Mabwell Therapeutics Announces Publication of Preclinical Data on Differentiated TREM2 Agonist Antibody 03O05 in Journal of Neuroinflammation

San Diego, CA – May 1, 2026 – Mabwell Therapeutics, a U.S.-based biotechnology company focused on developing innovative antibody-based therapies for serious diseases with high unmet medical need, today announced the publication of preclinical research on 03O05, a ligand-mimetic anti-TREM2 agonist antibody, in Journal of Neuroinflammation.

The article, titled “A ligand-mimetic anti-TREM2 agonist antibody elevates soluble TREM2 and ameliorates pathology in mouse models of Alzheimer’s disease and multiple sclerosis,” highlights a novel approach to activate TREM2, an important immune receptor involved in microglial function, tissue repair, and central nervous system homeostasis. The full article is available at: https://link.springer.com/article/10.1186/s12974-026-03733-2.

TREM2 signaling plays an important role in promoting disease-associated microglia and phagocytosis in neurodegenerative diseases. However, many traditional anti-TREM2 agonist antibodies are designed to block receptor shedding, reducing levels of soluble TREM2 (sTREM2), which has been associated with beneficial biological effects.

03O05 was designed to take a differentiated approach. Rather than blocking TREM2 shedding, 03O05 activates TREM2 while preserving the receptor’s natural shedding process and increasing sTREM2 levels. This shedding-permissive mechanism may offer a more balanced way to engage TREM2 biology, supporting protective microglial activity without driving sustained or excessive inflammatory activation.

In the published study, 03O05 demonstrated activity across multiple preclinical models. In a mouse model of Alzheimer’s disease, chronic treatment with 03O05 increased sTREM2, promoted clearance of disease-associated amyloid plaques, enhanced microglial phagocytic activity, and reduced markers of neuronal injury. In a demyelination model relevant to multiple sclerosis, 03O05 enhanced microglial clearance activity and supported remyelination during recovery.

“We are pleased to see this work published in Journal of Neuroinflammation,” said Xin Du, Ph.D., CEO of Mabwell Therapeutics. “The data support 03O05 as a differentiated TREM2 agonist antibody with a mechanism designed to activate protective microglial function while preserving soluble TREM2 biology. We believe this represents an important and potentially meaningful direction for therapeutic development in neurodegenerative and neuroinflammatory diseases.”

The publication underscores Mabwell Therapeutics’ antibody discovery and translational research capabilities, as well as the company’s commitment to developing innovative biologic therapies that address complex disease biology through differentiated mechanisms.