ESMO 2026 Gyn Cancer Slides

[Slide 1] Progression-Free Survival by BICR Sac-TMT reduced the risk of progression or death by 41%, extending median PFS by 3.3 months Pts w/ Event | Median, mo (95% CI) Sac-TMT TPC 6-mo 12-mo Percentage of Participants Median follow-up: 14.0 months Time, months No. at risk Response assessed per RECIST v1.1 by BICR. aThe observed 1-sided log-rank test P-value met the pre-specified boundary for significance (P[illegible]0.0025) at this interim analysis. Data cutoff date: March 23, 2026. Survival table Endpoint: PFS by BICR (RECIST v1.1) Arm | N | Median | Median CI Sac-TMT | 386 | 7.2 mo | 5.6–7.6 TPC | 390 | 3.9 mo | 3.7–5.3 HR: 0.59 HR CI: 0.50–0.70 P: P <0.0001 (1-sided log-rank; interim analysis) 6-mo PFS: 51.2% vs 31.9% 12-mo PFS: 29.4% vs 12.4% [Slide 2] Treatment-Related AEs With Incidence ≥15%: Hematological Grade 1 2 3 4 Sac-TMT TPC Incidence, % Anemia: Sac-TMT 62.5 | TPC 39.8 Neutropeniab: Sac-TMT 20.8 | TPC 15.3 Neutrophil count decreased: Sac-TMT 18.5 | TPC 17.2 WBC count decreased: Sac-TMT 12.5 | TPC 15.8 | Anemia (Sac-TMT, TPC) | Neutropenia (Sac-TMT, TPC) | Neutrophil count decreased (Sac-TMT, TPC) | WBC count decreased (Sac-TMT, TPC) Grade 1 | 13.0, 10.1 | 3.6, 1.4 | 1.8, 0.5 | 3.1, 2.5 Grade 2 | 28.6, 16.3 | 7.6, 4.6 | 7.8, 5.7 | 7.0, 4.1 Grade 3 | 20.3, 13.4 | 5.7, 6.3 | 6.5, 5.2 | 1.6, 6.0 Grade 4 | 0.5, 0 | 3.9, 3.0 | 2.3, 5.7 | 0.8, 3.3 aFebrile neutropenia: 2.3% with sac-TMT and 5.2% with TPC; any G-CSF use: 27% with sac-TMT vs 32% with TPC. Data cutoff date: March 23, 2026. [Slide 3] Treatment-Emergent AEs of Special Interest for Sac-TMT Crude Incidence Anemia | 71.4 | 46.6 Oral mucositis/stomatitis | 57.0 | 17.4 Neutropeniaa | 41.1 | 36.2 Ocular surface toxicityb | 30.5 | 6.8 Leukopenia | 18.2 | 19.9 Thrombocytopenia | 12.8 | 10.1 Hypersensitivity/IRR ≤2 days | 4.2 | 2.5 ILD/pneumonitis | 1.8 | 0.5 Sac-TMT | TPC Participants, % Events were based on predefined categories of preferred terms intended to capture known risks of sac-TMT regardless of attribution to treatment by the investigator. aNeutropenia included the preferred terms neutropenia, neutrophil count decreased, and febrile neutropenia. G-CSF use: 27.1% with sac-TMT vs 31.9% with TPC. bMost commonly dry eye (21.4%) and increased lacrimation (8.6%) with sac-TMT; ocular symptom assessment at each visit was protocol-mandated only in the sac-TMT group and routine assessment was not required in the TPC group. cAfter exposure adjustment, event rates were generally similar between groups, except for higher oral mucositis/stomatitis and ocular surface toxicity with sac-TMT vs TPC. Data cutoff date: March 23, 2026. [Slide 4] Treatment-Related AEs With Incidence ≥15%: Non-hematological Incidence, % Grade^a 1 2 3 Sac-TMT TPC Stomatitis 54.9 14.4 Alopecia 43.8 32.4 Nausea 35.9 28.9 Fatigue 25.9 22.6 Dry eye 18.5 3.0 Vomiting 17.7 10.4 Asthenia 17.2 12.8 Diarrhea 17.2 7.9 Grade 1: Stomatitis 28.4 7.6 | Alopecia 23.4 11.4 | Nausea 23.2 18.3 | Fatigue 12.5 11.7 | Dry eye 15.9 2.7 | Vomiting 11.7 5.2 | Asthenia 9.1 5.7 | Diarrhea 10.4 6.3 Grade 2: Stomatitis 16.7 5.2 | Alopecia 20.3 21.0 | Nausea 12.0 10.1 | Fatigue 10.2 8.7 | Dry eye 2.3 0.3 | Vomiting 4.9 4.1 | Asthenia 5.5 5.2 | Diarrhea 4.9 1.4 Grade 3: Stomatitis 9.9 1.6 | Alopecia 0 0 | Nausea 0.8 0.5 | Fatigue 3.1 2.2 | Dry eye 0.3 0 | Vomiting 1.0 1.1 | Asthenia 2.6 1.9 | Diarrhea 1.8 0.3 ^aNone of the non-hematological treatment-related AEs with incidence ≥15% were grade 4 or 5. Data cutoff date: March 23, 2026.

[Slide 1] Proffered Paper session LBA11 - Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study Speakers Domenica Lorusso (Pieve Emanuele, Italy) Lecture Time 17:18 - 17:30 Abstract Background Trophoblast cell-surface antigen 2 (TROP2) is overexpressed in endometrial cancer, making it a promising target. Sacituzumab tirumotecan (sac-TMT) is a TROP2-directed antibody-drug conjugate with a unique, bifunctional linker that stabilizes the drug-to-antibody ratio (7.4) in circulation and maximizes payload delivery to tumor cells. TroFuse-005/ENGOT-en23/GOG-3095 (NCT06132958) evaluated sac-TMT in advanced or recurrent endometrial cancer after immunotherapy. [Slide 2] Methods Eligible participants (pts) had endometrial carcinoma, including carcinosarcoma, measurable or non-measurable disease, and prior platinum and anti–PD-1/PD-L1 therapy, separately or in combination, with up to 3 total prior lines. Pts were randomized 1:1 to sac-TMT 4 mg/kg Q2W or treatment of physician's choice (TPC; doxorubicin 60 mg/m2 Q3W or paclitaxel 80 mg/m2 on days 1, 8, and 15 Q4W) until progression or unacceptable toxicity. Randomization was stratified by MMR status, TROP2 expression, prior lines of therapy, and baseline disease status. Dual primary endpoints were PFS by BICR and OS; ORR by BICR was the key secondary endpoint. [Slide 3] Results 776 pts were randomized to sac-TMT (n=386) or TPC (n=390). At data cutoff (March 23, 2026), median follow-up was 14.0 months. Statistically significant improvements in PFS (HR, 0.59 [95% CI, 0.50–0.70]; P<0.0001) and OS (HR, 0.68 [95% CI, 0.55–0.84]; P=0.0001) were observed with sac-TMT vs TPC; ORR was also significantly improved vs TPC (Table). Grade ≥3 TRAEs occurred in 54.4% of sac-TMT and 41.4% of TPC pts (Table), with anemia most common in both groups (20.8% vs 13.4%). Global health status/QoL was maintained over time in both groups. Conclusions Sac-TMT provided statistically significant and clinically meaningful improvements in PFS, OS, and ORR vs TPC in previously treated advanced or recurrent endometrial cancer with manageable safety, supporting it as a new treatment option for this population. Table: LBA11 [Slide 4] Proffered Paper session Efficacy and safety Sac-TMT N=386 | TPC N=390 Efficacy Median PFS, mo (95% CI) | 7.2 (5.6–7.6) | 3.9 (3.7–5.3) PFS HR (95% CI) | 0.59 (0.50–0.70); P<0.0001* Median PFS gain vs TPC, mo | 3.3 Median OS, mo (95% CI) | 19.0 (16.1–NR) | 12.1 (11.0–15.2) OS HR (95% CI) | 0.68 (0.55–0.84); P=0.0001* Median OS gain vs TPC, mo | 6.9 Response | N=376 | N=375 ORR, (%) | 35.1 | 17.3 ORR diff., percentage points (95% CI) | 17.8 (11.6–23.9); P<0.00001 Median DoR, mo (95% CI) | 11.1 (9.2–13.0) | 6.9 (5.4–9.1) ≥6 mo, % | 69.0 | 53.2 ≥12 mo, % | 42.9 | 35.1 Safety | N=384 | N=367 Median tx duration, wk (range) | 31.1 (0.1–96.7) | 15.0 (0.1–94.1) Any TRAE, % | 97.1 | 89.6 Grade ≥3 TRAE, % | 54.4 | 41.4 Discontinued due to TRAE, % | 3.1 | 4.9

Progression-Free Survival by BICR Sac-TMT reduced the risk of progression or death by 41%, extending median PFS by 3.3 months Pts w/ Event | Median, mo (95% CI) Sac-TMT | 70.2% | 7.2 (5.6–7.6) TPC | 73.1% | 3.9 (3.7–5.3) HR 0.59 (95% CI, 0.50–0.70) P <0.0001a 6-mo 51.2% / 31.9% 12-mo 29.4% / 12.4% Median follow-up: 14.0 months Percentage of Participants Time, months No. at risk Survival table Endpoint: PFS by BICR Arm | N | Median | Median CI Sac-TMT | 386 | 7.2 mo | 5.6-7.6 TPC | 390 | 3.9 mo | 3.7-5.3 HR: 0.59 HR CI: 0.50-0.70 P: <0.0001 6 mo: 51.2% vs 31.9% 12 mo: 29.4% vs 12.4%

[Slide 1] Progression-Free Survival by BICR Sac-TMT reduced the risk of progression or death by 41%, extending median PFS by 3.3 months 6-mo: 51.2% (Sac-TMT) | 31.9% (TPC) 12-mo: 29.4% (Sac-TMT) | 12.4% (TPC) Pts w/ Event | Median, mo (95% CI) Sac-TMT: 70.2% | 7.2 (5.6–7.6) TPC: 73.1% | 3.9 (3.7–5.3) HR 0.59 (95% CI, 0.50–0.70) P <0.0001ᵃ Median follow-up: 14.0 months Percentage of Participants Time, months No. at risk 386 300 244 186 143 101 63 38 19 13 3 0 0 390 244 163 95 52 28 18 10 6 6 2 0 0 Response assessed per RECIST v1.1 by BICR. ᵃThe observed 1-sided log-rank test P-value met the pre-specified boundary for significance (P=0.0025) at this interim analysis. Data cutoff date: March 23, 2026. Domenica Lorusso Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study Survival table Endpoint: PFS by BICR Arm | N | Median | Median CI Sac-TMT | 386 | 7.2 mo | 5.6–7.6 TPC | 390 | 3.9 mo | 3.7–5.3 HR: 0.59 HR CI: 0.50–0.70 P: <0.0001 6-mo: 51.2% vs 31.9% 12-mo: 29.4% vs 12.4% [Slide 2] Overall Survival Sac-TMT reduced the risk of death by 32%, extending median overall survival by 6.9 months 6-mo: 85.7% (Sac-TMT) | 74.8% (TPC) 12-mo: 63.4% (Sac-TMT) | 50.8% (TPC) Pts w/ Event | Median, mo (95% CI) Sac-TMT: 40.7% | 19.0 (16.1–NR) TPC: 52.3% | 12.1 (11.0–15.2) Information fraction, 67.5% HR 0.68 (95% CI, 0.55–0.84) P=0.0001ᵃ Median follow-up: 14.0 months Percentage of Participants Time, months No. at risk 386 377 360 330 290 231 166 108 77 42 14 3 1 0 390 365 323 286 240 190 132 86 56 32 13 6 1 0 ᵃThe observed 1-sided log-rank test P-value crossed the pre-specified significance boundary (P=0.00636) at this interim analysis. At this time, subsequent anticancer therapy was received by 35.0% of participants in the sac-TMT group and 49.0% in the TPC group; of those, 4.9% and 12.1%, respectively, had received ADCs. Data cutoff date: March 23, 2026. Survival table Endpoint: OS Arm | N | Median | Median CI Sac-TMT | 386 | 19.0 mo | 16.1–NR TPC | 390 | 12.1 mo | 11.0–15.2 HR: 0.68 HR CI: 0.55–0.84 P: 0.0001 6-mo: 85.7% vs 74.8% 12-mo: 63.4% vs 50.8% [Slide 3] Antitumor Activity by BICR Sac-TMT doubled the ORR and improved DCR vs TPC, with median DOR of 11.1 months DCR: 74.5% sac-TMT vs 57.3% TPC (Δ 17.2 pp; 95% CI: 10.5–23.7) Δ 17.8 pp (95% CI, 11.6–23.9) P <0.00001ᵃ Sac-TMT: 35.1% (30.3–40.2); PR: 29.0%; CR: 6.1% TPC: 17.3% (13.6–21.6); PR: 12.8%; CR: 4.5% Confirmed ORR, % ORR by Histology | Sac-TMT n/N (%) | TPC n/N (%) Non-endometrioid | 57/138 (41.3%) | 23/145 (15.9%) Endometrioid | 71/208 (34.1%) | 40/209 (19.1%) Carcinosarcoma | 4/27 (14.8%) | 2/21 (9.5%) DOR, % 6-mo: 42.9% | 35.1% 12-mo: 42.9% | 35.1% Median, mo (95% CI) Sac-TMT: 11.1 (9.2–13.0) TPC: 6.9 (5.4–9.1) Time, months No. at risk 132 128 102 75 54 32 21 9 5 2 0 0 0 65 63 41 29 16 9 7 6 4 1 0 0 0 Response assessed per RECIST v1.1 by BICR. ᵃThe observed P-value crossed the pre-specified significance boundary (P=0.025) at this interim analysis. pp, percentage points. Data cutoff date: March 23, 2026.

