NGM Discloses Third Oncology Development Candidate, NGM438, a Novel Antagonist Antibody Inhibiting LAIR1 for the Treatment of Advanced Solid Tumors
- LAIR1, through interactions with tumor-associated collagens, may form a stromal checkpoint that imposes signaling-based immune suppression and impedes anti-tumor immunity
- NGM plans to initiate first-in-human testing of NGM438 in 4Q21
- NGM featured NGM438 today at its first R&D Day, along with its diverse pipeline of drug candidates for liver and metabolic diseases, retinal diseases and cancer
SOUTH SAN FRANCISCO, Calif., Dec. 09, 2020 (GLOBE NEWSWIRE) -- NGM Biopharmaceuticals, Inc. (NGM) (Nasdaq: NGM), a biotechnology company focused on discovering and developing transformative
therapeutics for patients, today disclosed its third oncology development candidate, NGM438, a novel antagonist antibody that inhibits Leukocyte-associated immunoglobulin-like receptor 1 (LAIR1).
NGM438 was featured earlier today during NGM’s first R&D Day. The event highlighted the company’s diverse portfolio of therapeutic candidates for liver and metabolic disease, retinal diseases
and cancer. All presentations from the R&D Day can be found in the Investors & Media section of NGM’s website here.
LAIR1 is a collagen-binding inhibitory receptor expressed on immune cells1-2 that is implicated in immune suppression. LAIR1 and collagens are upregulated in multiple cancer types3-7 where collagens are produced by activated stromal cells. These stromal-derived suppressive factors are associated with poor responses to checkpoint inhibitors. For such tumors, formation of the LAIR1-collagen complex may act as a stromal checkpoint to both physically exclude immune cells from the tumor and impose signaling-based immune suppression8-9. Consequently, inhibiting this stromal checkpoint represents a potentially promising new therapeutic strategy to treat cancer by promoting the remodeling of the tumor architecture that restricts T cell infiltration of the tumor cell mass and reversing immune suppression in the tumor microenvironment.
Designed to inhibit LAIR1 interactions with stromal-derived collagens, NGM438 has the potential to block this stromal checkpoint and restore anti-tumor immune responses. In preclinical studies, NGM438 demonstrated the ability to reprogram collagen-suppressed myeloid cells to a stimulatory phenotype, induce inflammatory cytokine production by myeloid and T cells, and relieve collagen-based suppression of T cell proliferation. Reinvigoration of collagen-suppressed immune cells may address a key resistance mechanism that limits responses to current immunotherapies.
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