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FDA Grants Orphan Drug Designation to Leukogene's M2T-CD33 for Acute Myeloid Leukemia Treatment

a day ago3 min read

Key Insights

  • The U.S. FDA has granted orphan drug designation to M2T-CD33 (LTI-214), Leukogene Therapeutics' lead immunotherapy candidate for treating acute myeloid leukemia.

  • The designation recognizes the significant unmet medical need in AML and provides development incentives including tax credits, fee waivers, and potential seven-year market exclusivity.

  • M2T-CD33 utilizes Leukogene's novel M2T platform technology that functions as an antigen-presenting cell engager targeting CD33-positive leukemic blasts and stem cells.

The U.S. Food and Drug Administration has granted orphan drug designation to M2T-CD33 (LTI-214), a novel immunotherapy developed by Leukogene Therapeutics for the treatment of acute myeloid leukemia (AML). The designation underscores the significant unmet medical need for AML patients and recognizes the therapeutic potential of LTI-214 as a differentiated approach for this aggressive blood cancer.
The orphan drug designation provides Leukogene with several development incentives, including eligibility for tax credits on qualified clinical trial costs, waiver of certain FDA fees, and potential U.S. market exclusivity of approximately seven years upon approval.

Novel M2T Platform Technology

M2T-CD33 is built on Leukogene's proprietary M2T platform, which represents a completely new approach to cancer immunotherapy. The M2T platform is a novel, recombinant, high-affinity Major Histocompatibility Complex Class II (MHCII) binding protein conjugated to tumor-associated antigens. The platform functions as an antigen-presenting cell engager that directly stimulates MHCII and generates a powerful T and B cell response against the chosen antigen.
LTI-214 is specifically designed to selectively eliminate CD33-positive leukemic blasts and leukemic stem cells that drive disease progression in AML. The CD33 targeting approach aims to address the root causes of disease progression by targeting both the bulk leukemic population and the stem cell compartment.

Promising Preclinical Results

Preclinical studies have demonstrated robust anti-leukemic efficacy in AML models, with significant reduction in leukemic burden and prolonged survival. Importantly, LTI-214 has shown a favorable safety profile, with minimal off-target toxicity and no evidence of cytokine release storm in preclinical studies.
"We are honored that the FDA has recognized the therapeutic promise of LTI-214 by granting Orphan Drug Designation," said Dr. Sandeep Gupta, CEO of Leukogene. "AML remains one of the most challenging hematologic cancers, and outcomes for relapsed or refractory patients remain poor. The LTI-214 program embodies our commitment to advancing new immunotherapy approaches that are both potent and safer for patients."

Clinical Development Timeline

Leukogene expects to initiate first-in-human clinical evaluation of LTI-214 in AML patients in the near term. The company is also developing LTI-002, targeting tumor antigen mesothelin, as its second M2T platform candidate for treating pancreatic, ovarian, and other solid tumors.
Nathan Dolloff, PhD, Founder and Chief Scientific Officer of Leukogene, emphasized the significance of the FDA recognition: "This is an important step forward for Leukogene and the company's Major Histocompatibility Complex Class II engager technology. The M2T platform is a completely new approach to cancer immunotherapy and the endorsement from FDA is a testament to its high impact potential."

AML Disease Burden

According to the American Cancer Society, approximately 22,010 people in the United States will receive an AML diagnosis in 2025, with around 11,090 expected deaths from the disease. AML accounts for about one-third of leukemias in adults and approximately 1% of all cancers. The disease starts in the bone marrow and most often quickly moves into the blood, sometimes spreading to other body parts including lymph nodes, liver, spleen, central nervous system, and testicles.
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