TroFuse-005/ENGOT-en23/GOG-3095: a Randomized Phase 3 Study Key Eligibility Criteria • Advanced or recurrent histologically confirmed diagnosis of endometrial carcinoma, including carcinosarcoma (capped at 4% by central histology) • Radiologically apparent measurable or non-measurable disease • Prior platinum exposure and prior anti-PD-1/PD-L1 exposure (given separately or in combination) in any setting, including neoadjuvant or adjuvant therapy • No more than 3 total prior lines of systemic therapy • Recurrence of endometrial cancer <12 months after completing platinum-based adjuvant therapy or regardless of platinum-free interval if received platinum or an immunotherapy-based regimen in the metastatic setting R 1:1 N=776 Sac-TMT 4 mg/kg IV Q2W TPC Doxorubicin 60 mg/m2 IV Q3Wa or Paclitaxel 80 mg/m2 IV on Days 1, 8 and 15 of each 28-day cycle PD by BICR PD by BICR Dual Primary Endpoints • PFS (BICR) • OS Secondary Endpoints • ORR (BICR) • DOR (BICR) • QoL • Safety/Tolerability Stratification Factors • MMR (deficient vs. proficient) • TROP2 expressionb (low [0 to <50% 2+/3+] vs. medium-high [≥50% 2+/3+]) • Prior lines of therapy (≤2 vs. 3) • Disease status at baseline per RECIST 1.1 assessed by BICR (measurable vs. non-measurable) [illegible]ubicin was capped at a lifetime cumulative dose of 450 mg/m2, unless continuation was consistent with institutional standard and was requested by the investigator. b% 2+/3+ [illegible] the % of tumor cells with moderate (2+) or strong (3+) membrane staining using an IHC assay (TROP2 EPR20043 Formulation Locked Assay) developed by Roche Tissue [illegible]stics. TroFuse-005/ENGOT-en23/GOG-3095 ClinicalTrials.gov identifier, NCT06132958.

CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Progression-Free Survival in Subgroups by BICR Subgroup | Number of Events/Number of Participants (%) | Hazard Ratio (95% CI) Overall | 556/776 (71.6) | 0.59 (0.50 to 0.70) Age <65 years | 259/358 (72.3) | 0.63 (0.49 to 0.81) ≥65 years | 297/418 (71.1) | 0.56 (0.44 to 0.70) Race White | 333/467 (71.3) | 0.65 (0.52 to 0.81) All Others | 167/239 (69.9) | 0.54 (0.40 to 0.74) Ethnicity Hispanic or Latino | 57/78 (73.1) | 0.93 (0.54 to 1.59) Not Hispanic or Latino | 443/626 (70.8) | 0.59 (0.48 to 0.71) ECOG Perfomance Status 0 | 282/412 (68.4) | 0.73 (0.58 to 0.93) 1 | 272/361 (75.3) | 0.47 (0.37 to 0.60) MMR Status Deficient | 89/122 (73.0) | 0.72 (0.47 to 1.09) Proficient | 467/654 (71.4) | 0.57 (0.47 to 0.69) TROP2 Expression Low | 127/159 (79.9) | 0.84 (0.60 to 1.20) Medium-High | 429/617 (69.5) | 0.54 (0.44 to 0.65) Prior Lines of Therapy ≤2 | 417/581 (71.8) | 0.56 (0.46 to 0.68) 3 | 139/194 (71.6) | 0.68 (0.49 to 0.96) Measurable Disease at Baseline Yes | 545/751 (72.6) | 0.59 (0.50 to 0.70) Histology (Local) Carcinosarcoma | 40/48 (83.3) | 1.52 (0.80 to 2.90) Endometrioid | 300/429 (69.9) | 0.56 (0.44 to 0.70) Non-Endometrioid | 213/296 (72.0) | 0.54 (0.41 to 0.72) 0.1 1 10 Sac-TMT better TPC better Response assessed per RECIST v1.1 by BICR. Data cutoff date: March 23, 2026. Domenica Lorusso Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study

[Slide 1] CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Treatment-Related AEs With Incidence ≥15%: Non-hematological Incidence, % Gradea 1 2 3 Sac-TMT TPC Stomatitis 54.9 14.4 Alopecia 43.8 32.4 Nausea 35.9 28.9 Fatigue 25.9 22.6 Dry eye 18.5 3.0 Vomiting 17.7 10.4 Asthenia 17.2 12.8 Diarrhea 17.2 7.9 | Stomatitis | Alopecia | Nausea | Fatigue | Dry eye | Vomiting | Asthenia | Diarrhea Grade 1 | 28.4 7.6 | 23.4 11.4 | 23.2 18.3 | 12.5 11.7 | 15.9 2.7 | 11.7 5.2 | 9.1 5.7 | 10.4 6.3 Grade 2 | 16.7 5.2 | 20.3 21.0 | 12.0 10.1 | 10.2 8.7 | 2.3 0.3 | 4.9 4.1 | 5.5 5.2 | 4.9 1.4 Grade 3 | 9.9 1.6 | 0 0 | 0.8 0.5 | 3.1 2.2 | 0.3 0 | 1.0 1.1 | 2.6 1.9 | 1.8 0.3 aNone of the non-hematological treatment-related AEs with incidence ≥15% were grade 4 or 5. Data cutoff date: March 23, 2026. Domenica Lorusso Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study [Slide 2] CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Treatment-Related AEs With Incidence ≥15%: Hematological Incidence, % Grade 1 2 3 4 Sac-TMT TPC Anemia 62.5 39.8 Neutropeniab 20.8 15.3 Neutrophil count decreased 18.5 17.2 WBC count decreased 12.5 15.8 | Anemia | Neutropenia | Neutrophil count decreased | WBC count decreased Grade 1 | 13.0 10.1 | 3.6 1.4 | 1.8 0.5 | 3.1 2.5 Grade 2 | 28.6 16.3 | 7.6 4.6 | 7.8 5.7 | 7.0 4.1 Grade 3 | 20.3 13.4 | 5.7 6.3 | 6.5 5.2 | 1.6 6.0 Grade 4 | 0.5 0 | 3.9 3.0 | 2.3 5.7 | 0.8 3.3 aFebrile neutropenia: 2.3% with sac-TMT and 5.2% with TPC; any G-CSF use: 27% with sac-TMT vs 32% with TPC. Data cutoff date: March 23, 2026. Domenica Lorusso Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study

[Slide 1] Proffered Paper session LBA12 - KEYNOTE-C93/GOG-3064/ENGOT-en15: Phase 3, randomized, open-label study of first-line (1L) pembrolizumab (pembro) vs carboplatin (C) + paclitaxel (P) in mismatch repair-deficient (dMMR) advanced or recurrent endometrial carcinoma (a/rEC) Speakers Brian M. Slomovitz (Miami Beach, United States of America) Lecture Time 17:42 - 17:54 Abstract Background Preferred 1L therapy for dMMR a/rEC is CP + ICI then maintenance ICI. An unmet need exists for a CTx-free option in this setting. The phase 3 KEYNOTE-C93/GOG-3064/ENGOT-en15 study (NCT05173987) assessed 1L pembro vs CP for dMMR a/rEC. [Slide 2] Methods Participants (pts) had inoperable, stage III/IV, a/rEC that was radiologically evaluable (measurable or non-measurable by investigator unless stage IVB then no evidence of disease was allowed following surgical resection) and centrally confirmed dMMR. Prior systemic therapy was not allowed (except for [neo]adjuvant therapy if recurrence ≥6 mo after last dose). Pts were randomized 1:1 to pembro Q6W for 18 cycles or CP Q3W for 6 cycles. Primary endpoints were PFS by BICR and OS. QoL was assessed by EORTC QLQ-C30 global health status (GHS)/QoL scale. [Slide 3] Table: LBA12 Pembro (n = 149) | CP (n = 150) PFS Median (95% CI), mo | 38.2 (17.9–NR) | 8.4 (6.8–10.4) HR (95% CI)a | 0.57 (0.42–0.79) 36-mo rate (95% CI), % | 52.8 (44.2–60.7) | 30.0 (22.4–37.9) OS Median (95% CI), mo | NR (NR–NR) | NR (38.9–NR) HR (95% CI) | 0.77 (0.52–1.15) 36-mo rate (95% CI), % | 70.7 (62.4–77.5) | 62.0 (53.1–69.8) ORR (95% CI),b % | 64.1 (55.8–71.9) | 62.1 (53.6–70.0) CR, % | 33.8 | 26.2 PR, % | 30.3 | 35.9 DORc Median, mo | NR | 10.2 ≥24 mo, % | 77.0 | 41.3 ≥36 mo, % | 70.7 | 40.0 NR, not reached. aPrespecified statistical criterion p-value boundary of 1-sided 0.025 was met (P = 0.0002) bIn pts with measurable disease per BICR at baseline (n = 145 per arm). cIn responders with measurable disease per BICR at baseline (pembro, n = 93; CP, n = 90). [Slide 4] Results 299 pts were randomized (median follow-up, 36.5 mo). Efficacy results at the prespecified IA (data cutoff: Apr 24, 2026) are in the table. In the CP arm, 85.2% of pts with BICR PD received crossover pembro or subsequent PD-(L)1 inhibitors off study; in the pembro arm, 47.6% of pts with BICR PD received subsequent platinum CTx off study. Clinically meaningful improvement in GHS/QoL scale scores was observed from baseline to week 12 (primary time point) with pembro vs CP, with a between-group difference of 7.02 (95% CI, 2.54–11.50). Grade ≥3 treatment-related AEs occurred in 18.1% in the pembro arm and 50.7% in the CP arm, with the most common being anemia (2.0% vs 18.1%). Grade ≥3 immune-mediated AEs and infusion reactions occurred in 7.4% and 3.5%, respectively. Conclusions 1L pembro showed a statistically significant, clinically meaningful, and durable improvement in PFS and a favorable trend in OS over traditional CTx in pts with dMMR a/rEC. There were no new safety signals in either arm. Single agent pembro can be an option for this patient population.

