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Here we conducted a preliminary embryo-fetal developmental toxicity study of pritelivir in CD1-IGS mice. Pritelivir was administered by oral gavage to time-mated mice at dose levels of 0, 10, 60 and 200\u00a0mg\/kg\/day from gestational day 6 through 15. Maternal food consumption, body weight and clinical observations were monitored throughout gestation. The mice were sacrificed at gestational day 18 and assessed based on embryo-fetal development and viability. Fetuses were weighed and examined for external and visceral variations and malformations. The results showed that exposure to pritelivir did not cause maternal or developmental toxicity in mice. Thus, both maternal and fetal no-observed-adverse-effect-level of pritelivir was determined to be 200\u00a0mg\/kg\/day. At this dose, the area under the concentration-time curve for pritelivir at steady state in maternal animals was 20 times greater than reported in humans at the clinical dose of 100\u00a0mg\/day. Placenta-to-maternal plasma and fetus-to-maternal plasma concentration ratios in mice were 0.4 and 0.2, respectively, indicating transfer but not accumulation of pritelivir in the fetoplacental compartment. Taken together, our findings support further preclinical studies of pritelivir for its use in pregnancy.<\/jats:p>","DOI":"10.1038\/s41598-026-57669-x","type":"journal-article","created":{"date-parts":[[2026,6,21]],"date-time":"2026-06-21T07:47:31Z","timestamp":1782028051000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Preliminary embryo-fetal developmental toxicity study of pritelivir in CD1-IGS mice"],"prefix":"10.1038","volume":"16","author":[{"given":"Tatiana N.","family":"Nanovskaya","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Svetlana L.","family":"Patrikeeva","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoming","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erik","family":"Rytting","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bandana","family":"Bera","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sydni C.","family":"Zacharias","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brendan","family":"Prideaux","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valentina F.","family":"Bryant","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"},{"role":"corresponding-author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,6,21]]},"reference":[{"issue":"9","key":"57669_CR1","doi-asserted-by":"publisher","first-page":"438","DOI":"10.15698\/mic2016.09.528","volume":"3","author":"D Jaishankar","year":"2016","unstructured":"Jaishankar, D. & Shukla, D. Genital herpes: Insights into sexually transmitted infectious disease. Microb. Cell. 3 (9), 438\u2013450. https:\/\/doi.org\/10.15698\/mic2016.09.528 (2016).","journal-title":"Microb. Cell."},{"key":"57669_CR2","doi-asserted-by":"publisher","unstructured":"Pinninti, S. G. & Kimberlin, D. W. Neonatal herpes simplex virus infections. Semin. Perinatol. 42(3), 168\u2013175. https:\/\/doi.org\/10.1053\/j.semperi.2018.02.004 (2018) (Epub 2018 Mar 12).","DOI":"10.1053\/j.semperi.2018.02.004"},{"key":"57669_CR3","unstructured":"Fernandes, N. D., Arya, K., Syed, H. A. & Ward, R. Congenital Herpes Simplex. In StatPearls. https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK507897\/ (StatPearls Publishing, 2025)."},{"issue":"5","key":"57669_CR4","doi-asserted-by":"publisher","first-page":"1092","DOI":"10.1172\/JCI119237","volume":"99","author":"A Wald","year":"1997","unstructured":"Wald, A. et al. Frequent genital herpes simplex virus 2 shedding in immunocompetent women. Effect of acyclovir treatment. J. 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