Lastly, even though I said BCMA is highly conserved, as with every target of every cancer, there is a possibility of resistance bilateral expression. However, a target that has been used to develop another bispecific, which is cevostamab.
Those targets include GPRC5D, against which we have bispecifics and CAR T-cell therapies, and FCRH5, which I was joking at the ASH meeting you could test the “myeloma doctor mini-mental status” with this because there are so many names to remember. However, we now have more targets for the bispecifics and the CAR T-cell therapies. “Can you use a BCMA agent, such as an ADC, before you use a CAR T-cell therapy?” And so forth, with the permutations of that. The first one is, given that BCMA has been at the forefront for targets that we developed agents against, immediately and practically, we’re facing questions about sequencing. But having said that, there are some important considerations. I think that holds true it’s not the same to talk about an ADC vs a bispecific or CAR T-cell therapy. We should be talking more about the mechanism of action. Some time ago, I used to say we shouldn’t talk about BCMA-targeting agents because that just tells you about the anchor, the target. This has proven to be an excellent target for a number of approaches. 2 But it turns out that BCMA is highly conserved in very large B cells and primarily in plasma cells and perhaps a little bit more in malignant, although the normal plasma cells do have this as part of normal signaling. This is a B-cell–specific antigen associated with signaling that normally occurs in B cells. How is utilizing the B-cell maturation antigen (BCMA) important to treating these patients? I would anticipate not quite what we have seen with CAR T-cell therapies in the areas of lymphoma, but still the possibilities are there for quite durable responses. The second is-although this is certainly not universal-with some of the immunotherapies, the duration of second or third or fourth or fifth remission might end up being as long as, if not longer than, some of the previous ones. 1 Our ability to induce long remissions is much greater than it has ever been. This still holds true to this day, but…1 is that the first remission can be significantly longer than anything that was published back in 2013.
peaks and intensity disease, but ultimately somewhat shorten the intervals between the various phases of disease control. This is relevant because that dictates essentially not just what happens because of several lines of therapy, but what we anticipate for the possibility of resistance to a specific drug. In fact, there was a meeting about a month ago with the FDA where the whole meeting was about the design of clinical trials.Ī big push at that meeting was that we should not talk about lines of therapy, but we should talk more about exposure to the various agents. More and more, we’re seeing patients in our practice who come with multiple lines of therapy, and probably more importantly now, multiple exposures to the various agents. Targeted Oncology TM: What are the latest discussion topics around the treatment of patients with relapsed/refractory multiple myeloma (RRMM)?įONSECA: this is typical for what we anticipate in a patient with multiple myeloma.
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