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1.
J Biomol Struct Dyn ; 37(6): 1616-1627, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-29633908

RESUMEN

In this work, the binding mechanism of new Polyketide Synthase 13 (Pks13) inhibitors has been studied through molecular dynamics simulation and free energy calculations. The drug Tam1 and its analogs, belonging to the benzofuran class, were submitted to 100 ns simulations, and according to the results obtained for root mean square deviation, all the simulations converged from approximately 30 ns. For the analysis of backbone flotation, the root mean square fluctuations were plotted for the Cα atoms; analysis revealed that the greatest fluctuation occurred in the residues that are part of the protein lid domain. The binding free energy value (ΔGbind) obtained for the Tam16 lead molecule was of -51.43 kcal/mol. When comparing this result with the ΔGbind values for the remaining analogs, the drug Tam16 was found to be the highest ranked: this result is in agreement with the experimental results obtained by Aggarwal and collaborators, where it was verified that the IC50 for Tam16 is the smallest necessary to inhibit the Pks13 (IC50 = 0.19 µM). The energy decomposition analysis suggested that the residues which most interact with inhibitors are: Ser1636, Tyr1637, Asn1640, Ala1667, Phe1670, and Tyr1674, from which the greatest energy contribution to Phe1670 was particularly notable. For the lead molecule Tam16, a hydrogen bond with the hydroxyl of the phenol not observed in the other analogs induced a more stable molecular structure. Aggarwal and colleagues reported this hydrogen bonding as being responsible for the stability of the molecule, optimizing its physic-chemical, toxicological, and pharmacokinetic properties.


Asunto(s)
Antituberculosos/química , Proteínas Bacterianas/química , Benzofuranos/química , Simulación del Acoplamiento Molecular , Simulación de Dinámica Molecular , Sintasas Poliquetidas/química , Aminoácidos , Antituberculosos/farmacología , Proteínas Bacterianas/antagonistas & inhibidores , Benzofuranos/farmacología , Sitios de Unión , Descubrimiento de Drogas , Enlace de Hidrógeno , Estructura Molecular , Sintasas Poliquetidas/antagonistas & inhibidores , Unión Proteica , Conformación Proteica , Relación Estructura-Actividad
2.
J Biomol Struct Dyn ; 37(7): 1843-1856, 2019 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-29697300

RESUMEN

Galantamine (Gnt) is a natural alkaloid inhibitor of acetylcholinesterase and is presently one of the most used drugs in the treatment against Alzheimer's disease during both the initial and intermediate stages. Among several natural Gnt derivatives, sanguinine (Sng) and lycoramine (Lyc) attract attention because of the way their subtle chemical differences from Gnt lead to drastic and opposite distinctions in inhibitory effects. However, to date, there is no solved structure for these natural derivatives. In the present study, we applied computational modeling and free energy calculation methods to better elucidate the molecular basis of the subtle distinctions between these derivatives and Gnt. The results showed that differences in the mobility of the non-aromatic ring carried by the Lyc-like sp2-sp3 modification display drastic conformational, vibrational, and entropic penalties at binding compared to Gnt. Additionally, the establishment of a stronger hydrogen bond network added enthalpic advantages for the linkage of the Sng-like methoxy-hydroxy substituted ligands. These results, which suggest an affinity ranking in agreement with that found in the literature, provided insights that are helpful for future planning and development of new anti-Alzheimer's disease drugs.


Asunto(s)
Acetilcolinesterasa/química , Inhibidores de la Colinesterasa/química , Conformación Molecular , Simulación del Acoplamiento Molecular , Simulación de Dinámica Molecular , Enfermedad de Alzheimer/tratamiento farmacológico , Sitios de Unión , Dominio Catalítico , Inhibidores de la Colinesterasa/farmacología , Humanos , Enlace de Hidrógeno , Ligandos , Estructura Molecular , Unión Proteica
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