drugset / Press release

Corporate Presentation April 2024

2024-04-30 · Ichnos Sciences SA · original iginnovate.com ↗

Collaboration propels innovation Corporate Presentation March, 2024 Forward-Looking Statements Ichnos Glenmark Innovation (“IGI”) is an alliance between Glenmark Pharmaceuticals Limited (“GPL”) and Ichnos Sciences Inc. (“Ichnos”) for the purpose of collaborating with each other on the discovery and development of new molecules by leveraging on each other capabilities to achieve synergies around developing innovative pharmaceutical products. These materials have been prepared by IGI solely for informational purposes and are strictly confidential and may not be taken away, reproduced, or redistributed to any other person. This presentation is on drugs in clinical development and includes information from experiments and information that might be considered forward-looking. While these forward- looking statements represent our current judgment based on current information, please be aware they are subject to risks and uncertainties as development progresses that could cause actual results to differ materially. These materials also contain material, non-public information. In addition, these materials contain forward-looking statements that are, by their nature, subject to significant risks and uncertainties. In these materials, the words “will,” “anticipate,” “expect,” “plan,” “potential,” and similar expressions identify forward-looking statements. Such forward-looking statements necessarily involve known and unknown risks and uncertainties, which may cause actual performance and financial results in future periods to differ materially from any projections of future performance or result expressed or implied by such forward-looking statements. Corporate Presentation | Mar 2024 Such forward-looking statements are based on numerous assumptions regarding IGI’s present and future business strategies and the environment in which IGI will operate in the future and must be read together with such assumptions. Predictions, projections, or forecasts of the economy or economic trends of the markets are not necessarily indicative of the future or likely performance of IGI, and the forecast financial performance of IGI is not guaranteed. IGI does not undertake any obligation to update these forward-looking statements to reflect events, circumstances, or changes in expectations after the date hereof or to reflect the occurrence of subsequent events. No representations or warranties are made as to the accuracy or reasonableness of such assumptions or projections or the forward- looking statements based thereon. This presentation does not constitute or form part of, and should not be construed as, directly or indirectly, any offer or intimation or inducement to sell or issue or an offer or any solicitation of any offer, to purchase or sell any securities, as defined. The information contained here is not a prospectus, statement in lieu of prospectus, advertisement, or any other offer. It is not IGI’s intention to provide, and you may not rely on these materials as providing, a complete or comprehensive analysis of the IGI’s financial position or prospects. The information contained in these materials has these materials has not been independently verified and is subject to verification, completion, and change without notice. The information contained in these materials is current as of the date hereof and is subject to change without notice, and its accuracy is not guaranteed. Accordingly, no representation or warranty, express or implied, is made or given by or on behalf of IGI, or any of its directors and affiliates or any other person, as to, and no reliance should be placed for any purposes whatsoever on, the fairness, accuracy, completeness or correctness of, or any errors or omissions in, the information contained herein or any other information, whether written or oral, transmitted or made available to you herewith. The IGI name and all related names, logos, product and service names and designs included in these materials are trademarks of IGI or its affiliates or licensors. All other names, logos, product and service names, and designs included in these materials are the trademarks of their respective owners. The distribution of these materials in certain jurisdictions may be restricted or affected by the laws of such jurisdictions. To the fullest extent permitted by applicable law, IGI disclaims any responsibility or liability for the violations of any such restrictions by any person. 