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Design, catalyst-free synthesis, DFT study and anticancer assessment of new 2,9-disubstituted purine-6-carboxamides.

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Bioorganic chemistry 📖 저널 OA 2.3% 2024: 0/13 OA 2025: 1/75 OA 2026: 4/129 OA 2024~2026 2026 Vol.172() p. 109529 Biochemical and Molecular Research
TL;DR Flow cytometric analysis demonstrated that compound 6E significantly reduced p-PI3K levels, comparably to erlotinib, indicating effective suppression of EGFR-AKT downstream signaling at the cellular level, and molecular docking and MD simulations of the 6E-EGFR complex highlighted key amino acid interactions, corroborating the observed in vitro EGFR inhibition.
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PubMed DOI OpenAlex Semantic 마지막 보강 2026-04-29
OpenAlex 토픽 · Biochemical and Molecular Research Chronic Lymphocytic Leukemia Research Quinazolinone synthesis and applications

Chatterjee J, Bhujbal SM, Joshi G, Mishra UK, Sharon A, Muskan, Singh S, Wahajuddin M, Bharatam PV, Dalal R, Kumar R

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Flow cytometric analysis demonstrated that compound 6E significantly reduced p-PI3K levels, comparably to erlotinib, indicating effective suppression of EGFR-AKT downstream signaling at the cellular l

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APA Joydeep Chatterjee, Shivkanya Madhavrao Bhujbal, et al. (2026). Design, catalyst-free synthesis, DFT study and anticancer assessment of new 2,9-disubstituted purine-6-carboxamides.. Bioorganic chemistry, 172, 109529. https://doi.org/10.1016/j.bioorg.2026.109529
MLA Joydeep Chatterjee, et al.. "Design, catalyst-free synthesis, DFT study and anticancer assessment of new 2,9-disubstituted purine-6-carboxamides.." Bioorganic chemistry, vol. 172, 2026, pp. 109529.
PMID 41643510 ↗

Abstract

A green, catalyst-free synthesis of seventeen new 2,9-disubstituted purine-6-carboxamides (5 and 6) designed as EGFR inhibitors in high yields (85-93%) was accomplished. DFT analysis revealed the formation of an energetically favorable oxazolidine transition state with a lower activation barrier compared to alternative pathways, supporting the experimentally observed selectivity. In vitro anticancer activity against A549 lung cancer cells demonstrated dose-dependent growth inhibition, with IC₅₀ values ranging from 4.35 to 22.1 μM, and compound 6E emerged as the most potent derivative. It exhibited superior activity compared to the reference drug erlotinib, with a cellular IC₅₀ of 4.35 μM vs 11.83 μM and an EGFR enzymatic IC₅₀ of 105.96 nM vs 218.47 nM, indicating approximately 2-fold enhanced potency. Flow cytometric analysis demonstrated that compound 6E significantly reduced p-PI3K levels, comparably to erlotinib, indicating effective suppression of EGFR-AKT downstream signaling at the cellular level. Mechanistic investigations demonstrated that 6E increased ROS generation, induced mitochondrial depolarisation, and promoted apoptotic cell death. Further, molecular docking and MD simulations of the 6E-EGFR complex highlighted key amino acid interactions, corroborating the observed in vitro EGFR inhibition.

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