Eli Lilly’s new JAK2 inhibitor—which it obtained from the recent acquisition of Ajax Therapeutics—reduced spleen volume by more than a third in 70% of patients with myelofibrosis.
Eli Lilly’s shiny new JAK2 inhibitor reduced spleen volume and symptom burden in an early-stage study of a rare chronic blood cancer called myelofibrosis, demonstrating a degree of efficacy that analysts said could position the drug as a “potentially best in class” asset.
At 12 weeks, 70% of patients on Lilly’s drug, acquired in April in the $2.3 billion buyout of Ajax Therapeutics, achieved a 35% reduction in spleen volume, according to a Phase 1 readout presented Saturday at the European Hematology Association’s 2026 meeting. The same percentage of treated patients similarly saw a 50% improvement in symptoms.
In addition, Lilly reported that 59% of patients who reached 24 weeks of treatment demonstrated at least a 20% decrease in driver mutation variant allele frequency—an indicator of how common disease-causing genetic alterations are. A reduction of at least half in these variants was documented in 35% of patients.
“While still early, these data appear highly competitive,” BMO Capital Markets wrote to investors on Sunday evening. With this Phase 1 performance, Lilly’s drug, known as AJI-11095, could become a “potentially best in class JAK2i,” the analysts continued.
The firm also called the drug’s safety profile “clean,” pointing to manageable cases of treatment-emergent anemia. There were no dose-limiting toxicities or treatment-related dropouts, though more than half had to have doses lowered due to side effects.
Lilly is currently running an expansion cohort to study AJI-11095 as a second-line option for myelofibrosis, the pharma said Saturday. The pharma also plans to test AJI-11095 for high-risk polycythemia vera and for myelofibrosis that had not previously been exposed to JAK2 inhibitors.
AJI-11095 is the centerpiece of Lilly’s Ajax acquisition. The drug, designed to be taken orally, works by binding to inactive JAK2, in turn “more completely” suppressing the signaling cascade that leads to myelofibrosis and other blood cancers linked to overactive blood cell production in the bone marrow, according to Lilly.
The pharma on Saturday also claimed that AJI-11095 “demonstrated superior activity compared to ruxolitinib”—Incyte’s drug marketed as Jakafi—“in preclinical models of myelofibrosis.”
Incyte CEO Bill Meury told BMO that there’s a place for both therapies on the market. “I think that it’s an apples-and-oranges comparison,” he said, according to the firm’s note on Sunday. “One’s a symptomatic therapy, optimizing or maximizing spleen volume reduction and symptoms versus potentially disease modifying therapy. I don’t think it’s an either or.”
Jakafi made nearly $3.1 billion in 2025, charting 11% year-on-year growth.
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