2 Corporate Presentation | Mar 2024 Our Mission To provide curative therapies that extend and improve lives. Our Vision We dare to imagine a world where cure is possible. 3 Clinical-Stage Biotechnology Company at the Forefront of Innovation in Oncology Corporate Presentation | Mar 2024 Complementary Biologics and Small Molecules Discovery engines • Proprietary protein engineering platform (BEAT®) allowing maximal flexibility and manufacturability of full length multispecific antibodies • Structure-based SMs and degrader discovery platform powered by computational chemistry to design molecular entities with desired binding mode, functional activity, selectivity and degradation • Dual-pronged research strategy based on multispecific immune cell engager antibodies that can engage multiple targets on cell surface and small molecules modulating intracellular pathways in cancer or immune cells • Clinical stage pipeline in Oncology • 6 initial programs targeting hematologic malignancies and solid tumors • Engaging different types of immune cells • Open to asset-level partnerships with global immuno-oncology leaders • Auto-immune programs led by Alliance Partners • Core capabilities in biologics and small molecules: discovery, antibody engineering, clinical development • Global footprint: U.S., Switzerland and India • Ongoing discussions for divesting the biologics manufacturing plant Fully Integrated Biotech Robust Pipeline 4 BEAT®: Bispecific Engagement by Antibodies based on the TCR Highly Experienced Leadership Team Corporate Presentation | Mar 2024 110+ Years combined experience in biotech and pharmaceuticals 30+ Products developed or launched 40+ Mergers, acquisitions, IPOs and other transactions LEADERSHIP PREVIOUS EXPERIENCE BY THE NUMBERS CYRIL KONTO, M.D. President and Chief Executive Officer KARISHMA SIPAHIMALANI, Ph.D. Head of Human Resources DEAN THOMAS, J.D. General Counsel LIDA PACAUD, M.D. Chief Medical Officer EVA YUEN Head of Finance MARIO PERRO, Ph.D. Head of Biologics Research NAGARAJ GOWDA Head of Small Molecule Research SEBASTIEN CHENUET, Ph.D. Head of Business Development 5 Accomplished Governance Board With Track Record of Success Corporate Presentation | Mar 2024 GLENN SALDANHA Chairman and Managing Director, Glenmark Pharmaceuticals Limited DAVID LUBNER Former CFO of Ra Pharma V S MANI Global CFO of Glenmark Pharmaceuticals Limited LAWRENCE OLANOFF, M.D., Ph.D. Former President and COO of Forest Laboratories ALIND SHARMA Global CHRO of Glenmark Pharmaceuticals Limited CYRIL KONTO, M.D. President and Chief Executive Officer Ichnos Glenmark Innovation DENNIS PURCELL Founder of Aisling Capital and Former Senior Managing Partner 6 Corporate Presentation | Mar 2024 Multispecific antibodies and SM Modulators are Complementary and Will Drive the Next Wave of Innovation in Oncology TARGETED THERAPIES IMMUNO-ONCOLOGY BISPECIFIC ANTIBODIES CAR-T CELLS Fc Function-based Tumor Killing Checkpoint and Innate Immunity Modulators CD3 T-Cell Engagers Engineered T-Cells MULTISPECIFICS AND SM MODULATORS Targeting simultaneously multiple cell surface antigens on cancer and immune cells while modulating their intracellular pathways ISB 1442 ISB 2001 GRC 65327 IRAK-M 2010s1990s 2014 2017 Next Wave 7 Sudhakar A. J Cancer Sci Ther. 2009;1:1-4; Checkpoint inhibitors image: Reprinted from Immunity, Vol 39, Chen DS, Mellman I. Oncology Meets Immunology: The Cancer-Immunity Cycle, Pages 1-10, Copyright 2013, with permission from Elsevier Multispecifics: Strategy Starts with a Validated Target in Multiple Myeloma, hen Expands MULTIPLE MYELOMA ISB 1342, a CD38 X CD3 BEAT® bispecific antibody Corporate