IndraLab

Statements

Escitalopram inhibits KCNH2. 7 / 7
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"Escitalopram block of hERG potassium channels."
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"Fluoxetine and its metabolite, norfluoxetine, citalopram and escitalopram prolong the QT interval by directly inhibiting the hERG potassium channels and by disrupting channel protein trafficking reducing the number of channels on the cell membrane [XREF_BIBR]."
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"The blocking of hERG by escitalopram was voltage dependent, with a steep increase across the voltage range of channel activation."
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"citalopram/escitalopram) among others can block HERG channels, inhibiting rapid potassium influx and prolonging the repolarization phase, thereby increasing the risk for possible QT-interval prolongation [21, 22]."
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"Both escitalopram and citalopram produced a reduction of hERG channel protein trafficking to the plasma membrane but did not affect the short-term internalization of the hERG channel."
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"These results suggest that escitalopram blocked hERG currents at a supratherapeutic concentration and that it did so by preferentially binding to both the open and the inactivated states of the channels and by inhibiting the trafficking of hERG channel protein to the plasma membrane."
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"Since both citalopram and escitalopram can inhibit hERG K + channels ( Chae et al., 2014 ; Witchel et al., 2002 ), hERG K + channels might be main molecular targets of them for cardiotoxicity inducing[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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