[Slide 1] 16:30 - 18:15 Presidential Symposium III CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Phase III Trials in dMMR Endometrial Carcinoma KN-C93 GOG-3064 MMRd Pembrolizumab Carbo/Paclitaxel ENGOT-en13 DOMENICA MMRd Dostarlimab Carbo/Paclitaxel ENGOT-en9 LEAP-001 MMRd and MMRp Pembrolizumab+ Lenvatinib Carbo/Paclitaxel Is chemo only an adequate control Arm? Christian Marth Invited Discussant LBA12 [Slide 2] 16:30 - 18:15 Presidential Symposium III CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Pembrolizumab +/- Chemotherapy in First-line MMRd Endometrial Cancer: 24 months PFS NRG- GY018 Time from randomization (months) KN C93 Progression-Free Survival, % Time, mo 35 patients progress irrespective any treatment +24 patients without progression with chemo plus pembro or pembro alone 31 patients treated with chemo or pembro or combination without progression Chemo plus pembro: +10 patients without progression at 24 months Ramez N. Eskander et al. Nature Medicine 2025; Brian M. Slomovitz et al. ESMO 2026 Christian Marth Invited Discussant LBA12 [Slide 3] 16:30 - 18:15 Presidential Symposium III CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH MMRd is not the target, but a predictive factor for better immune-response MMRd EC is not a homogeneous group: - ORR in TMB-low MMRd EC: 23% vs. 46% in TMB-high (Dostarlimab in Garnet-Trial)1 - Immune predictors of response to immune checkpoint inhibitors2: High Tinf cluster (21%): 100% ICI-Responder Intermediate Tinf (62%): 87% ICI-Responder Desert cluster (28%): 13% ICI-Responder - Low WES-Aneuploidy score (W-AS) as predictive biomarker for Atezolizumab in MMRd population and AtTEnd-trial3 - Promoter-hypermethylation vs. mutation–associated MMRd (Lynch and pseudo-Lynch) differ in prognosis and pembrolizumab response4 1. Oaknin et al. ESMO 2021, 2. Grau Bejar JF, Alexandra Leary, et al. Journal for ImmunoTherapy of Cancer 2024; 3. Luca Mazzarella et al. ESMO 2025; 4. Michael D. Toboni, et al. Gynecologic Oncology 2023 Christian Marth Invited Discussant LBA12 [Slide 4] 16:30 - 18:15 Presidential Symposium III CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Take home messages - “KN C93 suggest pembrolizumab monotherapy can be a clinically relevant, chemotherapy-free, first-line treatment option for patients with dMMR advanced or recurrent endometrial carcinoma who prioritize tolerability and quality of life” ©BS - IO plus chemo results in better oncological outcome than pembro alone but with the price of a higher toxicity - Translational research should focus on identification of primary pembrolizumab-resistant EC - New treatment options beyond the combination with chemotherapy should be investigated to prevent early progressions and improve long-term results Christian Marth Invited Discussant LBA12

Progression-Free Survival by BICR | Events, n (%) | Median (95% CI), mo | Difference in median, mo Pembrolizumab | 69 (46.3) | 38.2 (17.9–NR) | 29.8 Carbo + Pac | 94 (62.7) | 8.4 (6.8–10.4) HR, 0.57 (95% CI, 0.42–0.79) P = 0.0002a 24-mo rate 55.4% / 31.0% 36-mo rate 52.8% / 30.0% Progression-Free Survival, % Time, mo No. at Risk Pembrolizumab Carbo + Pac • Pembrolizumab significantly improved PFS in the ITT population aThe observed 1-sided log-rank test P value successfully crossed the prespecified boundary of 0.025 at this prespecified IA. Data cutoff: April 24, 2026. Survival table Endpoint: PFS by BICR (ITT) Arm | N | Median | Median CI Pembrolizumab | 149 | 38.2 mo | 17.9-NR Carbo + Pac | 150 | 8.4 mo | 6.8-10.4 HR: 0.57 HR CI: 0.42-0.79 P: 0.0002 (1-sided) 24 mo: 55.4% vs 31.0% 36 mo: 52.8% vs 30.0%

16:30 - 18:15 Presidential Symposium III CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH Antitumor Activityᵃ and Durability of Response CR PR SDᵇ Pembrolizumab (n = 145) Carbo + Pac (n = 145) Objective Response Rate: Pembrolizumab 64.1 (55.8–71.9) [49 (33.8%); 44 (30.3%)] | Carbo + Pac 62.1 (53.6–70.0) [38 (26.2%); 52 (35.9%)] Disease Control Rate: Pembrolizumab 70.3 (62.2–77.6) | Carbo + Pac 69.0 (60.8–76.4) Response Rate (95% CI), % Pembrolizumab (n = 93) | Carbo + Pac (n = 90) Median DOR (range), mo: NR (2.0+ to 40.7+) | 10.2 (1.9+ to 43.8+) ≥24 mo: 77.0% | 41.3% ≥36 mo: 70.7% | 40.0% Duration of Response, % Time, mo No. at Risk Pembrolizumab: 93 85 76 69 61 42 15 0 0 Carbo + Pac: 90 56 40 36 32 19 8 2 0 "+" indicates no PD by the time of last disease assessment. ᵃORR and DCR were assessed in participants with measurable disease per BICR at baseline; DOR was assessed in responders with measurable disease per BICR at baseline. ᵇIncluded participants with SD for ≥24 weeks. Data cutoff: April 24, 2026. Brian Slomovitz KEYNOTE-C93/GOG-3064/ENGOT-en15: Phase 3, randomized, open-label study of first-line (1L) pembrolizumab (pembro) vs carboplatin (C) + paclitaxel (P) in mismatch repair-deficient (dMMR) advanced or recurrent endometrial carcinoma (a/rEC) ALICANTE AUDITORIUM - HALL 6 Survival table Endpoint: Duration of response (responders) Arm | N | Median | Median CI Pembrolizumab | 93 | NR | range 2.0+ to 40.7+ Carbo + Pac | 90 | 10.2 mo | range 1.9+ to 43.8+ ≥24 mo: 77.0% vs 41.3% ≥36 mo: 70.7% vs 40.0%

1 96% of tumours were B7-H4+ and Mo-Rez responses were seen across B7-H4 expression levels 2 Cathepsin B (CTSB), which cleaves the linker, was elevated in responders 3 TOP1 expression, involved in payload sensitivity, tended to be higher in responders 4 Matrix remodelling, which enables ADC penetration into the tumour, and immune-related pathways were associated with response Legend: Mo-Rez; Linker-payload; B7-H4; Immune cell

08:30 - 10:00 Rapid oral 2: Gynaecological cancers CHAIRS: PHILIPP HARTER, CAMILLA NERO, ELS VAN NIEUWENHUYSEN Mo-Rez was associated with rapid and deep responses at the 5.8 mg/kg Q3W dose Mo-Rez 2.8 mg/kg Q3W (N=45): cORR* (95% CI): 36% (21.9, 51.2); CR: 2 (4%) patients; PR: 14 (31%) patients Mo-Rez 4.8 mg/kg Q3W (N=46): cORR* (95% CI): 57% (41.1, 71.1); CR: 4 (9%) patients; PR: 22 (48%) patients Mo-Rez 5.8 mg/kg Q3W (N=45): cORR* (95% CI): 62% (46.5, 76.2); CR: 5 (11%) patients; PR: 23 (51%) patients [Waterfall plots per dose; Y axis: Best Percent Change from Baseline in Sum of Target Lesion Diameters] Mo-Rez dose, mg/kg Q3W 2.8 4.8 5.8 mTTR, days (IQR) 80.0 (42.5, 85.5) 80.0 (43.0, 121.0) 42.0 (41.5, 50.5) mDpR†, % (IQR) −28.6 (−51.1, −11.1) −38.2 (−60.0, −21.4) −45.5 (−78.3, −27.3) Responses were observed across a range of B7-H4 expression levels (scan QR code) [Footnote small:] DCO: 30 June 2026. Efficacy analysed in all randomised patients. [rest illegible] BEHOLD-1 [logo] Vanda Salutari Mocertatug rezetecan (Mo-Rez) in patients with platinum-resistant ovarian cancer (PROC): Updated results with longer follow-up from the global BEHOLD-1 study BURGOS AUDITORIUM - HALL 3

Genes linked to ADC MoA were elevated in responders WTS used to characterise differential gene/pathway expression (all Mo-Rez dose levels combined) CTSB, responsible for cleaving the linker to release the TOP1i payload, was elevated* [Box plot: CTSB expression, log2(1+TPM); Responders (CR/PR) vs Non-responders (SD/PD/NE); p=0.02] TOP1, involved in payload sensitivity, tended to be higher† [Box plot: TOP1 expression, log2(1+TPM); Responders (CR/PR) vs Non-responders (SD/PD/NE); p=0.094] Matrix remodelling, which enables ADC penetration into the tumour, was elevated‡ [Box plot: GSVA scores; Responders (CR/PR) vs Non-responders (SD/PD/NE); p=0.00065] Nominal p-values. Data were analysed using the Wilcoxon rank-sum test. *Correlations between CTSB RNA levels and Mo-Rez response (responders, n=34; non-responders, n=35). †Correlations between TOP1 RNA levels and Mo-Rez response (responders, n=34; non-responders, n=35). ‡GSVA was applied to WTS data to analyse 29 TME signatures in Mo-Rez responders (n=34) and non-responders (n=35). ADC, antibody-drug conjugate; CR, complete response; CTSB, cathepsin B; GSVA, gene set variation analysis; MoA, mechanism of action; Mo-Rez, mocertatug rezetecan; NE, not evaluable; PD, progressive disease; PR, partial response; RNA, ribonucleic acid; SD, stable disease; TME, tumour microenvironment; TOP1, topoisomerase 1; TOP1i, topoisomerase 1 inhibitor; TPM, transcripts per million; WTS, whole-transcriptome sequencing.

