A new approach in a challenging disease
A New Approach
Stopping eosinophils before they can cause damage.
Like other blood cells, eosinophils originate as stem cells in the bone marrow. They differentiate and mature into eosinophils through complex molecular signaling and interactions with surrounding tissues, primarily in the bone marrow. Inflammatory signals—from the asthmatic lung, for example—may increase production of mature eosinophils. This increases eosinophil counts in the blood and ultimately in the lungs, causing tissue remodeling, mucus secretion, airway trapping, and asthma attacks.
If approved, dexpramipexole will be a first-in-class eosinophil maturation inhibitor that targets eosinophilic inflammation by lowering blood and tissue eosinophils.
Like other blood cells, eosinophils originate as stem
cells in the bone marrow. They differentiate and mature
into eosinophils through complex molecular signaling
and interactions with surrounding tissues, primarily in
the bone marrow. Inflammatory signals—from the
asthmatic lung, for example—may increase production
of mature eosinophils. This increases eosinophil counts
in the blood and ultimately in the lungs, causing tissue remodeling, mucus
secretion, airway trapping, and
asthma attacks.
Dexpramipexole inhibits the maturation of eosinophils at an early stage, preventing their travel through the blood to the lung, according to evidence from cell cultures and human biopsies.
Not treated.
Large epidemiology studies have shown that eosinophil counts in the bloodstream may predict the risk of asthma exacerbations. Eosinophilic inflammation causes damage to the bronchi (breathing tubes in the lungs), ultimately leading to the symptoms of asthma.
Treated with dexpramipexole.
Across five clinical trials, dexpramipexole significantly reduced eosinophils in blood and inflamed tissue and improved lung function in patients with eosinophilic asthma.
How Did We Get Here?
The eosinophil-targeting effects of oral dexpramipexole were discovered during its clinical development. Across five clinical trials, dexpramipexole showed a significant reduction in eosinophil counts in both the blood and in inflamed tissue.
Most recently, we reported positive topline results from the Phase III EXHALE-4 clinical trial of dexpramipexole in participants with eosinophilic asthma. In the EXHALE-4 trial, dexpramipexole met the primary endpoint with statistically significant improvement in lung function compared with placebo and statistically significant reduction in blood absolute eosinophil count (AEC) compared with placebo. In this study, dexpramipexole was well tolerated, with a safety profile similar to previous studies.
Areteia is also advancing dexpramipexole through the EXHALE-2 and EXHALE-3 Phase III clinical trials. Together, these three studies will potentially support approval of dexpramipexole for the treatment of eosinophilic asthma. To our knowledge, dexpramipexole is the only late-stage oral treatment in development for eosinophilic asthma.
Pipeline
Phase III development is underway.
Following the successful Phase II EXHALE-1 trial of dexpramipexole in moderate-to-severe eosinophilic asthma, Areteia is conducting three Phase III trials in patients with eosinophilic asthma. We have reported positive topline results for the EXHALE-4 trial and continue to advance the EXHALE-2 and EXHALE-3 trials.
