AB Science webcast of October 16, 2025

Web-Conference AB8939 Clinical Development Update October 2025 2 Disclaimer This presentation, together with the material set forth herein, does not constitute an offer of securities for sale nor the solicitation of an offer to purchase securities in any jurisdiction. Distribution of such presentation in certain jurisdiction may constitute a breach of applicable laws and regulation. This document is solely for your information on a confidential basis and may not be reproduced, redistributed or sent, in whole or in part, to any other person, including by email or by any other means of electronic communication. In particular, neither this document nor any copy of it may be taken, transmitted or distributed, directly or indirectly, in the United States, Canada, Japan or Australia. 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Participants 3 OLIVIER HERMINE, MD, PhD Head of Haematology Department, Paris Necker and Cochin Hospital Chief Scientific Officer and Chaiman of Scientific Committee Member of the French Academy of Science AB SCIENCE MANAGEMENT AML EXPERTS ALAIN MOUSSY Co-founder and CEO LAURENT GUY Chief Financial Officer NICHOLAS SHORT, MD, PhD Associate Professor, Department of Leukemia, MD Anderson Cancer Center CHRISTIAN AUCLAIR, PharmD, PhD Professor Emeritus Cofounder and former director of the PhD program in oncology at Institut Gustave Roussy, Paris-Saclay University Former director of the biology department and CNRS UMR8113 at Ecole Normale Supérieure de Cachan/Paris-Saclay Today’s objective it to update the market on the second platform AB8939 4 (1) Collaborative programme with Assistance Publique - Hôpitaux de Paris (AP-HP) as sponsor, publicly funded as part of the "hospital-university health research " projects under the Future Investment Programme. Platform Drug / Target Therapeutic area Indication Development Stage Tyrosine Kinase Inhibitor Masitinib (Oral) Neuro- degenerative Diseases (NDD) Amyotrophic Lateral Sclerosis Phase 3 Authorized Progressive Forms of Multiple Sclerosis Phase 3 Sites initiated Alzheimer’s Disease Phase 3 Authorized Mast Cell Diseases Indolent Systemic Mastocytosis Phase 3 Initiated Mast Cell Activation Syndrome Phase 2 Initiated Blood diseases Sickle Cell Disease Phase 2 To be authorized ALDH / Microtubule AB8939 (IV) Hematology Acute Myeloid Leukemia (AML) Phase 1 Initiated AB12319 (Oral) Oncology Sarcoma, Solid Tumors Preclinical Tyrosine Kinase Inhibitor Masitinib (Veterinary) Oncology Canine Mast Cell Tumor Registered in the EU (>1M€ annual sales) Proprietary Drug Portfolio Development of AB8939, a new drug targeting ▪ Tumor cells (Tubulin disruption) And ▪ Tumor stem cells (ALDH inhibition) 5 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 6 In AML, there are several registered drugs but 70% of patients relapse and die creating a persistant unmet medical need. AML remains the most lethal leukemia in humans 1st Line AML AML treatment Complete Remission + Allogeneic stem cell transplant Survival long-term 2nd Line (RR/AML) ~ 30% Refractory / Relapse Patients eligible to high dose chemotherapy (HDC) ▪ Anthracyclines + cytarabine (3x7) Patients with specific genetic profile ▪ CD33+ : Gemtuzumab ozogamycin ▪ FLT3- ITD : Midostaurin, Quizartinib ▪ IDH1-mutated: Ivosidenib ▪ Menin inhibitors: KMT2Ar/11q23: Revumenib, Ziftomenib Relapse and death OS depending on genetic risk profile ~ 70% ▪ CD33+ : Gemtuzumab ozogamycin ▪ FLT3- ITD : Gilteritinib ▪ IDH1-mutated: Ivosidenib ▪ IDH2-mutated: Enasidenib, Olutasidenib ▪ Menin inhibitors : KMT2Ar/11q23: Revumenib, Ziftomenib ▪ High dose chemotherapy or ▪ Low dose chemotherapy or ▪ Azacitidine / venetoclax Patients ineligible to high dose