GlycoMimetics begins dosing in Phase II portion of GMI-1271 trial to treat AML

6th June 2016 (Last Updated June 6th, 2016 18:30)

US-based biotechnology company GlycoMimetics has started dosing in the Phase II portion of its Phase I/II clinical trial of its new E-selectin antagonist, GMI-1271, combined with induction chemotherapy to treat patients with relapsed / refractory acute myeloid leukemia (AML).

AML

US-based biotechnology company GlycoMimetics has started dosing in the Phase II portion of its Phase I/II clinical trial of its new E-selectin antagonist, GMI-1271, combined with induction chemotherapy to treat patients with relapsed / refractory acute myeloid leukemia (AML).

It is reported that in this portion, patients will be administered to a simultaneous pre-determined dosage of GMI-1271, as well as the chemotherapy regimen to assess the safety and efficacy of GMI-1271.

Enrolment in this portion of the trial is limited to patients at least 18 years old with relapsed or refractory AML and who would be treated with mitoxantrone, etoposide, and cytarabine (MEC).

During the phase II portion, the patients will be subjected to an additional cycle of treatment as compared to a single cycle of treatment in the Phase I portion of the study.

GlycoMimetics chief medical officer Helen Thackray said: "The data from the first cohorts point to both the safety and potential efficacy of GMI-1271 as a treatment for AML.

"The data from the first cohorts point to both the safety and potential efficacy of GMI-1271 as a treatment for AML."

"In the second half of this trial, we will further assess if patients with relapsed or refractory AML respond well to this combination approach while also including those who have been newly diagnosed with the disease in a separate arm of the study.

"If the second half confirms our earlier preclinical and clinical findings, we believe that GMI-1271 could well address the unmet needs of AML patients, beyond what can be done with currently available therapies."

GMI-1271 works by blocking E-selectin, an adhesion molecule on cells in the bone marrow, from bonding with AML cells disrupt the leukemic cell resistance within the bone marrow microenvironment.

Earlier clinical research has revealed the drug's ability to move cancerous cells out of the protective environment of the bone marrow where they take refuge to avoid the effects of chemotherapy.


Image: Bone marrow aspirate displays AML. Photo: courtesy of VashiDonsk.