#EHA2026 @EHA_Hematology has just wrapped up in Stockholm. The congress delivered a strong set of hematology readouts across multiple myeloma, lymphoma, myelofibrosis and acute myeloid leukemia.
I used
@LARVOL CLIN data to identify the ten most exciting trial results discussed by oncologists on X. Here they are:
MonumenTAL-3: talquetamab plus daratumumab in relapsed/refractory multiple myeloma
MonumenTAL-3 was arguably the most important multiple myeloma readout at EHA 2026. Talquetamab plus daratumumab, with or without pomalidomide, was tested in relapsed/refractory multiple myeloma and showed a strong benefit versus daratumumab, pomalidomide and dexamethasone.
Two-year progression-free survival was 81.3% with talquetamab, daratumumab and pomalidomide, 77.6% with talquetamab and daratumumab, and 51.2% in the control arm. The PFS hazard ratios were 0.28 and 0.33 respectively. Overall survival also favoured the talquetamab-containing arms, with OS hazard ratios of 0.47 and 0.51.
The strategic message is clear: GPRC5D-directed bispecific therapy is moving earlier in the myeloma pathway. This raises important sequencing questions against BCMA-directed bispecifics, CAR-T therapy and other emerging combinations.
Pola-R-ICE: polatuzumab vedotin in second-line large B-cell lymphoma
Pola-R-ICE tested whether adding polatuzumab vedotin to R-ICE could improve outcomes in second-line large B-cell lymphoma.
The all-comer result was not a clean win. At two years, event-free survival was 26% with Pola-R-ICE versus 30% with R-ICE. However, progression-free survival was 47% versus 41%, and overall survival was 75% versus 64%.
This is the kind of readout where the headline does not tell the whole story. The trial does not establish a broad new standard for all patients, but the PFS and OS signal may remain relevant in selected patient groups. From a forecasting perspective, the key issue will be whether any subgroup signal is strong enough to influence real-world treatment behaviour.
MajesTEC-3: TECVAYLI plus DARZALEX in relapsed/refractory multiple myeloma
MajesTEC-3 delivered one of the clearest efficacy signals in relapsed/refractory multiple myeloma.
Teclistamab plus daratumumab produced a striking three-year PFS benefit versus standard daratumumab-based regimens. In standard-risk patients, three-year PFS was 87.4% versus 37.1%. In patients with high-risk cytogenetics, three-year PFS was 77.7% versus 11.5%.
This is a very strong signal for moving BCMA-directed bispecific therapy earlier in the myeloma pathway. The clinical question is increasingly shifting from “does it work?” to “how should we sequence it?” Infection management, outpatient feasibility and competition with CAR-T therapy will be central to will be central to adoption.
Beat AML / OPTI-AML: venetoclax duration in newly diagnosed AML
Beat AML / OPTI-AML addressed a highly practical question in older patients with newly diagnosed AML: can venetoclax exposure be shortened from 28 days to 14 days when combined with azacitidine?
The answer was not straightforward. Complete remission after two cycles was 43% with the 14-day venetoclax schedule versus 49% with the 28-day schedule. Non-inferiority was not met.
This matters because venetoclax-based AML therapy is widely used, and schedule optimization has major implications for cytopenias, infections, hospital burden and quality of life. The trial suggests that shortening therapy may be attractive in practice, but should not be assumed to preserve efficacy across all patients.
AJX-101: type II JAK2 inhibition in pretreated myelofibrosis
AJX-101 is an early but important signal in myelofibrosis. AJ1-11095 is a first-in-class type II JAK2 inhibitor being evaluated in patients previously treated with type I JAK2 inhibitors.
The EHA data showed no dose-limiting toxicities or adverse event-related discontinuations. Spleen volume reduction of at least 35% was seen in 65% of patients, while symptom score improvement of at least 50% was reported in 74%.
These are still early-phase data, but the mechanism is strategically interesting. The programme aims to address incomplete pathway suppression after conventional JAK inhibition. Durability, anemia effects and randomized validation will be crucial, but this is clearly a programme to watch.
HOVON 156 AML: gilteritinib versus midostaurin in frontline FLT3-mutated AML
HOVON 156 AML compared gilteritinib with midostaurin in newly diagnosed FLT3-mutated AML eligible for intensive therapy.
The trial missed its primary overall survival endpoint. Median OS was not reached in either arm, with a hazard ratio of 1.02. Event-free survival was 51.1 months versus 19.9 months, while complete remission was 79% versus 83%. Relapse after complete remission was lower with gilteritinib, at 21% versus 36%.