Presentation | Mar 2024 T-Cell Bispecific Engager HEMATOLOGIC MALIGNANCIES • ISB 1442, a first-in-class CD38 X CD 47 2+1 Biparatopic BEAT® bispecific antibody • ISB 2001, BCMA X CD38 X CD3 TREAT trispecific antibody Myeloid and T-Cell Multispecific Engagers SOLID TUMORS ISB 2301, BEAT® NK-Cell Engaging Multispecific Platform Multispecific Engagers 8 BEAT®: Bispecific Engagement by Antibodies based on the TCR TREAT : Trispecific Engagement by Antibodies based on the TCR Portfolio Addresses Unmet Needs in Multiple Myeloma, Overcomes Limitations of Select Therapies HIGH UNMET NEED AND LARGE MARKET Global multiple myeloma cases annually1 LIMITATIONS OF SELECT THERAPIES • Decreased CD38 expression limits efficacy of CD38-targeted therapies3 • Resistance to Complement Dependent Cytotoxicity • CD47-targeted therapies not suitable as single agents • Few options following failure of BCMA-targeted therapies Corporate Presentation | Mar 2024 160000 Low Responses for Triple Refractory Patients2 3.4 9.3 31% ORR with subsequent therapy Median OS (months) Median PFS (months) 99 1 Oncologist. 2020 September;25(9):e1406-e1413 | 2 Gandhi UH et al. Leukemia 2019; 33: 2266 –75. 3 Saltarella I. et al. CELLS 2020 Following Proteasome inhibitors, Immunomodulators, and Anti-CD38 therapies. ISB 1442 Addresses Unmet Needs in Acute Myeloid Leukemia, Overcomes Limitations of Current and Developing Therapies HIGH UNMET NEED AND LARGE MARKET (2020) New AML patients in the U.S., France, Germany, Italy, Spain, UK and Japan1 LIMITATION OF CURRENT AND DEVELOPING THERAPIES • Few late stage, emerging agents for AML • Standard of care for R/R AML lacks desired efficacy and durability • Multiple, persistent and/or emerging mechanisms of resistance may be overcome by co-targeting CD38 and CD47 Corporate Presentation | Mar 2024 41000+ High rates of resistance and recurrence2 Half Relapse Refractory Percent of Total Patient Population ~33% Primary Refractory ~33% Refractory ~33% Relapsed ~67% Respond 10 1 DelveInsight, "Acute Myeloid Leukemia (AML) - Market Insight, Epidemiology and Market Forecast – 2032” 2 American Cancer Society, “Treatment Response Rates for Acute Myeloid Leukemia (AML)” Pipeline 11 Diversity of Immune Cell Engagement and Indications Across Hematologic and Solid Tumors Corporate Presentation | Mar 2024 ASSET DESCRIPTION INDICATION PRECLINICAL PHASE 1 PHASE 2 PHASE 3 STATUS ISB 1342* CD38 x CD3 BEATTM bispecific antibody Multiple Myeloma PHASE 1 ORPHAN DRUG ISB 1442 CD38 x CD47 BEATTM bispecific antibody Multiple Myeloma; AML planned PHASE 1 ORPHAN DRUG ISB 2001 BCMA x CD38 x CD3 TREATTM trispecific antibody Multiple Myeloma PHASE 1 ORPHAN DRUG GRC 65327 Cbl-b Inhibitor Solid Tumors PRE-CLINICAL ISB 2301 IMMUNITE NK-cell engager Solid Tumors DISCOVERY IRAK-M Interleukin-1 receptor associated Kinase-3 inhibitor Solid Tumors DISCOVERY CLINICAL ASSETS CANDIDATES 12 * Open for partnership Out-Licensing Autoimmune Disease Programs to Enable Greater Focus on Oncology Clinical Studies Corporate Presentation | Mar 2024 $320 million for upfront payment, development, regulatory and sales milestone payments, plus tiered royalties on global sales €20.8 million for upfront payment. Plus development, regulatory and sales milestone payments, and tiered royalties on global sales Atopic Dermatitis Autoimmune Disease PRODUCTS TARGET PRECLINICAL PHASE 1 PHASE 2 PHASE 3 STATUS Licensed to Telazorlimab and ISB 830-X8 OX40 antagonist monoclonal antibody SUCCESSFUL PHASE 2B* Licensed to ISB 880 / ALM27134 IL-1RAP antagonist monoclonal antibody PHASE 1 * A US IND for rheumatoid arthritis and other autoimmune indications is active 13 BEAT® Platform 14 BEAT® Combines TCR Interface-Based Hc Pairing and Common Lc to Streamline the Creation and Development of Multispecific Antibodies Corporate Presentation | Mar 2024 Fab Common Light Chain Heavy Chain Heterodimerization Interface T cell receptor T cell Cell membrane TCR α TCR β Biased Heterodimer Purification Fc Proprietary plug -and-play modular platform enables a plurality of multispecific configurations BEAT® TREATTM BEAT®: Bispecific