Thiophenes
Apexbio Technology LLC Vatalanib (PTK787) 2HCl 212141-51-0 50mg
Vatalanib (PTK787) 2HCl (CAS 212141-51-0) is a small molecule inhibitor targeting vascular endothelial growth factor (VEGF) receptor tyrosine kinases including VEGFR/KDR (IC50 0 037 M) VEGFR/Flt-1 (IC50 0 077 M) and VEGFR/Flk (IC50 0 27 M) It also inhibits other receptor tyrosine kinases such as PDGFR- (IC50 0 58 M) c-Kit (IC50 0 73 M) and c-Fms (IC50 1 4 M) Through blockade of these pathways Vatalanib suppresses VEGF-mediated signaling and angiogenesis It is utilized in research investigating mechanisms of angiogenesis and has potential applications in studies of solid tumors and other angiogenesis-dependent diseases
Apexbio Technology LLC 4-Methylhistamine dihydrochloride 36376-47-3 1mg
4-Methylhistamine dihydrochloride (CAS 36376-47-3) is a selective agonist for the histamine H4 receptor (H4R) displaying a pEC50 of 7 4 0 1 at human H4R It exhibits over 100-fold selectivity for H4R relative to H3R and H2R and over 100 000-fold compared to H1R While affinity for human H4R is moderate it binds rat and mouse H4R with higher affinity (Ki values of 73 nM and 55 nM respectively) In in vivo models 4-Methylhistamine dihydrochloride modulates inflammatory signaling elevating TNF- and NF- B expression via JAK/STAT pathways in response to LPS-induced joint inflammation It serves as a valuable tool in studies of H4R-mediated immune regulation and inflammatory mechanisms
Apexbio Technology LLC 4-Methylhistamine dihydrochloride 36376-47-3 5mg
4-Methylhistamine dihydrochloride (CAS 36376-47-3) is a selective agonist for the histamine H4 receptor (H4R) displaying a pEC50 of 7 4 0 1 at human H4R It exhibits over 100-fold selectivity for H4R relative to H3R and H2R and over 100 000-fold compared to H1R While affinity for human H4R is moderate it binds rat and mouse H4R with higher affinity (Ki values of 73 nM and 55 nM respectively) In in vivo models 4-Methylhistamine dihydrochloride modulates inflammatory signaling elevating TNF- and NF- B expression via JAK/STAT pathways in response to LPS-induced joint inflammation It serves as a valuable tool in studies of H4R-mediated immune regulation and inflammatory mechanisms