The result is strategically important because gilteritinib is a highly active later-line FLT3 inhibitor. However, superiority over midostaurin in frontline intensive therapy was not demonstrated. This reinforces how difficult it can be to replace an established standard, even with a mechanistically attractive next-generation agent.
SENTRY: selinexor plus ruxolitinib in JAK inhibitor-naïve myelofibrosis
SENTRY tested selinexor plus ruxolitinib in JAK inhibitor-naïve myelofibrosis.
The combination significantly improved spleen volume reduction. SVR35 was 49.8% with selinexor plus ruxolitinib versus 28.0% with ruxolitinib alone. The overall survival hazard ratio was 0.43. However, the symptom score result was less convincing, with -9.9 versus -10.9.
This is a classic myelofibrosis development dilemma: a strong spleen signal, but a more complicated positioning question if symptom improvement is not clearly differentiated. The commercial narrative will depend on whether longer follow-up can support a broader disease-modification argument.
KEYFORM-008: favezelimab plus pembrolizumab in PD-1-refractory Hodgkin lymphoma
KEYFORM-008 evaluated favezelimab plus pembrolizumab versus chemotherapy in relapsed/refractory classical Hodgkin lymphoma after PD-1 exposure.
The combination improved PFS numerically, with median PFS of 6.4 versus 5.7 months and a hazard ratio of 0.757. ORR was lower than chemotherapy, at 44.2% versus 67.7%, but duration of response was longer, at 11.0 versus 5.4 months.
Scientifically, this is an interesting signal for LAG-3 plus PD-1 biology after PD-1 failure. Commercially, the result is less straightforward. A modest PFS difference, lower response rate and programme-level development decisions all complicate the read-through.
EPCORE NHL-1: EPKINLY in relapsed/refractory large B-cell lymphoma
EPCORE NHL-1 added another important data point for epcoritamab in relapsed/refractory large B-cell lymphoma.
The trial showed an objective response rate of 59%, a complete response rate of 41%, median duration of complete response of 37.7 months, and median overall survival of 18.5 months.
These are meaningful data in a heavily pretreated lymphoma population. The key strategic point is that CD3xCD20 bispecific antibodies are now firmly established as part of the lymphoma innovation landscape. The next phase will be about combinations, earlier-line use, treatment duration and differentiation versus CAR-T therapy.
KOMET-007: ziftomenib plus 7 3 in newly diagnosed AML
KOMET-007 delivered striking early data for ziftomenib combined with intensive 7 3 chemotherapy in newly diagnosed AML with NPM1 mutation or KMT2A rearrangement.
Composite complete remission rates were 96% in NPM1-mutated AML and 90% in KMT2A-rearranged AML. MRD negativity was 83% and 82% respectively. One-year overall survival was 94% in NPM1-mutated AML and 70% in KMT2A-rearranged AML.
This is still early, non-randomized data, but the signal is impressive. Menin inhibitors are becoming one of the most interesting targeted therapy classes in AML, particularly in molecularly defined populations. The next question is whether randomized phase 3 data can confirm the magnitude and durability of benefit.
Several patterns stand out.
First, EHA 2026 reinforced the continued movement of highly active therapies into earlier treatment settings. This was particularly visible in multiple myeloma, where both MonumenTAL-3 and MajesTEC-3 point to earlier use of bispecific antibody combinations.
Second, sequencing is becoming one of the central strategic questions in hematology. In myeloma and lymphoma, clinicians increasingly have to choose between bispecific antibodies, CAR-T therapy, antibody-drug conjugates and established targeted combinations. The forecast is therefore no longer only about market share within a line of therapy, but about treatment order, eligibility, logistics and duration.
Third, AML is becoming more molecularly defined. HOVON 156, Beat AML / OPTI-AML and KOMET-007 all show different aspects of this evolution: targeted FLT3 inhibition, optimization of venetoclax-based therapy, and the emerging role of menin inhibition in NPM1-mutated and KMT2A-rearranged AML.
Fourth, myelofibrosis remains a field where spleen response, symptom benefit, anemia, survival and disease modification all need to be balanced carefully. AJX-101 and SENTRY both produced interesting signals, but both will need further validation before their full commercial relevance becomes clear.
Overall, EHA 2026 showed a hematology landscape that is becoming more precise, more competitive and more complex.
The strategic question is no longer simply whether a drug works. It is where it fits, how early it can move, how it sequences with adjacent modalities, and whether the clinical signal is strong enough to change real-world treatment behaviour.
That is where forecasting becomes difficult — and interesting.
© Robert F. Siegmund, PhD MBA | Life Code GmbH
I deliver strategic insights and product forecasting models to biopharma companies. Reach out to me!