Engagement by Antibodies based on the TCR TREAT : Trispecific Engagement by Antibodies based on the TCR Common variable light chain domain TCR constant beta TCR constant alphaIgG1 IgG3 Common constant light chain domain T cell receptor TCR a TCR b 15 BEAT® Enables Production of Multispecific Antibodies with Competitive Developability Properties BEAT® (2 + 1) TREAT TRISPECIFIC Enables design and development of bi/multispecific antibodies that unlock new biology (e.g., T-cell, NK cells, macrophage engagers) by optimizing: • Affinity: low-medium-high combinations • Epitope: target/test several epitopes • Architecture: avidity, immune synapse size • Fc function: T-cell: silent; non T-cell: active – enhanced • Improved druggability and developability – rapid engineering Corporate Presentation | Mar 2024 ISB 1442 ISB 2001 Platform welcome partnerships to: • Establish collaboration leveraging our BEAT® technology, discovery and development capabilities • Create new opportunities in therapeutic areas within oncology, autoimmune diseases and beyond • Collaborate through discovery and license agreements, co-development or company creation. 16 MHC: Major histocompatibility complex, CDC: Complement-Dependent Cytotoxicity ADCC: Antibody-Dependent Cell-mediated Cytotoxicity ISB 1342 17 ISB 1342 - Executive Summary Corporate Presentation | Mar 2024 • Phase I, first-in-class, bispecific CD38xCD3 antibody developed in RRMM • Designed to overcome Daratumumab resistance mediated by low CD38-expressing tumor cells and resistance to CDC and ADCC: + ISB 1342 demonstrated cytotoxic potency and tumor growth inhibition superior to daratumumab + ISB 1342 demonstrated killing of multiple myeloma cells resistant to Daratumumab + ISB 1342 does not compete with Daratumumab for the same binding epitope on CD38 thus not requiring a wash out period in clinic • ISB 1342-101 Study in Triple Refractory Patients with R/R MM demonstrated a favorable safety profile and preliminary anti-myeloma effect in a heavily pre-treated patient population • Available for partnerships due to pipeline strategic reprioritization 18 ISB 1342 (CD38 x CD3) Bispecific Antibody: Potential First-in-Class Therapy in Relapsed/Refractory Multiple Myeloma • CD38 is expressed on the surface of multiple myeloma cells and is a clinically validated target • ISB 1342 is a bispecific antibody that redirects T cells to kill CD38-expressing tumor cells in MHC-antigen-independent manner • ISB 1342 binds to a proprietary anti-CD38 epitope, which is different from that of daratumumab • ISB 1342 is designed to overcome: + Daratumumab resistance by killing low CD38-expressing tumor cells + Resistance to CDC and ADCC mediated by daratumumab • ISB 1342 was Granted Orphan Drug Designation for Multiple Myeloma by U.S. FDA Corporate Presentation | Mar 2024 KEY ATTRIBUTES ISB 1342 (CD38 X CD3) bispecific antibody 19 ISB 1342 Effectively Controls Tumor Growth In Vivo and demonstrates tumor growth inhibition superior to daratumumab NOD-SCID mice were xenografted subcutaneously with human peripheral blood mononuclear cells and Daudi cells. ISB 1342 or daratumumab were injected intravenously weekly when tumor reached 100 mm3 and tumor growth monitored over two weeks (left panel). (Mann Whitney test). * = p<0.05 Corporate Presentation | Mar 2024 6 8 10 12 14 16 18 20 22 0 100 200 300 400 500 600 700 800 900 1000 1100 1200 1300 Days after xenograft Tumor volume (mm3 mean +/- SEM) Control ISB 1342 at 2.5mg/kg Daratumumab at 16mg/kg * * -10 0 10 Days after xenograft 20 0 500 1500 1000 2000 Tumor volume (mm3) Vehicle ISB 1342 at 0.5 mg/kg daratumumab at 16 mg/kg ✱✱✱✱ Pouleau B. et al. Blood 2023 20 Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021) 8044-8044 ISB 1342 retains cytotoxic potency in the presence of Daratumumab, which obviates the need for a wash out period in clinic Epitope mapping of daratumumab and ISB 1342 on CD38 demonstrates distinct epitope binding sites ISB 1342 does not compete with daratumumab and can engage CD38 prebound by daratumumab Corporate Presentation | Mar 2024 ISB 1342 Cytotoxicity of NCI-H929 MM