Cytarabine

PRESS RELEASE AB SCIENCE REPORTS COMPLETION OF THE STEP 3 OF PHASE 1, EVALUATING THE COMBINATION OF AB8939 WITH VENETOCLAX FOR THE TREATMENT OF REFRACTORY OR RELAPSED ACUTE MYELOID LEUKEMIA THE COMBINATION OF AB8939 WITH VENETOCLAX GENERATED A 67% OVERALL RESPONSE RATE (ORR) AND A 100% DISEASE CONTROL RATE (DCR), WITH NO DOSE-LIMITING TOXICITIES (DLT) OBSERVED, IN A POOR-PROGNOSIS POPULATION WITH ADVERSE GENETICS TREATED IN THE SECOND - TO FOURTH-LINE RELAPSED OR REFRACTORY SETTING Paris, June 29, 2026, 8am CET AB Science SA (Euronext - FR0010557264 - AB) today provides an update on the Phase 1 study of the molecule AB8939 and the completion of Step 3, evaluating the combination of AB8939 + venetoclax in patients with acute myeloid leukemia (AML) associated with a very unfavorable genetic profile. Step 3 evaluated the combination of AB8939 plus venetoclax administered over a 14-day cycle. A total of six patients were treated across two dose levels of AB8939 (16 mg/m² and 21.3 mg/m²), each in combination with venetoclax. The combination was well-tolerated, with no dose-limiting toxicity (DLT) and no hematological toxicity observed at either dose level, allowing selection of the recommended Phase 2 dose (RP2D). Encouraging preliminary signs of efficacy were observed. Of the six patients treated, four achieved an objective response (one complete remission with incomplete hematologic recovery and three partial responses), corresponding to a 67% overall response rate (ORR). The two remaining patients achieved stable disease, resulting in a 100% disease control rate (CDR). These responses were achieved after a single cycle of treatment (14 days) in heavily pre-treated patients receiving second- to fourth-line therapy. Notably, two of the responding patients had previously progressed on venetoclax in combination with other chemotherapies. The patients treated all have very difficult to treat cytogenetic pro including complex karyotype, TP53 mutation, NRAS mutation, monosomy 5 and 7 and MECOM-rearrangement, that typically have a poor prognosis due to their aggressive disease course and treatment resistance This is a high response rate in a population where standard-of-care therapies achieve ORR of 10–30% in adverse-risk, multiply pre-treated AML (Gill H, et al. Cancer Med. 2020;9(10):3371-3382). Response after the first 14 days cycle in the six patients treated in Step 3 (AB8939 + venetoclax) Patient AB8939 dose Line of therapy Key adverse genetics Best response Patient 1 16 mg/m² 2nd RUNX1 and NRAS mutations CRi Patient 2 16 mg/m² 2nd MECOM-rearrangement, complex karyotype, monosomy 5 and 7 PR Patient 3 16 mg/m² 4th TP53 mutation, complex karyotype, monosomy 5 and 7 PR Patient 4 21.3 mg/m² 3rd TP53 mutation, complex karyotype, monosomy 5 and 7 PR Patient 5 21.3 mg/m² 2nd TP53 mutation SD Patient 6 21.3 mg/m² 2nd TP53 mutation (very high-risk MDS) SD Complete remission (CRc) is defined as CRc = CR + CRh + CRi + CRp CR=Bone marrow blasts 50% increase in marrow blasts over baseline (a minimum 15% increase is required in cases <30% blasts at baseline). This diversity of responsive patients appears to corroborate the mechanism of action of AB8939, which is capable of destabilizing microtubules while evading multi-drug resistance and also targeting cancer stem cells without eliminating non tumoral stem cells These results corroborate the positioning of AB8939 in patients with adverse genetics, complex karyotypes, TP53 mutations, NRAS and KRAS mutations, monosomy 5 and 7, and MECOM-rearrangement, which represents the highest unmet medical need. Nicholas J. Short, MD, Associate Professor and Co-Lead of the Section of Developmental Therapeutics, Department of Leukemia, MD Anderson Cancer Center, said, " This new data is very encouraging, particularly considering the very adverse risk pro this patient’s leukemia. These early efficacy and safety data suggest that AB8939 can be combined with venetoclax and could have significant activity in the highest-risk subtypes of AML. There is a strong interest in continuing the development of this combination in patients whose AML has high-risk features that are expected to lead to resistance to venetoclax + azacitidine. " Professor Olivier Hermine, MD, President of the Scientific Committee of AB Science and member of the Académie des Sciences in France, said, " There is a strong rationale to combine AB8939 and venetoclax as both molecules have low hematologic toxicity and complementary mode of actions. These first results are supportive of this rationale." With Step 3 completed, the next step is Step 4, evaluating the triple combination of AB8939 + venetoclax + azacitidine. About AB8939 AB8939 is a drug candidate that targets (i) cancer cells by destabilizing microtubules (essential for cell division) and (ii) cancer stem cells by