Amphivena Presents Translational Data Highlighting the Cytokine Profile for its Lead Clinical Candidate, AMV564 at the AACR 2021 Virtual Annual Meeting | Financial Buzz

Amphivena Presents Translational Data Highlighting the Cytokine Profile for its Lead Clinical Candidate, AMV564 at the AACR 2021 Virtual Annual Meeting

Amphivena Therapeutics, a clinical-stage immuno-oncology company focused on developing immuno-therapeutics that restore anti-cancer immunity, today presents translational data for the Company’s lead clinical candidate from a Phase 1 study in patients with advanced solid tumors. The poster, entitled “MDSC Suppress the T Cell Repertoire and Contribute to a Pathologic Cytokine Milieu in Cancer Patients,” (Abstract 528) is presented today at the American Association for Cancer Research (AACR) 2021 Virtual Annual Meeting.

“The translational data we are presenting today at AACR continue to highlight the unique properties of AMV564 and our broader platform technology. AMV564 relieves immune suppression via MDSC depletion which results in the expansion of anti-tumor T-cells, while attenuating the biological responses that contribute to cytokine release syndrome. These findings are consistent with both the clinical activity and safety profile that we have observed in our phase 1 dose escalation in solid tumor patients, with no CRS at doses of 5 – 50 mcg. As our work advances, we are confident that these data signal an opportunity for AMV564 as a new, safe treatment paradigm for solid tumors,” said Victoria Smith, Ph.D., Chief Scientific Officer of Amphivena Therapeutics.

The poster’s authors conclude:

  • AMV564 selectively depletes M- and G-MDSC with concomitant activation of T cells, thereby relieving systemic immune suppression and preventing pathologic levels of myeloid cytokines
  • Control of MDSC by AMV564 yields a pro-inflammatory cytokine profile that is favorable for anti-tumor immunity, without excessive production of myeloid cytokines such as IL6 which are associated with cytokine release syndrome (CRS)
  • Treatment with AMV564 yields significant expansion of the T cell repertoire including T cell clones not detectable at baseline, and expansion of anti-tumor T cells, in cancer patients

Poster Details:

Session Title: Immunomodulatory Agents and Interventions

Session Start Date/Time: Saturday, April 10, 2021, 8:30 AM – 11:59 PM ET

Title: MDSC suppress the T cell repertoire and contribute to a pathologic cytokine milieu in cancer patients

Authors: Sterling C. Eckard, et al.

Abstract: 528

The abstract is available on the AACR Annual Meeting website, and in addition, the poster is available on the Presentations & Publications page on the Amphivena website.

About AMV564

AMV564 relieves immune suppression via targeted depletion of MDSC and drives T cell activation and polarization to restore anti-cancer immunity. To date, over 90 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, immuno-oncology company based in South San Francisco, CA that is developing a novel platform of dual-action biologics to selectively relieve immune suppression and drive T-cell activation/polarization, to restore anti-cancer immunity in patients. The company’s lead therapeutic candidate, AMV564, induces selective T-cell mediated killing of myeloid derived suppressor cells (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 with limited evidence of CRS and combinability with checkpoint inhibition and represents a unique opportunity to bring new treatment options to cancer patients underserved by immunotherapy.


Alicia Chung, Corporate Development

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Mike Beyer, President and Chief Media Officer

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