IndraLab

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"This study highlights the complexity of dissecting sunitinib mediated cardiotoxicity from adverse conduction effects, as an extensive electrophysiological analysis of sunitinib mediated inhibition of the sodium and hERG channels and examination of field potential changes were performed."

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"In these studies, sunitinib decreased cardiomyocyte viability, inhibited AMPK, increased lipid accumulation, disrupted beat pattern, and blocked hERG activity); in contrast, erlotinib demonstrated only minor changes (increased acetyl-CoA carboxylase (ACC) phosphorylation, the rate limiting step in fatty acid biosynthesis), did not impact ROS, caspase, or lipid levels, and did not affect beat patterns [XREF_BIBR]."

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