Antisense presses on with asthma therapeutic
Monday, 21 March, 2005
Melbourne's Antisense Therapeutics (ASX:ANP) is pressing ahead with development of its ATL1102 inhalant inflammation inhibitor for asthma, despite voluntarily suspending research into the drug's potential as a therapy for multiple sclerosis early this month.
Antisense is presenting data from animal trials of its antisense therapy for asthma at the annual meeting of the Thoracic Society of Australia and New Zealand in Perth today.
Antisense CEO Mark Diamond said his company was mindful of the fact that the US Food and Drug Administration was monitoring companies developing anti-inflammation therapies targeting VLA-4 receptor on inflammatory lymphocytes, after Irish biotech Elan Pharmaceuticals and its US partner Biogen Idec withdrew a monoclonal antibody therapy for multiple sclerosis, Tysabri.
Tysabri blockades the VLA-4 receptor on T-cells, monocytes and macrophages that cause inflammatory reactions in the brains of MS patients. ATL1102 was designed to achieve the same result, by targeting the messenger RNA sequence coding for the CD49d sub-unit of the VLA-4 protein.
Asked if Antisense's ATL1102 gene-suppression therapy might expose asthma patients to the same risk of brain infection, Diamond said the company was encouraged by the results of its animal trials in a mouse model of asthma, and believed ATL1102 offered advantages - including its safety - over monoclonal antibodies, peptides and synthetic VLA-4 inhibitors.
"It's active at very low doses in mice," he said. "It we extrapolate that result, it's also likely to work at very low doses in humans, and there's nothing in our mouse data to indicate any risk of adverse side effects.
In contrast to Tysabri and peptide blockers of VLA-4, which were administered via the systemic circulation, inhaled ATL1102 was likely to have much more localized effects on inflamed lung tissues
"We think it's going to be an important factor in competitive profiling, which will distinguish between our technologies and others.
Antisense's research director, Dr Christopher Wraight, said the company's presentation to the Perth conference would include data indicating that ATL1102, delivered as an aerosol directly into the lungs of mice, significantly reduces the infiltration of inflammatory cells called eosinophils from the bloodstream into the lung tissues affected by asthma.
At this early stage, it was not clear whether the effect was due to a change in the activation state of the eosinophils, or to loss of the cells' ability to move from the bloodstream into adjacent lung tissues.
The end-effect is that by restricting the entry of eosinophils, low-dose, inhaled ATL1102 significantly reduces the airway constriction caused by asthma attacks.
Wraight said the company would continue pre-clinical experiments in mice, and had no plans yet to take the asthma therapy into Phase 1 human clinical trials.
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