On November 11, 2021 GlycoMimetics, Inc. (Nasdaq: GLYC) reported that two abstracts relating to GMI-1359, the Company’s dual antagonist of CXCR4 and E-selectin, have been accepted for poster presentations at the 63rd American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition, to be held December 11-14, 2021 (Press release, GlycoMimetics, NOV 11, 2021, View Source [SID1234595244]).

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"The data to be presented at ASH (Free ASH Whitepaper) provide further support for targeting both CXCR4 and E-selectin as a novel treatment strategy for patients with AML, particularly patients with FLT-3 ITD mutations. Both posters detail preclinical studies conducted at the MD Anderson Cancer Center at the University of Texas in Houston, under the direction of Dr. Michael Andreeff. The first poster (#1171) describes the unexpected activities of FLT-3 inhibitors such as quizartinib and sorafenib to upregulate the expression of E-selectin ligands (sialyl Lex) and CXCR4 thereby increasing adhesion to protective niches in the bone marrow microenvironment and inducing chemoresistance. The addition of GMI-1359 to quizartinib in a PDX mouse model from a relapsed patient broke this induced chemoresistance, leading to a dramatic reduction in leukemic burden and a near-doubling of survival time. The second (#3348) demonstrates that GMI-1359 reduced adhesion and stimulated mobility of leukemic stem cells within the bone marrow microenvironment. In AML mouse models, GMI-1359 increased the efficacy and extended survival time in engrafted mice treated with venetoclax/HMA while protecting the hematopoietic stem cells and the bone marrow components from this treatment," said John Magnani, GlycoMimetics’ Chief Scientific Officer.

Details on GlycoMimetics posters at the ASH (Free ASH Whitepaper) Meeting are as follows:

1. Poster# 1171

Title: FLT3 Inhibitors Upregulate CXCR4 and E-selectin Ligands and CD44 Via ERK Suppression in AML Cells, and Blockade of CXCR4 and E-selectin Signaling with GMI-1359 Overcomes AML Resistance to Quizartinib In Vitro and In Vivo.
Authors: Y. Jia, M. Basyal, L. Ostermann, W.E. Fogler, J.L. Magnani, T. Seki, W. Zhang, M. Andreeff
Session Name: 604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster I
Date/Time: Saturday, December 11, 5:30-7:30 p.m. ET, Georgia World Congress Center, Hall B5

2. Poster# 3348

Title: Co-targeting E-selectin/CXCR4 with GMI-1359 Facilitates AML Stem Cell Mobilization and Protects BM Niches from Anti-leukemia Therapy.
Authors: K.-H. Chang, T. Zal, M. Basyal, L. Ostermann, M. Muftuoglu, P. Y. Mak, Y. Jia, W. Tao, A. Zal, W.E. Fogler, J.L. Magnani, W. Zhang, B.Z. Carter, M. Andreeff
Session Name: 604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster III
Date /Time: Monday, December 13, 6:00-8:00 p.m. ET, Georgia World Congress Center, Hall B5

The accepted abstracts are available online through the ASH (Free ASH Whitepaper) meeting website.

About GMI-1359

GMI-1359 is designed to simultaneously inhibit both E-selectin and CXCR4 — both adhesion molecules involved in tumor trafficking and metastatic spread. Preclinical studies indicate that targeting both E-selectin and CXCR4 with a single compound could improve efficacy in the treatment of cancers that involve the bone marrow such as AML and multiple myeloma or in solid tumors that metastasize to the bone, such as prostate cancer and breast cancer, as well as in osteosarcoma, a rare pediatric tumor. GMI-1359 has received Orphan Drug Designation and Rare Pediatric Disease Designation from the FDA for the treatment of osteosarcoma, a rare cancer affecting about 900 adolescents a year in the United States.