MediciNova Updates MN-001 Data At The 18th International Colloquium on Lung and Airway Fibrosis

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18th International Colloquium on Lung and Airway Fibrosis

18th International Colloquium on Lung and Airway FibrosisMediciNova, a biopharmaceutical company focused on developing therapies to fulfill unmet needs in respiratory, neurological, and liver diseases, recently announced that it will present at the 18th International Colloquium on Lung and Airway Fibrosis (ICLAF) on September 23rd in Mont Tremblant, Canada.

According to a recent press release, the presentation will focus on “MN-001 (tipelukast), a nonselective phosphodiesterase, 5-lipoxygenase, leukotriene, phospholipase C and thromboxane A2 inhibitor, demonstrates anti-fibrotic effects in the Bleomycin-induced idiopathic pulmonary fibrosis mouse model.”

Bleomycin is an anti-cancer drug that may have a side effect, pulmonary fibrosis, a progressive and eventually fatal disease (about two-thirds of PF patients’ die within 5 years) represented by the scarring of the lungs, with consequent loss of oxygen transportation.

According to the press release, during the presentation, the company expects to provide information on the mechanism by which MN-001 is thought to may have a positive effect in idiopathic pulmonary fibrosis (IPF), as well as how it can have an impact on curtailing Bleomycin-induced idiopathic pulmonary fibrosis.

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MN-001 is a small molecule compound able to produce its anti-inflammatory activity through several mechanisms in preclinical models like leukotriene (LT) receptor antagonism or inhibition of phosphodiesterase 3 e 4 and of 5-lipoxygenase.

In June, MediciNova had already announced positive data from an animal model study for the treatment of pulmonary fibrosis. Earlier, it had also observed positive findings in the analysis of MN-001’s potential efficacy in asthma.

The ICLAF gathers students, scientists, and patient advocates for lung fibrosis, among others, and focuses on top research in basic and clinical science, according to the event’s webpage.

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