SML3198
Ac2-26 trifluoroacetate
≥98% (HPLC)
别名:
Ac2-26 TFA, LC1 trifluoroacetate, Lipocortin 1- trifluoroacetate, 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, Annexin A1 trifluoroacetate, AnxA1 trifluoroacetate
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About This Item
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一般說明
Ac2-26 is a Lipocortin 1/Annexin 1 Peptide Mimetic, derived from the N-terminal region of annexin A1 (AnxA1). It contains residues 2–26 of AnxA1. Ac2-26 activates formyl peptide receptor family members formyl peptide receptor (FPR), FPR-like (FPRL) 1 and FPRL2. It exhibits an anti-inflammatory effect by inhibiting the adhesion and transmigration of leukocytes (leukocyte extravasation). This facilitates the growth and migration of epithelial cells, aiding in tissue repair. Ac2-26 also serves as a cardioprotective peptide. It is observed that Ac2-26 reduces acute lung injury caused by ischemia and reperfusion.
儲存類別代碼
11 - Combustible Solids
水污染物質分類(WGK)
WGK 3
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Diabetes, 70(10), 2192-2203 (2021-06-10)
Inflammation and abnormal metabolism play important roles in the pathogenesis of diabetic nephropathy (DN). Annexin A1 (ANXA1) contributes to inflammation resolution and improves metabolism. In this study, we assess the effects of ANXA1 in diabetic mice and proximal tubular epithelial
The Journal of biological chemistry, 287(41), 34101-34109 (2012-08-11)
Neutrophil serine proteases play an important role in inflammation by modulating neutrophil effector functions. We have previously shown that neutrophils deficient in the serine proteases cathepsin G and neutrophil elastase (CG/NE neutrophils) exhibit severe defects in chemokine CXCL2 release and
Cells, 10(1) (2021-01-15)
This study evaluated the role of endogenous and exogenous annexin A1 (AnxA1) in the activation of the NLRP3 inflammasome in isolated peritoneal neutrophils. C57BL/6 wild-type (WT) and AnxA1 knockout mice (AnxA1-/-) received 0.3% carrageenan intraperitoneally and, after 3 h, the
Journal of neuroinflammation, 17(1), 325-325 (2020-10-31)
Bacterial meningitis is still a cause of severe neurological disability. The brain is protected from penetrating pathogens by the blood-brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G-protein-coupled formyl peptide
Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury
International Journal of Molecular Sciences, 18(8) (2017)
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