SOHO 2025 | Immune-based strategies in AML: current limitations and novel targets being explored

Yeah, so I think we’re all trying to catch up to our lymphoma and myeloma colleagues where, you know, bispecific CAR-T have really been the biggest paradigm-changing therapies, even potentially getting incorporated in frontline therapy. So we’re trying to get there. I think unfortunately, we’ve had a lot of negative trials, trials abandoned early, trials without either efficacy or toxicity challenges. So we’re really thinking, you know, what is our next step? So I think an out-of-the-box approach. And so there are a number of novel targets. So for example, FLT3 receptor, which is not specific to the mutation, can be expressed on the surface of the majority of blasts or some bispecific trials that are ongoing and hopefully we’ll see some data in the near future. There’s also targets that are typically not ever expressed on the outside of cells. And one unique one is called cathepsin G. It’s usually only in the granules of neutrophils, but in AML patients gets extracellularly expressed. So there’s a T-cell engager therapy that has recently activated. I think in the CAR-T space, what’s gonna be needed is more out-of-the-box approaches. I really think a CAR-T that can target multiple antigens, two or even three is probably what’s needed. Because I think what we need to take off the table, if we really cover all of the surface phenotype of blasts, will we get response or not? Single antigen CAR is not enough. And so in that regard, there’s a couple of recent therapies. One is an off-the-shelf CAR-NK that targets both FLT3 and CD33 with some exciting data at AACR and expected some updated data at ASH, as well as one that we’ll be involved in soon targeting both 33 and 123. So again, these are just a couple of examples, but really different approaches are gonna be needed so that we can really have immune breakthroughs in patients with acute myeloid leukemia.

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