Our lead product for severe pneumonia, rhu-pGSN, has application for COVID19.

Plasma Gelsolin's Biological Role: Protect and Defend

Plasma gelsolin (pGSN) is an ancient, highly conserved human protein that is a highly abundant plasma protein in healthy individuals. Its role is to keep inflammation localized to the site of injury and to boost the body’s ability to clear pathogens.

It regulates the pathogen clearance by enhancing NOS3 and scavenger receptor activity in macrophages and thereby improves antimicrobial defense in multiple gram positive and negative resistant and sensitive bacterial strains, as well as pneumonia secondary to influenza. 

Plasma gelsolin’s efficacy is not limited to bacterial infection.  Its non-immunosuppressive anti-inflammatory addresses the inflammatory component of infection, including severe flu, as well as multiple inflammatory, autoimmune and degenerative diseases.

Key Component of Innate Immunity:

Macrophage Regulation by Plasma Gelsolin

NORMAL CIRCUMSTANCES

Macrophage receptor with collagenous structure (MARCO) binds with pathogens. Macrophage absorbs and destroys them, maintaining homeostasis.

INJURY OR INFECTION

Actin released from cellular injury or infection binds to MARCO preventing it from binding with pathogens. Without your macrophage defense system, pathogens can build up making a small infection severe.

PLASMA GELSOLIN IN ACTION

Plasma Gelsolin overcomes the actin inhibition which increases pathogen binding and uptake. Plasma Gelsolin also stimulates NOS3 activation via Akt phosphorylation to improve killing of the pathogen inside the cell.

Efficacy Demonstrated in >20 Models in Independent Labs

   Enhanced Microbial Uptake and Killing in Human Alveolar Macrophages

   Gram Positive

   Gram Negative

   Influenza

   Infectious Peritonitis

INFECTION

Inflammation/CV/Metabolic

    Ischemic Stroke Model

    Inflammatory Bowel Disease

    Diabetes Type 2: Multiple Models

    Pain: Central/Periheral Models

    Alzheimer’s Disease

    Multiple Sclerosis (EAE)

    Neuroinflammation

Neurological

INJURY/TRAUMA

    Burns – Lung Microvascular Permeability

    Radiation Exposure

    Hyperoxia Acute Lung Injury

Collaborating With Over 20 Institutions Worldwide

Hotspots Background

BOSTON, MA

Harvard TH Chan School of Public Health

Brigham and Womens Hospital

Beth Israel Deaconess Hospital

Mass General Hospital

BETHESDA/BALTIMORE, MD

NIA - National Institute on Aging

University of Maryland

NIAID - National Institute of Allergy and Infectious Disease

CHICAGO, IL

Feinberg School of Medicine, Northwestern University

PENNSYLVANIA

University of Pennsylvania, Philadelphia

University of Pittsburgh, Pittsburgh

TENNESSEE

St. Jude Children's Research Hospital, Memphis

Vanderbilt University School of Medicine, Nashville

MICHIGAN

Central Michigan University

CALIFORNIA

University of California San Diego

NEW YORK

Weill Cornell Medical Center, New York City

Syracuse VA Medical Center, Syracuse

TORONTO

University of Toronto

KENTUCKY

University of Louisville

FINLAND

University of Helsinki, Helsinki

POLAND

Medical University of Bialystok, Bialystok

SOUTH KOREA

Hangyang University, Seoul

BioAegis has established collaborations with a number of leading investigators. These collaborations enhance the ability to recognize additional commercial opportunities, extend the research effort that is ongoing in its own laboratory, and refine and drive current programs forward.