OUR SCIENCE
Targeting the Key Drivers of Neutrophilic Airway Inflammation
Our products represent a new class of protein therapeutics for treating neutrophilic lung diseases such as COPD, non-T2 asthma, bronchiectasis, ARDS, infections, and other conditions. They are based on a proprietary recombinant version of human alpha-1 antitrypsin (AAT) that has multimodal anti-protease effects in combination with immunomodulation and anti-infective properties. This combined activity broadly addresses key disease drivers in neutrophilic respiratory diseases.
In neutrophilic lung diseases, patients are trapped in a vicious vortex, a self-perpetuating cycle where a rapid influx of neutrophils leads to persistent inflammation, recurrent infections, irreversible tissue damage and impaired mucus clearance. Key disease drivers are massive amounts of aggressive serine proteases from neutrophils and bacteria causing complex and non-resolving inflammatory processes in the airways.
Therapeutic approaches to treat neutrophilic inflammation by inhibiting single targets have not been successful due to the complexity of the diseases. The effective therapy of complex lung diseases requires a broader treatment modality. As a new, broader approach, DPP1 inhibitors have shown efficacy in bronchiectasis. However, the efficacy is limited due to incomplete reduction of disease drivers and side effects.
AATec’s products overcome the limitations by multimodal effects, providing broad activity against several key drivers of inflammation. They reduce neutrophil serine proteases, inflammatory cytokines, bacterial proteases, and viral host factors. Our approach is designed to not just manage symptoms, but provide causative treatment. For optimal effects, we deliver our products by inhalation using a new handheld nebulizer with state-of-the-art protein nebulization technology. It provides high deposition in the lungs while the overall doses are low and systemic exposure is minimal.
Our lead program ATL-105 is under development for non-cystic fibrosis bronchiectasis (NCFB). Clinical development is planned to start in 2026. A scalable industrial manufacturing process and broad preclinical efficacy and safety data are available, and the development strategy has been agreed with regulatory authorities in Europe and the US.
Broad inhibition
of neutrophil proteases
ATL-105 protects lung tissue by blocking harmful enzymes such as neutrophil elastase, proteinase-3, and cathepsin G. When these enzymes bind to ATL-105, they are permanently inactivated, preventing them from driving inflammation and tissue damage in the lungs.
Immuno-
Modulation
ATL-105 modulates the immune response by decreasing pro-inflammatory cytokines (e.g., IL-8) while promoting anti-inflammatory signals (e.g., IL-10), effectively restoring the airway’s immunological balance.
Anti-
Infective
Beyond inflammation, ATL-105 provides bacteriostatic effects against common pathogens, and antiviral protection by inhibiting host factors required for viral entry.
