Forty Seven Inc. to Present New Preclinical Data on 5F9 at the 60th American Society of Hematology (ASH) Annual Meeting
-- 5F9 Priming Dose Results in CD47 Pruning, Removing CD47 from Surface of Red Blood Cells to Mitigate Risk of Anemia --
The presentation on Forty Seven’s proprietary 5F9 priming and maintenance dosing strategy will include preclinical data providing additional mechanistic insight into why this dosing strategy mitigates on-target anemia caused by the clearance of aged red blood cells (RBCs). This study demonstrates that the initial priming dose of 5F9 results in a near complete loss of CD47 on surviving, younger RBCs – a phenomenon termed CD47 pruning. As a result, these cells are less susceptible to phagocytosis, contributing to a decreased risk of CD47 antibody-induced anemia during subsequent maintenance dosing. These findings are
The presentation on 5F9 plus azacitidine, a standard of care therapy for AML, will include preclinical data demonstrating that the combination increases the phagocytic elimination of AML blast cells by human macrophages in vitro, enhances clearance of AML in vivo, and prolongs survival compared to single-agent treatment with either 5F9 or azacitidine alone.
"We are pleased to unveil these preclinical results, which provide important insights supporting our proprietary priming dose strategy and underscore our belief in 5F9 as a safe and tolerable option for patients," said
The accepted abstracts are listed below and are now available online on the ASH website: http://www.hematology.org/Annual-Meeting/Abstracts/.
RBC-Specific CD47 Pruning Confers Protection and Underlies the Transient Anemia in Patients Treated with Anti-CD47 Antibody 5F9
Presentation Date & Time:
Poster Session Title: 101. Red Cells and Erythropoiesis, Structure and Function, Metabolism, and Survival, Excluding Iron: Poster II
Abstract Number: 2327
Combination Treatment with 5F9 and Azacitidine Enhances Phagocytic Elimination of Acute Myeloid Leukemia
Presentation Date & Time:
Poster Session Title: 616. Acute Myeloid Leukemia: Novel Therapy, excluding Transplantation: Poster II
Abstract Number: 2729
5F9 is a monoclonal antibody against CD47 that is designed to interfere with recognition of CD47 by the SIRPα receptor on macrophages, thus blocking the “don’t eat me” signal used by cancer cells to avoid being ingested by macrophages.
Forward Looking Statements:
Statements contained in this press release regarding matters that are not historical facts are "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "may," "will," "expect," "anticipate," "estimate," "intend," “potential,” and similar expressions (as well as other words or expressions referencing future events, conditions, or circumstances) are intended to identify forward-looking statements. These statements include those related to the effectiveness of the Company’s dosing strategy to mitigate on-target anemia; the potential of 5F9 as a safe and tolerable treatment option for patients; the effectiveness of 5F9 for the treatment of AML and high-risk myelodysplastic syndrome single-agent treatment and in combination with azacitidine. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. The product candidates that Forty Seven develops may not progress through clinical development or receive required regulatory approvals within expected timelines or at all. In addition, clinical trials may not confirm any safety, potency or other product characteristics described or assumed in this press release. Such product candidates may not be beneficial to patients or successfully commercialized. The failure to meet expectations with respect to any of the foregoing matters may have a negative effect on Forty Seven's stock price. Additional information concerning these and other risk factors affecting Forty Seven's business can be found in Forty Seven's periodic filings with the
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Source: Forty Seven, Inc.