Design and optimization of peptidomimetics as PD-1/PD-L1 modulators for the management of triple-negative breast cancer

设计和优化肽模拟物作为PD-1/PD-L1调节剂用于三阴性乳腺癌的治疗

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Abstract

Immunotherapy has garnered significant attention as a promising alternative treatment modality for triple-negative breast cancer because of its immunogenic nature. Of late, the modulation of programmed cell death-1 (PD-1) and its ligand programmed cell death ligand-1 (PD-L1) has shown potency in combating TNBC. Till date, several monoclonal antibodies and peptides are being used as PD-1/PD-L1 modulators. Nevertheless, the limitations associated with these molecules necessitate the development of potent alternative therapeutics. Thus, the present study aimed to employ a series of virtual screening strategies to derive peptidomimetic molecules as PD-1 modulators. Initially, a short peptide sequence (p-ADKYR) that disrupts the PD-1/PD-L1 dyad was designed. Subsequently, alanine scanning was conducted to analyse the critical residues on the designed peptide. The obtained results were then utilised for screening of peptidomimetics from the pep: MMs: MIMIC. The binding of the 200 peptide-mimicking molecules with the PD-1 protein was determined using AutoDock Vina. Further, the binding free energy and machine learning-based scoring analysis were used to re-score the docked pose of the complexes. Then, interaction analysis and ADMET properties were assessed for the obtained peptidomimetics, which resulted in one molecule, MMs01069049, as a potent PD-1 modulator. Finally, molecular dynamics simulation was performed for 200 ns, and the equilibrated structure from the last 5 ns was subjected to binding free energy analysis using MM-GBSA, which confirmed the enhanced stability and affinity of MMs01069049 at the PD-1 interface compared to the designed peptide. Collectively, we propose that MMs01069049 may serve as an efficient PD-1 modulator for the management of TNBC in the near future. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40203-025-00528-w.

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