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Egle Therapeutics to present novel immunocytokine preclinical data for EGL-001 with poster presentation at the 2024 AACR Annual Meeting

Egle Therapeutics, a biotechnology company focused on advancing the next generation of regulatory T cell-focused therapies for oncology and auto-immunity, will present a poster at the American Association for Cancer Research Annual Meeting (AACR) 2024 being held on April 5-10, 2024.

In the poster, entitled “EGL-001 is a novel immunocytokine designed to specifically target and disarm T regulatory cells in the tumor microenvironment”.

Egle scientists present evidence that EGL-001, a CTLA-4 targeted IL-2 dominant negative mutein, selectively binds to T regulatory (Treg) cells and inhibits Treg IL-2 signaling.

The resulting reduction of Treg frequencies and functionality, as observed in ex vivo human tumor cultures and in vivo mouse models, promotes effector T cell responses. Accordingly, EGL-001 induces anti-tumor responses in combination with anti-PD-1 treatment in mouse models.

EGL-001 is the first drug candidate to emerge from Egle’s discovery platform, and it’s being developed for treatment of advanced solid tumors and to restore responsiveness to PD-1 inhibition.

Session Category: Immunology; Session Title: Immune Modulation with Cytokines; Session Date and Time: Tuesday Apr 9, 2024 9:00 AM - 12:30 PM; Location: Poster Section 4; Poster Board Number: 23 Published Abstract Number: 4079

About Egle Therapeutics SAS (Egle)

Egle Therapeutics is a biotechnology company focused on developing immunotherapies targeting suppressive regulatory T cells. Egle is leveraging a proprietary discovery platform to unveil novel Treg specific targets and to develop innovative Treg-focused drug candidates for oncology and autoimmune diseases. Egle aspires to advance toward the clinic its most advanced drug candidates, EGL-001 (a Treg-selective anti-CTLA4-IL-2m) and EGL-003 (non-targeted IL-2 Treg engager), which are currently developed in IND-enabling studies.

Find out more at www.egle-tx.com.

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