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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
C141H210N32O44S
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一般描述
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.
WGK
WGK 3
闪点(°F)
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法规信息
新产品
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
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
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
Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury
International Journal of Molecular Sciences, 18(8) (2017)
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
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