PhorMed, Inc.

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—Inflammation
"Innovating ARDS care to breathe life back into patients."

ARDS is a severe lung condition leading to respiratory failure. PhorMed’s RP-323 works by reducing inflammation and promoting the repair of lung tissues, thereby improving respiratory function and offering new hope for recovery.

Acute Respiratory Distress Syndrome (ARDS)
WHAT WE HAVE DETERMINED IN OUR ARDS STUDIES
ARDS is a lung disorder where fluid collects in the air sacs of the lungs, depriving organs of oxygen. We have determined through our studies that RP-323 significantly reduces the influx of inflammatory cells into the lungs, thereby limiting damage to the lungs. In addition, RP-323 has shown the ability to block over-active/over-productive pro-inflammatory chemokines (eotaxin) and cytokines (interleukins: IL-1, IL-2, IL-9, and IL-10). These markers have been shown to be key effectors that comprise the “cytokine storm syndrome” (CSS) consistently observed in severe ARDS associated with respiratory infections, including COVID-19, influenza and bacterial pneumonia.

ARDS presents in a variety of ways including sudden acute respiratory syndrome (SARS).  In severe and fatal ARDS, disease severity is directly associated with the extent of inflammatory cell (neutrophil and macrophage) infiltration into the lungs.  When ARDS occurs, these inflammatory cells are profoundly elevated in the blood vessels, alveoli and other lung tissue. This results in congestion, hypoxia, vascular destruction and thrombosis (clotting), swelling, and is reflected in histology in ARDS tissue.

In our on-going studies, the results demonstrate that RP-323 safely and effectively reduces pulmonary inflammation. The ARDS animal system that we used is a validated model that is predictive of clinical drug efficacy and widely accepted in the industry. This study therefore represents a milestone advancement towards PhorMed’s goal of initiating human clinical trials of RP-323 for treating ARDS a symptom of COVID-19..

A Promising Solution for ARDS

RP-323 has demonstrated significant potential in combating ARDS by effectively reducing inflammation in the lungs, as shown in preclinical studies using a validated ARDS animal model. The therapeutic effects of RP-323 target the underlying mechanisms responsible for severe lung damage and inflammation, making it a groundbreaking candidate for treating ARDS.

  • Cytokine Induction: RP-323 has shown the ability to counteract pro-inflammatory cytokines and stimulate the production of anti-inflammatory cytokines by infiltrating neutrophils. This balanced cytokine profile aims to restore a healthy immune response and promote lung tissue repair.
  • Anti-Inflammatory Action through Cytokine Induction: RP-323 reduces inflammation and limits lung damage caused by ARDS by regulating cytokine production, specifically targeting pro-inflammatory cytokines like IL-1, IL-2, IL-9, IL-10 and Eotaxin, which can trigger a harmful “Cytokine Storm Syndrome” in ARDS.
  • Apoptosis: RP-323 promotes apoptosis, the natural process of programmed cell death, to eliminate hyperactive immune cells contributing to inflammation and tissue damage in ARDS. This selective approach minimizes collateral tissue damage.
Addressing Cytokine Storm Syndrome

Various infections, including flu, COVID-19, and bacterial pneumonia, can trigger a surge of pro-inflammatory cytokines, leading to CSS—a major contributor to ARDS severity. By controlling this cytokine storm, RP-323 provides significant anti-inflammatory benefits and minimizes lung damage.

New hope for ARDS patients

RP-323’s ability to modulate cytokines, reduce inflammation, and promote apoptosis offers a multifaceted approach to managing ARDS. The company plans to validate these findings in Phase 2 clinical trials, paving the way for innovative treatments that address this life-threatening condition.