So we know that we’ve treated some patients of teclistamab on a clinical trial in smoldering myeloma, high-risk smoldering myeloma, and we presented this last year. We also know that in relapsed refractory myeloma, single-agent teclistamab, is also very effective. But the question is, how effective are they? And can you really look at the T-cell population or the immune cell population in those two extreme settings, smoldering myeloma versus relapsed refractory, and try to understand how teclistamab would work in those patients...
So we know that we’ve treated some patients of teclistamab on a clinical trial in smoldering myeloma, high-risk smoldering myeloma, and we presented this last year. We also know that in relapsed refractory myeloma, single-agent teclistamab, is also very effective. But the question is, how effective are they? And can you really look at the T-cell population or the immune cell population in those two extreme settings, smoldering myeloma versus relapsed refractory, and try to understand how teclistamab would work in those patients.
So here we’re doing single-cell RNA sequencing and TCR sequencing, looking at the spectrum of those patients, those from high-risk smoldering myeloma, those from relapsed refractory myeloma treated on teclistamab. And we’re showing data that before therapy, you can actually predict the T-cell function and the T-cell fitness of those patients and how it can actually make a difference in response and depth of response in patients receiving teclistamab, but also post-therapy, how the T-cell repertoire expands. And by doing that, you can potentially predict who will be the patient who will respond to teclistamab or potentially give them something else if you know already that they may not respond, but also giving you further evidence that if you use your best therapies, if you use immunotherapy earlier in the smoldering myeloma setting, you will probably have a deeper remission because your immune cells are actually much better and much more fit.
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