IndraLab

Statements

Erlotinib inhibits KCNH2. 3 / 3
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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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"Data in XREF_FIG reveal that at 6 microM concentration, erlotinib does not block the hERG K+ channel, as should be expected for an approved drug."
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"In contrast, erlotinib, the least cardiotoxic of the 4 drugs tested, was a less potent inhibitor of hERG and only inhibited 35% (mean) of hERG current at the concentration of 10 muM, which was the sol[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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