inhibiting ALDH1A1 and ALDH2 (enzymes essential for maintaining their physiological state and survival). AB8939 has shown in vitro activity in Ara-C (cytarabine, which is one of the standards of care) resistant patient cell lines, including adverse genetic MECOM and TP53 mutations. Analysis of cell lines responsive to AB8939 showed that AB8939 is effective in cell lines with TP53 mutations, MECOM, and complex karyotypes, whereas ARAC and azacitidine are not effective. AB8939 increased survival and had an additive effect in combination with venetoclax (another standard of care) in vivo in a MECOM-grafted PDX mouse model. AB8939 increased survival and had an additive effect in combination with Vidaza (azacitidine, another standard of care) in vivo in the MECOM PDX#C1005 mouse model of leukemia. AB8939 eradicated Leukemia Cancer Stem Cells in vivo in a human PDX AML mouse model, which is compatible with targeting stem cells via ALDH. AB8939 is currently being evaluated in a Phase 1 clinical trial (study AB18001, NCT05211570) in patients with refractory and relapsed AML. The Phase 1 clinical trial of AB8939 has completed its first three steps. The first two steps determined the maximum tolerated dose (MTD) after 3 and 14 consecutive days of monotherapy. In both cases, the MTD was 21.3 mg/m². The third step, now completed, evaluated the combination of AB8939 and venetoclax. Six patients were treated across two dose levels (AB8939 14 days at a dose of 16 mg/m² + venetoclax 14 days, then AB8939 14 days at a dose of 21.3 mg/m² + venetoclax 14 days), with no dose-limiting toxicity observed, supporting selection of the recommended Phase 2 dose. The next step (Step 4) will evaluate the triple combination of AB8939 + venetoclax + azacitidine. Medical need in AML and AB8939 mechanism of action Although several drugs have been registered for AML, 70% of patients still relapse and die, creating a persistent unmet medical need for effective treatments. Acute myeloid leukemia remains the most lethal form of leukemia in humans. AML is a heterogeneous disease, and its outcome is highly dependent on genetic factors. TP53 mutation has a very poor prognosis, with a median overall survival (OS) of 5.5 months. NRAS and KRAS mutants have a poor prognosis, with a median OS of 12.1 months. MECOM also has a very poor prognosis in AML, with a median OS of 5.5 months in relapsed or refractory settings. The challenge in AML is the recurrence of tumors due to a combination of two factors: the resistance of cancer cells to chemotherapy and relapse due to the persistence of cancer stem cells. This challenge may be overcome by AB8939’s dual mechanism of action. First, AB8939 blocks the proliferation of leukemia cells through microtubule disruption. It is not subject to multi-drug resistance as it does not bind to PgP, which is responsible for efflux outside the cells, and is not degraded by myeloperoxidase. Second, AB8939 targets leukemia cancer stem cells by inhibiting ALDH and promotes bone marrow repopulation of normal progenitors. AB8939 + venetoclax combination There is a strong rationale to combine AB8939 with venetoclax Both molecules exhibit low hematologic toxicity. This combination is expected to be less toxic than azacitidine + venetoclax as first-line treatment for AML These molecules have different and complementary targets in cancer cells. There is an additive, even synergistic, efficacy potential for the combination, with three mechanisms of action in a single treatment. Venetoclax’s mechanism of action inhibits the BCL2 pathway, a protein that prevents apoptosis (programmed 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-apoptotic, destabilizing microtubules, and would benefit from 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 Next steps Following completion of Step 3, the next step is to initiate Step 4, evaluating the triple combination of AB8939 + venetoclax + azacitidine, and to launch an expansion study in approximately 15 AML patients eligible for AB8939 + venetoclax at the appropriate dose. The expansion phase is expected to generate robust preliminary evidence of efficacy in the AML label, sufficient to support the clinical development plan and a beneficial partnership agreement. AB Science has started to discuss three possibilities for registration studies, which are not mutually exclusive, with the European Medicines Agency (EMA) and US Food and Drug Administration (FDA): AB8939 + venetoclax as first-line treatment, with aged patients and/or patients with adverse genetics (complex karyotypes, TP53 mutations, NRAS and KRAS mutations, monosomy 5 and 7, and MECOM-rearrangement) AB8939 + venetoclax as a second- or third-line treatment, in all patients or patients with adverse genetics AB8939 as a single agent in MECOM as a second or third-line treatment. Addressable