How Might IMiD Holding Therapy Impact Outcomes in R/R Multiple Myeloma?

In a retrospective USMIRC analysis of 363 patients with relapsed/refractory multiple myeloma who received commercial CAR T-cell therapy, immunomodulatory drug (IMiD)– holding therapy before leukapheresis was associated with a significant overall survival (OS) benefit among recipients of idecabtagene vicleucel (ide-cel; Abecma; hazard ratio [HR], 0.52; 95% CI, 0.28-0.94; P = .032), but not among those who received ciltacabtagene autoleucel (cilta-cel; Carvykti; HR, 1.12; 95% CI, 0.56-2.26; P = .70).¹

Study investigator Al-Ola A. Abdallah, MD, an associate professor of medicine and the director of the Plasma Cell Disorder Clinic in the Division of Hematologic Malignancies and Cellular Therapeutics at the University of Kansas Medical Center, spoke with CancerNetwork® about his leading explanation for why holding therapy appeared to matter more for one CAR T-cell product over the other. These findings were presented at the 23rd Annual International Myeloma Society (IMS) Meeting & Exposition.

Transcript:

CancerNetwork: This analysis showed that IMiD-containing holding therapy was associated with a significant OS benefit in ide-cel recipients, but not in cilta-cel recipients. What’s your leading explanation for why holding therapy would matter for one CAR T product and not the other?

Abdallah: We have to be very careful about that interpretation. We’re talking about 45 patients who received an IMiD in the ide-cel group, so it’s a small number. It’s a retrospective, nonrandomized [analysis] that could be impacted by a lot of things: treatment selection bias, differences in disease biology, center-specific therapies, and subsequent therapies. Many factors can play a role in that result, and we have to be very careful about it.

Now, if we want to look for a biological reason, there might be something that explains why ide-cel recipients benefited from IMiDs in the holding therapy [more than cilta-cel recipients]. It’s possible that it’s because the cilta-cel construct has 2 binding domains targeting BCMA and doesn’t need the IMiD to help it out, whereas ide-cel has only a single anti-BCMA binding domain with somewhat lower efficacy, and the IMiD may have pushed those [patients] toward a better survival benefit. That might be a biological explanation. But as I said, statistically, we’re talking about 45 patients, so we can’t make a big assumption based on that. It needs more study, and more prospective study, to evaluate that.

Reference

Krishnan V, Chopra R, Shaikh H, et al. Does IMiD-based holding therapy improve outcomes after CAR-T? Presented at: 23rd International Myeloma Society Annual Meeting; September 23-26, 2026; Glasgow, Scotland. Poster PA-242.