If you reduce dose, frequency and or duration you may not ‘spend’ bcma. Not treating to resistance is the key. Unfortunately these types of trials don’t test limited duration therapy
Another BCMA bispecific beats standard of care at early relapse. This is turning into a pattern, and I mean that in a good way.View quoted post on X
Pfizer's topline from MagnetisMM-32: elranatamab monotherapy vs investigator's choice of EloPd, PVd or Kd in 523 pts with 1 to 4 prior lines, all len and anti-CD38 exposed, BCMA-naive. PFS by blinded central review met at a prespecified interim analysis.
- 18-mo PFS 68% with elra, median not reached. That lands right next to tec in MajesTEC-9. Different trials and controls, but the class effect at first relapse is getting hard to argue with
- Grade ≥3 infections 27.5% vs 18.1%.
- Grade 5 infections 0.8% vs 1.6%, lower than the control arm. Infection prophylaxis was built in from the start of the study. If that holds in the full data, it may be the most useful line in the whole release
- OS still immature
Not presented, the HR, control arm PFS, response depth, MRD, CRS and ICANS rates. Waiting for the full presentaion.
The bigger challenge is translational, and it's about sequencing more than efficacy. Tec mono, tec-dara and now likely elra are all competing for the same len/dara-exposed pt at first relapse. Each of those choices spends BCMA early, and we still have very little prospective data on what BCMA CAR-T delivers once a BCMA bispecific has failed.
For my MM colleagues, at first relapse, what actually makes you pick tec vs elra, beyond what your infusion center is used to? Expect a lof of this at ASH !
#mmsm #Myeloma #Elranatamab
