Addex Therapeutics Advances Promising New Treatment for Severe Chronic Cough
Geneva, Wednesday, 29 April 2026.
On April 29, 2026, Addex Therapeutics announced a novel drug candidate that not only suppresses severe chronic cough but remarkably improves underlying lung health in preclinical respiratory disease models.
Unpacking the Preclinical Efficacy
On April 28, 2026, Addex Therapeutics detailed encouraging preclinical data regarding its positive allosteric modulator (PAM) targeting GABAB receptors [1]. In a bleomycin-induced model of idiopathic pulmonary fibrosis (IPF), chronic once-daily dosing of the candidate yielded robust and sustained antitussive efficacy [1]. The data demonstrated significant reductions in cough frequency alongside an increased latency to cough over the treatment period [1]. Beyond symptom suppression, the treatment actively improved underlying lung pathology compared to untreated control subjects [1]. Assessments at Day 7 and Day 28 revealed lower Ashcroft scores—a standard histological measure of pulmonary fibrosis [GPT]—and a reduced percentage of affected lung tissue, indicating a potential disease-modifying effect [1].
Strategic Pipeline and Financial Context
The advancement of this candidate addresses a critical gap in respiratory care. According to Addex CEO Tim Dyer, persistent coughing in IPF patients substantially degrades their quality of life and exacerbates the overall disease burden, making chronic cough a significant unmet medical need [1]. The Geneva-headquartered biopharmaceutical firm, which also maintains a research presence in Cambridge, Massachusetts, is leveraging its proprietary drug-discovery platforms to build a diverse pipeline of allosteric modulators [2]. Beyond respiratory conditions, Addex’s partner Indivior has successfully completed IND-enabling studies for a different GABAB PAM candidate aimed at substance use disorders [1]. Concurrently, Addex’s lead clinical candidate, dipraglurant, is undergoing evaluation for brain injury recovery [1] and levodopa-induced dyskinesia in Parkinson’s disease [2].