RE: Senti Bio26 May 2025 12:45
I understand why comparisons are drawn with Senti Bio’s SENTI-202 and how it stack's up against Hemogenyx’s HEMO-CAR-T, and while both are targeting AML, the similarities largely stop there. SENTI-202 is a CAR-NK therapy that uses a logic-gated design to target CD33 or FLT3, while avoiding endothelial markers like EMCN to try and spare healthy cells. It’s a clever synthetic biology approach, and in theory, it offers some tumour selectivity — but the reality is that the early results while promising on paper, come with important caveats. According to Senti’s April 2025 press release- 4 out of 7 patients achieved what they called “composite complete remission” or cCR, which likely includes patients with incomplete count recovery. That’s not the same as a deep, molecular remission or full count recovery and crucially, three of those responders went on to receive a bone marrow transplant shortly after SENTI-202. That tells you something important: the therapy on its own wasn’t considered curative, or at the very least, the clinicians felt the response wouldn’t be durable without HSCT. That’s not a criticism — bridging patients to transplant can be clinically valid — but it does suggest that SENTI-202 is functioning more as a disease-reducing tool than a stand-alone solution.
Now contrast that with Hemogenyx. While they haven’t released official efficacy data yet, we do know from public statements that the first patient treated with HEMO-CAR-T — a FLT3+ r/r AML case — is doing well three months post-infusion. That in itself is a meaningful signal, because in this population, survival beyond two or three months without active therapy is incredibly rare. Unlike Senti’s off-the-shelf CAR-NK platform, HEMO-CAR-T is an autologous, third-generation CAR-T product that targets FLT3 directly — a well-validated AML driver mutation present in some of the most aggressive and treatment-resistant disease. The FLT3 targeting approach used by Hemogenyx is not reliant on logic gates or indirect antigen filtering; it’s direct, precise, and designed to eradicate both leukemic blasts and stem cells without damaging healthy hematopoiesis, due to the selectivity of FLT3 expression.
There’s also the issue of persistence. CAR-NK therapies like SENTI-202, by their nature, are short-lived. NK cells don’t persist long in the body, and even when modified, they tend to offer short bursts of cytotoxic activity — useful for initial debulking, but unlikely to maintain long-term immune pressure on minimal residual disease. That’s probably part of the reason those patients needed transplant: once the NK cells disappear, so does the anti-leukaemic effect. CAR-T therapies, on the other hand — particularly autologous ones like HEMO-CAR-T — can persist for weeks or months, offering prolonged surveillance and the potential to achieve molecular clearance. That’s a big part of why CAR-Ts in general have been curative in other blood
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