-- Regenerative Medicine Company Advances Development of Fibroblast-Based 
Product as an "Off the Shelf" Cell-Treatment for Coronavirus Acute Respiratory 
Distress Syndrome (ARDS)

FibroGenesis announced today identification of molecular mechanisms associated 
with the potent reduction of lung inflammation previously reported by the 
Company in an animal model of COVID-19 lung failure.  

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The Company disclosed data demonstrating that administration of PneumoBlast(TM) 
resulted in dramatic alterations of immunological signaling molecules called 
"cytokines".  The studies showed that PneumoBlast(TM) reduced concentrations of 
the inflammatory cytokines interleukin-1 beta, interleukin-6, interleukin-8, 
interleukin-17, interleukin-18, and Tumor Necrosis Factor alpha, TNFa.  
Supporting the inflammation-inhibiting properties of PneumoBlast(TM), Company 
scientists observed an increase in anti-inflammatory cytokines interleukin-4, 
interleukin-10, interleukin-13 and interleukin-35, as well as 
regeneration-associated cytokines FGF-2 and HGF-1.  The cytokines found to be 
manipulated by PneumoBlast(TM) are known to be associated with survival and 
recuperation from COVID-19.  

Interleukin-1 beta (IL-1Beta): Mortality from acute respiratory distress 
syndrome (ARDS), is associated with increased IL-1Beta.  Studies have shown 
that administration of Anakinra, a drug specifically designed to block 
IL-1Beta, reduces mortality in patients with a COVID-19 associated cytokine 
storm, one of the other causes of death. 

Interleukin-6 (IL-6):  In a review of 1,426 COVID-19 patients in nine separated 
studies, interleukin-6 levels were more than three times higher in patients 
with complicated COVID-19 compared with those with a non-complicated disease.  
Furthermore, it was shown that higher levels of interleukin-6 correlated with 
death.   Supporting a causative role of interleukin-6 in pathology of COVID-19, 
studies have shown that administration of blocking antibodies to interleukin-6 
reduces pathology of this disease. 

Interleukin-8 (IL-8): Patients with ARDS show that elevated levels of IL-8 are 
associated with higher mortality.  IL-8 is known to recruit and activate 
neutrophils in the lung. Under normal circumstances, neutrophils serve to fight 
infections.  In the case of COVID-19, excessive neutrophils in the lung are 
believed to be associated with lethality.

Interleukin-17 (IL-17): Most of diseases associated with the immune system 
(Autoimmune diseases) have upregulated levels of both IL-17 and the cells which 
produce it, the Th17 cells. Patients with COVID-19 have dysfunctional blood 
vessels which predispose to excessive coagulation, believed to be caused by 
IL-17.  Additionally, IL-17 stimulates neutrophil infiltration into lungs. 

Previously reported by the Company:

In one set of experiments, control-untreated-mice possessed a lung wet weight 
to body weight ratio (LWW/BW) of 3.7 mg/g.  Mice treated with 
lipopolysaccharide; an agent that induces COVID-19-like lung inflammation 
caused an increase of the LWW/BW ratio of 12.5 mg/g.  Administration of bone 
marrow mesenchymal stem cells (BMSCs) to lipopolysaccharide-treated-mice only 
reduced the LWW/BW ratio to 9.9 mg/g.  In strong contrast, PneumoBlast(TM) 
administration significantly reduced the LWW/BW ratio to 5.2 mg/g in 
lipopolysaccharide-treated-mice (p < .001).  PneumoBlast(TM) showed a 37% 
improvement in outcome compared to BMSCs, which was statistically significant 
(p < .005). More importantly, after the introduction of PneumoBlast(TM) 
fibroblast cell therapy, average LWW/BW ratios returned to baseline control 
numbers of healthy lungs, which resulted in no statistical difference between 
recovered lungs and normal/healthy lungs using PneumoBlast(TM).

When the lung inflammation marker interleukin-6 was assessed, control mice 
possessed 532.3 pg/ml of the cytokine, whereas lipopolysaccharide 
administration caused an increase to 4400.1 pg/ml.  Treatment with BMSCs 
resulted in a slight 26% decrease of IL-6 in the 
lipopolysaccharide-treated-mice to 3317.7 pg/ml, whereas PneumoBlast(TM) 
significantly reduced IL-6 by 80% to 896.2 pg/ml, which was highly significant 
(p < .001).  The use of PneumoBlast(TM) resulted in a 54% improvement over 
BMSCs (p < .001).  The introduction of PneumoBlast(TM) cell therapy resulted in 
a reduction of inflammation back to normal/healthy lung levels in just 24 hours.

"Expanding our research continues to build a compelling scientific 
justification for use of fibroblasts in treatment of COVID-19 ARDS," said Tom 
Ichim, Ph.D., Chief Scientific Officer of FibroGenesis.  PneumoBlast(TM) 
appears to offer new hope to patients suffering from COVID-19 associated lung 
disease."

"We continue to be impressed with the potency of fibroblasts and their ability 
to effectively halt fluid accumulation in the lungs and repair the damage," 
said Pete O'Heeron, President and CEO of FibroGenesis. "Compared to stem cells, 
fibroblasts appear to be a more robust and potent cell source."

About FibroGenesis

Based in Houston, Texas, FibroGenesis, is a regenerative medicine company 
developing an innovative solution for chronic disease treatment using human 
dermal fibroblasts. Currently, FibroGenesis holds 220+ U.S. and international 
issued patents/patents pending across a variety of clinical pathways, including 
Disc Degeneration, Multiple Sclerosis, Parkinson's, Chronic Traumatic 
Encephalopathy, Cancer, Diabetes, Liver Failure and Heart Failure. Funded 
entirely by angel investors, FibroGenesis represents the next generation of 
medical advancement in cell therapy. 

Visit www.Fibro-Genesis.com.

SOURCE  FibroGenesis

CONTACT: info@Fibro-Genesis.com