chemotherapy ▪ Azacitidine Venetoclax ▪ Decitabine ▪ Glasdegib ▪ Low dose chemotherapy or Best supportive care 7 AML is a heterogenous disease with outcome highly dependent on genetic factors. TP53 mutation has a very poor prognosis, NRAS, KRAS mutant has a poor prognosis ▪ HIGH RISK TP53 MUTATION ▪ INTERMEDIATE RISK KRAS, NRAS, FLT3 ITD ▪ LOW RISK others Döhner et al. Genetic risk stratification and outcomes among treatment-naive patients with AML treated with venetoclax and azacitidine. Blood (2024) 144 (21): 2211–2222. Outcomes with Venetoclax + Azacitidine by Genetic Risk in treatment-naive AML patients 3 prognostic risk signatures, defined by the mutational status of just 4 genes *Excluding patients with t(15;17), t(8;21), inv(16), t(9;11), t(6;9),inv(3)/t(3;3). **Excluding patients with any other abnormalities listed previously. 8 MECOM has the worst prognosis in AML, with a median OS of 5.5 months (1) in relapsed or refractory setting MECOM Grimwade et al. Blood. 2010 Jul 22;116(3):354-65. doi: 10.1182/blood-2009-11-254441. Impact of cytogenetic entities recognized in 2008 WHO classification24 on survival . Survival of AML with 3q abnormality treated with AZA according to prior treatments. Survival was expressed in months and calculated using Kaplan Meier estimate. AML: acute myeloid leukemia; IC: intensive chemotherapy. Wanquet et al. Am. J. Hematol. 90:859–863, 2015. (1) Wanquet A, et al. Azacitidine treatment for patients with myelodysplastic syndrome and ac ute myeloid leukemia with chromosome 3q abnormalities. Am J Hematol. 2015 Oct;90(10):859-63. 9 AB8939 targets proliferating leukemia blasts and leukemia stem cells BLOCKING PROLIFERATING LEUKEMIA CELLS THROUGH MICROTUBULES DISRUPTION TARGETING OF LEUKEMIA CANCER STEM CELLS THOUGH ALDHS INHIBITION THIS DUAL EFFECT RESULTS IN THE DECREASE OF TUMOR RECURRENCE CANCER CELLS ARE RESISTANT TO CHEMOTHERAPY RELAPSING DUE TO PERSISTENCE OF CANCER STEM CELLS Problem in AML is recurrence of tumor This problem may be solved by the dual Moa of AB8939 ▪ Destabilizes microtubules a well kown MoA in cancer but that suffers for known drugs (taxol, taxoter, vincristine, vinblastine) from multi drug resistance and rapid metabolization ▪ AB8939 is not subjected to multidrug resistance (no PgP binding) ▪ AB8939 is not degraded by myeloperoxidase ▪ ALDH plays critical role in cancer stem cells ▪ AML cells with high ALDH activity are more resistant to chemotherapeutic agents ▪ ALDH is over-expressed in MECOM 10 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 11 In vitro, AB8939 has shown activity in Ara-C (cytarabine is one of the standard of care) resistant patients cell lines, including adverse genetic MECOM, TP53 mutated ▪ Among the blasts isolated from a cohort of 99 AML patients, ~70% are resistant to standard AraCytine-based chemotherapy ▪ Among blasts isolated from this cohort that are resistant to Ara-C, 66% remain sensitive to AB8939, including with adverse genetic (MECOM, TP53 mutated) 12 Analysis of cell lines responsive to AB8939 shows that AB8939 is effective in cell lines with TP53 muation, MECOM and complex karyotypes, when ARAC and azacitidine is not effective karyotype NUM_INCLUSIO N complex TP53 FLT3 FLT3- NPM1 IDH1 IDH2 TET2 RAS RUNx1 IKZF1 BARD1 PTPN11 DNMT3 NPM1 PHF6 NF 1 JAK2 WT1 NOTCH2 ETV6 MECOM RAD21 APC AB8939 ARAC AZA C1012 P3 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0,013 7,9 9,7 C1018 0 0 0 0 0 1 0 0 0 0 0 0 1 0 1 1 0 0 0 0 0 0 0 0,04 13,1 50 C1005-P2 0 0 0 0 0 0 1 1 1 1 1 0 0 0 0 0 0 0 0 0 1 0 0 0,05 4,1 NT C1022 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 1 0 0 0 0 0,06 >20 16,7 C1015 0 0 0 0 0 0 0 0 0 1 0 1 0 0 0 0 0 0 0 0 0 0 0 0,08 >20 39,1 C1024 0 1 0 0 0 0 0 1 0 0 0 0 0 0 0 