Galapagos NV a clinical stage Belgium-based biotech company, recently announced the last rheumatoid arthritis patients in its DARWIN 1 and 2 dose finding studies with filgotinib have completed their final visit.
Both studies completed 24 weeks of treatment, and will be followed by a final database lock and analysis. Topline results from the final analysis will be released in by August 2015. Patients who completed the study will now be enrolled in DARWIN 3, a long-term extension, open-label study with filgotinib.
Twelve-week results of both studies showed that the primary endpoint was achieved at 12 weeks of treatment with the selective JAK1 inhibitor filgotinib: symptom improvement of active RA. Both studies have also met their efficacy endpoints after 12 weeks of treatment with the drug, specifically ACR50 scores were accomplished with all dose regimens and dose levels. There were also improvements in DAS28(CRP) after one week of treatment.
At 12 weeks, the drug was found to be well tolerated and to meet the necessary safety profile. Consistent with JAK1 selectivity, the results showed an increase in haemoglobin levels.
A global Phase 2B program (DARWIN 1, 2 and 3) in a total of 886 patients with RA will further analyse the results of 24 weeks of treatment with Filgotinib.
“We really look forward to the 24 weeks’ topline results starting in July,” said in a recent press release Dr Piet Wigerinck, Chief Scientific Officer of Galapagos. “After having met the primary endpoint and secondary endpoints in both studies at 12 weeks, with a differentiated safety picture, we eagerly anticipate seeing how well this potential best-in-class profile holds up with 24 weeks’ treatment. Knowing that 98% of eligible patients who completed DARWIN 1 and 2 also enrolled in DARWIN 3 gives confidence, as investigators and patients saw benefit in continuing treatment with filgotinib.”
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. An external trigger (eg, cigarette smoking, infection, or trauma) that activates an autoimmune reaction leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is thought to occur in genetically susceptible individuals.