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MedChemExpress - Model Cryptochlorogenic acid -905-99-7
Cryptochlorogenic acid (4-Caffeoylquinic acid) is a naturally occurring phenolic acid compound with oral effectiveness, anti-inflammatory, antioxidant and anti-cardiac hypertrophy effects. Alleviating LPS (HY-D1056) and ISO (HY-B0468) by regulating proinflammatory factor expression, inhibiting NF-κB activity, promoting Nrf2 nuclear transfer, and regulating PI3Kα/Akt/ mTOR / HIF-1α signaling pathway Induced physiological stress response[1][2][3].MCE products for research use only. We do not sell to patients.
Cryptochlorogenic acid
MCE China:Cryptochlorogenic acid
Brand:MedChemExpress (MCE)
Cat. No.HY-N0787
CAS:905-99-7
Synonyms:4-Caffeoylquinic acid; 4-O-Caffeoylquinic acid
Purity:99.87%
Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Shipping:Room temperature in continental US; may vary elsewhere.
Description:Cryptochlorogenic acid (4-Caffeoylquinic acid) is a naturally occurring phenolic acid compound with oral effectiveness, anti-inflammatory, antioxidant and anti-cardiac hypertrophy effects. Alleviating LPS (HY-D1056) and ISO (HY-B0468) by regulating proinflammatory factor expression, inhibiting NF-κB activity, promoting Nrf2 nuclear transfer, and regulating PI3Kα/Akt/ mTOR / HIF-1α signaling pathway Induced physiological stress response.
In Vitro:Cryptochlorogenic acid (0-150 μM, 12, 24 or 48 h) shows low toxicity to RAW264.7 cells and does not significantly affect the viability of RAW264.7 cells at specific concentrations[2]. Cryptochlorogenic acid (20-80 μM, 2 h) can dose-dependent inhibit lipopolysaccharide (LPS: 1 μg/mL, 24 h) in RAW264.7 cells. induced the production of nitric oxide (NO), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), blocking the expression of iNOS, COX-2, TNF-α and IL-6[2]. Cryptochlorogenic acid (20-80 μM, 2 hours) inhibits the phosphorylation of IκB kinase (IKK), degrades I-κB, and reduces the nuclear translocation of NF-κB. At the same time, CCGA downregulates the phosphorylation level of MAPKs. Overall, CCGA effectively controls the expression of pro-inflammatory factors, thereby alleviating LPS-induced (1 μg/mL, 24 h) inflammation. It also promotes the nuclear translocation of Nrf2 to inhibit oxidative stress[2]. Cryptochlorogenic acid (1-200 μM, 48 hours) can effectively reduce the myocardial hypertrophy of H9c2 cells caused by ISO at a certain concentration. Cryptochlorogenic acid regulates the PI3Kα/Akt/mTOR/HIF-1α signaling pathway by significantly inhibiting the phosphorylation expression level of mTOR and over-expression of p-Akt and HIF-1α induced by ISO[3].
In Vivo:Pharmacokinetic parameters of Cryptochlorogenic acid after intragastric administration of Cryptochlorogenic acid at three dosages[2] Dose (mg/kg) Cmax (μg/L) tmax (h) t1/2 (h) AUC0-t (μg•h/L) AUC0-∞ (μg•h/L) MRT0-t (h) MRT0-∞ (h) 100 630 0.33 2.00 1938.91 1977.70 3.21 3.51 200 1270.09 0.47 1.97 3071.87 3179.41 3.23 3.39 400 2582.68 0.44 2.34 8825.32 9139.54 3.47 3.93
IC50 & Target:HIF-1α
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References:
[2]. Zhao XL, et al. Cryptochlorogenic acid attenuates LPS-induced inflammatory response and oxidative stress via upregulation of the Nrf2/HO-1 signaling pathway in RAW 264.7 macrophages. Int Immunopharmacol. 2020;83:106436. [Content Brief]
[3]. Li J, et al. Cryptochlorogenic acid and its metabolites ameliorate myocardial hypertrophy through a HIF1α-related pathway. Food Funct. 2022;13(4):2269-2282. Published 2022 Feb 21. [Content Brief]
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