0 1 0 0 1 0 1 0 0,12 2,3 20,4 C1028 1 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0,38 11,5 41,7 C1021 0 0 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 1 0 0 0 0 0 0,94 >20 38,5 mutations Drug sensitibity (IC50 µM) 13 In vivo in mice, in a Mecom grafted PDX model, AB8939 increased survival and has an additive effect in combination with Venetoclax (another standard of care) BLOOD CTRL AB8939 Venetoclax AB/Venetoclax 0 50 100 150 5000 10000 15000hCD33 (cell/µL) SPLEEN CTRL AB8939 Venetoclax AB/Venetoclax 0 2×105 4×105 6×105 8×105 1×106 2×1074×1076×1078×1071×108 hCD33 (cell/µL) BONE MARROW CTRL AB8939 Venetoclax AB/Venetoclax 0 1000000 2000000 3000000 4000000 hCD33 (cell/µL) C. AB8939/ Venetoclax combination allows the clearing of leukemia blasts in blood, spleen and bone marrow without adding toxicities. B. AB8939 monotherapy or combined with Venetoclax is well-tolerated: absence of any toxicity (left: weight curves) or hematotoxicity (right: hematopoietic progenitors mCD45) A. Study Design 0 10 20 30 80 90 100 110 CTRL AB8939 Venetoclax AB8939/Venetoclax Days post treatment % weight before treatment control AB8939 VENETOCLAX AB8939/VENETOCLAX 0 500 1000 1500mCD45 (cell/µL) ns ✱ ns 14 In vivo in mice, in the same Mecom PDX#C1005 model, AB8939 increased survival and has an additive effect in combination with Vidaza (another standard of care) 0 10 20 80 90 100 110 Weight Curve Days post treatment % weight before treatment AB8939/VIDAZA VIDAZA AB8939 CTRL Spleen CTRL AB8939 VIDAZA AB/VIDAZA 0 10 20 30 40 50 9092949698100 % hCD33/µL Blood CTRL AB8939 VIDAZA AB/VIDAZA 0 5 10 15 20 40 60 80 100 % hCD33/µL Bone Marrow CTRL AB8939 VIDAZA AB/VIDAZA 0.00.20.40.60.81.0 20 40 60 80 100 % hCD33/µL ControlAB8939VIDAZA AB8939/VIDAZA 0 500 1000 1500 2000mCD45/µL A. Study Design B. AB8939 monotherapy or combined with Azacytidine is well-tolerated: absence of any toxicity (left: weight curves) or hematotoxicity (right: hematopoietic progenitors mCD45) C. Treatment response ▪ AB8939/ vidaza combination allows the clearing of leukemia blasts in blood, spleen and bone marrow (C) without adding toxicities (B left panel weight). ▪ Unlike Vidaza, AB8939 does not induce any hematotoxicity (B right panel mCD45). 15 In vivo in mice, AB8939 was able to eradicate Leukemia Cancer Stem Cells in a human PDX AML animal model, which is compatible with the ALDH MoA targeting stem cells ▪ AB8939 reduced the re-occurrence of leukemia following re-transplanted of leukemia cells indicating that AB8939 treatment eradicated both leukemic blast and leukemia cancer stem cells(Step 2). ▪ AB8939 is believed to kill highly dividing blasts through microtubule disruption while it kills resting cancer Stem cells through inhibition of ALDHs. 16 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 17 Phase 1 in monotherapy has been completed and phase 1 in combination has begun Step 1 MTD* 3 DAYS AB8939 alone Step 2 MTD 14 DAYS AB8939 alone # Dose Patients DLT 1 0.9 mg/m 2 3 0 2 1.8 mg/m 2 3 0 3 3.6 mg/m 2 3 0 4 6.0 mg/m 2 3 0 5 9.0 mg/m 2 3 0 6 12.0 mg/m 2 3 0 7 16.0 mg/m 2 3 0 8 21.3 mg/m 2 4 1 MTD 3D 9 28.3 mg/m 2 3 2 Completed 28 patients randomized (some patients received several cycles at increased dose following observed clinical benefit) Step 3 MTD 14 DAYS AB8939 Combination ▪ AB8939 + Venetoclax ▪ AB8939 + Venetoclax + Azacitidine On-Going StepsCompleted 13 patients randomized # Dose Patients DLT 1 16.0 mg/m 2 7 1 2 21.3 mg/m 2 6 1 MTD 14D 18 AB8939 in monotherapy has shown activity in MECOM, based on non-clinical data and early clinical data, with long OS benefit Clinical evidence in MECOM ▪ 50% response rate in early phase 1 o 2 out of 4 patients with MECOM after 1 cycle of 3 days or 14 days AB8939 