market with AB8939 in relapsed/refractory AML Treatments for relapsed or refractory AML represent an estimated market size potential of greater than EUR 2 billion per annum. Region Incidence Case (1) % Relapse or Refractory (2,3) % Insured Patients (4) Drug Price (€) Market Size (per 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 EUROPE = EU27 + Norway + United Kingdom + Switzerland ; APAC = Australia, People’s Republic of China , Japan, New Zealand, Singapore, Taiwan ; LATAM = Argentina, Brazil, Chile, Colombia, Costa Rica, Mexico ; MENA = Algeria, Bahrain, Egypt, Israel, Kuwait, Morocco, Oman, Qatar, Saudi Arabia, Tunisia, United Arab Emirates (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) Ravandi F. Relapsed acute myeloid leukemia: Why is there no standard of care Best Pract Res Clin Haematol. 2013;26(3):253-9 (3) Walter RB et al. Resistance prediction in AML: analysis of 4601 patients from MRC/NCRI, HOVON/SAKK, SWOG and MD Anderson Cancer Center. Leukemia (2015) 29:312–20. . (4) Estimated (5) Choi M. et al. Costs per patient achieving remission with venetoclax-based combinations in newly diagnosed patients with acute myeloid leukemia ineligible for intensive induction chemotherapy. Journal of Managed Care & Specialty Pharmacy Volume 28, Number 9. Intellectual property AB8939 intellectual property rights in AML are secured until 2036 through a ‘composition of matter’ patent and potentially until 2041 with a 5 years extension. Two additional ‘second medical use’ patent applications have been filed to protect the use of AB8939 in the treatment of AML with specific chromosomal abnormalities. If these applications are accepted, the protection for AB8939 will be extended until 2044 and 2046 for these AML subpopulations. AB8939 has also received orphan drug designation for AML by both the EMA and FDA. This orphan drug designation confers 10 and 7 years of marketing exclusivity in Europe and the US, respectively, from the date of product registration. AB Science is the sole proprietary holder of AB8939 and its family of compounds. About AB Science Founded in 2001, AB Science is a pharmaceutical company specializing in the research, development and commercialization of protein kinase inhibitors (PKIs), a class of targeted proteins whose action are key in signaling pathways within cells. Our programs target only diseases with high unmet medical needs, often lethal with short term survival or rare or refractory to previous line of treatment. AB Science has developed a proprietary portfolio of molecules and the Company’s lead compound, masitinib, has already been registered for veterinary medicine and is developed in human medicine in oncology, neurological diseases, inflammatory diseases and viral diseases. The company is headquartered in Paris, France, and listed on Euronext Paris (ticker: AB). Further information is available on AB Science’s website: . Forward-looking Statements - AB Science This press release contains forward-looking statements. These statements are not historical facts. These statements include projections and estimates as well as the assumptions on which they are based, statements based on projects, objectives, intentions and expectations regarding financial results, events, operations, future services, product development and their potential or future performance. These forward-looking statements can often be identified by the words "expect", "anticipate", "believe", "intend", "estimate" or "plan" as well as other similar terms. While AB Science believes these forward-looking statements are reasonable, investors are cautioned that these forward-looking statements are subject to numerous risks and uncertainties that are difficult to predict and generally beyond the control of AB Science and which may imply that results and actual events significantly differ from those expressed, induced or anticipated in the forward-looking information and statements. These risks and uncertainties include the uncertainties related to product development of the Company which may not be successful or to the marketing authorizations granted by competent authorities or, more generally, any factors that may affect marketing capacity of the products developed by AB Science, as well as those developed or identified in the public documents published by AB Science. AB Science disclaims any obligation or undertaking to update the forward-looking information and statements, subject to the applicable regulations, in particular articles 223-1 et seq. of the AMF General Regulations. For additional information, please contact: AB Science Financial Communication & Media Relations investors@ab-science.com Attachment CP_AB8939_STEP3_VENG VF

