Intramolecular Interactions of Twenty-Eight Amide Derivatives with the C-ALB Kinase using a Theoretical Model as a Therapeutic Alternative to Treat Cancer

Abstract

Background

Several studies have shown that some drugs can slow the growth of cancer cells by inhibiting the c-Abl kinase. However, some of these drugs can cause side effects such as gynecomastia, pulmonary toxicity, and lentiginosis, among others. In the search for a therapeutic alternative, some amide derivatives have been developed to treat cancer. However, their interaction with the c-Abl kinase is not clear.

Objective

The aim of this study was to evaluate the interaction of 28 amide derivatives with the c-Abl kinase as a therapeutic alternative to treat cancer cells.

Methods

The theoretical interaction of amide derivatives with the c-Abl kinase was carried out using the 1iep protein as a theoretical model. Besides, bosutinib, dasatinib, imatinib, nilotinib, and radotinib were used as controls in the DockingServer program.

Results

The results displayed different types of aminoacid residues involved in the interaction of amide derivatives with the 1iep protein surface compared to the controls. In addition, the inhibition constant (Ki) was lower for compounds 15, 16, and 18 compared to radotinib. Finally, the Ki for amide derivatives 1, 19, and 21 were lower compared with bosutinib, dasatinib, imatinib, and nilotinib.

Conclusions

Theoretical data indicate that amide derivatives such as 1, 15, 16, 18, 19, and 21 might have a higher affinity for the 1iep protein surface. This phenomenon could be translated as c-Abl kinase inhibition, resulting in a decrease in cancer cell growth.

Keywords

Cancer - c-Alb kinase - theoretical model - amide derivatives

Publication History

Received: 06 December 2025

Accepted after revision: 20 January 2026

Article published online:
03 February 2026

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