[Slide 1] Interim OS: dMMR subpopulation Favourable OS trend with CP+D and CP+D+O vs CP; mOS not reached 24 months: 86.9% (CP+D+O), 82.3% (CP+D), 58.6% (CP) 36 months: 82.1% (CP+D+O), 73.4% (CP+D), 51.6% (CP) | CP (N=49) | CP+D (N=46) | CP+D+O (N=48) Events, n (%) | 24 (49.0) | 17 (37.0) | 13 (27.1) mOS (95% CI),a months | 50.2 (17.3–NR) | NR (NR–NR) | NR (NR–NR) HR (95% CI) vs CPb | | 0.57 (0.30–1.05) | 0.43 (0.21–0.83) HR (95% CI) vs CP+Db | | | 0.74 (0.35–1.51) Data maturity 37.8% Curves: Durvalumab + olaparib arm; Durvalumab arm; Control arm OS (%) ; Time since randomisation (months) 0-66 No. at risk Durvalumab + olaparib arm: 48 47 45 40 40 40 39 37 37 36 35 34 34 34 32 30 27 21 14 8 2 1 0 Durvalumab arm: 46 44 44 43 41 40 39 37 37 35 34 34 32 28 28 27 25 20 14 9 4 2 0 Control arm: 49 46 40 36 34 33 29 27 25 25 25 23 22 22 22 21 16 14 9 5 3 0 0 Footnote (small, partly blurred): Prespecified exploratory analysis. The median (range) duration of follow-up in dMMR patients censored for OS was 52.1 months [range partly illegible] in the control arm, 52.1 months [range partly illegible] in the durvalumab arm and 52.2 months [range partly illegible] in the durvalumab + olaparib arm. OS rates were estimated by the Kaplan-Meier method. aCI for median OS derived based on the Brookmeyer-Crowley method; bThe HRs and CIs were estimated from an unstratified Cox proportional hazards model. Shannon N. Westin Survival table Endpoint: Interim overall survival, dMMR subpopulation (prespecified exploratory) Arm | N | Median | Median CI CP (control) | 49 | 50.2 mo | 17.3–NR CP+D (durvalumab) | 46 | NR | NR–NR CP+D+O (durvalumab + olaparib) | 48 | NR | NR–NR HR: CP+D vs CP 0.57; CP+D+O vs CP 0.43; CP+D+O vs CP+D 0.74 HR CI: 0.30–1.05; 0.21–0.83; 0.35–1.51 Landmark rates: 24 months: CP+D+O 86.9% | CP+D 82.3% | CP 58.6% 36 months: CP+D+O 82.1% | CP+D 73.4% | CP 51.6% [Slide 2] TFST: ITT population (secondary endpoint) Favourable mTFST with CP+D and CP+D+O vs CP | CP (N=241) | CP+D (N=238) | CP+D+O (N=239) Events, n (%) | 190 (78.8) | 168 (70.6) | 159 (66.5) mTFST (95% CI),a months | 10.8 (10.2–12.7) | 13.6 (11.3–16.6) | 21.4 (18.1–30.2) HR (95% CI) vs CPb | | 0.79 (0.64–0.97) | 0.61 (0.49–0.75) Data maturity 72.0% Curves: Durvalumab + olaparib arm; Durvalumab arm; Control arm Patients free from first subsequent therapy or death (%) ; Time since randomisation (months) 0-69 No. at risk Durvalumab + olaparib arm: 239 229 210 184 167 147 132 116 107 102 97 88 82 75 70 65 49 40 28 16 9 3 1 0 Durvalumab arm: 238 221 204 170 123 107 95 85 81 74 67 64 63 58 55 55 49 36 21 14 8 4 0 0 Control arm: 241 226 200 147 108 82 69 61 55 53 51 47 45 42 38 35 29 23 14 7 3 2 1 0 mTFST, median time from randomisation to first subsequent therapy or death. TFST rates were estimated by the Kaplan-Meier method. aCI for median TFST derived based on the Brookmeyer-Crowley method; bThe HRs were estimated from a stratified Cox proportional hazards model. The CI was calculated using a profile likelihood approach. Shannon N. Westin Survival table Endpoint: Time to first subsequent therapy or death (TFST), ITT, secondary endpoint Arm | N | Median | Median CI CP (control) | 241 | 10.8 mo | 10.2–12.7 CP+D | 238 | 13.6 mo | 11.3–16.6 CP+D+O | 239 | 21.4 mo | 18.1–30.2 HR: CP+D vs CP 0.79; CP+D+O vs CP 0.61 HR CI: 0.64–0.97; 0.49–0.75 [Slide 3] Interim OS: ITT population (key secondary endpoint) Clinically meaningful improvement in mOS of 11.5 months with CP+D+O vs CP Favourable OS trend for CP+D vs CP 24 months: 71.4% (CP+D+O), 64.0% (CP+D), 61.1% (CP) 36 months: 63.4% (CP+D+O), 55.5% (CP+D), 52.0% (CP) | CP (N=241) | CP+D (N=238) | CP+D+O (N=239) Events, n (%) | 136 (56.4) | 123 (51.7) | 115 (48.1) mOS (95% CI),a months | 39.6 (30.3–49.2) | 40.7 (34.7–57.9) | 51.1 (44.2–NR) HR (95% CI) vs CPb | | 0.87 (0.68–1.11) p=0.259 | 0.77 (0.60–0.98) p=0.037 HR (95% CI) vs CP+Db | | | 0.87 (0.67–1.12) p=0.282 Overall data maturity 52.1% Curves: Durvalumab + olaparib arm; Durvalumab arm; Control arm OS (%) ; Time since randomisation (months) 0-69 No. at risk Durvalumab + olaparib arm: 239 234 227 209 204 193 180 174 162 157 150 146 139 131 125 117 96 71 46 31 13 6 2 0 Durvalumab arm: 238 228 222 206 194 185 171 152 144 137 131 126 121 114 106 104 93 75 54 32 14 4 0 0 Control arm: 241 229 215 201 186 173 157 147 140 132 130 124 119 114 109 106 82 63 41 23 11 5 1 0 OS rates were estimated by the Kaplan-Meier method. aCI for median OS derived based on the Brookmeyer-Crowley method; bThe HRs were estimated from a stratified Cox proportional hazards model. The CI was calculated using a profile likelihood approach. P-values were calculated using a stratified log-rank test. Two-sided significance levels were 0.0184 (CP+D vs CP) and 0.0165 (CP+D+O vs CP). Shannon N. Westin Survival table Endpoint: Interim overall survival, ITT (key secondary endpoint) Arm | N | Median | Median CI CP (control) | 241 | 39.6 mo | 30.3–49.2 CP+D | 238 | 40.7 mo | 34.7–57.9 CP+D+O | 239 | 51.1 mo | 44.2–NR HR: CP+D vs CP 0.87; CP+D+O vs CP 0.77; CP+D+O vs CP+D 0.87 HR CI: 0.68–1.11; 0.60–0.98; 0.67–1.12 P: CP+D vs CP p=0.259; CP+D+O vs CP p=0.037; CP+D+O vs CP+D p=0.282 Landmark rates: 24 months: CP+D+O 71.4% | CP+D 64.0% | CP 61.1% 36 months: CP+D+O 63.4% | CP+D 55.5% | CP 52.0% [Slide 4] Conclusions • DUO-E met its dual primary PFS endpoints, leading to regulatory approvals for CP + durvalumab followed by durvalumab and CP + durvalumab followed by durvalumab + olaparib for advanced/recurrent EC • At this second interim OS analysis, statistical significance was not met, however: – OS was favourable with CP+D vs CP in the ITT and dMMR populations – There were clinically meaningful mOS improvements with CP+D+O vs CP of 11.5 and 8.0 months in the ITT and pMMR populations, respectively, and a favourable OS trend in the dMMR subpopulation • Consistent benefits in TFST, TSST and TDT were observed in the ITT population with both treatment arms vs control • Safety across treatment arms continues to be generally consistent with the known profiles of each individual agent, with no new safety signals identified since DCO1 • OS will be formally retested at the final analysis Favourable DUO-E interim OS results and post-progression endpoints further support CP + durvalumab followed by durvalumab or durvalumab + olaparib as treatments for advanced/recurrent endometrial cancer Scan for: • Plain-language infographic • Slides Copies of this presentation obtained through QR code are for personal use only and may not be reproduced without written permission of the authors. Shannon N. Westin

[Slide 1] Proffered paper: Gynaecological cancers 14:45 - 16:15; Chairs: Antonio González-Martín, Vicky Makker Conclusions - DUO-E met its dual primary PFS endpoints, leading to regulatory approvals for CP + durvalumab followed by durvalumab and CP + durvalumab followed by durvalumab + olaparib for advanced/recurrent EC - At this second interim OS analysis, statistical significance was not met, however: - OS was favourable with CP+D vs CP in the ITT and dMMR populations - There were clinically meaningful mOS improvements with CP+D+O vs CP of 11.5 and 8.0 months in the ITT and pMMR populations, respectively, and a favourable OS trend in the dMMR subpopulation - Consistent benefits in TFST, TSST and TDT were observed in the ITT population with both treatment arms vs control - Safety across treatment arms continues to be generally consistent with the known profiles of each individual agent, with no new safety signals identified since DCO1 - OS will be formally retested at the final analysis Favourable DUO-E interim OS results and post-progression endpoints further support CP + durvalumab followed by durvalumab or durvalumab + olaparib as treatments for advanced/recurrent endometrial cancer Shannon N. Westin Side panel: Shannon Westin - Durvalumab (D) plus carboplatin/paclitaxel (CP) followed by D with or without olaparib (O) in advanced/recurrent endometrial cancer (a/rEC): Interim overall survival (OS) and safety from the randomised phase 3 DUO-E/GOG-3041/ENGOT-EN10 study [Slide 2] Interim OS: ITT population (key secondary endpoint) Clinically meaningful improvement in mOS of 11.5 months with CP+D+O vs CP Favourable OS trend for CP+D vs CP 24 months: 71.4% / 64.0% / 61.1% 36 months: 63.4% / 55.5% / 52.0% | CP (N=241) | CP+D (N=238) | CP+D+O (N=239) Events, n (%) | 136 (56.4) | 123 (51.7) | 115 (48.1) mOS (95% CI),a months | 39.6 (30.3-49.2) | 40.7 (34.7-57.9) | 51.1 (44.2-NR) HR (95% CI) vs CPb | | 0.87 (0.68-1.11) p=0.259 | 0.77 (0.60-0.98) p=0.037 HR (95% CI) vs CP+Db | | | 0.87 (0.67-1.12) p=0.282 Overall data maturity 52.1% Legend: Durvalumab + olaparib arm; Durvalumab arm; Control arm. OS (%); Time since randomisation (months) 0-69 No. at risk Durvalumab + olaparib arm | 239 234 227 209 204 193 180 174 162 157 150 146 139 131 125 117 96 71 46 31 13 6 2 0 Durvalumab arm | 238 228 222 206 194 185 171 152 144 137 131 126 121 114 106 104 93 75 54 32 14 4 0 0 Control arm | 241 229 215 201 186 173 157 147 140 132 130 124 119 114 109 106 82 63 41 23 11 5 1 0 OS rates were estimated by the Kaplan-Meier method. aCI for median OS derived based on the Brookmeyer-Crowley method; bThe HRs were estimated from a stratified Cox proportional hazards model. The CI was calculated using a profile likelihood approach. P-values were calculated using a stratified log-rank test. Two-sided significance levels were 0.0184 (CP+D vs CP) and 0.0165 (CP+D+O vs CP). Shannon N. Westin Survival table Endpoint: Overall survival (ITT, interim, key secondary) Arm | N | Median | Median CI CP | 241 | 39.6 mo | 30.3-49.2 CP+D | 238 | 40.7 mo | 34.7-57.9 CP+D+O | 239 | 51.1 mo | 44.2-NR HR: CP+D vs CP 0.87; CP+D+O vs CP 0.77; CP+D+O vs CP+D 0.87 HR CI: 0.68-1.11; 0.60-0.98; 0.67-1.12 P: 0.259; 0.037; 0.282 (two-sided significance levels 0.0184 CP+D vs CP and 0.0165 CP+D+O vs CP - not met) Landmark rates: 24 months: CP+D+O 71.4% | CP+D 64.0% | CP 61.1% 36 months: CP+D+O 63.4% | CP+D 55.5% | CP 52.0% [Slide 4] Interim OS: dMMR subpopulation Favourable OS trend with CP+D and CP+D+O vs CP; mOS not reached 24 months: 86.9% / 82.3% / 58.6% 36 months: 82.1% / 73.4% / 51.6% | CP (N=49) | CP+D (N=46) | CP+D+O (N=48) Events, n (%) | 24 (49.0) | 17 (37.0) | 13 (27.1) mOS (95% CI),a months | 50.2 (17.3-NR) | NR (NR-NR) | NR (NR-NR) HR (95% CI) vs CPb | | 0.57 (0.30-1.05) | 0.43 (0.21-0.83) HR (95% CI) vs CP+Db | | | 0.74 (0.35-1.51) Data maturity 37.8% Legend: Durvalumab + olaparib arm; Durvalumab arm; Control arm. OS (%); Time since randomisation (months) 0-66 No. at risk Durvalumab + olaparib arm | 48 47 45 40 40 40 39 37 37 36 35 34 34 34 32 30 27 21 14 8 2 1 0 Durvalumab arm | 46 44 44 43 41 40 39 37 37 35 34 34 32 28 28 27 25 20 14 9 4 2 0 Control arm | 49 46 40 36 34 33 29 27 25 25 25 23 22 22 22 21 16 14 9 5 3 0 0 Prespecified exploratory analysis. The median (range) duration of follow-up in dMMR patients censored for OS was 52.1 months (2.4 to 62.6) in the control arm, 52.1 months (6.7 to 55.7) in the durvalumab arm and 52.2 months (1.1 to 63.5) in the durvalumab + olaparib arm. OS rates were estimated by the Kaplan-Meier method. aCI for median OS derived based on the Brookmeyer-Crowley method; bThe HRs and CIs were estimated from an unstratified Cox proportional hazards model. Shannon N. Westin Survival table Endpoint: Overall survival, dMMR subpopulation (interim, exploratory) Arm | N | Median | Median CI CP | 49 | 50.2 mo | 17.3-NR CP+D | 46 | NR | NR-NR CP+D+O | 48 | NR | NR-NR HR: CP+D vs CP 0.57; CP+D+O vs CP 0.43; CP+D+O vs CP+D 0.74 HR CI: 0.30-1.05; 0.21-0.83; 0.35-1.51 Landmark rates: 24 months: CP+D+O 86.9% | CP+D 82.3% | CP 58.6% 36 months: CP+D+O 82.1% | CP+D 73.4% | CP 51.6%

Preliminary Efficacy in PROC • Median follow-up was 7.4 months • ORR 48% (95% CI: 27, 69); confirmed ORR 43% (95% CI: 23, 66) — 10 of 11 patients had a confirmed response – Prior PD with PARPi (n=14): ORR 43% (95% CI: 18, 71) – Prior bevacizumab (n=19): ORR 42% (95% CI: 20, 67); confirmed ORR 37% (95% CI: 16, 62) • DCR 91% (95% CI: 72, 99) • Median DOR 5.7 months (95% CI: 3.7, 9.4); median PFS 7.4 months (95% CI: 5.7, 9.3) Waterfall: Best Percentage Change From Baseline in Sum of Target Lesions, % (Dose escalation / Dose expansion) Swimmer plot legend: PR, SD, PD, PD at EOT, Ongoing, Death, PARPi discontinuation due to PD, Prior bevacizumab, Dose escalation, Dose expansion; x-axis Days *Including RECIST-evaluable patients with PROC who received INCB123667 50 mg bid orally + bevacizumab 10 mg/kg q2w intravenously in dose escalation and dose expansion.

