Novel AML patient selection assay for AMV564, Amphivena's lead therapeutic in hematology, presented at the 62nd American Society of Hematology (ASH) 2020 Annual Meeting
Amphivena Therapeutics, a clinical-stage oncology company focused on developing immunotherapeutics that restore anti-cancer immunity in patients, today presented data on a novel assay for selection of acute myeloid leukemia (AML) patients for treatment with AMV564, at the 62nd Annual American Society of Hematology Meeting and Exposition (ASH 2020), taking place virtually from December 5-8, 2020.
This novel assay could identify patients most likely to experience deeper and more durable responses with AMV564 therapy
AMV564 is the lead candidate from the AMPHIVENA ReSTORETM (Relieve Suppression of T cells in Oncology and Reinvigorate Effectors) platform of bivalent T-cell engagers, and has been studied in 2 Ph1 clinical studies in relapsed/refractory AML (NCT03144245) and in patients with advanced solid tumor malignancies (NCT04128423). AMV564 selectively depletes both myeloid derived suppressor cells (MDSC) and leukemic blasts via avid binding to clustered CD33, has been well tolerated with no dose-limiting toxicities reported and has shown single-agent activity across both R/R AML and solid tumors.
The assay leverages the selectivity of AMV564 in a screening format to identify AML patients in whom leukemic blasts are expressing CD33 in a predominantly clustered configuration. "While AMV564 has demonstrated early signs of efficacy and anti-leukemic blast activity across an unselected relapsed/refractory AML population, this novel assay could identify patients most likely to experience deeper and more durable responses with AMV564 monotherapy", said Curtis Ruegg, Ph.D., President and CEO of Amphivena.
Details of the Presentation:
 | Title: Selectivity of T Cell Engager AMV564 Against Different Leukemic Blast Populations and Potential Application for Patient Selection Authors: Sarde, A. et al. Abstract Number: 1976 Session: Acute Myeloid Leukemia: Novel Therapy, excluding Transplantation: Poster II Poster Viewing: Sunday, December 6, 2020: 7:00 AM-3:30 PM EST | |
The abstract and presentation are available on the ASH Annual Meeting, and Amphivena websites.
About AMV564
AMV564 relieves immune suppression via targeted depletion of immunosuppressive myeloid derived suppressor cells (MDSC) and drives T cell activation and polarization to restore anti-cancer immunity. To date, over 95 patients have received AMV564 across three Phase 1 clinical trials for patients with solid tumors, acute myeloid leukemia (AML), and myelodysplastic syndromes (MDS).
About Amphivena Therapeutics, Inc.
Amphivena Therapeutics, Inc. is a privately held, clinical-stage, oncology company based in South San Francisco, CA with a mission to restore anti-cancer immunity in patients and to take cancer treatment beyond the limits of immunotherapy. Our proprietary Amphivena ReSTORETM (Relieve Suppression of T cells in Oncology and Reinvigorate Effectors) platform of bivalent T-cell engagers is designed to selectively relieve immune suppression and drive T-cell activation/polarization in patients. The company's lead therapeutic candidate, AMV564, induces selective T-cell mediated killing of MDSC, known to be associated with immune suppression and poor outcomes to immunotherapy. In parallel, it drives improved T cell effector function. AMV564-induced immune restoration is optimized by targeting the lymphoid tissues, through subcutaneous delivery, where immunoregulation occurs. AMV564 has exhibited an excellent clinical safety profile and combinability with checkpoint inhibition and represents a unique opportunity to offer new treatment options to cancer patients underserved by immunotherapy.
Amphivena has raised $88.5 M to date in Series A, B and C venture financings led by NanoDimension, Qiming Venture Partners USA, MPM Capital and funds managed by Tekla Capital Management LLC.
Contact:Alicia Chung, Corporate Developmentachung@amphivena.com +1 650 499-3178info@amphivena.com
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SOURCE Amphivena Therapeutics
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