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480-20-6

中文名称 香橙素
英文名称 DIHYDROKAEMPFEROL
CAS 480-20-6
分子式 C15H12O6
分子量 288.25
MOL 文件 480-20-6.mol
更新日期 2024/05/20 10:34:39
480-20-6 结构式 480-20-6 结构式

基本信息

中文别名
黄杞苷苷元
二氢山柰酚
二氢莰非醇
二氢化萜醇
二氢山奈酚
香橙素,香树素
香橙素(标准品)
香橙素(二氢山奈酚 )
(2R,3R)-3,5,7-三羟基-2-(4-羟基苯基)四氢苯并吡喃-4-酮
英文别名
Katuranin
aromadedrin
AROMADENDRIN
DIHYDROKAEMPFEROL
(+)-dihydrokaempferol
DIHYDROKAEMPFEROL-CMPD
3,5,7,4'-TETRAHYDROXYFLAVANONE
Aromadendrin >=95% (LC/MS-ELSD)
AroMadendrin (DihydrokaeMpferol)
(2R,3R)-3,4′,5,7-Tetrahydroxyflavanone
所属类别
天然产物:黄酮类化合物

物理化学性质

熔点237~241℃
沸点139-140 °C
密度1.599±0.06 g/cm3(Predicted)
储存条件Sealed in dry,2-8°C
溶解度DMSO:2.88(Max Conc. mg/mL);10.0(Max Conc. mM)
酸度系数(pKa)7.42±0.60(Predicted)
形态neat
InChIKeyPADQINQHPQKXNL-LSDHHAIUSA-N
LogP2.860 (est)

安全数据

危险性符号(GHS)
GHS07
警示词警告
危险性描述H302
危险品标志N,Xn
危险类别码50-22
安全说明61
危险品运输编号UN 3077 9 / PGIII
WGK Germany3

常见问题列表

生物活性
Dihydrokaempferol 是从紫荆花 Bauhinia championii (Benth) 中分离得到的。 Dihydrokaempferol 诱导 apoptosis 并抑制 Bcl-2 和 Bcl-xL 的表达。Dihydrokaempferol 可以作为抗关节炎新药的良好候选。
靶点

Apoptosis; Bcl-2; Bcl-xL

体外研究

Dihydrokaempferol (0.3-300 μM; 48 hours) has no significant effect on normal synoviocytes, but dependently decreases the viability of RA-FLSs. Dihydrokaempferol (3-30 μM; 48 hours) increases the percentage of apoptotic cells (including early and late apoptotic cells; ~3.8% and ~9.6%, respectively). Dihydrokaempferol (3-30 μM; 48 hours) promotes Bax and Bad expression and inhibits Bcl-2 and Bcl-xL expression, increases the cleaved fragments of caspase-3, caspase-9 and cleaved PARP.

Cell Proliferation Assay

Cell Line: Normal synoviocyte cells; RA-FLS cells
Concentration: 0.3 μM, 3 μM, 30 μM, 300 μM
Incubation Time: 48 hours
Result: Decreased the proliferation of RA-FLSs.

Apoptosis Analysis

Cell Line: RA-FLS cells
Concentration: 3 μM, 30 μM
Incubation Time: 48 hours
Result: Induced apoptosis in RA-FLSs.

Western Blot Analysis

Cell Line: RA-FLS cells
Concentration: 3 μM, 30 μM
Incubation Time: 48 hours
Result: Promoted Bax and Bad expression, increased the cleaved fragments of caspase-3, caspase-9 and cleaved PARP and inhibited Bcl-2 and Bcl-xL expression.
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