Muratspahić Edin, Aslanoglou Despoina, White Andrew M, Draxler Claudia, Kozisek Xaver, Farooq Zara, Craik David J, McCormick Peter J, Durek Thomas, Gruber Christian W
Center for Physiology and Pharmacology, Institute of Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.
Institute for Molecular Bioscience, Australian Research Council Centre of Excellence for Innovations in Peptide and Protein Science, The University of Queensland, Brisbane, Queensland 4072, Australia.
ACS Pharmacol Transl Sci. 2023 Sep 26;6(10):1373-1381. doi: 10.1021/acsptsci.3c00090. eCollection 2023 Oct 13.
G protein-coupled receptors are among the most widely studied classes of drug targets. A major challenge in this field is to develop ligands that will selectively modulate a single receptor subtype to overcome the disadvantages of undesired "off target" effects caused by lack of target and thus signaling specificity. In the current study, we explored ligand design for the melanocortin 4 receptor (MC4R) since it is an attractive target for developing antiobesity drugs. Endogenously, the receptor is activated by peptide ligands, i.e., three melanocyte-stimulating hormones (α-MSH, β-MSH, and γ-MSH) and by adrenocorticotropic hormone. Therefore, we utilized a peptide drug design approach, utilizing "molecular grafting" of pharmacophore peptide sequence motifs onto a stable nature-derived peptide scaffold. Specifically, protegrin-4-like-peptide-1 (Pr4LP1) and arenicin-1-like-peptide-1 (Ar3LP1) fully activated MC4R in a functional cAMP assay with potencies of 3.7 and 1.0 nM, respectively. In a nanoluciferase complementation assay with less signal amplification, the designed peptides fully recruited mini-Gs with subnanomolar and nanomolar potencies. Interestingly, these novel peptide MC4R ligands recruited β-arrestin-2 with ∼2-fold greater efficacies and ∼20-fold increased potencies as compared to the endogenous α-MSH. The peptides were inactive at related MC1R and MC3R in a cAMP accumulation assay. These findings highlight the applicability of animal-derived disulfide-rich scaffolds to design pathway and subtype selective MC4R pharmacological probes. In the future, this approach could be exploited to develop functionally selective ligands that could offer safer and more effective obesity drugs.
G蛋白偶联受体是研究最为广泛的一类药物靶点。该领域的一个主要挑战是开发能够选择性调节单一受体亚型的配体,以克服因缺乏靶点特异性而导致的不良“脱靶”效应的缺点。在本研究中,我们探索了黑皮质素4受体(MC4R)的配体设计,因为它是开发抗肥胖药物的一个有吸引力的靶点。内源性地,该受体由肽配体激活,即三种促黑素细胞激素(α-MSH、β-MSH和γ-MSH)以及促肾上腺皮质激素。因此,我们采用了一种肽药物设计方法,将药效团肽序列基序“分子嫁接”到一个稳定的天然来源的肽支架上。具体而言,在功能性cAMP测定中,protegrin-4样肽-1(Pr4LP1)和沙蚕毒素-1样肽-1(Ar3LP1)分别以3.7 nM和1.0 nM的效力完全激活了MC4R。在信号放大较少的纳米荧光素酶互补测定中,设计出的肽分别以亚纳摩尔和纳摩尔的效力完全募集了微型Gs。有趣的是,与内源性α-MSH相比,这些新型肽MC4R配体募集β-抑制蛋白2的效力提高了约20倍,功效提高了约2倍。在cAMP积累测定中,这些肽对相关的MC1R和MC3R无活性。这些发现突出了动物来源的富含二硫键的支架在设计途径和亚型选择性MC4R药理学探针方面的适用性。未来,这种方法可用于开发功能选择性配体,从而提供更安全、更有效的肥胖药物。