| Description | PKA Regulatory Subunit II Substrate (RII phosphopeptide) is a tool peptide derived from the regulatory subunit Type II (RII) of cyclic AMP-dependent protein kinase (PKA). PKA Regulatory Subunit II Substrate is commonly used to mimic the phosphorylation of protein kinases and as a specific substrate PKA Regulatory Subunit II Substrate (RII phosphopeptide) is a tool peptide derived from the regulatory subunit Type II (RII) of cyclic AMP-dependent protein kinase (PKA). PKA Regulatory Subunit II Substrate is commonly used to mimic the phosphorylation of protein kinases and as a specific substrate for protein phosphatases to assess the activities of these enzymes[1]... Read More | α-Bungarotoxin is a competitive antagonist at nicotinic acetylcholine receptors (nAChRs). α-Bungarotoxin, a selective α7 receptor blocker, blocks α7 currents with an IC50 of 1.6 nM and has no effects on α3β4 currents at concentrations up to 3 µM[1][2] | α-MSH (α-Melanocyte-Stimulating Hormone) TFA, an endogenous neuropeptide, is an endogenous melanocortin receptor 4 (MC4R) agonist with anti-inflammatory and antipyretic activities. α-MSH TFA is a post-translational derivative of pro-opiomelanocortin (POMC)[1][2] | 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] |