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However, a greater chemical variety of readthrough inducers is required to broaden the medical applications of this therapeutic strategy. In this study, we developed a reporter cell line and performed high-throughput screening (HTS) to identify potential readthrough inducers. After three successive assays, we isolated 2-guanidino-quinazoline (TLN468). We assessed the clinical potential of this drug as a potent readthrough inducer on the 40 PTCs most frequently responsible for Duchenne muscular dystrophy (DMD). We found that TLN468 was more efficient than gentamicin, and acted on a broader range of sequences, without inducing the readthrough of normal stop codons (TC).<\/jats:p>","DOI":"10.1073\/pnas.2122004119","type":"journal-article","created":{"date-parts":[[2022,8,22]],"date-time":"2022-08-22T15:14:57Z","timestamp":1661181297000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":18,"title":["2-Guanidino-quinazoline promotes the readthrough of nonsense mutations underlying human genetic diseases"],"prefix":"10.1073","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3973-4058","authenticated-orcid":false,"given":"Laure","family":"Bidou","sequence":"first","affiliation":[{"name":"Institute for Integrative Biology of the Cell, Universit\u00e9 Paris-Saclay, CEA, CNRS, 91198 Gif-sur-Yvette, France"},{"name":"Sorbonne Universit\u00e9, CNRS, 75006 Paris, 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