ROCKVILLE, Md.–(BUSINESS WIRE)–Apr 22, 2019–GlycoMimetics, Inc. (NASDAQ: GLYC) today announced the publication of a paper in Nature Cell Biology that describes how tumor cells engage specific stromal components, most notably E-selectin, for propagation and outgrowth. 1 The paper provides further scientific support for the clinical trial in breast cancer patients with bone metastasis that was recently announced by GlycoMimetics.
Specifically, Esposito et. al. identify an E-selectin ligand expressed on tumor cells that is necessary for inducing mesenchymal-epithelial transition (MET) and that drives metastatic progression within the bone marrow microenvironment. Of note, in preclinical animal models of human breast cancer, inhibition of E-selectin with GlycoMimetics’ compound uproleselan (GMI-1271) prevented bone metastases progression and significantly attenuated bone metastases-associated bone degradation, resulting in a significant survival advantage in treated tumor-bearing mice. Previously published work also demonstrates a complimentary role for CXCR4. Together these observations support the testing of GMI-1359, GlycoMimetics’ dual-function antagonist, which targets both mechanisms.
“The scientific rationale for potential uses of GMI-1359 in oncology indications continues to build,” said John L. Magnani, PhD, Chief Scientific Officer of GlycoMimetics. “This most recent paper contributes additional understanding to the critical role of E-selectin and to the potential uses of compounds that target this mechanism in cancer, in particular in cancers that metastasize to bone.”
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