cell line is not impacted by pre-treatment of daratumumab 0.1 1 10 100 Tumor cell Killing EC50 (pM) ns 0 20 40 60 80 100 120 140 Maximum (%) ns Day: 0 1 PBMC + Tumor Dose range of ISB 1342 3 readoutsingle dose of daratumumab (EC50) 4.0 3.5 3.0 2.5 2.0 1.5 1.0 0.5 0 0 200 400 600 800 1000 1200 1400 Time(s) nm hCD3 8-biot SA sensor daratumumab + ISB 1342 daratumumab daratumumab daratumumab ISB 1342 21Pouleau B. et al. Blood 2023 -25 0 25 50 75 100 125 MaximumKilling of T-ALLcells(%) ✱✱ ISB 1342 Demonstrates Superior Cytotoxic Potency relative to Daratumumab in Several CD38+ patient-derived hematological malignancies Waldenstrom Macroglobulinemia dara-naive Plasma Cell Leukaemia dara-naive Corporate Presentation | Mar 2024 T-Acute Lymphocytic Leukaemia -50 -25 0 25 50 75 100 Antibody Concentration (nM) % Killingof CD138+ cells ISB 1342 EC50 = 12.54 PM daratumumab EC50 = 229 pM % Killing of CD138+ cells 22Pouleau B. et al. Blood 2023 ISB 1342 Kills Multiple Myeloma Cells That Are Resistant to Daratumumab Corporate Presentation | Mar 2024 • Demonstrated Efficacy: Many patients relapse when they become resistant to anti-CD38 therapies (e.g., daratumumab). ISB1342 was designed to be active regardless of CD38 expression. • In vivo – ISB 1342 induced complete tumor eradication in mice models • In vitro – ISB 1342 maintains high potency to kill tumor cells in bone marrow samples from patients previously treated with daratumumab (figure at right) • Acceptable toxicology profile in cynomolgus monkeys Results suggest ISB 1342 may be an option for patients whose multiple myeloma is resistant to anti-CD38 therapies. • Demonstrated Safety: Maximal cytotoxicity of CD138+ tumor cells with ISB 1342 (10-100 nM) or daratumumab (100 nM) in samples from dara-naïve patients (filled symbols) vs dara-exposed (open symbols). Dots represent individual samples, and data are mean ± SD compared using 1-way ANOVA followed by Dunnett multiple comparison analysis to daratumumab on dara-naïve samples. -25 0 25 50 75 100 125 Maximum Killing of CD138+ cells (%) ns ✱ ISB 1342: dara-naive ISB 1342: dara-exposed daratumumab: dara-naive daratumumab: dara-exposed *=p <0.05 23Pouleau B. et al. Blood 2023 ISB 1342-101 Clinical Trial Design Corporate Presentation | Mar 2024 ISB 1342-101 Study in Triple Refractory Patients with R/R MM Primary endpoint: ORR Part 2 Dose Expansion • Pivotal single arm Phase 2 study in R/R MM, monotherapy in 4th line Other Studies • Phase 2 combination studies • Phase 2 in other CD38-expressing hematologic malignancies Phase 3 Confirmatory Studies Clinical Proof-of-Concept for BEAT® Primary endpoint: MTD Further DevelopmentPart 1 • Steroids premedication • Step up dosing Enrollment Closed 29 patients enrolled in biweekly dosing cohorts 52 patients enrolled in weekly dosing cohorts 3+3 Dose Escalation Enrolling Patients at 16 µg/kg IV NCT03309111 24 ISB 1342-101 Clinical Trial Corporate Presentation | Mar 2024 • First-in-human, open-label study, including a dose escalation part (Part 1), and a disease-specific expansion part (Part 2) in subjects with relapsed and/or refractory multiple myeloma (RRMM) who received prior proteasome inhibitors (PIs), immunomodulators (IMiDs) and CD38. • Primary objective to assess the safety profile of ISB-1342 and determine the maximal tolerated dose (MTD) and/or recommended phase 2 dose (RP2D). • Data from earlier cohorts were previously reported at the ASH Annual Meeting 2022 (Blood(2022) 140 (Supplement 1): 7264–7266). • Here we report findings from the Q1W dose-escalation portion from Cohorts 108, 109 and 110 (4, 8 and 16 μg/kg, respectively, as a full dose on Day 8, preceded by a priming dose on Day 1 for each dose level). Data extraction was performed on 10/23/23 (ongoing database) 25 Presented at American Society of Hematology 2023 Annual Meeting Adverse Events of Special Interest Corporate Presentation | Mar 2024 • CRS occurred in 16/28 (57%) subjects; all were low grade (25% Grade 1, 28% Grade 2, no Grade 3 or higher). CRS generally started between days 1-2, resolved within 4.75 days. Five of 16 subjects had more then one episode of CRS. Tocilizumab was used in 8/28 (28.6%) subjects. • Injection site reactions were observed in 7/8 (87%) subjects with subcutaneous (SC) administration; all were grade 1 or 2. Two subjects had skin biopsies showing neutrophilic dermatoses. • 2/28 had related infection (one grade 2 herpes virus reactivation, one grade 4 sepsis, bothresolved). • Grade 3-4 neutropenia was observed in 11/28 (39%) of patients in Cohorts 109 and 110 IV (expected range for TCE). Neutropenia risk did not translate into the infectious risk. • No immune effector cell associated neurotoxicity syndrome (ICANS) observed. 