Yeah, I think again, this is the question for the future. Menin inhibitors currently are mainly studied in the relapsed/refractory setting. We saw a couple of attempts to bring them earlier in the treatment paradigm in the upfront setting as well, either in combination with 7+3 in some trials for the fit population or HMA-VEN for the unfit population. These are all great alternatives and we have to see first how to do that in a safe manner to identify you know potential toxicity signals that we might need to be aware of...
Yeah, I think again, this is the question for the future. Menin inhibitors currently are mainly studied in the relapsed/refractory setting. We saw a couple of attempts to bring them earlier in the treatment paradigm in the upfront setting as well, either in combination with 7+3 in some trials for the fit population or HMA-VEN for the unfit population. These are all great alternatives and we have to see first how to do that in a safe manner to identify you know potential toxicity signals that we might need to be aware of. But certainly if that works out, if the combination is safe and if that combination produces high-quality responses, I think we’re gonna face a good problem to have. How do we choose between, you know, let’s say 7+3 venetoclax or 7+3 and a menin inhibitor down there on for the subset of patients that menin inhibition is relevant, obviously, NPM1 or KMT2A or any of the other more rare genetic lesions that could be potentially targeted by menin inhibition. So I think there is a lot for the future. It’s too early to be able to make any prediction or compare any of those approaches. But I think it opens up a lot of opportunity for the future.
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