Bright Peak Therapeutics to Present Innovative Best-in-Class and Multifunctional Regulatory T Cell (Treg) Enhancers at the 10th International Conference on Autoimmunity: Mechanisms and Novel Treatments
– First presentation of BPT264, the only Treg-targeting IL-2 for autoimmune disease that is both IL2Rα-enhanced and IL2Rβ-dead, displaying best-in-class preclinical properties —
– Introduction of BPT323, a cutting-edge, multifunctional immunocytokine combining TNFα blockade and selective Treg expansion for the treatment of autoimmune disease —
October 20, 2022 — SAN DIEGO, California & BASEL, Switzerland — Bright Peak Therapeutics, a privately held biotechnology company developing next-generation multifunctional precision immunotherapies, today announced the presentation of two posters showcasing the potential of its unique chemical protein engineering platform at the 10th International Conference on Autoimmunity: Mechanisms and Novel Treatments taking place October 20-25, 2022, in Chania, Crete.
“We are excited to share, for the first time, details of our innovative IL-2-based therapeutics that selectively activate and enhance Treg expansion for the treatment of patients with autoimmune diseases,” said Dr. Bertolt Kreft, Chief Scientific Officer of Bright Peak Therapeutics. Tregs are essential for maintaining peripheral tolerance, preventing autoimmunity and limiting chronic inflammatory diseases. IL-2 is an essential cytokine critical for Treg activation and proliferation, and low-dose IL-2 has demonstrated promising preliminary clinical efficacy in several autoimmune diseases.
Dr. Kreft continued, “Our chemical protein synthesis platform enabled us to create an optimized IL-2 payload that is uniquely IL2Rα-enhanced as well as IL2Rβ-dead, with the further capacity to be chemically conjugated. Using this fully synthetic IL-2 payload, we created a PEGylated, half-life-extended molecule with best-in-class preclinical properties as well as a cutting-edge multifunctional immunocytokine combining TNFα blockade and selective Treg expansion.”
Details of the abstracts are as follows:
Dates and Times: October 21-24, 2022, 10:00 AM – 11:30 AM (CET)
Title: Identification of BPT264 – a potent alpha-enhanced/beta-dead and half-life-extended IL-2 Treg enhancer for treatment of autoimmune diseases
Abstract Highlights: Using our chemical protein synthesis technology, we rationally designed an enhanced cytokine payload harboring a site-specific chemical conjugation handle and specific sequence variations that retune the biological properties of IL-2 for the treatment of patients with autoimmune disease. Bright Peak’s optimized cytokine payload is engineered to uniquely augment binding to IL2Rα and ablate binding to IL2Rβ for the precise and potent activation of Treg over other immune cell types. Conjugation to a 30 kDa PEG generates a fully synthetic cytokine with optimal pharmacokinetic properties that is able to selectively expand Tregs in cynomolgus monkeys up to 60-fold and to strongly suppress antigen-specific T cell-mediated inflammation in mice. Based on these best-in-class properties, IND-enabling studies have been initiated and a first in human trial is planned to start early 2024.
Title: Identification of BPT323 – An immunocytokine for treatment of autoimmune diseases combining orthogonal modes of action of TNFα blockade and selective Treg expansion
Abstract Highlights: Bright Peak has developed a cell-free chemical protein synthesis and conjugation platform to rapidly generate optimized antibody-cytokine (immunocytokine, IC) therapeutics within weeks. We have sitespecifically conjugated a single IL-2 variant that selectively activates and expands Tregs to the Fc region of the well-characterized anti-TNFα antibody adalimumab to generate an anti-TNFα-IL2 IC that fully retains the functions of the parent molecules in vitro and in vivo. TNFα-IL2 IC is apparently able to leverage an additional mode-of-action as its ability to activate and expand Tregs is augmented in the presence of TNFα. This suggests that TNFα-IL2 IC may exhibit higher local activity in inflamed tissues where TNFα is present at high levels.
The abstracts are available for viewing on Bright Peak’s website, www.brightpeaktx.com, and online at: https://www.aegeanconferences.org/src/App/sessions/posters/155
About Bright Peak Therapeutics
Bright Peak is a privately held biotechnology company based in Basel, Switzerland and San Diego, CA. We are rapidly advancing a robust portfolio of next generation, multifunctional, cytokine-based immunotherapies for the treatment of patients with cancer and autoimmune disease. We accomplish this by leveraging our world class protein engineering capabilities and our unique cell-free technology platform to chemically synthesize and conjugate novel protein therapeutics that reflect state-of-the-art insights into cytokine and immune checkpoint biology. Our pipeline stretches from discovery to INDenabling and encompasses enhanced cytokines, antibody-cytokine conjugates and other novel formats. Bright Peak is funded by a syndicate of leading healthcare investors.