In a post hoc analysis, patients treated with roxadustat showed a durable and clinically meaningful improvement in transfusion independence (TI) in patients with LR-MDS and high transfusion burden (HTB) compared to placebo Similar rates of TI for patients treated with roxadustat were observed in both ring sideroblast positive (RS+) and ring sideroblast negative (RS-) disease Pivotal Phase 3 trial protocol of roxadustat for the treatment of anemia in patients with LR-MDS and high transfusion burden is being finalized based on feedback received from the Food and Drug Administration (FDA) SAN FRANCISCO, June 11, 2026 (GLOBE NEWSWIRE) -- Kyntra Bio (Nasdaq: KYNB) today announced additional data from the Phase 3 MATTERHORN trial showing improvements in transfusion independence in patients with anemia associated with lower - risk myelodysplastic syndromes (LR-MDS) treated with roxadustat will be presented as a poster at the European Hematology Association (EHA) Congress 2026, taking place June 11-14, 2026 in Stockholm, Sweden. “In addition to roxadustat demonstrating clinically meaningful efficacy in patients with lower-risk MDS and high transfusion burden, improvements in transfusion independence in both RS+ and RS- disease were also observed in this post-hoc analysis, which is an important finding given the limited effectiveness of currently available treatment options for patients with RS - disease,” said Thane Wettig, Chief Executive Officer of Kyntra Bio. “These findings underscore the potential of roxadustat to elevate the standard of care for patients with lower-risk MDS who are in need of additional treatment options. We are finalizing the protocol for the pivotal Phase 3 trial, which we expect to initiate in the second half of 2026, with the aim to build upon and confirm these findings in patients with lower-risk MDS and high transfusion burden, including both RS+ and RS - disease.” “Through this novel MOA, stabilizing HIF1-⍺, thereby normalizing erythroid precursor development and improving hemoglobin production, these findings highlight the potential for roxadustat to address a significant unmet need, providing a convenient, well-tolerated and effective treatment option for anemia in patients with LR-MDS independent of RS histology,” said Amer Zeidan, MD, Professor of Medicine at Yale School of Medicine and Chief of the Division of Hematologic Malignancies at Yale Cancer Center. “This post-hoc analysis from the MATTERHORN trial shows clinically meaningful RBC transfusion independence among high transfusion burden patients, as well as clear evidence of hemoglobin increase among patients who received roxadustat compared to placebo. I am excited to be able to share this data with the MDS community at the EHA meeting and believe they provide strong rationale for the planned randomized Phase 3 trial in anemic patients with LR-MDS and high RBC transfusion burden,” concluded Dr. Zeidan, who is also the global principal investigator of the planned randomized Phase 3 trial. As previously disclosed, the initial analysis with all of the patients who participated in the Phase 3 MATTERHORN trial showed that more patients receiving roxadustat achieved transfusion independence vs. placebo (48% vs. 33%; p=0.22). The presentation highlights data from a post hoc analysis of the entire trial population, demonstrating that roxadustat led to similar rates of transfusion independence in both RS+ and RS - patients. In RS - patients, which comprised 84 of the 140 patients enrolled in the trial, treatment with roxadustat led to transfusion independence for ≥8 weeks over 28 weeks in 48% of patients vs. 28% for placebo. The presentation at EHA also provides additional details on the subgroup of patients (n=37) who met the criteria of HTB (≥ 4 units pRBCs per 8-week period for 2 consecutive 8-week periods) per IWG-2018, where roxadustat achieved clinically meaningful efficacy in patients with LR-MDS and HTB with higher rates of ≥8 - , 12 - , 16 - week RBC TI vs placebo. TEAEs were generally lower grade and managed medically with no new safety signals. The poster presentation, titled “Roxadustat improves transfusion independence in LR-MDS patients with anemia and high transfusion burden and in ring sideroblast positive and negative disease: post-hoc analysis of MATTERHORN study” is scheduled for the poster session taking place on June 12, 2026 at 18:45 CEST. The pivotal Phase 3 trial protocol of roxadustat for the treatment of anemia in patients with LR-MDS and high transfusion burden is being finalized based on feedback received from the FDA. About Myelodysplastic Syndromes Anemia Myelodysplastic syndromes (MDS) are a group of disorders characterized by dysfunctional progenitor blood cells and stem cells, resulting in chronic anemia in most patients. Annual incidence rates of MDS are estimated to be 4.9/100,000 adults in the U.S., thereof 77% are considered lower-risk MDS. Approximately 80% of patients with