Researchers for GlaxoSmithKline are launching a clinical program for a RIP1 kinase drug in pancreatic cancer after nailing down a positive look at how this drug worked in mice for pancreatic cancer.
Scientists at NYU School of Medicine and its Perlmutter Cancer Center partnered with investigators at GSK on the study, concluding that the RIP1 approach added to checkpoint inhibitors doubled the survival time of mice — from 25 days to 50 days.
There’s always a big question mark over rodent studies for cancer, but the team here felt that GSK547 provided the kind of early validation they needed to jump into human studies with an upgraded drug dubbed GSK095.
By inhibiting the RIP1 enzyme, the researchers believe they can thwart what ultimately becomes an immune cell suppressor — and that’s a target attracting deep and wide attention in a variety of fields. And the mouse study provided evidence of killer T cell activation with less suppressor activity. The news also signals fresh evidence of GSK’s amped up ambitions in oncology now that Hal Barron has taken the lead in R&D. GSK’s oncology group is headed up by Axel Hoos.
“If clinical trials prove successful, this could be really promising for many people with end-stage disease,” says George Miller, a professor at NYU Langone Health.
There’s been a growing focus on the role of RIP1 in disease. Sanofi recently signed up to partner on Denali’s RIP1K program, taking the anti-inflammatory route while the biotech sticks with its targets in the brain. And GSK has done its own work in RIP1.
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