UK-based Xention has initiated Phase II trial of XEN-D0103, a potent and selective oral modulator of the cardiac potassium channel Kv1.5, to treat atrial fibrillation (AF).
In 2013, Servier secured a contract from Xention for the development and commercialisation of XEN-D0103 for the treatment of AF.
Xention holds the US and Japanese rights to XEN-D0103, while Servier has commercialisation rights in all other territories of the world.
The two firms are undertaking a joint programme of clinical development for XEN-D0103, including two Phase II clinical trials aimed at showing the efficacy of the compound in AF.
The XAPAF study, the first of the planned Phase II trials, is being managed by Xention and is designed to evaluate the efficacy and safety of XEN-D0103 in patients with paroxysmal AF.
Dr Neil Sulke is serving as the principal investigator of the trial, which is being undertaken at Eastbourne General Hospital.
Dr Sulke said: "XEN-D0103 is a potent and selective blocker of the potassium channel Kv1.5, and this is the first time a highly selective Kv1.5 blocker is being assessed in patients with AF."
A total of 20 patients suffering from paroxysmal AF who also have implanted pacemakers will be enrolled in this a double-blind, randomised, placebo-controlled, crossover trial.
Xention CEO Tim Brears said: "We are delighted to report that our partnership with Servier is progressing extremely well and that XEN-D0103 is being evaluated in the first of two planned studies in AF."
Servier Research and Development vice-president and Cardiovascular and Metabolism Therapeutic Innovation Departments head Dr Isabelle Tupinon-Mathieu said: "We are pleased to announce that the second study 'DIAGRAF-IKur', managed by Servier, is in the process of being approved by the competent authorities and should start in the near future."
Apart from its Kv1.5 programme, the company is also developing antagonists of Kir3.1/3.4 (IKACh), a second exciting target for AF.
The company said that both Kv1.5 and Kir3.1/3.4 (IKACh) are expressed only in the atria and represent exciting targets for the development of atrial-selective therapeutics to treat AF.