MDS have anemia at the time of diagnosis, and around 60% of patients with MDS will experience severe anemia (hemoglobin <8 g/dL) at some point during the course of their disease. Anemia in patients with MDS is associated with increased risk of cardiovascular complications and the need for blood transfusion. Approximately 50% of patients with MDS require regular red blood cell transfusions. Transfusion dependent MDS patients suffer higher rates of cardiac events, infections, and iron overload with the related complications. In addition, anemia frequently leads to significant fatigue, cognitive dysfunction, and decreased quality of life. Today, patients are routinely treated with erythropoiesis-stimulating agents (ESAs), luspatercept, imetelstat, or lenalidomide in lower-risk MDS with isolated del(5q), and hypomethylating agents (HMAs) in higher-risk disease. Only 35-40% of patients respond to current treatments and the durability of response is short. Moreover, these treatments are challenging to dose-calibrate and can only be administered via subcutaneous injection or through IV infusion. There remains a high unmet need for the treatment of anemia associated with MDS, and new strategies that provide durable response and the convenience of oral administration are highly desired in managing patients with MDS. About Roxadustat Roxadustat, an oral medication, is the first in a new class of medicines comprising HIF-PH inhibitors that promote erythropoiesis, or red blood cell production, through increased endogenous production of erythropoietin, improved iron absorption and mobilization, and downregulation of hepcidin. Roxadustat is approved in Europe, Japan, and numerous other countries for the treatment of anemia of CKD in adult patients on dialysis (DD) and not on dialysis (NDD). Kyntra Bio has the sole rights to roxadustat in the United States, Canada, Mexico, and in all markets not held by AstraZeneca or licensed to Astellas. Astellas and Kyntra Bio are collaborating on the commercialization of roxadustat for the treatment of anemia in territories including Japan, Europe, Turkey, Russia, and the Commonwealth of Independent States, the Middle East, and South Africa. About Kyntra Bio Kyntra Bio is a biopharmaceutical company focused on development of novel therapies in oncology and rare disease. Roxadustat (爱瑞卓 ® , EVRENZO™) is currently approved in Europe, Japan, China, and numerous other countries for the treatment of anemia in chronic kidney disease (CKD) patients on dialysis and not on dialysis. The Company continues to evaluate the development plan for the Phase 3 trial of roxadustat in anemia associated with lower-risk myelodysplastic syndromes (LR-MDS) in the U.S. FG-3246 (also known as FOR46), a first-in-class antibody-drug conjugate (ADC) targeting CD46, is in Phase 2 development for the treatment of metastatic castration-resistant prostate cancer. This program also includes the development of FG-3180, an associated CD46-targeted PET biomarker. For more information, please visit . Note: Amer Zeidan’s views are his own personal views and do not necessarily represent his employer’s views. He has also consulted and received honoraria and travel support from Kyntra Bio. Forward-Looking Statements This release contains forward-looking statements regarding Kyntra Bio’s strategy, future plans and prospects, including statements regarding its commercial products and clinical programs . These forward-looking statements include, but are not limited to, statements regarding the efficacy, safety, and potential clinical or commercial success of Kyntra Bio products and product candidates, and statements about Kyntra Bio’s plans and objectives. These forward-looking statements are typically identified by use of terms such as “may,” “will”, “should,” “on track,” “could,” “expect,” “plan,” “anticipate,” “believe,” “estimate,” “predict,” “potential,” “continue” and similar words, although some forward-looking statements are expressed differently. Kyntra Bio’s actual results may differ materially from those indicated in these forward-looking statements due to risks and uncertainties related to the continued progress and timing of its various programs, including the enrollment and results from ongoing and potential future clinical trials, and other matters that are described in Kyntra Bio’s most recent Annual Report on Form 10-K and Quarterly Report on Form 10-Q, each as filed with the Securities and Exchange Commission (SEC), including the risk factors set forth therein. Investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this release, and Kyntra Bio undertakes no obligation to update any forward-looking statement in this press release, except as required by law. For Investor Inquiries: David DeLucia, CFA Senior Vice President and Chief Financial Officer ir@kyntrabio.com