Identification | Back Directory | [Name]
SAFFLOMIN A | [CAS]
78281-02-4 | [Synonyms]
HSYA SAFFLOMIN A Hydroxysafflor yellow Hydroxysafflor yellow A Hydroxysafflor yellow A,Safflomin A Hydroxysafflor yellow A,SaffloMin A,HSYA Safflomin A, 98%, from Carthamus tinctorius L. 2,5-Cyclohexadien-1-one, 2,4-di-β-D-glucopyranosyl-3,4,5-trihydroxy-6-[(2E)-3-(4-hydroxyphenyl)-1-oxo-2-propen-1-yl]- 2,5-Cyclohexadien-1-one, 2,4-di-beta-D-glucopyranosyl-3,4,5-trihydroxy-6-((2E)-3-(4-hydroxyphenyl)-1-oxo-2-propenyl)- | [Molecular Formula]
C27H32O16 | [MDL Number]
MFCD08435942 | [MOL File]
78281-02-4.mol | [Molecular Weight]
612.533 |
Chemical Properties | Back Directory | [Melting point ]
184-186 °C | [Boiling point ]
1015.8±65.0 °C(Predicted) | [density ]
1.851±0.06 g/cm3(Predicted) | [solubility ]
DMF: 1 mg/ml; DMSO: 1 mg/ml; PBS (pH 7.2): 1 mg/ml | [form ]
powder | [pka]
4.50±1.00(Predicted) | [color ]
Yellow-orange | [LogP]
1.688 (est) |
Hazard Information | Back Directory | [Definition]
ChEBI: Hydroxysafflor yellow A is a C-glycosyl compound that is 3,4,5-trihydroxycyclohexa-2,5-dien-1-one which is substituted by beta-D-glucosyl groups at positions 2 and 4, and by a p-hydroxycinnamoyl group at position 6. It is the main bioactive compound of a traditional Chinese medicine obtained from safflower (Carthamus tinctorius). It has a role as an anti-inflammatory agent, an antioxidant, a platelet aggregation inhibitor, an antineoplastic agent, a radical scavenger, an EC 3.2.1.48 (sucrose alpha-glucosidase) inhibitor, a neuroprotective agent and a plant metabolite. It is a C-glycosyl compound, a member of phenols, an enone and an enol. | [Biological Activity]
Hydroxysafflor yellow A is a pigment that has been found in C. tinctorius and has diverse biological activities. It inhibits LPS-induced increases in NF-κB levels and production of nitric oxide (NO), IL-1β, and TNF-α in primary mouse embryonic mesencephalic cultures when used at concentrations of 40 and 160 μM. | [in vivo]
Hydroxysafflor yellow A (1 and 3 mg/kg) decreases mean arterial pressure (MAP) and heart rate in anesthetized normotensive or spontaneously hypertensive rats. It reduces infarct volume and serum superoxide dismutase (SOD) activity in a rat model of focal transient cerebral is chemia induced by middle cerebral artery occlusion (MCAO) when administered at doses of 2, 4, and 8 mg/kg. |
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