Anti-<i>Trypanosoma cruzi</i> Potential of New Pyrazole-Imidazoline Derivatives

Chagas disease, caused by <i>Trypanosoma cruzi</i>, poses a significant public health challenge due to its widespread prevalence, limited therapeutic options, and adverse effects associated with available medications. In this study, we developed 13 novel pyrazole-imidazoline derivatives,...

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Main Authors: Edinaldo Castro de Oliveira, Leonardo da Silva Lara, Lorraine Martins Rocha Orlando, Sarah da Costa Lanera, Thamyris Perez de Souza, Nathalia da Silva Figueiredo, Vitoria Barbosa Paes, Ana Carolina Mazzochi, Pedro Henrique Myra Fernandes, Maurício Silva dos Santos, Mirian Claudia de Souza Pereira
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Molecules
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Online Access:https://www.mdpi.com/1420-3049/30/15/3082
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Summary:Chagas disease, caused by <i>Trypanosoma cruzi</i>, poses a significant public health challenge due to its widespread prevalence, limited therapeutic options, and adverse effects associated with available medications. In this study, we developed 13 novel pyrazole-imidazoline derivatives, inspired by a previously identified cysteine protease inhibitor, and evaluated their antiparasitic activity. Our in silico analyses predicted favorable physicochemical profiles and promising oral bioavailability for these derivatives. Upon phenotypic screening, we observed that these new derivatives exhibited low cytotoxicity (CC<sub>50</sub> > 100 µM) and marked efficacy against intracellular amastigotes. Derivative <b>1k</b> showed high activity (IC<sub>50</sub> = 3.3 ± 0.2 µM), selectivity (SI = 73.9), and potency (pIC<sub>50</sub> = 5.4). In a 3D cardiac microtissue model, <b>1k</b> significantly reduced parasite load, matching the efficacy of benznidazole (Bz) even at lower concentrations. Both <b>1k</b> and Bz effectively prevented parasite recrudescence; however, neither resulted in parasite sterility under the experimental conditions employed. The combination of <b>1k</b>–Bz yielded an additive interaction, highlighting its potential for in vivo combination therapy. While structural changes abolished cysteine protease inhibition, incorporating a CF<sub>3</sub> substituent at the <i>para</i> position and excluding the amino group enhanced antiparasitic activity. These findings reinforce the promise of the pyrazole-imidazoline scaffold and support further structural optimizations to develop innovative candidates for treating Chagas disease.
ISSN:1420-3049