Preliminary Efficacy in PROC • Median follow-up was 7.4 months • ORR 48% (95% CI: 27, 69); confirmed ORR 43% (95% CI: 23, 66) — 10 of 11 patients had a confirmed response – Prior PD with PARPi (n=14): ORR 43% (95% CI: 18, 71) – Prior bevacizumab (n=19): ORR 42% (95% CI: 20, 67); confirmed ORR 37% (95% CI: 16, 62) • DCR 91% (95% CI: 72, 99) • Median DOR 5.7 months (95% CI: 3.7, 9.4); median PFS 7.4 months (95% CI: 5.7, 9.3) [Waterfall plot: Best Percentage Change From Baseline in Sum of Target Lesions, %; legend Dose escalation / Dose expansion; reference lines 20 and −30; bar labels left to right: PD, PD, SD, SD, SD, SD, SD, SD, SD, SD, SD, PR, PR, PR, PR, PR, PR, PR, PR, PR, PR, PR] [Swimmer plot, x-axis Days 0–700; legend: PR, SD, PD, PD at EOT, Ongoing, Death, PARPi discontinuation due to PD, Prior bevacizumab, Dose escalation, Dose expansion] *Including RECIST-evaluable patients with PROC who received INCB123667 50 mg bid orally + bevacizumab 10 mg/kg q2w intravenously in dose escalation and dose expansion. RECIST-evaluable patients had a baseline scan and met at least 1 of the following criteria: ≥1 postbaseline scan, ≥63 days of treatment or study discontinuation. bid, twice a day; CI, confidence interval; DCR, disease control rate; DOR, duration of response; EOT, end of treatment; ORR, objective response rate; PARPi, poly(ADP-ribose) polymerase inhibitor; PD, progressive disease; PFS, progression-free [cut off]

Cyclin E1 Positivity by IHC Predicts Clinical Response and Is Associated With Improved Outcomes With Azenosertib Treatment Cyclin E1 IHC positive (n=48): waterfall, best % change from baseline; ORR in response-evaluable patients 37.2%; CCNE1 status: Amplified / Non-amplified / Not evaluable Cyclin E1 IHC positive (n=48) ORR, % (n/N; 95% CI) | 33.3 (16/48; 20.4–48.4) ORR in response-evaluable patients, % (n/N; 95% CI) | 37.2 (16/43; 23.0–53.3) Median DOR, months (95% CI) | 5.5 (4.5–15.9) Median PFS, months (95% CI) | 4.1 (2.8–6.8) Overall survival, Cyclin E1 IHC positive (n=48) vs Cyclin E1 IHC negative (n=46) Subjects at risk (0, 6?, ...): IHC positive 48 35 25 15 5 1 0; IHC negative 46 26 14 9 4 0 | Cyclin E1 IHC positive (n=48) | Cyclin E1 IHC negative (n=46) Median OS, months (95% CI) | 15.9 (8.7–21.2) | 7.5 (5.8–12.3) Events, n (%) | 31 (65) | 34 (74) Cyclin E1 positivity predicted longer OS with azenosertib Data cutoff: May 22, 2026. Fiona Simpkins, MD

[Slide 1] Where does more treatment earn its place? Three verdicts — and what each means for standard of care (SOC) TRIAL / SETTING | VERDICT | WHAT THE DATA SHOW | STANDARD-OF-CARE IMPLICATION GY020 (Stage I–II HIR dMMR, RT backbone) | Not earned | 3-y recurrence-free 73% vs 77%, P=.306. 21% stopped pembrolizumab for toxicity. OS immature; both curves superimpose at >90% at 5y. RT alone remains the standard. | RT alone remains adjuvant SOC for stage I–II HIR dMMR endometrioid EC. Pembrolizumab: no role B21 (Resected high-risk dMMR, Chemo ± RT backbone) | Earned — still descriptive | 3-y DSFS 95% vs 80%, HR 0.25, after DFS alpha was spent. Updated DFS and OS still needed. | Strengthens chemo + pembrolizumab ± RT for completely resected HR dMMR EC. ctDNA should not yet guide selection, de-escalation or intensification as SOC DUO-E (Advanced / recurrent, Chemo-IO backbone) | Durvalumab: supported in dMMR; Olaparib: unresolved | dMMR OS HR 0.57 with durvalumab; pMMR 0.95. Olaparib's increment HR 0.87 (0.89 pMMR), CI spans 1, at ~50% grade ≥3 maintenance toxicity. | dMMR: chemo + durvalumab → durvalumab remains the standard. pMMR: adding olaparib is an approved EU option on PFS; await biomarker and final OS Vicky Makker, MD [Slide 2] DUO-E: informing first-line treatment choices Durvalumab: an approved EU option for eligible advanced/recurrent dMMR endometrial cancer Durvalumab–olaparib: an approved EU option for eligible advanced/recurrent pMMR endometrial cancer Evidence shaping first-line care RUBY Part 1 ITT OS HR 0.69 (0.54–0.89) OS HR 0.32 (dMMR) / 0.79 (pMMR, CI 0.60–1.04) NRG-GY018 (OS update 2026) PFS HR 0.30 (dMMR) / 0.54 (pMMR) OS HR 0.56 (dMMR) / 0.86 (pMMR, NS) RUBY Part 2 PFS benefit, no observed OS benefit ITT OS HR 1.20 (0.81–1.78) PARP contribution not separately assessed DUO-E: established PFS benefit ITT PFS HR 0.71 (D) / 0.55 (D+O) vs CP Numerical interim OS improvement: D+O vs CP 51.1 vs 39.6 months OS HR 0.77 (0.60–0.98) P=.037 (prespecified threshold P<.0165) OS significance not yet reached Exploratory D+O versus D comparison OS HR 0.87 (0.67–1.12) pMMR OS HR 0.89 (0.67–1.16) Additional survival contribution under evaluation Maintenance grade ≥3 AEs: 49.5% with D+O vs 26.8% with D Established PFS benefit with further OS follow-up Treatment choice integrates risk to benefit assessment, MMR status, tolerability and patient preferences Mirza 2023; Powell 2024/2026; Eskander 2023/ASCO 2026; Westin 2024/ESMO 2026 LBA37; EMA. Full sources in notes. Cross-trial comparisons are descriptive. HRs with 95% CIs where shown. CP=carboplatin/paclitaxel, D=durvalumab, O=olaparib, NS=nonsignificant Vicky Makker, MD [Slide 3] Olaparib maintenance adds toxicity Maintenance recipients: D n=183; D+O n=192 Grade ≥3 AEs | Durvalumab 26.8% | Durvalumab + olaparib 49.5% AE discontinuation | 8.7% | 20.3% Grade ≥3 anemia | 0.5% | 20.3% Interruption / delay | 38.3% | 64.1% +22.7 percentage points in grade ≥3 AEs Exposure differs. Cumulative toxicity requires context. Patient-reported benefit, dose intensity and persistent toxicity are needed Maintenance recipients are a post-randomization subset. Rates are not a separately randomized maintenance comparison. Vicky Makker, MD [Slide 4] Durvalumab drives the dMMR OS benefit; olaparib's increment is modest and imprecise in both subgroups pMMR: ≈80% of patients dMMR: 54 deaths overall, 30 in active arms [two small KM curve thumbnails, text illegible] Updated OS HR (95% CI) | CP+D vs CP | CP+D+O vs CP | CP+D+O vs CP+D pMMR | 0.95 (0.73–1.24) | 0.85 (0.65–1.11) | 0.89 (0.67–1.16) 36-mo OS, Δ points (arm values) | −1.0 (52.1 → 51.1) | +6.9 (52.1 → 59.0) | +7.9 (51.1 → 59.0) dMMR | 0.57 (0.30–1.05) | 0.43 (0.21–0.83) | 0.74 (0.35–1.51) 36-mo OS, Δ points (arm values) | +21.8 (51.6 → 73.4) | +30.5 (51.6 → 82.1) | +8.7 (73.4 → 82.1) Earlier direct active-arm PFS HR (95% CI): ITT 0.78 (0.61–0.99) pMMR 0.76 (0.59–0.99) dMMR 0.97 (0.49–1.98) Olaparib's OS increment: HR 0.89 pMMR, 0.74 dMMR, neither excludes 1; no dMMR PFS increment (HR 0.97) Vicky Makker, MD Westin SN et al. J Clin Oncol 2024;42:283–99 (PFS). Westin SN et al. ESMO 2026, LBA37 (updated OS). Survival table Endpoint: Updated OS (DUO-E) by MMR status Landmark rates: 36 mo: pMMR CP 52.1 | pMMR CP+D 51.1 | pMMR CP+D+O 59.0 | dMMR CP 51.6 | dMMR CP+D 73.4 | dMMR CP+D+O 82.1

[Slide 1] R-DXd + Bevacizumab Showed Promising Antitumor Activity Confirmed ORR per RECIST Version 1.1 by BICR and Best Percentage Change From Baseline in Target Lesionsª R-DXd 4.8 mg/kg + Bev (n = 10): DCR: 100% (95% CI, 69%–100%); SD 2 (20%); PR 7 (70%); CR 1 (10%); ORR: 80% (95% CI, 44%–98%) Median (range) follow-up: 5.8 (2.6–8.8) mo R-DXd 5.6 mg/kg + Bev (n = 15): DCR: 100% (95% CI, 78%–100%); SD 7 (47%); PR 8 (53%); ORR: 53% (95% CI, 27%–79%) Median (range) follow-up: 4.1 (0.8–7.0) mo [Waterfall plot: Change From Baseline, %; 20% tumor growth; 30% tumor reduction] R-DXd 4.8 mg/kg + Bev (n = 10) | R-DXd 5.6 mg/kg + Bev (n = 15) ªIncludes participants treated on or before November 19, 2025. *Indicates that percent change from baseline in target lesion sum diameters was 0% for 1 participant in the R-DXd 5.6-mg/kg group. Data cutoff: February 3, 2026. [Slide 2] Raludotatug Deruxtecan + Bevacizumab in Participants With Platinum-Resistant Recurrent Ovarian Cancer Results for Cohort B-1 of the Phase 1b/2 REJOICE-Ovarian02 Study Ana Oaknin¹; Marta Gil-Martin²; Ora Rosengarten³; Carmen García-Duran⁴; Ronnie Shapira-Frommer⁵; Luis Manso Sánchez⁶; Linda R. Duska⁷; Antonio González Martín⁸; Susana Banerjee⁹; Justin Call¹⁰; Rebecca Redman¹¹; Bernard Doger de Spéville Uribe¹²; Paul Johannet¹³; Qing Zhao¹⁴; Sandra Re[illegible]¹⁵; Carmen Gonzalez¹⁴; Karin Yamada¹⁴; Ruth Perets¹⁶ [Affiliations, small text: Hospital Universitario Puerta de Hierro-Majadahonda, Madrid; Institut Català d'Oncologia L'Hospitalet, Barcelona; Shaare Zedek Medical Center, Jerusalem; Vall d'Hebron University Hospital / VHIO, Barcelona; Sheba Medical Center; University of Virginia School of Medicine; Cancer Center Clínica Universidad de Navarra, Madrid; Royal Marsden NHS Foundation Trust and Institute of Cancer Research, London; START Mountain Region, West Valley City, UT; The University of Louisville, Brown Cancer Center; START Madrid-FJD, Hospital Fundación Jiménez Díaz; Memorial Sloan Kettering Cancer Center, New York; Merck & Co., Inc., Rahway, NJ; Daiichi Sankyo, Inc., Basking Ridge, NJ; Rambam Health Care Campus, Haifa — partially legible] Podium: MADRID SPAIN 23-27 OCTOBER 2026

