A roundtable discussion, moderated by Thomas Martin, MD, Blood Cancers Today Associate Editor, of the University of California, San Francisco, focused on bispecific therapeutics for the treatment of multiple myeloma. Dr. Martin was joined by Ajay Nooka, MD, MPH, FACP; Ajai Chari, MD; and Angela Dispenzieri, MD.
In the next segment of the roundtable series, the panel discusses where they think bispecifics have “the best role” in the myeloma treatment paradigm.
Watch the next segment in this series.
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Dr. Martin: I want to ask one more question before we talk about operations of the bispecific, operationally, how you’ve enrolled patients and how you’ve basically rolled out this therapeutic for your institution. But one question is, where do you think the optimal place for this therapy is going to sit? Where do you think bispecifics are going to have their best role? I’ll start with you, Angela.
Dr. Dispenzieri: Oh boy, I don’t know. I mean I think the strategy in myeloma is earlier is better for everything and that’s the way perhaps you’re going to cure people, but I just don’t know. Do you do everything kind of at once and sort of use everything up or what’s the intelligent way to go about it? I like them a lot in the relapse setting in truth because they are so convenient in the sense of off the shelf, but it’s hard for me to predict what the next 10 years are going to bring, 10, 15 years are going to bring.
Dr. Martin: But it’s exciting.
Dr. Dispenzieri: It is. Oh, without a doubt. Oh, it’s amazing. I mean it’s a good problem. I tell patients, the good news is there are a lot of options. The bad news, there are a lot of options because you can’t be dogmatic. You can’t say, we’re going to do this, because this is the answer because so much is changing.
Dr. Martin: How about you? What do you think?
Dr. Chari: I think one of the challenges is currently we only have single-arm studies. For the ability for drugs to move up, you need to understand relative to control arm what the value add is. If we look at examples of drugs that moved very quickly upfront, daratumumab is a great example. Very easy, predictable toxicities, very combinable, so it blew upfront. Carfilzomib still doesn’t have a frontline indication, and it just shows the complexity of the dosing, the schedule. I think where I see bispecifics going up very early is the unmet needs. So extramedullary, renal failure, high risk, areas where our current drugs are not enough. Those will get moved much faster. But for the standard risk, I think we need that randomized data to make sure, for example, that infectious deaths don’t offset any other issues.
Dr. Martin: Yeah. Any other thoughts?
Dr. Nooka: I think Ajai has mentioned before about the T-cell fitness. When is the most optimal time for the T-cell collection, probably is going to play a huge role. We may not have any data as we speak, but if we can take the surrogates, showing in the smoldering myeloma patients where the T-cell fitness is the best is after starting the treatment, even in the smoldering myeloma space where the T cells are really healthy at the eight-month or nine-month mark. I would argue this in two ways. Number one, is that related to the choice of the treatment that we make or is it related to the effect of myeloma on the T cells?
Both of them, right now, if we take the best analogy, we collect the stem cells after a brief period of induction therapy and that is a time where we have the lowest disease burden. At the same time, we probably could collect the healthiest CD34 cells for stem cell transplant in the same way. Could that be the right place where we could collect the T cells with an intent to use them at a later stage and later stage in the sense, so in the maintenance phase, there’s a huge opportunity for us to explore and expand the benefit of PFS [progression-free survival] that we are already achieving. I feel like there’s a huge amount of potential in that space in the future.
Dr. Martin: Excellent.