treatment below the MTD o Historical control shows 14% response rate(1) ▪ 2 patients with 18 months and 11 months OS benefit Patient ID AB8939 Best Response ES-12-001 0,9 mg/m2, 3 days Early discontinuation ES-07-001 1.8 mg/m2, 3 days, Response (BM blast from 55% to 5%) ES-07-002 16 mg/m2, 14 days Stable disease GR-04-001 16 mg/m2,14 days Response (BM blast from 13% to 3%) ▪ 50% response rate in in-vitro tests In-vitro, AB8939 was effective (IC50 of 50nM and 13nM) against 2 out of 4 patient blasts with MECOM rearrangement Non clinical in vitro evidence Drug sensitivity (IC50 µM) in MECOM Karyotype Patient ID AML type AraC AB8939 Azacitidine 1135 M0 >20 >2 49,90 1156 M0 >20 >5 >50 C1005 M1 refractory 4,1 0,05 NT C1012 M4 refractory 7,9 0,013 9,7 (1) G. Richard-Carpentier et al. Characteristics and clinical outcomes of patients with acute m yeloid leukemia with inv(3)(q21q26.2) or t(3;3)(q21;q26.2). Haematologica | 108 September 2023. 19 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 20 There is a strong rationale to combine AB8939 with Venetoclax 1. BOTH MOLECULES HAVE LOW HEMATOLOGIC TOXICITY 2. BOTH MOLECULES HAVE DIFFERENT AND COMPLEMENTARY TARGETS IN CANCER CELLS ▪ This combination is less toxic than azacitidine + venetoclax as first-line treatment for AML ▪ There is an additive, even synergistic, efficacy potential for the combination, with 3 MoA in one treatment - Venetoclax MoA is to inhibit BCL2 pathway, a protein that prevents apoptosis (progra mmed cell death) in cancer cells. BCL2 is a key factor in AML resistance, as it allows cancer cells to survive despite treatment - AB8939 is pro-aopototic, destabilizing microtubule, and would benefit fr om BCL2 inhibition to optimize apoptosis - In addition, AB8939 specifically targets cancer stem cells by inhibiting ALDH, reducing resistance to treatment and limiting the risk of relapse 21 In combination, AB8939 + Venetoclax remarkably generated responses in patients in Line 3 or 4 with high risk adverse profile, complex karyotypes, TP53, Mecom and NRAS mutation. There was no toxicity, no DLT Patient ID Treatment Line Prognostic Risk Response ES-07-301 3rd Line NRAS mutant Complete remission with incomplete hematologic recovery (CRi) ES-13-301 4th Line Complex karyotype , mecom Partial remission at D45 with no circulating blasts ES-13-302 4th Line Complex karyotype and TP53 mutation Partial remission (PR) 22 Patient 1: AB8939 (14 days, 16 mg/m²) + Venetoclax Baseline Characteristics RUNX1 with VAF del 86%. mutation RUNX1 with VAF: 9.7% mutations DNMT3A, NRAS, PRPF8, PTPN x 3 ▪ Cytogenetic, mutations details ▪ Prior treatments 74▪ Age Response Baseline D28 D49 BM Blasts 8% <1% na Blood Blasts 0% 0% 0% Neutrophils 4,4 3,6 5.2 Platelets 59 27 47 ▪ Response evaluation D28 Complete remission with incomplete hematologic recovery (CRi) Adverse▪ Cytogenetic risks category 1) Daunorubicine + cytarabine 2) Azacitidine 3) CLN-049-002 Cycle 1 (14 days) NRAS▪ Key Mutations ▪ Venetoclax dosing (mg) : D1 100, D2 200 and 400 until D8 and decreased to 100mg until D14 because of antifungal treatment ▪ Antifungal : posaconazole 23 Patient 2: AB8939 (14 days, 16 mg/m²) + Venetoclax Baseline Characteristics TET2, over expression Evi1▪ Key Mutation ▪ Cytogenetic details Complex karyotype: 45,XX,del(1)(34), add(2)(q22- 24),del(5)(q13q33), - 7,add(11)(p15),add(11)(q23),der(12)add(12)( p13)del(12)(q14q21-23),-18,- 20,add(21)(p11.2),+2mar[3]/46,XX[1] ▪ Prior treatments 1) Azacitidine 2) Cytarabin + venetoclax ; Refractory 73▪ Age ▪ FAB Classification M0 : Undifferentiated acute myeloblastic leukemia Response ▪ Response ▪ Stable disease (SD) at D28 ▪ Partial remission at D45 with no circulating blasts Adverse▪ Cytogenetic risks category Baseline