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Peer-reviewedCC BYBiosafety and Health

Early bactericidal activity of isoniazid: Advances and implications for dosage adjustment

  • Ningjian Cai1
  • Xiaoyi Jiang1
  • Chao Zhang1
  • Chaonan Xing2
  • Xinchun Chen3
  • Hairong Huang4
4 affiliations
  1. 1National Clinical Laboratory on Tuberculosis, Beijing Key Laboratory for Drug-Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Institute, Beijing 101149, China
  2. 2Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen 518000, China
  3. 3Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Department of Pathogen Biology, Shenzhen University Medical School, Shenzhen 518000, China; Corresponding authors: Beiguan St. No. 9, Beijing 101149, China (H. Huang); No.1066 Xueyuan Avenue, Nanshan District, Shenzhen 518000, China (X. Chen).
  4. 4National Clinical Laboratory on Tuberculosis, Beijing Key Laboratory for Drug-Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Institute, Beijing 101149, China; Corresponding authors: Beiguan St. No. 9, Beijing 101149, China (H. Huang); No.1066 Xueyuan Avenue, Nanshan District, Shenzhen 518000, China (X. Chen).
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Abstract

Isoniazid (INH) remains a cornerstone of tuberculosis (TB) treatment; however, its early bactericidal activity (EBA) and associated adverse effects vary substantially among individuals. Although personalized dosing has been proposed, its clinical implementation remains limited, largely due to incomplete characterization of the predictive factors. This review synthesizes evidence from PubMed-indexed EBA studies of INH to identify key determinants of its variable efficacy and to guide individualized dose selection across different clinical settings. We found that individual N-acetyltransferase 2 (NAT2) acetylator status is a critical predictor of both the EBA of INH and the risk of drug–induced liver injury (DILI). Geographic variation in NAT2 acetylator phenotypes likely explains a substantial proportion of the regional disparities in reported EBA. Additionally, escalating the INH dosage may overcome low–level resistance associated with inhA promoter mutations. In conclusion, personalizing INH dosage based on NAT2 acetylator type—especially for rapid acetylators—and increasing doses to address inhA –mediated resistance may improve therapeutic efficacy and safety. Integrating these host and pathogen factors into clinical practice could help optimize TB treatment outcomes across diverse populations and resistance profiles.

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Cite

BibTeXRIS
BibTeX
@article{cai2026early,
  title = {{Early bactericidal activity of isoniazid: Advances and implications for dosage adjustment}},
  author = {Ningjian Cai and Xiaoyi Jiang and Chao Zhang and Chaonan Xing and Xinchun Chen and Hairong Huang},
  journal = {Biosafety and Health},
  year = {2026},
  month = jul,
  doi = {10.1016/j.bsheal.2026.07.001},
  url = {https://doi.org/10.1016/j.bsheal.2026.07.001},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Early bactericidal activity of isoniazid: Advances and implications for dosage adjustment
AU  - Ningjian Cai
AU  - Xiaoyi Jiang
AU  - Chao Zhang
AU  - Chaonan Xing
AU  - Xinchun Chen
AU  - Hairong Huang
PY  - 2026
DA  - 2026/07/07
JO  - Biosafety and Health
DO  - 10.1016/j.bsheal.2026.07.001
UR  - https://doi.org/10.1016/j.bsheal.2026.07.001
AB  - Isoniazid (INH) remains a cornerstone of tuberculosis (TB) treatment; however, its early bactericidal activity (EBA) and associated adverse effects vary substantially among individuals. Although personalized dosing has been proposed, its clinical implementation remains limited, largely due to incomplete characterization of the predictive factors. This review synthesizes evidence from PubMed-indexed EBA studies of INH to identify key determinants of its variable efficacy and to guide individualized dose selection across different clinical settings. We found that individual N-acetyltransferase 2 (NAT2) acetylator status is a critical predictor of both the EBA of INH and the risk of drug–induced liver injury (DILI). Geographic variation in NAT2 acetylator phenotypes likely explains a substantial proportion of the regional disparities in reported EBA. Additionally, escalating the INH dosage may overcome low–level resistance associated with inhA promoter mutations. In conclusion, personalizing INH dosage based on NAT2 acetylator type—especially for rapid acetylators—and increasing doses to address inhA –mediated resistance may improve therapeutic efficacy and safety. Integrating these host and pathogen factors into clinical practice could help optimize TB treatment outcomes across diverse populations and resistance profiles.
SN  - 2590-0536
SN  - 2096-6962
ER  -