

AbbVie's experimental myeloma drug etentamig nearly doubled response rates compared to standard treatments in heavily pretreated patients. The Phase 3 results could reshape how doctors sequence therapies in one of blood cancer's toughest-to-treat populations.
Imagine you've tried every treatment your doctor has. Three rounds of therapy, maybe more. Each time, the cancer came back. Now your oncologist is flipping through a short list of options, and none of them are great.
That's the reality for tens of thousands of patients with relapsed, refractory multiple myeloma (a blood cancer that keeps bouncing back after treatment). There's no clear standard of care for these patients. Doctors essentially improvise. And the options that do exist? They work less than half the time.
AbbVie just dropped data that could change the math.
In the Phase 3 CERVINO trial, AbbVie's experimental drug etentamig achieved a 74% response rate in patients with refractory multiple myeloma. The comparator arm, where doctors picked from a menu of existing standard therapies, managed just 45.7%.
That's not a marginal improvement. That's nearly doubling the odds that a patient's cancer will shrink. In a population where patients had already been through a median of three prior lines of therapy, that gap is enormous.
But the response rate was only half the story. The trial also showed etentamig cut the risk of the cancer getting worse (or killing the patient) by 60%, with a hazard ratio of 0.40. For the non-statisticians: a hazard ratio below 1.0 means the drug is better, and 0.40 means it's a lot better.
Etentamig belongs to a class of drugs called bispecific antibodies, which is a fancy way of saying it has two arms that grab onto two different things. One arm latches onto a protein called BCMA on the surface of myeloma cells. The other arm grabs CD3 on T cells (your immune system's hit squad).
Think of it like a molecular bouncer dragging a troublemaker to security. The drug physically brings the T cell face-to-face with the cancer cell, forces an introduction, and lets nature take its course. The T cell activates, releases its toxic payload, and the myeloma cell dies.

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It's elegant. It's also not the only bispecific in town.
The multiple myeloma bispecific market in 2026 is getting packed. Teclistamab (Tecvayli) was the first to get FDA approval back in 2022. Elranatamab (Elrexfio) followed in 2023. Both target a protein called BCMA on myeloma cells. Then there's talquetamab (Talvey), which goes after a completely different target called GPRC5D.
Etentamig is still investigational, with no approval yet. So why should anyone care?
Because the CERVINO data look really good, even compared to this crowd. The trial didn't just test etentamig against a placebo or some straw-man comparator. The control arm let investigators pick from legitimate regimens: carfilzomib plus dexamethasone, elotuzumab-based combos, or selinexor-based combos. These are real drugs that real doctors actually prescribe. And etentamig still blew them away.
Every cancer drug comes with a toll, and bispecifics are no exception. The main concern with this class is cytokine release syndrome (CRS), which is basically your immune system throwing a tantrum: fever, low blood pressure, sometimes worse. In CERVINO, CRS occurred in about 28% of etentamig patients, but importantly, none of those cases were grade 3 or higher (the really dangerous kind).
Infections were a real issue, though. Grade 3 or 4 infections hit 27.7% of patients on etentamig, compared to 19.2% on standard therapy. That's a meaningful gap, and it's something doctors will weigh carefully. Revving up the immune system to fight cancer can leave the door open for opportunistic infections; it's the classic trade-off.
Still, the overall safety profile was described as manageable, and discontinuation rates were low. For a drug class that sometimes requires intensive hospital monitoring, that matters. If etentamig can be administered in community oncology settings (not just big academic centers), its commercial reach expands dramatically.
If there's one asterisk on the CERVINO data, it's overall survival. At 12 months, 87.9% of etentamig patients were alive versus 72.0% in the control arm. That looks impressive on its face, but AbbVie acknowledged that the study hadn't yet crossed its prespecified statistical boundary for overall survival at the data cutoff.
Translation: the survival trend is pointing in the right direction, but it's too early to call it definitive. The data simply need more time to mature. This is common in cancer trials where patients live long enough that you need years of follow-up to prove a survival benefit with statistical rigor.
Full results are expected at the 23rd International Myeloma Society Annual Meeting later this month, and AbbVie says it will discuss regulatory next steps after that.
Multiple myeloma is a disease of diminishing returns. Each line of therapy tends to work a little less well than the last. By the time patients are "triple-class exposed" (meaning they've already been treated with a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 antibody), the playbook gets thin.
That's exactly the population CERVINO enrolled: 393 patients who had been through the wringer. The fact that nearly three-quarters of them responded to etentamig is genuinely striking. Earlier data even suggested the drug works in patients who've already received other BCMA-directed therapies, which would give it a sequencing advantage that competitors can't easily match.
The bispecific antibody race in myeloma isn't a winner-take-all sprint. It's more like a relay, where each drug finds its spot in the treatment sequence. But CERVINO's results suggest etentamig might deserve one of the earlier legs, not just a last-resort anchor.
AbbVie still has to get it approved, of course. And the full data presentation will face intense scrutiny from the myeloma community. But for now, the message is clear: in a crowded field of cancer drugs, etentamig just elbowed its way to the front of the line.
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