- BPM31510 demonstrates immune-metabolic remodeling that enhances T-cell infiltration and reduces checkpoint expression in tumors
- BRG399 induces early immunogenic cell death independent of mitotic arrest, revealing a novel immune-sensitizing mechanism
BOSTON, Mass. — November 3, 2025 — BPGbio, Inc., a biology-first, AI-powered, clinical-stage biopharma focused on mitochondrial biology and protein homeostasis, today announced that it will present two scientific posters at the Society for Immunotherapy of Cancer (SITC) 2025 Annual Meeting, taking place November 5–9 in National Harbor, Maryland.
The presentations highlight how BPGbio’s investigational agents BPM31510 and BRG399 remodel the tumor microenvironment and stimulate immune activation through distinct biological mechanisms.
Poster Presentations
Title: BPM31510, a CoQ10-Lipid Nanoparticle, Remodels the Tumor Microenvironment Through Immuno-Metabolic Reprogramming in Syngeneic Models
Authors: Maria-Dorothea Nastke et al.
Poster #: 1191
Summary: BPGbio’s BPM31510, a novel lipid nanoparticle delivering oxidized CoQ10, drives coordinated immuno-metabolic remodeling within the tumor microenvironment (TME). In syngeneic murine tumor models, BPM31510 treatment enhanced infiltration of T cells, reduced suppressive immune cells, and lowered key immune checkpoint signals that often block effective immune responses. Spatial multi-omics revealed discrete immune-rich niches accompanied by metabolic changes, reflecting a shift from an immune-cold to an immune-active TME. These findings highlight BPM31510’s potential to sensitize resistant tumors to immune-checkpoint inhibitors through combined modulation of immunity and tumor metabolism.
Title: BRG399: A Novel Colchicine-Binding Microtubule Agent Inducing Early Immunogenic Cell Death Independent of Mitotic Arrest
Authors: Kaila M. Bennett et al.
Poster #: 1154
Summary: BPGbio’s BRG399 is a first-in-class, brain-penetrant microtubule-targeting agent that induces early immunogenic cell death (ICD) through a mechanism independent of mitotic arrest. At low nanomolar concentrations, BRG399 upregulated canonical ICD markers such as calreticulin, ATP, HMGB1, and HSP70, prior to any detectable cell cycle arrest. In vivo, BRG399 treatment favorably reshaped the TME, increasing immune-cell infiltration and enhancing antitumor immune activity. These findings support BRG399’s potential as an immune-sensitizing agent capable of improving responses to immunotherapy.
Executive Commentary
“BPM31510’s immuno-metabolic effects and BRG399’s induction of immunogenic cell death both highlight the power of our NAi® Interrogative Biology platform to reveal therapeutic mechanisms that traditional discovery methods often miss,” said Michael A. Kiebish, Ph.D., Vice President of Translational Research at BPGbio. “The findings further validate the potential of BPM31510 beyond GBM, pancreatic, and rare disease (PCQD) since metabolic reengineering also plays a role in immunogenic rewiring leading to therapeutic benefit.”
“By integrating spatial omics, immune profiling, and mitochondrial biology, we’re uncovering how therapies like BPM31510 and BRG399 rewire the immune-metabolic landscape of tumors” added Stephane Gesta, Ph.D., VP, Discovery and Translational Biology at BPGbio. “This approach and these data provide strong insights that are guiding the next generation of combination immunotherapies.”
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Media Contact: media@bpgbio.com
