Ac2-26 ammonium is the N-terminal peptide of annexin 1, and has anti-inflammatory activity. Ac2-26 ammonium induces a decrease in IKKβ protein in lysosomes by chaperone-mediated autophagy (CMA). Ac2-26 ammonium ameliorates lung ischemia-reperfusion injury. Ac2-26 ammonium also inhibits airway inflammation and perresponsiveness in an asthma rat model.
References:
[1]. Wang LM, et al. Annexin 1-derived peptide Ac2-26 inhibits eosinophil recruitment in vivo via decreasing prostaglandin D₂. Int Arch Allergy Immunol. 2011;154(2):137-48.
[2]. Gong J, et al. Ac2-26 ameliorates lung ischemia-reperfusion injury via the eNOS pathway. Biomed Pharmacother. 2019 Sep;117:109194.
[3]. Luo Z, et al. Annexin-1 Mimetic Peptide Ac2-26 Suppresses Inflammatory Mediators in LPS-Induced Astrocytes and Ameliorates Pain persensitivity in a Rat Model of Inflammatory Pain. Cell Mol Neurobiol. 2020 May;40(4):569-585.
[4]. 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.