26 Presented at American Society of Hematology 2023 Annual Meeting PK Profile with Q1W IV Dosing Regimen Corporate Presentation | Mar 2024 • In general, the Cmax was achieved at the end of the infusion followed by a bi-exponential decline of serum concentrations • The Q1W PK profile support weekly dosing regimen, maintained higher Ctrough with lower fluctuations relative to Q2W regimen • Limited data from SC injection suggested slow absorption and lower Cmax than IV Dose Linear Increase in Exposures 27 ISB 1342 Q1W Summary Immunogenicity Profile Corporate Presentation | Mar 2024 ISB 1342 -101 Total Subjects (Evaluable) Treatment Emergent ADA Treatment Boosted ADA ADA Titers ADA Positive at Baseline only Neutralizing Ab Persistent Q1W 48 12/48 (25%) 1/48 (2.1%) 10-655360 None 13/48 (27.1%) 12/48 (25%) • In the Q1W regimen, 12 out of 48 (25%) evaluable subjects tested positive for ADA with titers ranging from 10 to 655360 • ADA were neutralizing in nature in all 12 subjects • High ADA titers appeared to influence the serum exposures 28 Biomarker Profile Corporate Presentation | Mar 2024 T-Cell Activation Measured by Expression of CD69 in T-cells Following Treatment with ISB 1342 • T-cell expression of CD69 was assessed by flow cytometry of peripheral blood samples collected during Cycle 1 from patients in Cohorts 108-110 (target dose levels 4-16 mmg/kg). • Comparison of CD69 expression frequencies indicate increased T-cell activation levels at 24- 48h post-dose compared to the pre-dose samples. • Increased levels of T-cell activation were observed at higher dose levels, and this effect was reduced in patients receiving ISB 1342 subcutaneously compared to patients treated intravenously. CD4 T-Cells CD8 T-Cells Biomarker Changes Associated with Response in a Patient Treated with ISB 1342 (Cohort 109 IV) • Transient increases in several T-cell activation-related biomarkers were consistently observed following ISB 1342 dosing at target dose levels 4-16 mg/kg. • Increased expression of CD69 on T-cells was determined by flow cytometry analysis of peripheral blood (left panel); circulating cytokine levels (center panel, assessed by Meso Scale Discovery /MSD immunoassay ) and T-cell functional markers, granzyme B and perforin (right panel, assessed by ELISA) were measured in serum, indicating transient increases associated with T-cell activation. • Pre and post dosing samples were drawn at various time points within 48h following the first 2 doses. All other time points shown were collected prior to dosing. 29 Presented at American Society of Hematology 2023 Annual Meeting Clinical Responses Corporate Presentation | Mar 2024 Best Overall Response Cohort 108 IV 4 μg/kg (N=4) Cohort 109 IV 8μg/kg (N=10) Cohort 109 SC 8μg/kg (N=8) Cohort 110 IV 16 μg/kg (N=6) PR 0 1 ( 10%) 0 2 ( 33.3%)* MR 0 0 0 1 ( 16.7%) SD 2 ( 50%) 3 ( 30%) 3 ( 37.5%) 1 (16.7%) PD 2 ( 50%) 5 ( 50%) 2 ( 25%) 2 (33.3%) NE 0 1 ( 10%) 1 ( 12.5%) 0 Missing 0 0 2 (25%) 0 ^Data extract update from 5th December, 2023 *1 PR assessment based on central laboratory data NE: not evaluated 30 Presented at American Society of Hematology 2023 Annual Meeting Clinical Responses Corporate Presentation | Mar 2024 • The efficacy signals observed in Cohorts 108 -110 are consistent with the lower end of the predicted efficacy dose range (5.0 to 50 ug/kg) by quantitative systems pharmacology (QSP) based on preclinical data. Reduced Serum M-Protein Levels in Three Patients Treated with ISB 1342 (IV Cohorts) Patients