eClinical Technology and Industy News

Sonnet BioTherapeutics Presents Compilation of Data Highlighting the Potential of SON-1010 as a Monotherapy or a Combination Therapy to Improve the Treatment of Solid Tumors

Poster presented at the 2025 AACR:IO Conference

Company’s novel platform that delivers either mono- or bifunctional immunomodulators linked to a Fully-Human, Albumin Binding scFv domain (FHAB®provides enhanced targeting to the tumor microenvironment (TME) and prolonged retention in the tumor

Excerpt from the Press Release:

PRINCETON, N.J., Feb. 26, 2025 (GLOBE NEWSWIRE) — Sonnet BioTherapeutics Holdings, Inc. (the “Company” or “Sonnet”) (NASDAQ: SONN), a clinical-stage company developing targeted immunotherapeutic drugs, today announced the presentation of a compilation of data at the 2025 American Association for Cancer Research (AACR) IO Conference.

As part of the conference, Dr. Sant Chawla, Principal Investigator at the Sarcoma Oncology Center in Santa Monica, California, presented a poster entitled, “Combination immunotherapy with an albumin-binding interleukin-12 fusion protein that extends cytokine half-life, targets the tumor microenvironment, and enhances therapeutic efficacy.” This is the first time the overall strategy of Sonnet’s Fully Human Albumin Binding (FHAB®) platform has been compiled with existing data and presented in a poster. The presented poster is now available on the Publications page of the Company’s website.

SON-1010 is the Company’s proprietary version of recombinant human interleukin-12 (rhIL-12), configured using genetic fusion to the FHAB platform, which extends the half-life and bioactivity of the IL-12 component due to binding native albumin in the serum. Albumin binding to FcRn, GP60, and SPARC results in an improved PK profile, decreased toxicity risk, and a broader therapeutic index preclinically, with significant targeting of the tumor microenvironment and increases in activated NK, NKT, Th1, and cytotoxic CD8 T cells, as well as marked repolarization of pro-tumor M2 MDSCs to inflammatory M1 APCs.

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