| Description | K41498 TFA is a potent and highly selective CRF2 receptor antagonist with Ki values of 0.66 nM, 0.62 nM and 425 nM for human CRF2α, CRF2β and CRF1 receptors respectively. K41498 TFA is an analogues of antisauvagine-30 (aSvg-30), inhibits sauvagine-stimulated cAMP accumulation in hCRF2αK41498 TFA is a potent and highly selective CRF2 receptor antagonist with Ki values of 0.66 nM, 0.62 nM and 425 nM for human CRF2α, CRF2β and CRF1 receptors respectively. K41498 TFA is an analogues of antisauvagine-30 (aSvg-30), inhibits sauvagine-stimulated cAMP accumulation in hCRF2α- and hCRF2β-expressing cells. K41498 TFA can be used for hypotension study[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] | GLP-2(rat) is an intestinal growth factor. GLP-2(rat) stimulates cell proliferation and inhibits apoptosis. GLP-2(rat) enhances mucosal mass and function in residual small intestine after massive small bowel resection (MSBR)[1][2] | HEP-1 (Human ezrin peptide (324 - 337)) is an orally active peptide with antiviral, anti-inflammatory, and immunomodulatory activities. HEP-1 is effective against infections by various viruses such as HIV, HCV, herpes viruses, HPV, and influenza viruses. As an immunomodulator, HEP-1 can enhance the HEP-1 (Human ezrin peptide (324 - 337)) is an orally active peptide with antiviral, anti-inflammatory, and immunomodulatory activities. HEP-1 is effective against infections by various viruses such as HIV, HCV, herpes viruses, HPV, and influenza viruses. As an immunomodulator, HEP-1 can enhance the adaptive immunity mediated by B cells and T cells. HEP-1 can also increase the antibody titers after hepatitis B vaccination. HEP-1 can be used in the research of viral infections and inflammation-related diseases[1][2]... 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] |