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ChemicalBook--->CAS DataBase List--->68592-15-4

68592-15-4

68592-15-4 Structure

68592-15-4 Structure
IdentificationBack Directory
[Name]

4'-Methoxy-3',5-di-2-propenyl-(1,1'-biphenyl)-2-ol
[CAS]

68592-15-4
[Synonyms]

4-O-Methyl honokiol
4'-Methoxy-3',5-di-2-propenyl-(1,1'-biphenyl)-2-ol
2-(4-methoxy-3-prop-2-enylphenyl)-4-prop-2-enylphenol
[1,1'-Biphenyl]-2-ol, 4'-methoxy-3',5-di-2-propen-1-yl-
[Molecular Formula]

C19H20O2
[MDL Number]

MFCD19705288
[MOL File]

68592-15-4.mol
[Molecular Weight]

280.36
Chemical PropertiesBack Directory
[storage temp. ]

Store at -20°C
[solubility ]

DMF: 33 mg/ml; DMSO: 33 mg/ml; Ethanol: 33 mg/ml; Ethanol:PBS (pH 7.2) (1:2): 0.3 mg/ml
[form ]

Viscous Liquid
[color ]

Orange to red
Safety DataBack Directory
[Symbol(GHS) ]


GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319-H335
[Precautionary statements ]

P261-P305+P351+P338
Hazard InformationBack Directory
[Uses]

4-O-Methyl honokiol is a natural neolignan isolated from Magnolia officinalis, acts as a PPARγ agonist, and inhibtis NF-κB activity, used for cancer and inflammation research.
[in vivo]

4-O-Methyl honokiol (40 or 80 mg/kg, i.p. everyday for 4 weeks) inhibits the growth of SW620 and PC3 tumours in SW620 and PC3 xenograft model. 4-O-Methyl honokiol significantly increases the expression of p21 and PPARγ in the tumour tissues[1]. 4-O-Methyl honokiol (0.5 or 1 mg/kg/day daily for 3 weeks) significantly ameliorates LPS-induced memory impairment, and inhibits LPS-induced iNOS and COX-2 expression in mice. 4-O-Methyl honokiol also shows inhibitory activities against the Aβ1-42 accumulation, and activates astrocytes and microglia in LPS-injected mice brain[2].

[IC 50]

PPARγ; NF-κB
[References]

[1] Lee NJ, et al. 4-O-methylhonokiol, a PPARγ agonist, inhibits prostate tumour growth: p21-mediated suppression of NF-κB activity. Br J Pharmacol. 2013 Mar;168(5):1133-45. DOI:10.1111/j.1476-5381.2012.02235.x
[2] Lee YJ, et al. Inhibitory effect of 4-O-methylhonokiol on lipopolysaccharide-induced neuroinflammation, amyloidogenesis and memory impairment via inhibition of nuclear factor-kappaB in vitro and in vivo models. J Neuroinflammation. 2012 Feb 19;9:35. DOI:10.1186/1742-2094-9-35
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