Caftaric acid


CAS No. : 67879-58-7

(Synonyms: trans-Caftaric acid)

67879-58-7
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Cat. No. : HY-N0321
M.Wt: 312.23
Formula: C13H12O9
Purity: >98 %
Solubility: H2O : 50 mg/mL (ultrasonic);DMSO : 50 mg/mL (ultrasonic)
Introduction of 67879-58-7 :

Caftaric acid (trans-Caftaric acid) is a polyphenolic antidiuretic, antioxidant and anti-apoptotic agent that can be hydrolyzed by intestinal microbial esterases. Caftaric acid exerts its antioxidant and potential anti-inflammatory effects mainly through intestinal microbial metabolism. Caftaric acid can reduce renal damage, restore electrolyte balance, renal function indicators and antioxidant enzyme activities in a rat albinism model, and further exert anti-oxidative stress and anti-inflammatory activities[1][2][3]. In Vitro:In an in vitro human fecal microbial fermentation experiment, Caftaric acid (1 μmol; 2 h) is rapidly metabolized, and no free caffeic acid or tartaric acid was detected. The main metabolites were 3-hydroxyphenylpropionic acid (3-HPP) and benzoic acid (BA). 3-HPP reached a peak value (0.24 μmol) at 2 hours[1].
In the same experiment, Caftaric acid (1 μmol; 24 h) produces benzoic acid (BA) continuously, accounting for 4-5% of the initial dose at 24 hours[1].
In Vivo:Caftaric acid (40, 80 mg/kg; ip; once daily; 2 weeks) alleviates renal injury in the lead acetate-induced nephrotoxicity model in male albino Sprague Dawley rats through antidiuretic, antioxidant and antiapoptotic activities, restores electrolyte balance, renal function indicators and antioxidant enzyme activities, and improves histopathological changes[2].
Caftaric acid (80 mg/kg; ip; once daily; 2 weeks) does not cause obvious renal injury or electrolyte disturbances in normal male albino Sprague Dawley rats[2].
Caftaric acid (40, 80 mg/kg; ip; once before reperfusion) alleviates renal and lung tissue damage in the Wistar rat renal ischemia-reperfusion model by reducing oxidative stress (MDA, MPO, TOS, OSI), inhibiting apoptosis (caspase-3), autophagy (LC3) and inflammation (COX-2)[3].

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