by Cohort Anti - CD38 Last dose of anti - CD38 ISB 1342 C1D1 Cohort 110 Patient 2 Isatuximab 21-Jan-2022 10-Oct-2023 Cohort 109 patient Daratumumab 04-Jan-2023 08-Mar-2023 Cohort 110 Patient 1 Daratumumab 04-May-2023 03-Jul-2023 31 Presented at American Society of Hematology 2023 Annual Meeting Conclusions of the phase I dose escalation study Corporate Presentation | Mar 2024 • Treatment with ISB 1342 was well tolerated at the evaluated weekly 4, 8 and 16 μg/kg dose levels. • The observed CRS events were mild to moderate and manageable with supportive care. No new safety signal identified. • Serum M-protein decreased indicating PR has been seen in 3 subjects (based on ongoing dataset analysis). • Further dose-escalation (to 32 and 64 μg/kg) is warranted based on manageable safety profile, anti-myeloma activity observed, and supported by PK profile as well as T-cell activation biomarkers with current dose of 16 µg/kg IV. • Trials have paused enrolment due to strategic prioritisation. Program is open for partnership for further development. 32 ISB 1442 33 ISB 1442 - Executive Summary Corporate Presentation | Mar 2024 • Phase I, first-in-class, bispecific and biparatopic CD38xCD47 antibody developed in RRMM and AML • Novel approach for the treatment of CD38+ tumors by co-targeting CD38 and CD47 with a 2+1 biparatopic bispecific antibody, showing: + Triple Mechanism of Tumor Killing: ADCP, ADCC, CDC + Higher cytotoxic potency relative to daratumumab in CD38high/low in vitro tumor models + High cytotoxic potency in AML ex vivo • Barely detectable on-target off-tumor binding compared to anti-CD47 mAb (5F9) as per molecular design • Phase 1 dose-finding study of ISB 1442 in RRMM opened in the U.S., Australia and India. Favorable safety profile shown as of April data cut-off and clinical proof-of-mechanism demonstrated in patients • Phase 1 dose-finding study in relapsed/refractory AML planned in 2024 34 ISB 1442 Triple Mechanism of Tumor-Cell Killing Driven by Enhanced ADCP, ADCC and CDC • Dual binding to CD38 and CD47 epitopes, increasing avidity relative to daratumumab • Two Fab regions drive binding to distinct CD38 epitopes that don’t compete functionally with daratumumab • One arm blocks CD47-SIRPa binding on tumor cells to enhance ADCP + CD47 is over-expressed by hematologic tumors and associated with worse prognosis + Enhanced phagocytosis by blocking CD47 and increasing activation signaling through FcγR binding + Reduced potential for antigen sink with lower-affinity Fab binding to CD47 expressed on healthy cells • Potent ADCC, CDC and ADCP based on optimized affinity, architecture/avidity and enhanced Fc function • Optimized tolerability with low potential for adverse effects on red blood cells such as hemagglutination, platelet aggregation • ISB 1442 was granted Orphan Drug Designation for Multiple Myeloma by the U.S. FDA Corporate Presentation | Mar 2024 KEY ATTRIBUTESISB 1442 (CD38 x CD47) biparatopic bispecific antibody 35 ADCP: Antibody-Dependent Cellular Phagocytosis ADCC: Antibody-Dependent Cell Cytotoxicity CDC: Complement-Dependent Cytotoxicity ISB 1442 Blocks CD47/SIRPα Interactions & Induces Enhanced Phagocytosis of CD38 Low-Expressing Tumor Cells vs. Daratumumab Blocks CD47/SIRPα Interactions Higher Phagocytosis Relative to Daratumumab in CD38low Statistics: Tukey’s multiple comparison test. Corporate Presentation | Mar 2024 CD47/SIRPa inhibition (%) CD38 CD47 180,000 60,000 CD38high(Daudi) 0 20 40 60 80 10-5 10-4 10-3 10-2 10-1 100 101 102 103 Phagocytosisindex ISB 1442 anti-CD47 mAb (5F9) Daratumumab Antibody concentration(nM) CD38 CD47 180,000 60,000 CD38high(Daudi) CD38 CD47 5,000 210,000 CD38low(KMS-12-BM) Antibody concentration(nM) Phagocytosisindex 36Data presented at American Society of Hematology 2021 Annual Meeting. Author, Stefano Sammicheli, et. al ISB 1442 Shows Higher Killing Potency Across a Broad Range of CD38 Expression Levels Relative to Daratumumab Higher Complement Dependent Cell Cytotoxicity (CDC) Than Daratumumab Higher Potency Than Daratumumab in CD38low Antibody Dependent Cell Cytotoxicity (ADCC) Corporate