化学
受体
肽
组合化学
模板
跨膜蛋白
合理设计
领域(数学)
生物系统
微调
序列(生物学)
简单(哲学)
杠杆
纳米技术
生物物理学
选择性
班级(哲学)
小分子
G蛋白偶联受体
信号转导
公制(单位)
肽序列
跨膜结构域
计算生物学
芯(光纤)
计算机科学
作者
Damla Sürmeli,Kathleen M. Sicinski,Tristan C. Dinsmore,Venkata S. Raman,Vittorio Montanari,Martin Beinborn,Krishna Kumar
标识
DOI:10.1021/acs.jmedchem.6c00745
摘要
Unimolecular multiagonists integrating GLP-1R/GIPR, and increasingly GCGR agonism, have altered the landscape of peptide therapeutics for metabolic syndrome. This progress has shifted the field from optimizing individual ligands to engineering defined receptor selectivity (balance) and, in some cases, pathway-selective signaling (bias) within a single-peptide scaffold. Despite this momentum, tuning 'balance' and 'bias' remains difficult because small sequence changes can have receptor-dependent, nonintuitive effects, and meaningful retuning often requires wholesale scaffold redesign. Here, we implement a systematic strategy based on simple N-terminal chemical modifications across dual- and triagonist templates to decouple these variables. Because the peptide N-terminus is buried within the membrane-embedded transmembrane core of class B GPCRs, localized chemical edits at this site provide a sensitive lever for reweighting receptor activation. These minimal changes can alter signaling preference without loss of efficacy, expanding the design grammar and offer rapid tuning of potency, efficacy, and bias.
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