SNSP113
Mechanism of Action

Changing How Progressive Pulmonary Disease is Treated

SNSP113 is designed to target the underlying cascade of events that lead to progressive pulmonary disease or other life-threatening pulmonary conditions such as nontuberculous mycobacteria (NTM), Burkholderia cepacia complex (BCC), Pseudomonas aeruginosa or methicillin-resistant Staphylococcus aureus (MRSA) pulmonary infections.

SNSP113 has a rationally designed broad spectrum mechanism of action to (1) normalize mucin viscosity and improve mucus transport thereby increasing airway clearance, (2) interact with the cell walls of invading bacteria to increase their permeability, reduce their viability and potentiate the efficacy of antibiotics, (3) disrupt the cohesion of bacterial biofilms to reduce chronic antibiotic resistance and (4) reduce the inflammatory cascade of neutrophils that can lead to tissue damage and fibrosis.

Frequent pulmonary infections, mucus and biofilm accumulation, airway congestion and inflammation are key drivers of pulmonary exacerbations, symptoms and pulmonary decline.

SNSP113 is a novel positively charged glycopolymer that interacts with the negative charge of the bacterial cell surface as well as the structural integrity of mucins and biofilms.

Changing the course of progressive pulmonary disease

THE SNSP113 EFFECT:

SNSP113 breaks down biofilm layer, reducing antibiotic resistance.

  • SNSP113 has been shown in vitro to rapidly disrupt the cohesion of bacterial biofilms from both clinical and non-clinical strains of all tested bacteria including Pseudomonas aeruginosa, Staphylococcus aureus, methicillin resistant Staphylococcus aureus, Burkholderia strains and nontuberculous mycobacterium.
  • This effect results in rapid removal of biomass and permeabilization of bacteria within the biofilm. Disrupts the structure of biofilms by reducing cohesion and viscosity.

SNSP113 disrupts bacterial cell wall, increasing permeability; synergistic with antibiotics; protective effect on lung surface reduces re-colonization.

  • Bacteria treated with SNSP113 exhibit rapid permeabilization and leaking of the outer cell wall leading to membrane disruption of bacteria and allowing increased uptake of antibiotics.
  • This mechanism of action for SNSP113 allows for mediated killing of bacteria and also likely contributes to its synergistic activity with antibiotics.

SNSP113 normalizes mucin viscosity and improves mucus transport, increasing airway clearance.

  • SNSP113 is observed to interact with mucus and biofilms with a new mechanism of action, a physical interaction with the polymers that comprise the mucus (mucins).
  • SNSP113 disrupts the abnormal packing of mucus, making these substances more fluid and less viscous. This allows for more normal ciliary clearance and for antibiotics to reach the otherwise protected bacteria. SNSP113 breaks up the cohesion of both respiratory mucus to normalize mucociliary transport.

SNSP113 reduces inflammatory cascade of neutrophils, reducing tissue damage and fibrosis.

  • In vitro studies show reduction in the inflammatory cascade of neutrophils and serine elastases in the lungs.
  • Potential to slow progression of CF lung function data suggests that very low doses of SNSP113 can have significant anti-inflammatory therapeutic effects.