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Against pulmonary fibrosis

March 06, 2006

The biotech companies Digna Biotech and Biotherapix have signed an agreement to jointly apply their patented products towards the development of a treatment for pulmonary fibrosis. Digna Biotech is the commercial entity responsible for developing the intellectual property (patents) generated by the CIMA of the University of Navarra in its preclinical, clinical and commercial research.

The focal points of this agreement are the M3 protein owned by Biotherapix and the p17 peptide from Digna Biotech. It is hoped that these two compounds can work in common, taking advantage of the chemokyne inhibiting activity of M3 and the specific TGF-beta1 inhibiting activity of p17. Both TGF-beta1 as well as the chemokynes are key molecules in various inflammatory and degenerative processes. The researchers believe that the combined action of M3 and p17 will allow the development of a viable therapeutic alternative for treating pulmonary fibrosis.




The necessary studies for the development of the treatment us the p17 peptide and the M3 protein will be preferentially performed in centers of the University of Navarra: the CIMA, the University Hospital and the CIFA (Center for Research in Applied Pharmacobiology).

Combination of the p17 peptide and the M3 protein

The causes of pulmonary fibrosis are poorly known; this disease is characterized by an abnormal accumulation of collagen fibers in the lung, which causes structural deterioration. This deterioration causes progressive scarring in the lungs, which impedes the uptake of oxygen into the bloodstream, and thus impedes respiration. The European health authorities currently consider that pulmonary fibrosis is a rare or uncommon disease, with a prevalence of from 13 cases (in men) to 20 cases (in women) per 100,000 persons.

There do not currently exist effective treatments for this disease. The current treatments are based on the administration of oxygen and anti-inflammatories (glucocorticoids), some associated with immunosuppression and others not. These therapies have had limited success in reduction the progress of the fibrosis, and a contribute little to improving the quality of life of those affected.

The p17 peptide has demonstrated its effectiveness in the animal model which best reproduces pulmonary fibrosis. Currently, research is underway to confirm these findings with other models, and to begin toxicological studies. M3, on the other hand, is a protein of viral origin which has demonstrated its neutralizing effect against a wide set of molecules from the chemokyne family. Biotherapix is researching the use of derivatives of this molecule in order to slow certain inflammatory processes in which chemokynes play a key role. The M3 protein has shown advantages over other biological therapeutic molecules, such as its inhibiting activity against multiple chemokynes, as well as its low toxicity.

Elhuyar Fundazioa



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