Description

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 hyperresponsiveness in an asthma rat model[1][2][3][4].–80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture and light, under nitrogen)—-C141H210N32O44S.xNH3—-[3]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.|[4]Gong J, et al. Ac2-26 ameliorates lung ischemia-reperfusion injury via the eNOS pathway. Biomed Pharmacother. 2019 Sep;117:109194.|[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]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.—-3089.43 (free base)–97.22–C([C@@H](C(N[C@@H](CC1=CC=CC=C1)C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@@H](CC2=CC=C(O)C=C2)C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@@H](CCCCN)C(O)=O)=O)[C@H](C)C)=O)[C@@H](C)O)=O)CCC(N)=O)=O)C(C)C)=O)=O)CCC(O)=O)=O)CCC(N)=O)=O)CCC(O)=O)=O)CCC(O)=O)=O)CC(N)=O)=O)CCC(O)=O)=O)[C@H](CC)C)=O)=O)NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@H](CC3=CC=CC=C3)NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC([C@@H](NC(C)=O)C)=O)CCSC)=O)[C@@H](C)C)=O)CO)=O)CCC(O)=O)=O)=O)CC(C)C)=O)CCCCN)=O)CCC(N)=O)=O)C)=O)C=4C=5C(NC4)=CC=CC5.xN–Inflammation/Immunology–10 mM in DMSO–IKK—-NF-κB–Peptides