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Senti Biosciences (SNTI) investor relations material
Senti Biosciences Study Update summary
Complete event summary combining all related documents: earnings call transcript, report, and slide presentation.Study background and rationale
Senti 202/SENTI-202 is a first-in-class, off-the-shelf logic-gated CAR-NK cell therapy targeting CD33 or FLT3 with a NOT gate for endomucin, designed to selectively kill AML cells while sparing healthy cells.
The therapy addresses the challenge of finding clean targets in AML by using logic gates to enhance selectivity and reduce toxicity.
Senti 202 includes a calibrated release IL-15 to boost NK cell and host immune activity.
The product is manufactured from healthy adult donor NK cells, enabling rapid, scalable, allogeneic, off-the-shelf delivery.
The addressable market is broad, with potential expansion into newly diagnosed AML, pediatric AML, and myelodysplastic syndrome.
Clinical trial design and patient population
Phase 1, open-label, multinational, multicenter trial enrolled 20 heavily pretreated relapsed/refractory AML or MDS patients, including those with adverse risk genetics and poor prognosis.
Dose finding followed by expansion at the recommended phase 2 dose (RP2D) of 1.5 x 10⁹ CAR+ NK cells.
Patients had a median of 2 prior lines of therapy, with high rates of prior HCT and refractory disease.
Median age was 49, with most patients having received multiple prior lines of therapy, including chemotherapy and targeted agents.
The RP2D cohort had more heavily pretreated and refractory patients compared to dose level one.
Efficacy results
50% overall response rate (ORR) and 42% CR/CRh rate at RP2D in relapsed/refractory AML patients.
All complete remissions (CR) were MRD negative, with MRD negativity rates exceeding 80% across all response types.
Responses were rapid (median time to response 1.2 months) and durable, with estimated median duration of composite CR at 7.6 months; some responses lasted over a year.
Responses observed across diverse patient subgroups, including those with adverse risk genetics and prior refractory disease.
Efficacy was independent of FLT3 mutation status, benefiting both wild-type and mutant patients.
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