annexin a1

Hydrocortisone 17-butyrate (Cortisol 17-butyrate) is a synthetic glucocorticoid receptor agonist with antiinflammatory, antipruritic and vasoconstrictive effects.

Dexamethasone acetate (NSC 39471) is the acetate salt form of Dexamethasone, a synthetic adrenal corticosteroid with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone also interferes with NF-kB activation and apoptotic pathways. This agent lacks the salt-retaining properties of other related adrenal hormones.

Amcinonide (CL-34699) is a Corticosteroid. The mechanism of action of amcinonide is as a Corticosteroid Hormone Receptor Agonist.

Hydrocortisone acetate (Cortisol 21-acetate) is the synthetic acetate salt form of hydrocortisone, a corticosteroid with anti-inflammatory and immunosuppressive properties.

Ac2-26 ammonium is an Annexin-A1 (AnxA1) N-terminal derived peptide with anti-inflammatory activity and alleviates liver ischemia-reperfusion injury in mice by regulating IL-22 IL-22R1 STAT3 signaling and eNOS pathways.

A11, a cell-penetrating peptide, integrates the HIV-1 Tat protein transduction domain with an 11-amino acid segment from the annexin A1 N-terminus (residues 20-30). This compound disrupts the interaction between annexin A1 and the Eph receptor tyrosine kinase A2 (EphA2), leading to enhanced EphA2 ubiquitination in HK1 nasopharyngeal carcinoma (NPC) cells. At a concentration of 10 µM, A11 curtails proliferation, migration, and invasion of HK1 and 5-8F NPC cells. Furthermore, A11 demonstrably diminishes tumor volume in mouse xenograft models of 5-8F and HK1 NPC in vivo.

Tat-NTS peptide, a cell-penetrating compound, comprises the HIV-1 Tat protein transduction domain fused with a 10-amino acid sequence (residues 228-237) from the repeat III domain of annexin A1, serving as a nuclear translocation signal (NTS). This peptide hinders the interaction between annexin A1 and importin β, obstructing annexin A1's nuclear entry in primary mouse hippocampal neurons. Tat-NTS effectively prevents apoptosis triggered by glucose-oxygen deprivation and reperfusion in these neurons. When administered in vivo at a dosage of 10 mg/kg, it significantly reduces infarct size, minimizes neuronal apoptosis, and improves navigation performance in the Morris water maze test for mice subjected to ischemia-reperfusion injury via middle cerebral artery occlusion (MCAO).

Ac2-26 TFA, an active N-terminal peptide of annexin A1 (AnxA1), attenuates ischemia-reperfusion-induced acute lung injury. Ac2-26 also decreases AnxA1 protein expression, inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue.

Ac2-26, an annexin A1 mimetic peptide, was able to attenuate renal inflammatory injury in a diabetic mouse model through inhibition of p38MAPK/NF-κB, as well as sepsis-induced cardiomyocyte apoptosis through the LXA4/PI3K/AKT signalling pathway, and hepatic ischaemia-reperfusion injury in mice by modulating IL-22/IL-22R1/STAT3 signalling pathway.

Ac2-26 acetate is an active N-terminal peptide of annexin A1(AnxA1). Ac2-26 acetate decreases AnxA1 protein expression and inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue. Ac2-26 acetate attenuates ischemia-reperfusion-induced acute lung injury.