D28 D45 BM Blasts 18% 23% 8% Blood Blasts 44% 12% 0% Neutrophils 1,33 1,12 1,32 Platelets 21 15 11 Cycle 1 (14 days) ▪ Venetoclax dosing (mg) : D1 50, D2 100 and 200 until D14 ▪ Antifungal : Isavuconazole (ongoing during trial) + nystatin (only D1 and after D14 for mouth health care) 24 Patient 3: AB8939 (14 days, 16 mg/m²) + Venetoclax Baseline Characteristics TP53+▪ Key Mutation ▪ Cytogenetic details Complex Karyotype 44,XY ,del(5)(q13q33),add(12)(p11.2),-13,- 16,-20,+mar1[5]/ 43,idem,add(1)(q22-24),-7,- 18,-mar1,+mar2,+mar3[15 ▪ Prior treatments 1) Idarubicin + Cytarabine : Disease progression 2) FLAG+IDA ; Refractory 3) Azacitidine+ Venetoclax ; Refractory 75▪ Age ▪ FAB Classification M2 : Acute myeloblastic leukemia with maturation Response ▪ Response evaluation D28 Partial remission (PR) Adverse▪ Cytogenetic risks category Baseline D28 BM Blasts 31% 14% Blood Blasts 4% 2% Neutrophils 1,07 0,37 Platelets 13 21 Cycle 1 (14 days) ▪ Venetoclax dosing (mg) : D1 50, D2 100 and 200 until D14 ▪ Antifungal : Mycostatin (after D14 for mouth health care) 25 AB8939 + Venetoclax could become a new standard of care in particular for AML patients with adverse genetics ▪ Venetoclax + Vidaza is the standard of care for aged patient not eligible to high dose chemotherapy in Line 1 ▪ Venetoclax + Vidaza is known to be poorly effective in TP53 and NRAS mutant ▪ AB8939 preliminary data give credit to the hypothesis that the combination AB8939+venetoclax could become a new standard of care ▪ AB8939+venetoclax is less toxic than other combinations, in particular on hematoxicity AB8939 + Venetoclax : a potentially new standard of care 26 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 27 The next step is to finish phase 1 in combination and to launch an expansion study to maximize the chance of success of a registrational study Rationale ▪ Generate robust preliminary evidence of efficacy in the AML label to support the clinical development plan and trigger partnership agreement ▪ 15 AML patients eligible to AB8939 + Venetoclax at the right dose Implementation of the expansion study 28 There are 3 possibilities of registrational studies, not mutually exclusive, that we have started to discuss with FDA and EMA AB8939 + VENETOCLAX IN LINE 1 AGED PATIENTS, ADVERSE GENETICS TP53mut+NRAS+KRAS+complex K+monosomy 5/7 + Mecom ▪ (AB8939 + Venetoclax) Vs (Venetoclax + Vidaza) =standard of care) ▪ Primary endpoint: CR+CRi ▪ Secondary endpoint: Survival ▪ 200 patients, randomized 1:1 AB8939 + VENETOCLAX IN LINE 2/3, ALL PATIENTS OR ADVERSE GENETICS L2+L3, all patients or adverse genetics ▪ AB8939+venetoclax Vs best supportive care Vs AB8939 ▪ Primary Endpoint: CR+Cri ▪ Secondary endpoint: survival ▪ 240 patients, randomized 1:1:1 AB8939 IN MECOM L2+L3 ▪ AB8939 vs best supportive care ▪ Primary Endpoint: survival ▪ Secondary endpoint: CR+Cri ▪ 80 patients, randomized 1:1 AB8939 Positioning Clinical Study Design 1 2 3 29 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 30 CHRISTIAN AUCLAIR, PharmD, PhD Professor Emeritus, Cofounder and former director of the PhD program in oncology at Institut Gustave Roussy, Paris-Saclay University Concluding Pharmacological Remarks ▪ The AB8939 molecule was initially selected based on two criteria: o i) its extreme efficacy in inhibiting proliferative tumor cells, particularly leukemic cell lines, and o ii) its extreme efficacy on cells expressing the multidrug resistance phenotype ▪ Subsequent investigations have shown that AB8939 was able to limit tumor recurrence in experimental models. This remarkable property is due to its ability to inhibit aldehyde dehydrogenase (ALDH), enzymes that provide metabolic support in tumor stem cells. ▪ This dual property makes AB8939 a molecule of choice for the treatment of refractory acute leukemia by reducing the frequency of relapses. ▪ Finally, AB8939 is a perfectly tolerated molecule characterized by a lack of bone marrow toxicity. 31 NICHOLAS SHORT, MD, PhD Associate Professor, Department of Leukemia, MD Anderson Cancer Center ▪ TP53-mutated and MECOM rearranged AML are the worst subtypes of AML ▪ In older adults treated with HMA + venetoclax, NRAS/KRAS mutations is also associated with a poor prognosis ▪ Single-agent AB8939 showed activity in MECOM ▪ AB8939 + venetoclax appears safe + and able to generate significant blast reductions in ultra-high-risk AML • Limited response with standard therapies • Median OS ~6 months, no standard of care • Median OS ~12 months • Response in 2 of 4 patients with MECOM rearrangement • For reference, in other unmet needs (e.g. KMT2Ar leukemias), CR/CRh rate of ~20% sufficient for FDA approval in single-arm study • Significant blast reductions in ultra-high-risk AML with TP53-mutated AML after HMA + venetoclax) ▪ Early data suggest that AB8939 (monotherapy and/or combination) may have significant activity in the highest risk subtypes of AML ▪ If similar responses rates and safety are observed during trial expansion, AB8939 well-positioned for development in adverse-risk AML in frontline and salvage settings 32 Medical Need in AML and AB8939 Mechanism of Actions Clinical Data - Monotherapy Non Clinical Data Clinical Data – Combination Therapy Next Steps Concluding Statements from AML Experts Market Potential and Intellectual Property 33 The objective is to position AB8939 combination treatment to be the standard of care in AML with a high risk profile adverse genetic, which represents a market size potential above EUR 2 billions per annum (1) Zhou, Y et al. Global, regional, and national burden of acute myeloid leukemia, 1990 –2021: a systematic analysis for the global burden of disease study 2021. Biomark Res 12, 101 (2024). (2) estimated (3) Estimated (4) Choi M. et al. Costs per patient achieving remission with venetoclax-based combinations i n newly diagnosed patients with acute myeloid leukemia ineligible for intensive induction chemotherapy. Journal of Managed Care & Specialty Pharmacy Volume 28, Number 9. https://doi.org/10.18553/jmcp.2022.22021 Region Incidence Case (1) % high risk profile (2) % Insured Patients (3) Drug Price (€) Market Size (per in in Mio EUR) USA / CANADA 23,700 50% 90% 100,000(5) 1 000 000 EUROPE 27,600 90% 60,000 770 000 APAC 27,800 30% 60,000 250 000 INDIA 11,000 30% 60,000 100,000 LATAM 7,200 30% 60,000 65 000 MENA 3,900 30% 60,000 35 000 TOTAL 90,200 2 200 000 ▪ Adverse genetics regroup TP53 mutant, NRAS/KRAS mutant, complex karyotype, monosomy 5 and 7, Mecom ▪ It represents around 50% of patients. ▪ These patients are refractory to or relapsing the current standard of care. Median survival is less than 12 months 34 AB8939 intellectual property rights in AML are secured until 2036 through a ‘composition of matter’ patent and 2041 with extension, and potentially until 2044 in AML with chromosome abnormality through a ‘second medical use’ patent. Orphan drug status Composition of Matter patent Protection Exclusivity period Enforcement Until February 2036 + 5 years extension ▪ Granted in the USA ▪ To be filed with EMA ▪ Granted (United States / Europe / China / Hong Kong / Japan / South Korea / India / Mexico / Israel / Brazil / South Africa / Russia / Australia) 7-year protection as of FDA approval 10-year protection as of EMA approval Second Medical Use patent Until February 2044 (if granted) ▪ PCT patent application filed for AML subpopulation with chromosome abnormality

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