The platform originated from the observation that human astrovirus can cause infection without eliciting an inflammatory response—an uncommon feature among viral pathogens. Investigation of this phenomenon identified a short peptide sequence with dual activity as a complement modulator and inhibitor of MPO and NETosis, two key drivers of inflammatory tissue injury.
This discovery led to the development of pegtarazimod, which is now advancing in hypoxic ischemic encephalopathy, where convergent complement and neutrophil biology drive disease.
Pegtarazimod acts extracellularly to suppress neutrophil extracellular trap (NET) formation, limiting the release of extracellular DNA and associated inflammatory mediators that amplify inflammation and drive tissue and cellular damage.
Pegtarazimod binds myeloperoxidase (MPO) extracellularly, inhibiting MPO-driven reactive oxygen species (ROS) generation and thereby reducing oxidative stress and downstream tissue injury.
This extracellular mechanism reduces neutrophil-mediated inflammatory amplification and damage without interfering with intracellular neutrophil signaling or viability, preserving essential antimicrobial function.
Pegtarazimod acts on the earliest stages of the inflammation cascade, thus having an out-sized effect to inhibit all related downstream inflammatory signals
Steroids, immuno-modulatory drugs, and biologics target inflammation much further downstream in the immune response cascade
RLS-0071 (pegtarazimod) has had widespread scientific review and support. Scientists conducting research on pegtarazimod capabilities have published more than 25 peer-reviewed and indexed studies. A number of leading research organizations, including the NIH, National Multiple Sclerosis Foundation, Cystic Fibrosis Foundation, VA Catalyst and the Commonwealth Transfusion Foundation have provided grant funding to ReAlta.
