Chicoric acid

CAS No. : 6537-80-0

(Synonyms: Cichoric acid; Dicaffeoyltartaric acid)

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Cat. No. : HY-N0457
M.Wt: 474.37
Formula: C22H18O12
Purity: >98 %
Solubility: H2O : 100 mg/mL (210.81 mM; Need ultrasonic); DMSO : 1 mg/mL (2.11 mM; Need ultrasonic)
Introduction of 6537-80-0 :

Chicoric acid (Cichoric acid), an orally active dicaffeyltartaric acid, induces reactive oxygen species (ROS) generation. Chicoric acid inhibits cell viability and induces mitochondria-dependent apoptosis in 3T3-L1 preadipocytes through ROS-mediated PI3K/Akt and MAPK signaling pathways. Chicoric acid increases glucose uptake, improves insulin resistance, and attenuates glucosamine-induced inflammation. Chicoric acid has antidiabetic properties and antioxidant, anti-inflammatory effects[1][2][3]. In Vitro: Chicoric acid (Cichoric acid; 10-200 μM; for 24, 48, and 72 h) causes a dose- and time-dependent decrease in cell viability[1].
Chicoric acid (100 μM; 48 h) induces apoptosis through caspase-3-dependent pathway[1].
Chicoric acid (100 μM; 48 h) decreases the protein level of p-Akt[1].
Chicoric acid (25, 50, 100 µM; for 24 hours) dramatically improves glucose uptake in a dose-dependent manner, and Chicoric acid further enhances insulin-induced (100 nM; 30 min) glucose uptake by 57.7% in HepG2 cells[2].
Chicoric acid (100 µM; for 24 hours) restores glucosamine-induced impairment of GLUT2 translocation through activating PI3K/Akt pathway in HepG2 cells[2].
Chicoric acid (100 µM) has no effects on HepG2 cell viability[2].
In Vivo: Chicoric acid (Cichoric acid; 60 mg/kg/day; drinking water for 4 weeks) inhibits pancreas apoptosis and adjusts islet function in diabetic mice, leading to an increase in insulin generation and secretion in C57BL/6J mice with Streptozotocin (STZ; 50 mg/kg; ip; for consecutive 5 days)[3].

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