Conclusions: Torvu-Sam monotherapy in patients with PROC • Safety data from FONTANA are consistent with a TOP1i-ADC, showing a manageable safety profile of Torvu-Sam across 1.6, 2.0, and 2.4 mg/kg dose levels. • Torvu-Sam demonstrated clinically meaningful and durable efficacy across FRα expression subgroups. • ORR was robust, with deep molecular responses by ctDNA observed. • DoR and PFS results showed sustained efficacy in both FRα-high and -low expressing tumours. These encouraging FONTANA data supported the design of three Phase 3 OC studies: • TREVI-OC-01 (NCT07218809): Torvu-Sam versus mirvetuximab soravtansine in FRα-high and Torvu-Sam versus chemotherapy in FRα-low PROC. TREVI-OC-02 (NCT07851025): Torvu-Sam plus bevacizumab as 1L maintenance in HRD-negative epithelial OC. TREVI-OC-03 (NCT07816666): Torvu-Sam with or without bevacizumab as maintenance therapy in PROC. [footnote, partially cut off] ...ne; HRD, homologous recombination deficiency; OC, ovarian cancer

The reality of second-line Cervical Carcinoma in 2026 [Bar chart; y-axis Overall Survival (mo) 0-35] First-Line Therapy (recurrent or metastatic): GOG-060 (cisplatin), 2001: 6.1 GOG-0204 (cisplatin+paclitaxel), 2009: 12.0 GOG-0240 (doublet+bevacizumab), 2013: 17.0 KEYNOTE-826 (doublet+pembrolizumab), 2021: 24.4 BEATcc (doublet+bevacizumab+atezolizumab+bevacizumab [as printed]), 2023: 32.1 Second-Line (recurrent): EMPOWER (cemiplimab), 2021: 12.0 innovaTV 301 (tisotumab vedotin), 2023: 11.5 -> FDA and EMA approval Phase 3 Randomized Trial Hazard Ratio for Death: GOG-0240 0.71 (98% CI, 0.54-0.95); KEYNOTE-826 0.64 (95% CI, 0.50-0.81); BEATcc 0.68 (95% CI, 0.52-0.88); EMPOWER 0.69 (95% CI, 0.56-0.84); innovaTV 301 0.70 (95% CI, 0.54-0.89) Objective Response Rate - %: GOG-060 31.4; GOG-0204 29.1; GOG-0240 48.0; KEYNOTE-826 68.1 in PD-L1+; BEATcc 84.0; EMPOWER 18.0 in PD-L1+; innovaTV 301 17.8 Tewari K, N Eng J Med 2025; Vergote I, N Eng J Med 2024

[Slide 2] Summary and Conclusions • Sac-TMT is the first ADC to show statistically significant and clinically meaningful improvements in the dual primary endpoints of PFS and OS and the key secondary endpoint of ORR vs TPC in previously treated advanced endometrial cancer • At the pre-specified interim analysis (final formal analysis): • mPFS: 7.2 vs 3.9 months (HR 0.59 [95% CI, 0.50–0.70]; P <0.0001; Δ +3.3 months) • mOS: 19.0 vs 12.1 months (HR 0.68 [95% CI, 0.55–0.84]; P=0.0001; Δ +6.9 months) • ORR: 35.1% vs 17.3% (P <0.00001; Δ +17.8 percentage points [95% CI, 11.6–23.9]) • mDOR: 11.1 vs 6.9 months (Δ +4.2 months) • Efficacy with sac-TMT was observed across most pre-specified subgroups • Sac-TMT AEs were mostly low grade and manageable with supportive care and dose modifications, with low discontinuation rates • Stomatitis incidence and severity decreased following mitigations, including mouthwash prophylaxis • HRQoL was maintained over time with sac-TMT These findings support sac-TMT as a new standard of care for patients with endometrial cancer who have received platinum-based chemotherapy and immunotherapy and have limited effective treatment options [Slide 3] Conclusions • In KEYNOTE-C93, first-line pembrolizumab showed a statistically significant and clinically meaningful improvement in PFS and favorable quality-of-life benefit in participants with dMMR advanced or recurrent EC; HR for OS numerically favored pembrolizumab despite substantial use of subsequent ICI therapy in the carbo + pac group, but the prespecified significance criterion was not met – PFS: HR, 0.57 (95% CI, 0.42–0.79); P = 0.0002 – OS: HR, 0.77 (95% CI, 0.52–1.15); P = 0.1000 – ORR: 64.1% with pembrolizumab vs 62.1% with carbo + pac – DOR: median NR with pembrolizumab vs 10.2 months with carbo + pac • The PFS KM curves crossed at ~6 months, reflecting early disease control with carbo + pac vs long-term durable disease control with pembrolizumab • The CR rate was higher and DOR was substantially longer with pembrolizumab vs carbo + pac • The safety profile was consistent with those of each drug, with no new safety signals • Limitation: study did not evaluate against current standard of care (CT + IO) These data suggest pembrolizumab monotherapy can be a clinically relevant, chemotherapy-free, first-line treatment option that may broaden treatment choice beyond CT + IO for certain patients with dMMR advanced or recurrent EC [Slide 4] Endometrial Cancer Enters the ADC Era The Present TroFuse-005 validates the clinical activity of a Trop2 targeting Topo1i ADC in advanced endometrial cancer. The Future Target expression overlap and correlation with ADC activity are critical questions to guide future ADC selection. Side effect and safety profiles will shape patient and clinician preferences for ADCs, especially when efficacy is similar. Cross-resistance, timing, sequencing, and development of differentiated payloads remain important challenges in the ADC space. Joyce F. Liu, MD, MPH

Efficacy of elfe-D plus pumitamig Deep responses (>50% reduction) were observed across all 5 tumor types Best tumor responses (N=138†) HNSCC (n=38) | Melanoma (n=26) | HCC (n=21) | CC (n=22) | PROC (n=31) Y-axis: Best percentage change from baseline (%) *Percent change in target lesion is capped at +40% for visualization; the maximum observed % change was 105%. †All patients who received ≥1 dose of study drug and had ≥1 post-baseline efficacy assessment with evaluable SOD of target lesions. Ye Guo Elfetabart drozuntecan (Elfe-D; DB-1311/BNT324 [B7H3 ADC]) + pumitamig (PD-L1 x VEGF-A bsAb) in patients with advanced solid tumors: First results from a global phase 2 trial

[Slide 1] Pattern of failure Different histological subtypes Subtype | Study (n) | Recurrence rate | Local / pelvic | Distant (sites) | Time to recurrence Leiomyosarcoma | Gennari & Ignatov 2026 (n=155, population-based) | 47.8% of LMS metastasise | – | First met site (all uterine sarcoma): lung 68.5%, bone 25.9%, peritoneum 18.5%, liver 16.7% | – Low-grade ESS | Quan et al. 2024 (n=38, recurrent LG-ESS) | – | – | Distant mets 15.8% (lung 10.5%, liver 2.6%); multiple sites 34.2% | Median RFI 22 mo ESS incl. high-grade | Wang et al. 2018 (n=42: LG 24 / HG 16 / UUS 2) | 21.4% (9/42) | Pelvic only 66.7% | Extrapelvic only 11.1%; both 22.2% (specific sites not reported) | – Adenosarcoma | Yuan Z et al. 2019 (n=53; uterine 32) | Uterine 28.1%; overall 18.9% | Local 77.8% of uterine recurrences | Lung 11.1% of uterine recurrences | – [Slide 2] Expertise from two worlds Uterine sarcoma care belongs in a centre for gynaecological cancer AND for sarcoma [Venn diagram: Gynaecological oncology centre | Uterine sarcoma | Sarcoma centre] Pathology, imaging and surgery need both kinds of expertise IV, A | Centralisation and referral network IV, A | MDT treatment planning IV, A | Experienced team Who operates? Mostly the gynaecological oncologist; in selected cases the surgical oncologist, or both together (e.g. multivisceral or extra-pelvic resection, recurrence, metastasectomy) Where is the patient discussed? Every patient in both the sarcoma MDT and the gynaecological oncology MDT Who sits at the table? Gynaecological and surgical oncologists, medical and radiation oncologists, subspecialised radiologists and pathologists, specialist nurses Ray-Coquard I, et al. ESGO/EURACAN/GCIG guidelines for uterine sarcomas. Int J Gynecol Cancer 2024;34:1499–1521 [Slide 3] Morcellation: the strongest recommendation we have Avoid fragmentation whenever sarcoma is suspected II, A | Morcellation should always be avoided, especially with pre-operative suspicion of sarcoma (e.g. rapid growth, suspicious MRI) V, A | Patients undergoing morcellation for an apparently benign condition must be counselled on the low risk of unsuspected sarcoma 1 in 352 | women operated for presumed fibroids had an unsuspected uterine sarcoma | FDA safety communication, April 2014 * 11.4% | of sarcoma patients after hysterectomy had been morcellated | Roser E, Int J Gynecol Cancer 2023 (REGSA-NOGGO) 9.2% | tissue spillage despite intact containment bags (n=76) | Cohen SL, Curr Opin Obstet Gynecol 2016 52% vs 23% | recurrence after morcellation vs none in early LMS | Park JY, Gynecol Oncol 2011 44% vs 13% | abdominopelvic sarcomatosis at recurrence | Park JY, Gynecol Oncol 2011 ~3x | higher risk of death in LMS after morcellation (n=125) | Raspagliesi F, Gynecol Oncol 2017 (MITO) * References: Bogani G, Crit Rev Oncol Hematol 2016; Cao H, Cancer Manag Res 2019; Ebner F, J Turk Ger Gynecol Assoc 2019. * Not cited in the guideline Guideline: Ray-Coquard I, et al. Int J Gynecol Cancer 2024;34:1499–1521 [Slide 4] Histology drives the surgical plan Practical summary by subtype Subtype | Ovaries (pre-menopausal, stage I) | Uterus-sparing surgery | Surgery at recurrence Leiomyosarcoma | May be preserved (IV, C) | No | If complete resection feasible; metastasectomy in selected HG-ESS / UUS | May be preserved (IV, C) | No | Only without dissemination; consider chemo first LG-ESS | Weigh relapse risk vs QoL; BSO at recurrence (IV, B) | Highly selected, referral centre (V, C) | Repeated resection + endocrine therapy Adenosarcoma, no overgrowth | BSO without proven survival effect | Selected stage IA (V, C) | As LG-ESS Adenosarcoma with overgrowth | As high-grade sarcoma | No | As high-grade sarcoma Ray-Coquard I, et al. ESGO/EURACAN/GCIG guidelines for uterine sarcomas. Int J Gynecol Cancer 2024;34:1499–1521

