Apigenin CAS 520-36-5 4′, 5, 7-Trihydroxyflavone 5, 7, 4′-Trihydroxyflavone

• CAS No.: 520-36-5
• Formula: C15h10o5
• EINECS: 208-292-3
• Classification: Monosaccharides
• Appearance: Liquid
• Grade Standard: Food Grade
• Model NO.: SUREST-256
• Type: Aldose
• Monosaccharides: Glucose
• Disaccharides: Sucrose
• Polysaccharides: Starch
• Colour: Faint Yellow
• Stock: Available
• Molecular Weight: 270.24
• Density: 1.2319
• Melting Point: 345-350 ºC
• Transport Package: 1kg/Bag or 25kg/Drum
• Specification: 98%min
• Trademark: Surest
• Origin: China
• HS Code: 2942000000
• Production Capacity: 1000 Tons Yearly

Product Description

Product Description

 

Name	Apigenin
Synonyms	4',5,7-Trihydroxyflavone; 5,7,4'-Trihydroxyflavone
Molecular Structure
Molecular Formula	C15H10O5
Molecular Weight	270.24
CAS Registry Number	520-36-5
EINECS	208-292-3

Properties

Melting point	345-350 ºC

 

Main Uses:

The molecular structure of apigenin determines its unique physiological effects and biological characteristics, and has a good biological effect. A large number of domestic and foreign studies have found that apigenin is a natural antioxidant, which has the effects of lowering blood pressure, dilating blood vessels, preventing atherosclerosis and inhibiting tumors. Compared with other flavonoids (quercetin, chennetin), it has the characteristics of low toxicity and no mutagenicity. At present, apigenin has certain applications in medicine, food and other industries. However, due to the poor water solubility and intestinal absorption of apigenin, its oral bioavailability is low, and its activity in vivo is low, which limits its application to some extent.


Flavonoid, which can capture the G2/M phase of the cell cycle and inhibit cell expansion. Inhibit growth, induce apoptosis, used in cancer drugs. The flavonoid contained in apigenin is a plant flavonoid that has been found to inhibit cell proliferation by stopping the cell cycle during the G2/M phase. Inhibition of growth through cell cycle arrest and induced apoptosis appears to be related to the induction of p53. Pma-mediated tumor promotion is inhibited by inhibition of protein kinase C and the resulting inhibition of oncogene expression. The inhibition of topoisomerase catalyzed deoxyribonucleic acid reconnection and enhanced intercellular communication of gap junction were also reported.

 

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