Ac2-26
/ Synthetic N-acetylated 25-residue peptide derived from Annexin A1 N-terminusALIAS · Annexin A1 N-terminal peptide (residues 2-26) · AnxA1 mimetic peptide · Acetylated Annexin A1(2-26)
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Tier 3. Synthetic 25-residue acetylated peptide derived from the N-terminal active region of Annexin A1, an endogenous glucocorticoid-induced anti-inflammatory protein. Extensive preclinical literature in rodent models of inflammation; no human clinical trials.
Ac2-26 mimics the bioactive N-terminal region of Annexin A1, an endogenous anti-inflammatory protein induced by glucocorticoids. It signals through formyl peptide receptor 2 (FPR2/ALX), promoting resolution of acute inflammation by inhibiting neutrophil transmigration and inducing macrophage clearance of apoptotic cells. The downstream pro-resolution programme overlaps with that of resolvins and lipoxins, framing Ac2-26 within the broader 'specialised pro-resolving mediator' pharmacology.
Tier 3. Rodent and in-vitro literature in models of myocardial ischaemia-reperfusion, inflammatory bowel disease, peritonitis, and ocular surface inflammation. No published human Phase 1 trial of synthetic Ac2-26.
No human safety database. FPR2 is broadly expressed; off-target effects of chronic agonism on host defence and tissue homeostasis are not characterised.
Regulatory status
- FDA status:
- Not FDA-approved
The endogenous Annexin A1 system is bidirectional — the same N-terminal region can be cleaved by inflammatory proteases to produce different downstream effects depending on tissue context. Synthetic mimetic peptides do not recapitulate the full regulatory complexity of the parent protein.