Feinstein Institutes' scientists uncover 'paradigm-shifting' drug discovery strategy for sepsis, rheumatoid arthritis

Novel peptide-based treatment targets critical inflammatory pathway common to both serious conditions

Published on Feb. 21, 2026

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Scientists at Northwell Health's Feinstein Institutes for Medical Research have unveiled a novel drug discovery strategy that transforms a previously identified 'detrimental' immune element into a potent therapeutic for both sepsis and rheumatoid arthritis (RA). The research demonstrates that a peptide called P2-1, derived from an antibody epitope, effectively targets a critical inflammatory pathway common to both serious and potentially life-threatening conditions.

Why it matters

Sepsis and RA are two distinct but related inflammatory conditions commonly driven by the body's dysregulated, overactive immune responses and excessive cytokine/chemokine production. Sepsis accounts for nearly 20 percent of global deaths, while RA is a chronic autoimmune disease characterized by persistent inflammation and joint destruction. Despite extensive research, effective therapies for sepsis remain elusive, and existing RA treatments have limited efficacy and significant side effects.

The details

Challenging conventional wisdom, the researchers pursued a counterintuitive hypothesis: that a specific epitope - the part of an antigen that the host's immune system sees as foreign, thereby prompting an immune and inflammatory response - derived from an anti-tetranectin antibody previously linked to worsening sepsis outcomes, could be reengineered into a targeted therapeutic for both conditions. The team discovered that this specific epitope can be developed to create a treatment that precisely targets only the bad, overactive inflammatory pathways, while leaving the body's helpful immune signals alone. This new treatment is 'activated by disease,' meaning it only starts working where the problem is, making it much safer than other medicines that broadly weaken the body's entire immune system.

  • The research, published today in Military Medical Research, was led by Haichao Wang, PhD, professor in the Institute of Translational Research at the Feinstein Institutes.

The players

Haichao Wang

Professor in the Institute of Translational Research at the Feinstein Institutes and lead author of the published research.

Kevin J. Tracey

President and CEO of the Feinstein Institutes and Karches Family Distinguished Chair in Medical Research, as well as a co-author of the paper.

Ping Wang

Chief scientific officer of the Feinstein Institutes and co-author of the paper.

Feinstein Institutes for Medical Research

The home of the research institutes of Northwell Health, the largest health care provider and private employer in New York State.

Northwell Health

The largest health care provider and private employer in New York State, of which the Feinstein Institutes is a part.

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What they’re saying

“Despite the significant challenges in translating sepsis research, our motivation is energized by its proven potential to drive therapeutic options for other inflammatory disorders like RA.”

— Haichao Wang, Professor in the Institute of Translational Research at the Feinstein Institutes (Military Medical Research)

“For decades Dr. Wang has been a leader in identifying molecular mediators of sepsis and systemic inflammation. Historically, early insights into sepsis have fostered the development of new therapies for inflammation, something now that this new work may well accomplish.”

— Kevin J. Tracey, President and CEO of the Feinstein Institutes and Karches Family Distinguished Chair in Medical Research (Military Medical Research)

What’s next

The researchers plan to continue their work to further develop and test the P2-1 peptide-based treatment for potential clinical applications in sepsis and rheumatoid arthritis.

The takeaway

This novel drug discovery strategy represents a paradigm shift in how researchers approach treating inflammatory conditions like sepsis and rheumatoid arthritis, by transforming a previously identified 'detrimental' immune element into a targeted therapeutic that precisely addresses the underlying disease pathways while avoiding broad immune system suppression.