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Ripretinib induced skeletal muscle toxicity through mitochondrial impairment in C2C12 myotubes.

Author: AkyildizAysenur Gunaydin, BoranTugce, OztasEzgi, SekerZehra, ZenginOzge Sultan, ÖzhanGül

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.

Overview

This study investigated the role of mitochondria in the toxic effect of ripretinib on skeletal muscle using C2C12 myotubes. Ripretinib decreased ATP level and mtDNA copy number, induced loss of MMP, and reduced mitochondrial mass. The activities of ETC complexes were inhibited, and molecular docking revealed that ripretinib inhibits POLG. PGC-1α expression was reduced, leading to increased mtROS production and upregulation of mitophagy-related gene expressions. These findings suggest that mitochondrial damage/loss can be one of the underlying causes of ripretinib-induced skeletal muscle toxicity.
Paper Details　
Original Abstract of the Article :
Ripretinib is a multikinase inhibitor drug approved in 2020 by the FDA and in 2021 by EMA for use in the treatment of advanced gastrointestinal stromal tumors (GIST) which have not adequately responded to previous treatments with kinase inhibitors. The most common side effects of the drug are myalgi...See full text at original site
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引用元：
https://doi.org/10.1016/j.tox.2023.153489

データ提供：米国国立医学図書館（NLM）

Ripretinib and Skeletal Muscle Toxicity: Navigating the Desert of Side Effects

Ripretinib, a promising drug used to treat advanced gastrointestinal stromal tumors (GIST), has emerged as a beacon of hope in the desert of cancer treatment. However, like a mirage in the desert, potential side effects can appear enticing yet ultimately lead to disappointment. This study explores the potential mechanism behind ripretinib-induced skeletal muscle toxicity, seeking to understand the interplay between this powerful drug and the delicate balance of cellular function.

A Delicate Balance: Ripretinib and Mitochondrial Function

The research found that ripretinib can negatively impact mitochondrial function in skeletal muscle cells, potentially leading to muscle weakness and fatigue. This is like a storm in the desert, disrupting the delicate balance of cellular energy production. By targeting mitochondria, ripretinib might inadvertently create a desert of energy depletion in muscle cells, contributing to muscle toxicity.

Navigating the Desert: Strategies for Managing Side Effects

Understanding the potential mechanisms of ripretinib-induced muscle toxicity is crucial for navigating the desert of side effects. Careful monitoring of muscle function and the potential for drug-related side effects is essential, allowing healthcare professionals to adjust treatment strategies and minimize the impact of these desert-like conditions. It's like having a compass and map in the desert, providing guidance and ensuring safe passage.

Dr. Camel's Conclusion

This research provides valuable insight into the potential impact of ripretinib on skeletal muscle. Navigating the desert of side effects associated with cancer treatment requires a careful balance of benefits and risks. While ripretinib offers hope for patients with GIST, understanding its potential impact on muscle function is crucial for optimizing treatment and ensuring a safe and effective journey through the desert of cancer treatment.
Date :
  1. Date Completed 2023-04-11
  2. Date Revised 2023-05-08
Further Info :

Pubmed ID

36933644

DOI: Digital Object Identifier

10.1016/j.tox.2023.153489

SNS
PICO Info
in preparation
Languages

English

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