1311P Clinical management and treatment tolerance in older women with advanced ovarian cancer: a multicentre real-world study (ReWiGO) A. Castelo-Loureiro1, C. Pernaut2, M. Cavanagh3, I. Gallego4, P. Ibeas5, A. Martín6, L. Furones7, A. Madariaga1, T. Zumarraga1 Medical Oncology: 1H.U. 12 de Octubre; 2H.U. Severo Ochoa; 3H.U. de Getafe; 4H.U. de Móstoles; 5H.U. del Henares; 6H.U. Infanta Leonor. Geriatrics: 7H.U. Infanta Elena. Madrid, Spain. 1 Background & Methods Older women with ovarian cancer are underrepresented in clinical trials. ReWiGO is a multicentre, retrospective, real-world study describing the clinical-geriatric profile, treatment received and treatment tolerance of older women with advanced ovarian cancer. Retrospective observational study across 7 hospitals in the Community of Madrid, Spain (2020–2025). Eligible: women aged ≥70 years with FIGO stage II–IV epithelial ovarian cancer and basic performance-status/treatment data available. Excluded: missing key treatment or comorbidity data, or non-ovarian gynaecological tumours. 2 Population (N = 102) 77.3 Mean age, years 92.2% FIGO III–IV 39.2% ECOG ≥2 28.4% Geriatric assessment (GA) documented 86.2% of the 29 patients with frailty status recorded showed some degree of frailty 3 Initial treatment 49.0% Cytoreductive surgery (50/102) 82.0% R0 resection (of those operated) 48.0% Recurrence or progression (49/102) 4 Baseline Characteristics & Geriatric Assessment Characteristic | Global | Documented (n=29) | Not documented (n=73) Age, years, median (IQR) | 76.4 (73.4–80.6) | 79.9 (74.9–82.6) | 76.0 (72.1–79.2) Age ≥80 years, n (%) | 29/102 (28.4%) | 12/29 (41.4%) | 17/73 (23.3%) ECOG ≥2, n (%) | 40/102 (39.2%) | 14/29 (48.3%) | 26/73 (35.6%) FIGO IV, n (%) | 36/102 (35.3%) | 11/29 (37.9%) | 25/73 (34.2%) High-grade serous, n (%) | 78/102 (76.5%) | 24/29 (82.8%) | 54/73 (74.0%) Any comorbidity, n (%) | 61/102 (59.8%) | 23/29 (79.3%) | 38/73 (52.1%) Frailty classified, n (%) | 29/102 (28.4%) | 29/29 (100%) | 0/73 (0%) Malnutrition or risk*, n (%) | 35/62 (56.5%) | 18/25 (72.0%) | 17/37 (45.9%) Cytoreductive surgery, n (%) | 50/102 (49.0%) | 11/29 (37.9%) | 39/73 (53.4%) Chemotherapy received, n (%) | 81/102 (79.4%) | 25/29 (86.2%) | 56/73 (76.7%) Adapted chemo schedule†, n (%) | 22/81 (27.2%) | 13/25 (52.0%) | 9/56 (16.1%) Values are n/N (%) unless noted. Documented = an explicit GA note or a professional-assigned frailty category in the chart; not a standardised pathway. *Among patients with nutritional status recorded (n=62). †Among 81 treated. GA was documented in under 3 in 10 patients and varied by centre. It was strongly linked to interventions. Outcomes associated with documented geriatric assessment Not documented (n=73) | Documented (n=29) Physical exercise: 2/73 (2.7%) vs 16/28 (57.1%); aOR 51.32 (11.76–357.29) * Nutritional intervention: 17/70 (24.3%) vs 20/28 (71.4%); aOR 6.63 (2.58–18.36) * Adapted chemo schedule: 9/56 (16.1%) vs 13/25 (52.0%); aOR 3.52 (1.14–11.19) * 5 Molecular Profile & PARP Inhibitor Use 36/102 (35.3%) of the whole cohort received single-agent PARPi maintenance Any molecular testing was available in 67/102 (65.7%); 50/102 (49.0%) had complete testing (BRCA, plus HRD if BRCA wild-type). Molecular subgroup | n/N cohort (%) | Single-agent PARPi n/N (%) BRCA mutated | 10/102 (9.8%) | 8/10 (80.0%) BRCA wt / HRD positive | 10/102 (9.8%) | 5/10 (50.0%) BRCA wt / HRD negative | 30/102 (29.4%) | 16/30 (53.3%) BRCA wt / HRD unknown | 17/102 (16.7%) | 7/17 (41.2%) BRCA untested | 35/102 (34.3%) | 0/35 (0%) Total | 102/102 (100%) | 36/102 (35.3%) PARPi use was strongly associated with the availability of any molecular testing: 36/67 (53.7%) tested vs 0/35 (0%) untested; p < 0.0001. PARP inhibitor use by molecular subgroup Single-agent PARPi | PARPi + bevacizumab BRCA mutated (n=10): 8/10 (80%); 0/10 (0%) BRCA wt / HRD+ (n=10): 5/10 (50%); 4/10 (40%) BRCA wt / HRD- (n=30): 16/30 (53%); 1/30 (3%) BRCA wt / HRD unknown (n=17): 7/17 (41%); 0/17 (0%) BRCA untested (n=35): 0/35 (0%); 0/35 (0%) 6 Toxicity: PARP Inhibitors vs Other Treatments 14/36 vs 0/17 (p=0.002) Grade ≥3 haematological toxicity: PARPi vs bevacizumab-only maintenance Grade ≥3 toxicity by treatment Grade ≥3 haematological | Grade ≥3 non-haematological PARPi (n=36): 14/36; 5/35 PARPi+Beva (n=5)*: 0/4; 3/5 Bevacizumab (n=17): 0/17; 2/17 Chemotherapy (n=81): 17/81; 14/80 PARPi vs bevacizumab-only (Fisher's exact test): grade ≥3 haematological p = 0.002 * non-haematological p = 1.000 (ns); hospitalisation p = 0.412 (ns); ED visit p = 1.000 (ns). Adverse event | PARPi (n=36) | PARPi+Beva (n=5) | Beva only (n=17) | Chemo (n=81) Grade ≥3 haematological | 14/36 (38.9%) | 0/4 (0%) | 0/17 (0%) | 17/81 (21.0%) Grade ≥3 non-haematological | 5/35 (14.3%) | 3/5 (60.0%) | 2/17 (11.8%) | 14/80 (17.5%) Hospitalisation, treatment toxicity | 7/36 (19.4%) | 0/5 (0%) | 1/17 (5.9%) | 13/81 (16.0%) ED visit, treatment toxicity | 4/36 (11.1%) | 0/5 (0%) | 1/17 (5.9%) | 15/79 (19.0%) Treatment-related death | 0/31 (0%) | 0/3 (0%) | 0/13 (0%) | 2/74 (2.7%) Denominators are patients with an evaluable record for each variable. Columns are different, non-mutually-exclusive treatment phases (a patient may contribute to more than one), not a randomised or adjusted comparison. Chemotherapy-related deaths: 2/102 (2.0%) of the whole cohort. 7 Survival & Conclusions Overall survival by frailty status Classified in 29/102 patients (exploratory). Adjusted HR by age 4.58 (1.47–14.30); log-rank p<0.001. Robust or prefrail | Frail Months from diagnosis Overall survival by cytoreductive surgery Kaplan-Meier, adjusted HR vs no surgery (age, ECOG, FIGO IV, stage I–II, comorbidity): primary 0.27 (0.07–0.75); interval 0.36 (0.17–0.75) — not causal effect estimates (see poster text). Primary surgery | Interval surgery | No cytoreductive surgery Months from diagnosis Age drove treatment decisions, not outcomes: adapted chemotherapy rose sharply from age 80 (adjusted OR 7.37, 95% CI 2.20–27.55), yet age was not significantly associated with severe toxicity (aOR 0.91, 0.55–1.48) or survival. Frailty told the opposite story: it predicted survival strongly (HR 4.58, 95% CI 1.47–14.30) but was classified in only 29 of 102 patients (28.4%). Age was always available; a more informative frailty assessment rarely was. Geriatric assessment should guide decisions age alone cannot. SURVIVAL 53 deaths; median follow-up 45.8 months. Surgery: adjusted HR 0.25; selection bias cannot be excluded. FUNCTIONAL STATUS HR 1.94. ECOG ≥2 associated with worse survival. TOXICITY 14/36 vs 0/17. Grade ≥3 haematological: PARPi vs bevacizumab-only (p = 0.002). MOLECULAR PROFILE 36/67 vs 0/35. PARPi use by any testing status (tested vs untested; p < 0.0001).

1335TiP TROY (APGOT-OV14/ENGOT-ov92): A Phase II Randomized, Open-label, Multicenter Study of Trastuzumab Deruxtecan (T-DXd) versus Investigator's Choice of Platinum-based Chemotherapy in Patients with Recurrent Ovarian Cancer Progressing after PARP Inhibitor Therapy Jung-Yun Lee, Myong-Cheol Lim, Jeong-Yeol Park, Jung Bok Lee, Angel Chao, Peng-Hui Wang, Ainhoa Madariaga Urrutia, Maria Pilar Barretina-Ginesta, Marcos Iglesias Campos, Eunyeong Yang, Alfonso Cortés-Salgado STUDY SCHEMA Key inclusion criteria • PSOC (PFI ≥ 6m) • Progressed on prior PARP inhibitor (TFIb ≤ 6m) • HER2 1+/2+/3+ (1+ with cap) • Prior 1-2 lines of platinum-based chemotherapy • High-grade serous or endometrioid ovarian, primary peritoneal or fallopian tube cancer R 1:1 Arm A: T-DXd +/- bev IV q3w Arm B: Platinum-based chemotherapy +/- bev Crossover at PD Primary endpoint • PFS (by INV) Secondary endpoint • OS • ORR DCR CBR • DoR TFST TSST PFS2 • Safety Stratification factor • HER2 IHC expression (1+ or 2+ / 3+) • Planned use of bevacizumab (yes or no) Abbreviations: TFIb, biologic agent free interval; PFI, platinum-free interval; PFS, progression free interval; INV, investigator; OS, overall survival; ORR, objective response; DCR, disease control rate; CBR, clinical benefit rate; DoR, duration of response; TFST, time to first subsequent therapy; TSST, time to second subsequent therapy ENDPOINTS Primary endpoint Investigator-assessed PFS (Progression-free survival) per RECIST v1.1 Secondary endpoints OS (Overall Survival) · ORR (Objective Response Rate) · CBR (Clinical Benefit Rate) · DoR (Duration of Response) · DCR (Disease Control Rate) · TFST (Time to First Subsequent Treatment) · TSST (Time to Second Subsequent Treatment) · PFS2 (Progression Free Survival 2) · Safety and tolerability Exploratory endpoint Circulating genomic and tumor tissue biomarkers Enrolled 16 (FPI: 26Feb2026) Participant country & Collaborative groups Republic of Korea, Spain, Taiwan, China Sponsor Severance Hospital, Yonsei University Health System · Samsung Bioepis KEY ELIGIBILITY CRITERIA Key Inclusion Criteria • Female patients aged ≥ 18 years • Histologically confirmed recurrent High-Grade Serous or High-Grade Endometrioid ovarian, fallopian tube, or primary peritoneal cancer • HER2 Expression: HER2 IHC 1+, 2+, or 3+ by local testing • Documented disease progression during or within 180 days of prior PARPi maintenance therapy (1st or 2nd line) • Platinum-free interval (PFI) > 6 months • At least one measurable lesion per RECIST 1.1 • ECOG Performance Status 0 or 1 • LVEF ≥ 50% and adequate organ/bone marrow function Key Exclusion Criteria • Primary platinum-refractory or platinum-resistant disease • Prior exposure to Topoisomerase I inhibitor-based ADCs or any other HER2-targeted therapy • History of non-infectious ILD/pneumonitis requiring steroids, active ILD. • Significant cardiovascular disease (QTcF > 470 ms) • Active or pending bowel obstruction, or active/uncontrolled infections • Active CNS metastases (stable brain metastases are allowed if asymptomatic and off steroids for ≥ 7 days) Contact: TROY_KCRN@kcrnresearch.co.kr / Protocol: Version 2.0 - 27Jun2025 ClinicalTrials.gov: NCT07340164

Background - The standard of care for PSOC has remained unchanged for over a decade, but the patient characteristics have evolved - HRD-positive patients achieve longer progression-free survival with upfront platinum chemotherapy + PARPi(1), but those who do recur demonstrate modest response rates to subsequent platinum-based therapy after PARPi maintenance (ORR= ~41.2%)(2) - Those patients with tumors that are non-HRD positive have minimal benefit to PARPi(3) and overall have poorer prognosis - Despite differential outcomes for HRD vs non-HRD positive patients, PSOC treatment algorithms remain unchanged - Given that FRα is highly expressed in high-grade serous ovarian cancer(4), and FRα-directed ADCs have demonstrated clinically meaningful monotherapy activity(5), there is the potential to redefine the PSOC treatment paradigm and address a clinically significant unmet need 1. Ray-Coquard I, et al. N Engl J Med. 2019;381(25):2416-2428. 2. Zhang N, et al. J Ovarian Res. 2024;17:55. 3. González-Martín A, et al. N Engl J Med. 2019;381(25):2391-2402. 4. Zannoni GF, et al. Int J Mol Sci. 2025;26(11):5222. 5. Matulonis UA, et al. J Clin Oncol. 2023;41(13):2436-2445. Abbreviations: Platinum-sensitive ovarian cancer (PSOC); standard of care (SOC); PARPi, poly (ADP-ribose) polymerase inhibitor; PSOC, platinum-sensitive ovarian cancer; ORR, overall response rate; MIRV, Mirvetuximab soravtansine; cORR, confirmed overall response rate. Chrisann Kyi

