| Description | Acimtamig (AFM13) is a CD30/CD16A bispecific innate cell engager. Acimtamig binds to the CD16A expressed on natural killer (NK) cells and binds to CD30 on CD30-expressing tumor cells, thereby selectively cross-linking tumor and NK cells. Acimtamig can be used for the study of eripheral T-cell Acimtamig (AFM13) is a CD30/CD16A bispecific innate cell engager. Acimtamig binds to the CD16A expressed on natural killer (NK) cells and binds to CD30 on CD30-expressing tumor cells, thereby selectively cross-linking tumor and NK cells. Acimtamig can be used for the study of eripheral T-cell lymphoma (PTCL)[1]... Read More | Gap 26 TFA is a connexin mimetic peptide, composed of residue numbers 63-75 of the first extracellular loop of connexin 43 (gap junction blocker), containing the SHVR amino acid motif[1] | KALA is an amphiphilic peptide that forms an α-helical structure at physiological pH. KALA modifies a plasmid DNA-encapsulating liposomal membrane and is used as a fusogenic peptide in order to achieve effective liver targeting and transfection of DNA via galactose receptors[1] | Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist. Lixisenatide inhibits the inflammatory response through down regulation of pro-inflammatory cytokines, and suppresses of the Akt-MEK1/2 signaling pathway. Lixisenatide can inhibit oxidative stress, mitochondrial dysfunction and Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist. Lixisenatide inhibits the inflammatory response through down regulation of pro-inflammatory cytokines, and suppresses of the Akt-MEK1/2 signaling pathway. Lixisenatide can inhibit oxidative stress, mitochondrial dysfunction and apoptosis. Lixisenatide can be used for the researches of inflammation, metabolic disease, neurological disease and cardiovascular disease, such as rheumatoid arthritis, diabetes, Alzheimer's disease and atherosclerosis[1][2][3][4][5][6]... Read More | RKH acetate exerts protective effects against sepsis-induced death and organ damage. RKH acetate can directly bind to Toll-like receptor 4 (TLR4) and block TLR4 signal transduction in immune cells[1] |