ArticleCanadian journal of physiology and pharmacology2012
The EGFR tyrosine kinase inhibitor tyrphostin AG-1478 causes hypomagnesemia and cardiac dysfunction.
Article in Canadian journal of physiology and pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Phosphoproteomic analysis reveals the diversity of signaling behind ErbB-inhibitor-induced phenotypes.The FEBS journal · 2025Article
- Profiling of ERBB receptors and downstream pathways reveals selectivity and hidden properties of ERBB4 antagonists.iScience · 2024Article
- Treadmill Running Regulates Adult Neurogenesis, Spatial and Non-spatial Learning, Parvalbumin Neuron Activity by ErbB4 Signaling.Cellular and molecular neurobiology · 2024Article
- Contrastive learning in protein language space predicts interactions between drugs and protein targets.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Substance P receptor blocker, aprepitant, inhibited cutaneous and other neurogenic inflammation side effects of the EGFR1-TKI, erlotinib.Molecular and cellular biochemistry · 2020Article
- The role of neuropeptides in adverse myocardial remodeling and heart failure.Cellular and molecular life sciences : CMLS · 2017Review
- EGFR-TKI, erlotinib, causes hypomagnesemia, oxidative stress, and cardiac dysfunction: attenuation by NK-1 receptor blockade.Journal of cardiovascular pharmacology · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We determined whether the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) N-(3-chlorophenyl)-6,7-dimethoxy-4-quinazolinamine (tyrphostin AG-1478) causes hypomagnesemia and cardiac dysfunction in rats. Tyrphostin was administered (3 times per week, intraperitoneal injection, to achieve 21.4 mg·(kg body mass)(-1)·day(-1)) to normomagnesemic rats for 5 weeks. Levels of magnesium in the plasma of the tyrphostin-treated rats decreased significantly by the following amount: 17% at week 1, 27% at week 2, and 26%-35% between weeks 3 to 5. Levels of the plasma lipid peroxidation marker 8-isoprostane rose significantly: by 58% at week 1, 168% at week 3, and 113% at week 5. At week 5, blood neutrophils from the tyrphostin-treated group displayed a 2.26-fold higher basal level of O(2)(·-) generation; the ratio of oxidized glutathione (glutathione disulfide; GSSG) to reduced glutathione (GSH) in the red blood cells increased 2.5-fold. At week 5, echocardiography revealed that TKI treatment resulted in significant cardiac systolic dysfunction, with impaired diastolic function and dilated cardiomyopathy. Since hypomagnesemia alone can trigger oxidative stress and cardiac injury, we suggest that inhibition of EGFR-TK caused magnesium wasting, which partly contributed to decreased cardiac contractility.
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