Abstract :
Background: Chronic heart failure is a progressive disorder characterized by cardiac fibrosis and pathological hypertrophy, primarily mediated by dysregulated growth factors such as VEGF, PDGF, TGF-?, and FGF. While Sorafenib is a known multi-kinase inhibitor, the potential role of Telmisartan in modulating growth factor pathways remains underexplored.Objective: This study aimed to investigate the inhibitory potential of Telmisartan, an angiotensin II receptor blocker, in comparison with Sorafenib, a multi-kinase inhibitor, against key growth factor signaling pathways implicated in chronic heart failure (CHF).Materials and Methods: An in-silico molecular docking study was performed using AutoDock Vina, targeting FGFR1 (4QAL), PDGFR? (6JOL), TGF?1R (5QTZ), TGF?2R (5QIN), and VEGFR2 (6XVK). The binding affinities of Telmisartan and Sorafenib were calculated, and molecular interactions were visualized using Biovia Discovery Studio 2024.Results: Telmisartan demonstrated stronger binding to FGFR1 (–7.7 kcal/mol), TGF?1R (–11.1 kcal/mol), and VEGFR2 (-9.9 kcal/mol) compared to Sorafenib, suggesting a higher affinity for receptors involved in fibrosis and vascular remodeling. Conversely, Sorafenib showed superior binding to PDGFR? (–10.2 kcal/mol) and TGF?2R (-9.5 kcal/mol). Structural analysis revealed hydrogen bonds and van der Waals forces as the primary stabilizing interactions.Conclusion: The results indicate that Telmisartan may possess growth factor-inhibitory properties beyond its established antihypertensive role, particularly in pathways linked to cardiac fibrosis and hypertrophy. These findings highlight the therapeutic potential of Telmisartan in chronic heart failure, warranting further in vitro and preclinical validation.
Keyword :
Chronic heart failure, Growth factor, Telmisartan, Sorafenib, In-silico study