International Myeloma Society Annual Meeting | 2026

AbbVie's Etentamig Clears Key Bar in Late Stage Myeloma Study, Cutting Progression Risk by More Than Half

AbbVie has shared early but striking findings from a large late stage trial testing its experimental drug etentamig in people battling a form of blood cancer that keeps coming back despite multiple rounds of treatment. The Chicago area drugmaker reported that patients on the therapy responded at nearly double the rate seen in those given currently available treatment options, while also facing a substantially lower chance of their cancer worsening or proving fatal during the study window.

About CERVINO

The trial, known by the shorthand CERVINO, enrolled 393 people whose multiple myeloma had already returned or stopped responding after they had cycled through three separate lines of therapy on average. Everyone in the study had previously been exposed to all three of the major drug categories doctors typically reach for first: a proteasome inhibitor, an immune modulating agent, and an antibody that targets a protein called CD38.

After patients had been followed for a median of just over eleven months, the gap between the two study arms was hard to ignore. Nearly three in four patients on etentamig, 74 percent, saw a measurable response to treatment, compared with under half, 45.7 percent, of those on standard therapy.

Those on etentamig faced a 60 percent lower risk of their cancer advancing or of death during the study period compared with the comparison group, a result reflected in a hazard ratio of 0.40.

Survival data, while still developing, pointed in the same direction. A year after starting treatment, roughly 88 percent of patients on etentamig were still alive, versus 72 percent of those on standard care.

Etentamig Mechanism of Action

Etentamig works by targeting a protein called BCMA, which sits abundantly on the surface of the malignant plasma cells that define multiple myeloma and which those cells depend on to keep growing and to avoid the programmed cell death that would otherwise eliminate them. The drug is engineered with a bivalent binding arm that grips BCMA tightly, paired with a comparatively weak grip on CD3, the immune cell target, a combination scientists believe helps explain its relatively gentle side effect profile without sacrificing potency against the cancer.