Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cells.
L
L
Eadie
T P
TP
Hughes
D L
DL
White
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D001549:Benzamides; D004359:Drug Therapy, Combination; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D050811:Octamer Transcription Factor-1 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010879:Piperazines / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011743:Pyrimidines / Q000494:pharmacology*; D019789:Tetraethylammonium / Q000378:metabolism; D014407:Tumor Cells, Cultured
D000317:Adrenergic alpha-Antagonists; D001549:Benzamides; D050811:Octamer Transcription Factor-1; C494165:POU2F1 protein, human; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D019789:Tetraethylammonium; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases; C498826:nilotinib; D011224:Prazosin