In silico and in vitro assessments show that gemcitabine derivatives improve cancer treatment efficacy in MCF7, A549, and PC3 cell lines, suggesting potential as viable alternatives.
Cancer remains one of the leading causes of death globally and is expected to increase in incidence. The present investigation aimed to evaluate the anticancer efficacy of gemcitabine derivatives on MCF7, A549, and PC3 cell lines. Compounds Com. 10 and Com. 16 were the most potent, with IC₅₀ values of 9.45, 6.93, and 12.09 µM (Com. 10) and 12.23, 6.60, and 21.57 µM (Com. 16) for the three cell lines, showing a better response compared to the reference drug gemcitabine. Com. 9 and Com. 14 were also moderately active, preferentially on A549 and PC3. Com. 16 showed strong binding with the active residues as determined by molecular docking. Com. 16 bound to key cancer targets Vav1 (6NEW), ERK2 (4ZXT), and CYP3A4 (7LXL), with docking scores of −191.72, −187.66, and −221.08 kcal/mol, respectively. These interactions were electrostatic, hydrophobic, and π-type, similar to those induced by gemcitabine. Several other compounds also demonstrated good docking scores (−160 to −180 kcal/mol), and eight protein–ligand complexes emerged as leads. Moreover, ADME and physicochemical analyses of the top six active compounds indicated good drug-likeness and a favorable PK profile compared to gemcitabine.
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Radhi et al. (2025) studied this question.
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