BEST POSTER 1291P Tumor vascular context and immune infiltration are associated with pembrolizumab response in high-grade serous ovarian cancer: spatial insights from the GINECO NeoPembrOV randomized phase II trial Laetitia Collet [...] ARCAGY GINECO CENTRE LEON BERARD ULB INSTITUT JULES BORDET INTRODUCTION / BACKGROUND RESULTS (1) Tumor-vessels colocalization is associated with an immunosuppressive tumor microenvironment (2) Tumor-vessel signature is associated with survival outcome with [illegible] (3) Combination of tumor-vessel signature and tumor-infiltrating lymphocytes (TILs) identify 4 tumor phenotypes associated with distinct outcome with pembrolizumab MATERIAL AND METHODS References and acknowledgements

[Slide 1] Primary endpoint: PFS in Arm C vs Arm A | Ola (n=46) | Ola + durva + UV1 (n=94) No. of events (%) | 34 (74) | 64 (68) Median PFS, months (95% CI) | 5.9 (5.3–8.2) | 8.7 (6.1–11.3) HR (95% CI) | 0.83 (0.68–1.01), 2-sided p=0.066 [KM curve: PFS probability vs Time (months) 0–40] No. at risk (0 / 10 / 20 / 30 / 40): Arm A: 46 / 11 / 3 / 1 / 0 Arm C: 94 / 37 / 14 / 5 / 0 In post hoc analyses, restricted mean survival time at 22 months showed a 2.5-month difference between Arms C and A (95% CI 0.1–4.9; exploratory p=0.043)* *Adjusted for HRD status and prior PARPi Trine Jakobi Nøttrup Survival table Endpoint: PFS (primary endpoint), Arm C vs Arm A Arm | N | Median | Median CI Arm A: Olaparib | 46 | 5.9 months | 5.3–8.2 Arm C: Olaparib + durvalumab + UV1 | 94 | 8.7 months | 6.1–11.3 HR: 0.83 HR CI: 0.68–1.01 P: 2-sided p=0.066 [Slide 2] Subgroup analyses: PFS in Arm C vs Arm A Legend: Ola (grey) / Ola + durva + UV1 (red) HRD negative (n=104): HR 0.73 (95% CI 0.58–0.92) No. at risk Arm C (0/10/20/30/40): 70 / 26 / 11 / 4 / 0; Arm A: [faint, partly illegible] 34 / ... No prior PARPi (n=116): HR 0.81 (95% CI 0.65–1.01) No. at risk Arm C (0/10/20/30/40): 78 / 32 / 12 / 5 / 0; Arm A: [faint, partly illegible] 38 / ... HRD positive (n=36): HR 1.19 (95% CI 0.74–1.89) No. at risk Arm C (0/10/20/30/40): 24 / 9 / 3 / 1 / 0; Arm A: [faint] 12 / ... Prior PARPi (n=24): HR 0.95 (95% CI 0.58–1.54) No. at risk Arm C (0/5/10/15/20/25): 16 / 7 / 5 / 2 / 2 / 0; Arm A: [faint] 8 / ... [Four KM panels: PFS probability vs Time (months)] Trine Jakobi Nøttrup Survival table Endpoint: PFS subgroups, Arm C (olaparib + durvalumab + UV1) vs Arm A (olaparib) HRD negative (n=104) | 104 No prior PARPi (n=116) | 116 HRD positive (n=36) | 36 Prior PARPi (n=24) | 24 [Slide 3] Secondary endpoint: PFS in Arm C vs Arm B | Ola + durva (n=48) | Ola + durva + UV1 (n=94) No. of events (%) | 37 (77) | 64 (68) Median PFS, months (95% CI) | 7.4 (5.5–8.6) | 8.7 (6.1–11.3) HR (95% CI) | 0.77 (0.51–1.14) [KM curve: PFS probability vs Time (months) 0–40; three arms] No. at risk (0 / 10 / 20 / 30 / 40): Arm A: 46 / 11 / 3 / 1 / 0 Arm B: 48 / 14 / 2 / 1 / 0 Arm C: 94 / 37 / 14 / 5 / 0 Trine Jakobi Nøttrup Survival table Endpoint: PFS (secondary endpoint), Arm C vs Arm B Arm | N | Median | Median CI Arm B: Olaparib + durvalumab | 48 | 7.4 months | 5.5–8.6 Arm C: Olaparib + durvalumab + UV1 | 94 | 8.7 months | 6.1–11.3 HR: 0.77 HR CI: 0.51–1.14 [Slide 4] DOVACC conclusions • In BRCAwt ROC, adding UV1 to PARPi (± durva) maintenance did not significantly improve PFS at the 2-sided 0.05 level • Compared with ola alone, Arms B and C were associated with increased toxicity; only vaccine complications, headache and flu-like symptoms were increased by adding UV1 to durva + ola • Although negative for the primary endpoint, subgroup analyses from DOVACC suggest a signal of effect in Arm C in the HRD– and PARPi-naïve subgroups – These results warrant further evaluation of cancer vaccines in ovarian cancer • Translational research is planned using the large collection of tissue and blood samples from patients with BRCAwt platinum-sensitive ROC treated in the academic DOVACC study – Additional treatment outcome measures, resistance mechanisms and patient selection will be investigated Trine Jakobi Nøttrup

2. Impact of HPV Screening at Home KEY ISSUE Suboptimal cervical cancer screening uptake Barriers: limited access to healthcare services, inconvenience, discomfort and inequities in screening participation. KEY INSIGHT At-home HPV self-collection showed comparable sensitivity and safety for cervical cancer screening compared to in-clinic cervical cancer screening. ESMO COMMITMENT ESMO advocates for policies that improve equitable access to high-quality screening services for HPV-related cancers. Clinical Validation of a Vaginal Cervical Cancer Screening Self-Collection Method for At-Home Use: A Nonrandomized Clinical Trial Fitzpatrick, MB. et al., JAMA Network Open (2025)

Anaplastic transformation in differentiated thyroid cancer: a national retrospective analysis from the French ENDOCAN-TUTHYREF network MADRID SPAIN 23-27 OCTOBER 2026 AIM The aim of this study was to characterize patients with differentiated thyroid cancer (DTC) who subsequently underwent anaplastic transformation and to assess their clinical outcomes using data from the French national ENDOCAN-TUTHYREF network. METHODS This retrospective multicenter study used data from the French TUTHYREF database, a national clinico-biological registry dedicated to refractory thyroid cancers. Eligible patients had: > an initial diagnosis of differentiated or poorly differentiated thyroid carcinoma at ≥18 years of age; and > subsequent histologically confirmed anaplastic transformation between 2010 and 2025. Demographic, clinical, pathological, molecular, treatment, and outcome data were collected. Overall survival (OS), defined as the time from anaplastic transformation to death from any cause or last follow-up, was estimated using the Kaplan-Meier method. RESULTS The study population comprised 69 patients, including 38 women (55%), with a median age of 72 years (range, 43-88) at the time of ATC transformation. The initial thyroid carcinoma was papillary in 51 patients (74%), follicular in 13 (19%), poorly differentiated in 3 (4%), oncocytic in 1 (1.5%), and unknown in 1 (1.5%). [remainder of Results column partly obscured/illegible] Molecular profiling data were available for 55 patients. The most frequent driver alteration was BRAF V600E (Fig. 2). Following transformation, 21 patients (30%) received cervical external beam radiotherapy, 37 (54%) received chemotherapy (doxorubicin-based in 15 and paclitaxel-based in 20), 32 (46%) received kinase inhibitors, dabrafenib plus trametinib in 24 (35%), and 12 (17%) received immune checkpoint inhibitors. After a median follow-up of 31 months, the median overall survival (OS) from anaplastic transformation was 5.3 months (95% CI, 3.4-7.8) (Fig.3). Male sex (HR 1.77, 95% CI 1.01-3.11) and an NLR ≥ 5 (HR 2.66, 95% CI 1.36-5.21) were associated with worse OS. Fig.3 Overall survival from anaplastic transformation CONCLUSION In this large national real-world cohort, anaplastic transformation was associated with extremely poor outcomes. This study provides one of the largest contemporary descriptions of patients experiencing DTC-to-ATC transformation. The increasing number of documented cases over time may reflect more frequent use of biopsy and pathological confirmation, leading to improved recognition of this rare event.

1337TiP Symbiotic-GYN-18 (GOG-3145/ENGOT-EN37/APGOT-EN6/LACOG 0426-EVA): phase 3 study of tivunatamig (PF-08634404), a PD-1/VEGF bispecific antibody, in combination with chemotherapy in patients with advanced or recurrent mismatch repair proficient endometrial cancer Kathleen Moore, Yoland Antill, Fernanda Cano Casarotto, Ramez N. Eskander, Kosei Hasegawa, Thomas J. Herzog, Jung-Yun Lee, Brian Slomovitz, David Tan, Xiaohua Wu, Ewa Kalinka, Michalis Liontos, Ibrahim Yalçin, Xia Tao, Matko Kalac, Stella Lin, Philipp Harter Background • EC is one of the most common gynecologic malignancies globally, with an estimated 434,620 women diagnosed in 2024 – Prognosis in patients with advanced/recurrent EC is typically poor – However, the 5-year OS rate in recurrent/advanced EC is ≈20%, with long-term outcomes worse for those with pMMR disease, who represent 70% to 80% of the patient population • Tivunatamig (PF-08634404) is a novel and structurally distinct PD-1/VEGF bispecific engineered with augmented VEGF inhibition and enhanced cooperative binding with PD-1 to enable robust immune activation in the tumor microenvironment (Figure 1) • When combined with chemotherapy, tivunatamig has shown promising antitumor activity and manageable safety in phase 2 NSCLC and CRC studies • Encouraging efficacy and manageable safety have also been observed in a phase 2 study involving patients with advanced/recurrent EC treated with tivunatamig (5 or 10 mg/kg) plus chemotherapy, irrespective of MMR status – The disease control rate was 100% in both the 5- and 10 mg/kg groups; the confirmed ORR was 90.9% in the 10 mg/kg group with pMMR tumors – Based on these data, the 10 mg/kg dose was selected for this study involving patients with advanced/recurrent EC Figure 1. Proposed Mechanism of Action of Tivunatamig, a Bispecific Antibody Targeting PD-1 and VEGF Study Design and Enrollment Status • Symbiotic-GYN-18 (NCT07578649) is an ongoing phase 3 study evaluating the efficacy and safety of tivunatamig plus chemotherapy vs pembrolizumab plus chemotherapy Figure 2. Symbiotic-GYN-18 Study Design Key eligibility criteria • Age ≥18 years • pMMR per central testing • Newly diagnosed stage III (with RECIST 1.1 measurable disease), stage IV, or recurrent endometrial cancer • Known p53 status • Prior adjuvant systemic anticancer therapy is allowed if relapse occurred >6 months after the last dose • ECOG performance status 0/1 • No active CNS metastases or clinically significant risk of hemorrhage/fistula R 1:1 N≈600 Tivunatamig 10 mg/kg Q3W + chemotherapy Q3W (× 6 cycles), followed by tivunatamig maintenance 10 mg/kg Q3W (total of 35 cycles) Pembrolizumab 200 mg Q3W + chemotherapy Q3W (× 6 cycles), followed by pembrolizumab maintenance 400 mg Q6W (total of 20 cycles) Primary endpoint • PFS per RECIST 1.1 assessed by BICR Key secondary endpoint • OS Other secondary endpoints • PFS by investigator • ORR • DOR • Safety • Pharmacokinetics • Immunogenicity • Patient-reported outcomes Randomization stratification factors • Geographic region (Asia vs rest of world) • Prior chemotherapy (yes vs no) • p53 status per central testing (normal vs abnormal) • The study will enroll ≈600 patients who will be randomized 1:1 to receive either tivunatamig or pembrolizumab in combination with chemotherapy • Eligibility criteria and endpoints are shown in Figure 2 • The study is currently open for enrollment – Figure 3 shows the countries and regions with active study sites Figure 3. Countries and Regions With Active and Planned Study Sites Active study sites Planned study sites Presented at ESMO Congress 2026; October 23-27, 2026; Madrid, Spain