ArticleFrontiers in chemistry2026
Computational QSAR and structure-based identification of plerixafor-derived PIM-1 kinase inhibitors in diffuse large B-Cell lymphoma.
Article in Frontiers in chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Diffuse large B-cell lymphoma (DLBCL) is the most common and aggressive subtype of non-Hodgkin lymphoma, with a substantial proportion of patients developing resistance to standard chemotherapy. Chromosomal translocations resulting in overexpression of the serine/threonine kinase Proviral Integration site for Moloney murine leukemia virus (PIM-1) contribute to disease progression, therapeutic resistance, and poor clinical outcomes, establishing PIM-1 as a promising molecular target. Unlike many kinases, the ATP-binding site of PIM-1 lacks a backbone hydrogen bond donor within the hinge region due to the presence of Pro123, conferring unique structural features relevant for selective inhibitor design. Although R-CHOP is the first-line treatment for DLBCL, approximately 30%-40% of patients develop refractory disease, highlighting the need for novel targeted therapies. Methods: In this study, an in-silico drug repurposing strategy was employed to investigate plerixafor analogues as potential ATP-competitive PIM-1 inhibitors. Quantitative Structure Activity Relationship (QSAR) modeling demonstrated strong predictive performance (R Results: Additional MM/GBSA, Principal Component Analysis (PCA), Dynamic Cross-Correlation Matrix (DCCM), and free energy landscape (FEL) analyses further supported complex stability and restricted conformational dynamics. Discussion: Collectively, these findings identify plerixafor-derived compound 1 as a promising PIM-1 inhibitor and provide a robust computational framework for the development of targeted therapeutics against aggressive DLBCL, warranting further experimental validation.
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