DMB [GLP-1R Agonist] [281209-71-0]

AdipoGen Life Sciences

DMB [GLP-1R Agonist] [281209-71-0]

10

281209-71-0

Research Use Only

>98%

C13H15Cl2N3O2S

348.2

Chemical. CAS: 281209-71-0. Formula: C13H15Cl2N3O2S. MW: 348.2. DMB is a small molecule GLP-1 receptor agonist (GLP-1R; KB = 26.3 nM for the recombinant human receptor). DMB exerts its activating effect by forming hydrogen bonds with the Tyr42, Cys71 and Ser84 residues of GLP-1R. GLP-1 receptor signaling is a predominant mechanism for regulating glucose homeostasis. DMB represents a unique non-peptide tool for studying the role of GLP-1 in both in vivo and in vitro diabetes and obesity models. DMB is a selective small molecule gasdermin D (GSDMD) agonist for inducing pyroptosis and enhancing anti-tumor immunity. DMB can directly activate GSDMD-mediated cancer cell pyroptosis. Unlike traditional pathways requiring GSDMD cleavage, DMB induces pyroptosis without this step, effectively stimulating anti-tumor immune responses with minimal toxicity. It achieves this by covalently modifying the Cys191 residue in GSDMD, disrupting the interaction between the N-terminus (NT) and C-terminus (CT). This keeps GSDMD in an activated state without cleavage, promoting pore formation and inducing pyroptosis while preserving the overall GSDMD structure. - DMB is a small molecule GLP-1 receptor agonist (GLP-1R; KB = 26.3 nM for the recombinant human receptor). DMB exerts its activating effect by forming hydrogen bonds with the Tyr42, Cys71 and Ser84 residues of GLP-1R. GLP-1 receptor signaling is a predominant mechanism for regulating glucose homeostasis. DMB represents a unique non-peptide tool for studying the role of GLP-1 in both in vivo and in vitro diabetes and obesity models. DMB is a selective small molecule gasdermin D (GSDMD) agonist for inducing pyroptosis and enhancing anti-tumor immunity. DMB can directly activate GSDMD-mediated cancer cell pyroptosis. Unlike traditional pathways requiring GSDMD cleavage, DMB induces pyroptosis without this step, effectively stimulating anti-tumor immune responses with minimal toxicity. It achieves this by covalently modifying the Cys191 residue in GSDMD, disrupting the interaction between the N-terminus (NT) and C-terminus (CT). This keeps GSDMD in an activated state without cleavage, promoting pore formation and inducing pyroptosis while preserving the overall GSDMD structure.

ClC1=C(Cl)C=C(N=C(NC(C)(C)C)C(S(C)(=O)=O)=N2)C2=C1

-20°C,2°C to 8°C

12161509