Synairgen has reported more positive data from its LOXL2 (lysyl oxidase-like 2 enzyme) inhibitor programme against the lung disease idiopathic pulmonary fibrosis (IPF).
The trial conducted with Australian Pharmaxis will open door for the Phase I clinical trials in H2 this year as planned, said Synairgen.
Synairgen and Pharmaxis are working together to develop small molecule inhibitors of LOXL2 for the treatment of IPF and other fibrotic conditions including non-alcoholic steatohepatitis (NASH), kidney fibrosis and cardiac fibrosis.
Synairgen has previously reported that these inhibitors can reduce cross-linking of collagen fibres in an in vitro model of IPF developed with the University of Southampton. The company said this results in a reduction in tissue stiffness of around 50%. Synairgen also said that oral administration of one of these compounds reduced fibrosis score and improved lung function (elastance) in a preclinical model of lung fibrosis. Inhibition of LOXL2 using these novel inhibitors has the potential to improve lung function in patients with lung fibrosis by reducing tissue stiffness.
Commenting on the results, Richard Marsden, CEO of Synairgen, said that 2017 will be an important year for Synairgen. “Subject to the successful completion of on-going pre-clinical work, we expect to commence Phase I clinical trials of the LOXL2 inhibitor during the second half of 2017. The window for licensing the LOXL2programme to a pharmaceutical partner will open at the end of Phase I. We also expect to hear the outcome of the AstraZeneca Phase II trial of interferon beta during the first half of 2017,” Marsden said.
About IPF
IPF is a fatal lung disease which, with a median survival of 2 to 3 years, can be worse than many cancers. Synairgen noted it affects up to 132,000 people in the US and about 50,000 new cases are reported every year. The current products for IPF have generated global revenues in excess of $1 billion in 2016. The cause of the disease is not fully understood, but IPF results from the relentless build-up of scar tissue which damages the structure of the lung affecting normal uptake of oxygen into the blood. The resultant stiffening of the lungs makes it increasingly difficult to breathe. Scar tissue is formed largely of collagen. LOXL2 is a member of a family of enzymes that stiffen scar tissue by forming cross-links between the collagen molecules.