Uses
Ac2-26 is the N-terminal peptide of annexin 1, and has anti-inflammatory activity. Ac2-26 induces a decrease in IKKβ protein in lysosomes by chaperone-mediated autophagy (CMA). Ac2-26 ameliorates lung ischemia-reperfusion injury. Ac2-26 also inhibits airway inflammation and hyperresponsiveness in an asthma rat model[1][2][3][4].
References
[1] Wang LM, et al. Annexin 1-derived peptide Ac2-26 inhibits eosinophil recruitment in vivo via decreasing prostaglandin D?. Int Arch Allergy Immunol. 2011;154(2):137-48. DOI:
10.1159/000320228[2] Liu L, et al. Ac2-26 Induces IKKβ Degradation Through Chaperone-Mediated Autophagy Via HSPB1 in NCM-Treated Microglia. Front Mol Neurosci. 2018 Mar 15;11:76. DOI:
10.3389/fnmol.2018.00076[3] Gong J, et al. Ac2-26 ameliorates lung ischemia-reperfusion injury via the eNOS pathway. Biomed Pharmacother. 2019 Sep;117:109194. DOI:
10.1016/j.biopha.2019.109194[4] Luo Z, et al. Annexin-1 Mimetic Peptide Ac2-26 Suppresses Inflammatory Mediators in LPS-Induced Astrocytes and Ameliorates Pain Hypersensitivity in a Rat Model of Inflammatory Pain. Cell Mol Neurobiol. 2020 May;40(4):569-585. DOI:
10.1007/s10571-019-00755-8[5] Zheng Y, et al. Annexin A1 (Ac2-26)-dependent Fpr2 receptor alleviates sepsis-induced acute kidney injury by inhibiting inflammation and apoptosis in vivo and in vitro. Inflamm Res. 2023 Feb;72(2):347-362. DOI:
10.1007/s00011-022-01640-9[6] Qin CX, et al. Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, Ac2-26, Against Myocardial Infarction. Front Pharmacol. 2019 Apr 3;10:269. DOI:
10.3389/fphar.2019.00269
