2. Academic Validation
  3. Famciclovir Ameliorates Platelet Activation and Thrombosis by AhR-Regulated Autophagy

Famciclovir Ameliorates Platelet Activation and Thrombosis by AhR-Regulated Autophagy

  • Cardiovasc Toxicol. 2025 Mar;25(3):486-497. doi: 10.1007/s12012-025-09971-9.
Yue Ming # 1,  Qilong Zhou # 1,  Guang Xin 1,  Zeliang Wei 1,  Chengjie Ji 2,  Kui Yu 1,  Shiyi Li 1,  Boli Zhang 1 3,  Junhua Zhang 1 3,  Youping Li 1,  Hongchen He 1,  Wen Huang 4
Affiliations

Affiliations

  • 1 Department of Rehabilitation Medicine Center, Natural and Biomimetic Medicine Research Center, Tissue-Orientated Property of Chinese Medicine Key Laboratory of Sichuan Province, West China School of Medicine, West China Hospital, Sichuan University, Keyuan Road 4 No.1, Gaopeng Avenue, Gaoxin District, Chengdu, 610041, Sichuan, China.
  • 2 Department of Laboratory Medicine, The People's Hospital of Jianyang City, Chengdu, Sichuan, China.
  • 3 Tianjin University of Traditional Chinese Medicine, Tianjin, China.
  • 4 Department of Rehabilitation Medicine Center, Natural and Biomimetic Medicine Research Center, Tissue-Orientated Property of Chinese Medicine Key Laboratory of Sichuan Province, West China School of Medicine, West China Hospital, Sichuan University, Keyuan Road 4 No.1, Gaopeng Avenue, Gaoxin District, Chengdu, 610041, Sichuan, China. huangwen@scu.edu.cn.
  • # Contributed equally.
PMID: 39928275 DOI: 10.1007/s12012-025-09971-9
Abstract

Cardiovascular diseases (CVDs) and their severe complications have posed immense challenges to global healthcare systems. A significant obstacle in this field lies in the development of innovative targets, mechanisms, and drugs to mitigate the side effects associated with current antiplatelet therapies. Through screening relevant CVD targets in the Gene Card database, we found that AhR appears to be linked to CVDs. Computer-aided drug screening and molecular docking techniques identified famciclovir as a potential AhR inhibitor. Further experiments demonstrated that famciclovir suppresses AhR expression and platelet activation in thrombin-stimulated platelets, significantly reducing mitochondrial damage and oxidative stress. Notably, oral administration of famciclovir significantly inhibits thrombin-induced platelet aggregation without affecting coagulation factors or thrombolysis systems. Moreover, famciclovir mitigates FeCl3-induced carotid arterial thrombosis and cerebral thrombosis induced by middle cerebral artery occlusion. Our study suggests that inhibiting AhR expression with famciclovir effectively reduces platelet activation and thrombosis, offering promise as a potential therapeutic strategy for improving CVDs.

Keywords

AhR; Famciclovir; Mitochondria; Oxidative stress; Platelet.

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