Abstract The aim of this study was to demonstrate the in silico the potential of curcuminoids and curcumin metabolites to inhibit the polymerization of HbS. Ten molecules were analyzed, including curcuminoids (curcumin, bisdemethoxycurcumin, demethoxycurcumin and cyclocurcumin) and curcumin metabolites (dihydrocurcumin, glucuronocurcumin, hexahydrocurcumin, hexahydrocurcumin, curcumin sulphate and tetrahydrocurcumin). In silico screenings were carried out by molecular docking to determine the free enthalpies of complexation and the interactions between different ligands studied and HbS. Moreover, in silico screening using the ADMET test was carried out to determine the pharmacokinetic profile of various compounds studied. The findings revealed that all the ligands can form stable complexes with HbS. The binding energies of the complexes formed between the ligands and Hb S ranged from -5.8 Kcal/moL to -8.1 Kcal/moL. These bindings between curcumin glucuronide and cyclocurcumin with HbS were stable compared with the other compounds (-8.1 Kcal/moL and -8.0 Kcal/moL). The in silico toxicity screening showed that the majority of ligands fulfilled the Lipinski and Veber rules. Thus, we believe that curcuminoids can individually or synergistically inhibit HbS polymerization and sickle cell sickling.
No takes yet. Share an insight, caveat, or question.
Mbadiko et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: