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In preclinical research models, MT-2 has been characterized for its agonism at MC1R (the receptor governing melanocyte eumelanin synthesis) and at MC4R (a central receptor studied in energy-homeostasis and melanocortin-signaling research)
In addition to the acquirement of drug-resistant mutation, the development of cancer stem cells also causes CML persistence and relapse from TKI therapy 12,13,14
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