| Identification | Back Directory | [Name]
AC2-26 | [CAS]
151988-33-9 | [Synonyms]
AC2-26
Annexin A1 (1-25)
Annexin 1 (ANXA - 1, Ac 2 - 26)
Annexin-1 (2-26) (huMan), Lipocortin-1 (2-26), Calpactin II (1-25) (dephosphorylated) (huMan), Ac2-26
Ac-Ala-Met-Val-Ser-Glu-Phe-Leu-Lys-Gln-Ala-Trp-Phe-Ile-Glu-Asn-Glu-Glu-Gln-Glu-Tyr-Val-Gln-Thr-Val-Lys-OH
Annexin A1 (1-25) (dephosphorylated) (huMan)
Annexin-1 (2-26) (huMan), Lipocortin-1 (2-26), Calpactin II (1-25) (dephosphorylated) (huMan), Ac2-26
Annexin A1 (1-25) (dephosphorylated) (human) trifluoroacetate salt Ac-Ala-Met-Val-Ser-Glu-Phe-Leu-Lys-Gln-Ala-Trp-Phe-Ile-Glu-Asn-Glu-Glu-Gln-Glu-Tyr-Val-Gln-Thr-Val-Lys-OH trifluoroacetate salt
L-Lysine, N-acetyl-L-alanyl-L-methionyl-L-valyl-L-seryl-L-α-glutamyl-L-phenylalanyl-L-leucyl-L-lysyl-L-glutaminyl-L-alanyl-L-tryptophyl-L-phenylalanyl-L-isoleucyl-L-α-glutamyl-L-asparaginyl-L-α-glutamyl-L-α-glutamyl-L-glutaminyl-L-α-glutamyl-L-tyrosyl-L-valyl-L-glutaminyl-L-threonyl-L-valyl- | [Molecular Formula]
C141H210N32O44S | [MDL Number]
MFCD00792708 | [MOL File]
151988-33-9.mol | [Molecular Weight]
3089.43 |
| Chemical Properties | Back Directory | [Boiling point ]
2847.6±65.0 °C(Predicted) | [density ]
1.327±0.06 g/cm3(Predicted) | [storage temp. ]
Desiccate at -20°C | [solubility ]
Soluble to 1 mg/ml in PBS | [form ]
Solid | [color ]
White to off-white | [Sequence]
Ac-Ala-Met-Val-Ser-Glu-Phe-Leu-Lys-Gln-Ala-Trp-Phe-Ile-Glu-Asn-Glu-Glu-Gln-Glu-Tyr-Val-Gln-Thr-Val-Lys-OH |
| Hazard Information | Back Directory | [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]. | [in vivo]
Ac2-26 (1?mg/kg/d, i.v. since reperfusion until day 7) reduces cardiac necrosis and cardiac inflammation in mice 24 h/48 h post I-R injury model[6]. | [storage]
Store at -20°C | [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 |
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