Key result
A pyridoxine and fumaric acid derivative reduces doxorubicin cardiotoxicity in vivo via Nrf2 activation.
Why the study?
To evaluate the biological activity of a new type of cardioprotectors, activators of Nrf2, based on pyridoxine and fumaric acid derivatives in vitro and in vivo.
A novel pyridoxine and fumaric acid derivative shows promise as a cardioprotective agent against doxorubicin-induced cardiotoxicity via Nrf2 activation in preclinical models.
The aim of the study was to evaluate the biological activity of a new type of cardioprotectors, activators of Nrf2, based on pyridoxine and fumaric acid derivatives in vitro and in vivo. It was found that di(3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridinium) fumarate is an effective activator of Nrf2 transcription factor and exhibits cytoprotective and antioxidant activity in vitro on a cardiomyocyte model. In addition, this compound reduces the cardiotoxic effect of doxorubicin in vivo by suppressing the development of oxidative processes and activating the Nrf2-dependent antioxidant response in the heart. The studied pyridoxine and fumaric acid derivative has high potential as a candidate medication for reducing the side effects of anthracycline antibiotics, as well as for protecting heart cells in various cardiovascular diseases and age-related changes. The revealed effects are of great importance for the development of approaches to designing a new type of cardioprotective compounds, activators of the transcription factor Nrf2.
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Балакина et al. (2026) studied Doxorubicin-induced cardiotoxicity. di(3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridinium) fumarate was evaluated on Cytoprotective and antioxidant activity in vitro and reduction of doxorubicin cardiotoxicity in vivo. Di(3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridinium) fumarate activated Nrf2, exhibited cytoprotective activity in vitro, and reduced doxorubicin cardiotoxicity in vivo.
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