PR84628

HOUSTON, July 2, 2020 /PRNewswire=KYODO JBN/ --

   -- 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.  

Logo - https://mma.prnewswire.com/media/1121989/FibroGenesis_Logo.jpg

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