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This study investigated the inhibitory effect of isobavachalcone (IBC) on\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      growth and elucidated its mechanism. The antifungal activity of IBC was evaluated using minimum inhibitory concentration 90% (MIC\n                      <jats:sub>90<\/jats:sub>\n                      ) and minimum fungicidal concentration (MFC), combined with murine vaginitis and oral thrush models to assess\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      efficacy. An MTT assay was used to assess drug safety. Mechanistic investigations included cell membrane\/wall damage assessments, virulence factor inhibition, oxidative stress evaluation, ATP metabolism analysis, protein expression profiling, and target identification (including RT-qPCR, inhibitor intervention experiments, and related methodologies). The antifungal potency of IBC against\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      was demonstrated with a MIC\n                      <jats:sub>90<\/jats:sub>\n                      of 2 \u00b5g\/mL and an MFC of 8 \u03bcg\/mL. Against strain S393, IBC exhibited potent efficacy with median effective and effective concentrations of 1.301 \u00b5g\/mL and 1.449 \u00b5g\/mL, respectively.\n                      <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                      , IBC significantly alleviated vulvovaginal candidiasis and oropharyngeal thrush, outperforming fluconazole in therapeutic efficacy and mucosal protection. Mechanistic studies revealed that IBC prevented fungal invasion by inhibiting\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      adhesion and colonization on mucosal surfaces, mitigated inflammation through suppression of proinflammatory cytokine release, and downregulated the expression of\n                      <jats:italic toggle=\"yes\">ADE13<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">TPI1<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">ADK1<\/jats:italic>\n                      genes, with\n                      <jats:italic toggle=\"yes\">ADK1<\/jats:italic>\n                      demonstrating the most significant suppression. Furthermore, IBC specifically bound to ADK1, inhibiting ATP synthesis and disrupting cellular energy metabolism in\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      . IBC represents a promising antifungal drug that acts by downregulating the\n                      <jats:italic toggle=\"yes\">ADE13<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">TPI1<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">ADK1<\/jats:italic>\n                      genes. Its downregulation of ADK1 leads to impaired ATP synthesis, induced DNA damage, and suppressed fungal proliferation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/aac.00797-25","type":"journal-article","created":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T14:01:15Z","timestamp":1766152875000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["Isobavachalcone effectively inhibits the growth of\n                    <i>Candida albicans<\/i>"],"prefix":"10.1128","volume":"70","author":[{"given":"Ping","family":"Xie","sequence":"first","affiliation":[{"name":"Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities","place":["Baise, China"]},{"name":"Guangxi Zhuang Autonomous Region Engineering Research Center of Clinical Prevention and Control Technology and Leading 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