Therapeutic Mechanisms and Clinical Outcomes of Nintedanib in Idiopathic Pulmonary Fibrosis Management

Qilu Tang

doi:10.54254/2753-8818/2025.24883

Theoretical and Natural ScienceOpen access

Therapeutic Mechanisms and Clinical Outcomes of Nintedanib in Idiopathic Pulmonary Fibrosis Management

Research Article

Open Access

Therapeutic Mechanisms and Clinical Outcomes of Nintedanib in Idiopathic Pulmonary Fibrosis Management

Qilu Tang ^1*

¹ School of Shandong University, Jinan, Shandong, 250000, China

^*Corresponding author: 3249646057@qq.com

Published on 20 July 2025

TNS Vol.123

ISSN (Print): 2753-8826

ISSN (Online): 2753-8818

ISBN (Print): 978-1-80590-187-7

ISBN (Online): 978-1-80590-188-4

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Abstract

This review systematically examines the pharmacological mechanisms and therapeutic performance of nintedanib in treating idiopathic pulmonary fibrosis (IPF). Initially, the pathogenesis of IPF is delineated, including its pathological progression, molecular underpinnings, and the limitations of conventional therapies such as glucocorticoids and immunosuppressants. Subsequently, the multi-target tyrosine kinase inhibitory properties of nintedanib are elaborated, focusing on its capacity to antagonize PDGFR, FGFR, and VEGFR signaling pathways. Clinical trial data from the TOMORROW and INPULSIS studies are analyzed to validate its efficacy in slowing forced vital capacity (FVC) decline and improving patient-reported outcomes. Safety profiles, including common adverse events like diarrhea, are also critically assessed. As the first FDA-approved agent for IPF, nintedanib represents a paradigm shift in fibrosis management, though long-term survival benefits require further investigation.

Keywords:

Ninterdanib, idiopathic pulmonary fibrosis(IPF)

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References

[1]. Wang Yiran, Ye Qiao (2019)Efficacy and safety of nintedanib in the treatment of idiopathic pulmonary fibrosis Meta-analysis Chinese Journal of Practical Internal Medicine Vol. 39 No. 8, pp.701-703

[2]. JAYACHANDRAN A, KONIGSHOFF M, YU H, et al.(2009) SNAI transcription factors mediate epithelial-mesenchymal transition in lung fibrosis. Thorax, 64(12): 1053-1061. pp.2-3

[3]. Kong Wei (2024)Chin J Antituberc, December Vol.46, No.S2 pp.4-6

[4]. IN Y Q, PENG F, SITU H J, et al. (2020) Construction of prediction model of inflammation related genes in idiopathic pulmonary fibrosis and its correlation with immune microenvironment [J]. Front Immunol, 2022, 13: 1010345

[5]. Richeldi L, Cottin V, du BRM, et al. (2016) Nintedanib in patients with idiopathic pulmonary fibrosis: Combined evidence from the TOMORROW and INPULSIS (®) trials [J]. Respir Med, pp.74-79

References

[2]. JAYACHANDRAN A, KONIGSHOFF M, YU H, et al.(2009) SNAI transcription factors mediate epithelial-mesenchymal transition in lung fibrosis. Thorax, 64(12): 1053-1061. pp.2-3

[3]. Kong Wei (2024)Chin J Antituberc, December Vol.46, No.S2 pp.4-6

[5]. Richeldi L, Cottin V, du BRM, et al. (2016) Nintedanib in patients with idiopathic pulmonary fibrosis: Combined evidence from the TOMORROW and INPULSIS (®) trials [J]. Respir Med, pp.74-79

Cite this article

Tang,Q. (2025). Therapeutic Mechanisms and Clinical Outcomes of Nintedanib in Idiopathic Pulmonary Fibrosis Management. Theoretical and Natural Science,123,20-26.

Data availability

The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.

About volume

Volume title: Proceedings of the 5th International Conference on Biological Engineering and Medical Science

ISBN: 978-1-80590-187-7(Print) / 978-1-80590-188-4(Online)

Editor: Alan Wang

Conference website: https://2025.icbiomed.org/

Conference date: 24 October 2025

Series: Theoretical and Natural Science

Volume number: Vol.123

ISSN: 2753-8818(Print) / 2753-8826(Online)

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