Evidence map›Paper›PMID 42603444›Full record

ArticleInternational journal for parasitology. Drugs and drug resistance2026

Identification of new Trypanosoma cruzi-specific protein synthesis inhibitors by using a developed high-throughput in vitro translation assay.

Camila Colombari Mantovani, Flavia R Novais Freitas, Carolina Borsoi Moraes, Guilherme Rodrigo Reis Dos Santos, Luiza R Cruz, Jadel Muller Kratz, Bertal Huseyin Aktas, Sergio Schenkman

Abstract read
In one paragraph

Article in International journal for parasitology. Drugs and drug resistance, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Camila Colombari MantovaniDepartamento de Microbiologia, Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Flavia R Novais FreitasDepartamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, SP, Brazil.
Carolina Borsoi MoraesDepartamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, SP, Brazil.
Guilherme Rodrigo Reis Dos SantosDivision of Hematology, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA, 02115, United States.
Luiza R CruzDrugs for Neglected Diseases Initiative (DNDi), Rio de Janeiro, RJ, Brazil.
Jadel Muller KratzDrugs for Neglected Diseases Initiative (DNDi), Rio de Janeiro, RJ, Brazil.
Bertal Huseyin AktasDivision of Hematology, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA, 02115, United States. Electronic address: huseyin_aktas@hms.harvard.edu.
Sergio SchenkmanDepartamento de Microbiologia, Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil; Antimicrobial Research Institute of São Paulo State (ARIES), Universidade Federal de São Paulo, São Paulo, S.P, Brazil. Electronic address: sschenkman@unifesp.br.

Funding

Protein Synthesis Inhibitors as anti-T. Cruzi agentsR21AI154196 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI AKTAS, BERTAL H. · 2020 to 2021
$494k
NIAID NIH HHS R21 AI154196
6 · The paper itself

Abstract

There are restricted treatment options for Chagas disease, a global health risk causing 12,000 fatalities annually. This situation is exacerbated by environmental changes and migration, which is altering patterns of disease transmission, and by expansion of the vector range. The disease is caused by the protozoan parasite Trypanosoma cruzi, which possesses a divergent translation apparatus, characterized by enlarged ribosomes and a unique mRNA cap appended to the 5' end of a 39-nucleotide spliced leader sequence at the 5' end of all its mRNAs. Given that many antimicrobial agents are protein synthesis inhibitors and that there are significant differences between the T. cruzi protein synthesis machinery and that of its mammalian host, it is likely that T. cruzi-specific protein synthesis inhibitors could be employed for the treatment of Chagas disease. Such inhibitors can be identified by screening chemical libraries in an in vitro translation assay. However, lysates of T. cruzi cannot reinitiate translation of exogenous mRNAs. Here, we demonstrate that T. cruzi extracts derived from a strain deficient for hemin accumulation efficiently translated a capped and polyadenylated reporter mRNA. We optimized assay conditions and adapted them to a 384-well format. We further miniaturized this assay to a 5 μL volume, demonstrating its suitability for ultra-high throughput screening. Further, in a proof-of-principle pilot study, we identified quinazoline compounds that inhibit translation of reporter mRNAs by T. cruzi extracts. These compounds inhibited protein synthesis and proliferation of insect-derived forms and wild-type parasites growing in mammalian cells at a low micromolar range and a selectivity index higher than 200. This first-of-its-kind T. cruzi in vitro translation system will enable high-throughput screening of very large chemical libraries, while first-in-class hit compounds identified in the pilot study can be developed into lead compounds by design and synthesis of focused libraries to develop therapeutics for Chagas disease.

Indexed as

Chagas diseaseHigh-throughput screeningInhibitorTranslationTrypanosoma cruzi

Identifiers

PMID42603444
PMCPMC13499490

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.