Data shows that E-selectin is key to tumor growth and metastasis to bone and provides further support for upcoming clinical trial in patients with metastatic breast cancer
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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