GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE312nnn/GSE312602/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE312602GEOGSEfalseProtective effects of metformin against ponatinib-induced toxicity in iPSC-derived cardiomyocytesAims: Ponatinib is currently considered the most effective treatment for patients with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), who develop resistance or intolerance to first- and second-line therapy, particularly those with T315I "gatekeeper" mutation in BCR-ABL. However, ponatinib is also one of the most cardiotoxic tyrosine kinase inhibitors (TKIs), with toxicity stemming from a combination of contractile dysfunction and inflammatory effects. Our goal was to model and investigate this toxicity in human-induced pluripotent stem-cell derived cardiomyocytes (hiPSC-CMs) and to evaluate whether metformin, a clinically well-tolerated antidiabetic drug with known cardioprotective potential via AMPK pathway activation in various pathologies, can mitigate the damage.2026/06/02GSE312602GSM9349923GSM9349912GSM9349913GSM9349921GSM9349922GSM9349916GSM9349917GSM9349914GSM9349915GSM9349918GSM9349919GSM934992024676312602Homo sapiens