GSK commences phase III study of mepolizumab in severe HES patients
GlaxoSmithKline (GSK) has initiated a phase III study of its interleukin 5 (IL-5) antagonist, mepolizumab in hypereosinophilic syndrome (HES) patients.
The trial will feature 80-120 patients having the severe form of the disease who will be randomized to receive treatment with either mepolizumab or placebo when added to the standard of care.
It will compare the efficacy of subcutaneous mepolizumab 300mg given once in four weeks against placebo patients with severe HES who had a minimum of two HES flares within the past one year and a blood eosinophil count of 1000/µL or more.
GSK vice president and mepolizumab medicine development leader Steve Yancey said: “While limited treatments are available for patients with certain types of HES, current options for the majority are either inadequate or come with undesired side-effects associated with long-term use.
“The start of our phase III study is an important development in our work to explore whether mepolizumab could provide a potential alternative treatment option in this patient population.”
Primary endpoint of the 32-week trial has been defined as the portion of patients who are observed to have flare that is worsening of their HES symptoms, resulting in escalation in treatment.
On the other hand, secondary endpoints aim to record evidence that would support the benefit of treatment with mepolizumab in comparison to placebo. They would also feature time taken to experience first flare in HES, the patient proportion that was observed to have an HES flare from week 20 to week 32, along with fatigue severity.
According to GSK, Mepolizumab binds to IL-5 cykotine and blocks the activity of eosinophils which is necessary for the treatment of HES.
Mepolizumab holds the orphan drug status for HES in the US and the European Union (EU).
Branded as Nucala, mepolizumab has been approved in the US and EU and other countries as an additional treatment for patients having severe asthma, with an eosinophilic phenotype.