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Amifostine

Amifostine

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Substance Overview and History

Amifostine, originally developed to protect against chemotherapy and radiation toxicity, shows potential as a treatment for idiopathic pulmonary fibrosis (IPF). This chronic lung disease involves irreversible scarring and mitochondrial dysfunction. In studies, amifostine reduced fibrosis by targeting mitochondrial ROS and restoring energy balance. It activates SIRT1 and AMPK, crucial for maintaining mitochondrial health, highlighting its role in combating oxidative stress and fibrosis progression.

References:

Guo, F., Xu, F., Li, S., Zhang, Y., Lv, D., Zheng, L., Gan, Y., Zhou, M., Zhao, K., Xu, S., Wu, B., Deng, Z. and Fu, P., 2024. Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD+/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism. European Journal of Medical Research

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FAQ
What is Amifostine used for?
Amifostine is primarily used to protect against the toxic effects of chemotherapy and radiation. It’s also being studied for treating idiopathic pulmonary fibrosis (IPF) by reducing lung scarring.
References:

Guo, F., Xu, F., Li, S., Zhang, Y., Lv, D., Zheng, L., Gan, Y., Zhou, M., Zhao, K., Xu, S., Wu, B., Deng, Z. and Fu, P., 2024. Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD+/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism. European Journal of Medical Research

How does Amifostine work in IPF?
It reduces mitochondrial reactive oxygen species (ROS) and restores energy metabolism, helping to prevent fibrosis and maintain lung function.
References:

Guo, F., Xu, F., Li, S., Zhang, Y., Lv, D., Zheng, L., Gan, Y., Zhou, M., Zhao, K., Xu, S., Wu, B., Deng, Z. and Fu, P., 2024. Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD+/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism. European Journal of Medical Research

What are the key mechanisms of Amifostine?
Amifostine activates SIRT1 and AMPK, essential for improving mitochondrial health and reducing oxidative stress, which are crucial in combating fibrosis.
References:

Guo, F., Xu, F., Li, S., Zhang, Y., Lv, D., Zheng, L., Gan, Y., Zhou, M., Zhao, K., Xu, S., Wu, B., Deng, Z. and Fu, P., 2024. Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD+/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism. European Journal of Medical Research