO21
MDL Number	MFCD05663667
Molecular Weight	707.63
MOL File	75645-24-8.mol

Chemical Properties

Boiling point	1173.6±65.0 °C(Predicted)
density	1.72±0.1 g/cm3(Predicted)
pka	12.39±0.20(Predicted)

Hazard Information

Uses

Gangliotetraose (Gg4) is a tetrasccharide, exhibits major components including GM1 and its sialylated derivatives. GM1 facilitates efflux of nuclear Ca2+ and reduces the level of nuclear Ca2+ that characterizes the differentiated neuron. GM1 affects neuronal plasticity and repair mechanisms, as well as neurotrophin release in the brain[1][2].

in vivo

Gangliotetraose (GM1) (30 mg/kg; i.p.; 5, 11, 42, and 73 d) stimulates the regeneration of nigrostriatal dopaminergic neurons in the central nervous system of rats after unilateral hemitransection^[5].

Animal Model:	Unilateral semi-transection model in Sprague-Dawley rats (170-190 g)^[5]
Dosage:	5 mg/kg; 30 mg/kg
Administration:	Intraperitoneal injection; 5, 11, 42, 73 days; started on day 2 after surgery and finished 24 h before sacrifice
Result:	Increased the V_max of tyrosine hydroxylase (TH) in the lesioned side starting on day 14 dose-dependently with 73% (5 mg/kg/d) and 85% (30 mg/kg/d) of that of the unlesioned side, respectively.

References

[1] Okada H, et al. Complement-mediated cytolysis and azidothymidine are synergistic in HIV-1 suppression. Int Immunol. 1998 Jan;10(1):91-5. DOI:10.1093/intimm/10.1.91
[2] Ledeen RW, et al. The role of GM1 and other gangliosides in neuronal differentiation. Overview and new finding. Ann N Y Acad Sci. 1998 Jun 19;845:161-75. DOI:10.1111/j.1749-6632.1998.tb09669.x
[3] Zakharova IO, et al. GM1 ganglioside activates ERK1/2 and Akt downstream of Trk tyrosine kinase and protects PC12 cells against hydrogen peroxide toxicity. Neurochem Res. 2014 Nov;39(11):2262-75. DOI:10.1007/s11064-014-1428-6
[4] Toffano G, et al. GM1 ganglioside stimulates the regeneration of dopaminergic neurons in the central nervous system. Brain Res. 1983 Feb 14;261(1):163-6. DOI:10.1016/0006-8993(83)91298-2

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