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As expected, these signals were sensitive to imatinib treatment only in WT-Bcr-Abl-32D cells but not T315I-Bcr-Abl-32D cells, while ponatinib 27 treatment abolished these signals in both cell lines (Supplementary Fig

Outcome according to KRAS-, NRAS- and BRAF-mutation as well as KRAS mutation variants: pooled analysis of five randomized trials in metastatic colorectal cancer by the AIO colorectal cancer study group

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Stability and Pharmacokinetics Semax: - Demonstrates capability of passing the BBB when administered via subcutaneous injection or intranasal delivery [2, 3]