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Description: Cyclosporin H (CsH), a specific inhibitor of FPR1, inhibited lung inflammation in the ALI models. CsH significantly attenuated MTDs or NFP-induced inflammatory lung injury and activation of MAPK and AKT pathways. Cyclosporin H is a viral transduction enhancer which increases lentiviral transduction up to 10-fold in human cord blood-derived hematopoietic stem and progenitor cells (HSPCs). When combined with Rapamycin or Prostaglandin E2 Cyclosporin H displays an additive effect. Cyclosporin H lacks immunosuppressant activity of Cyclosporin A. Target: Others. Smiles: C\C=C\C[C@H](C)[C@H](O)C1N(C)C(=O)[C@@H](C(C)C)N(C)C(=O)[C@H](CC(C)C)N(C)C(=O)[C@H](CC(C)C)N(C)C(=O)[C@@H](C)NC(=O)[C@H](C)NC(=O)[C@H](CC(C)C)N(C)C(=O)[C@@H](NC(=O)[C@H](CC(C)C)N(C)C(=O)CN(C)C(=O)CCCNC1=O)C(C)C. References: Zhang X, et al. Mitochondrial peptides cause proinflammatory responses in the alveolar epithelium via FPR-1, MAPKs, and AKT: a potential mechanism involved in acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2018,315(5):L775-L786.
This website uses cookies, which are necessary for the technical operation of the website and are always set. Other cookies, which increase the usability of this website, serve for direct advertising or simplify interaction with other websites and social networks, will only be used with your consent.
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