Presentation | Mar 2024 100 101 102 103 120 100 80 60 40 20 0 -20 Specific killing (%) ISB 1442 Daratumumab Is. Control P<0.0005 CD38 CD47 180,000 60,000 CD38high(Daudi) 100 10110-4 10-3 10-2 10-1 20 40 60 NCI-H929 EC50 (nM) P-value ISB 1442 0.001 <0.05 Daratumumab 0.012 Antibody concentration(nM) Specific killing (%) 0 CD38 CD47 31,000 94,000 CD38low-int (NCI-H929) Antibody concentration (nM) 37 Statistics: Tukey’s multiple comparison test. EC50: Half Maximal Effective Concentration ISB 1442 Shows Superior Tumor Cell Killing Compared to 5F9 and Daratumumab, as Monotherapies or in Combination Corporate Presentation | Mar 2024 Multiple Mode of Action of Killing (MMoAK) ISB 1442 Compared to Anti-CD47 (5F9) and Daratumumab Monotherapy ISB 1442 Compared to Combination of Anti-CD47 (5F9) and Daratumumab % Specifickilling P<0.05 10-4 Antibody concentration (nM) % Specific killing ISB 1442 Daratumumab + anti-CD47 mAb (5F9)* Statistics: Tukey’s multiple comparison test. • MMoAK assay shown above is run in the presence of irrelevant competing IgGs from serum, more closely representing the environment in patient serum • The enhanced Fc in ISB 1442 activates macrophages regardless of the presence of competing IgGs, resulting in greater monotherapy efficacy than anti-CD47 (5F9) CD38 CD47 31,000 94,000CD38low-int (NCI-H929) -20 0 20 40 60 80 10-2 100 102 104 Antibody concentration (nM) 38 Data presented at American Society of Hematology 2021 Annual Meeting. Author, Stefano Sammicheli, et. al ISB 1442 Shows Higher Tumor Growth Inhibition In Vivo vs. Daratumumab Corporate Presentation | Mar 2024 • 10 million Raji cells were implanted subcutaneously into CB17/SCID mice • Animals were randomized when tumor volume reached ~100 mm3 • Doses: ISB 1442 and 5F9 (anti CD47) dosed IV QW at 10 mg/kg, daratumumab dosed IV BIW at 16 mg/kg Improved Tumor Growth Inhibition Compared to Daratumumab (in vivo) 1500 Days after xenograft PBS ISB 1442 Daratumumab First Dose *** ** Statistics: 1-way ANOVA w. Tukey post hoc testing ** p<0.01; *** p<0.001 Tumors Volume (m3) Raji Model 1000 500 0 2 5 8 12 15 19 22 26 29 33 36 39 Data presented at American Society of Hematology 2021 Annual Meeting. Author, Stefano Sammicheli, et. al ISB 1442 Shows Higher Cytotoxic Potency Against AML Cell Lines Compared to Anti-CD38 and Anti-CD47 Mono-Targeting Antibodies Corporate Presentation | Mar 2024 Antibody Dependent Cell Phagocytosis (ADCP) 0 20 40 60 80 ✱ ✱✱ ✱✱✱✱ Max phagocytosis (%) Control ISB 1442 Daratumumab Anti-CD47 (5F9) 0.001 0.01 0.1 ✱✱ EC50 (nM) ISB 1442 Daratumumab Antibody Dependent Cell Cytotoxicity (ADCC) Multiple Mechanisms Of Action Of Killing (MMoAK) P < 0.05 ** P < 0.01 *** P < 0.001 **** P < 0.0001 40 Statistics: Not Significant (NS) AML: Acute Myeloid Leukemia Cell used: MOLM-13 (CD38int CD47low) Presented at American Society of Hematology 2022 Annual Meeting ISB 1442 Showed More Frequent Killing of AML Blasts and a Trend Towards Higher Cytotoxic Potency as Compared to Monospecific Anti-CD38 Daratumumab or Anti-CD47 (5F9) Ex Vivo Corporate Presentation | Mar 2024 Killing of AML Blasts from Patients’ Bone Marrow Aspirates Ant-CD47 (5F9) Control ISB 1442 Daratumumab Potency Compared to Anti-CD38 or Anti-CD47 Monospecifics 41 DARA: Daratumumab Presented at American Society of Hematology 2022 Annual Meeting ISB 1442 Only Binds to CD47 After Engaging CD38, Reducing On- Target, Off-Tumor Depletion of Red Blood Cells Corporate Presentation | Mar 2024 Reduced Binding to RBC Minimal RBC Depletion Antibody concentration (nM) Statistics: 2-way ANOVA with multiple comparisons 100 101 102 103 0 1.5×104 Antibody binding (GeoRFI) ISB 1442 ** * ** *** **** **** ns p≥ 0.05; * p<0.05; ** p<0.01; *** p<0.001; **** p<0.0001 Anti-CD47 mAb (5F9) 5×102 1×103 1.5×103 2×103 1×104 5×103 100 101 102 103 104 0 20 40 60 80 100 Antibody concentration (nM) % RBC vs baseline ISB 1442 anti-CD47 mAb (5F9) * ** **** **** ****ns Statistics: 2-way ANOVA with multiple comparisons Antibody concentration (nM) 42 Statistics: Not Significant (NS) AML: Acute Myeloid Leukemia Cell used: MOLM-13 (CD38int CD47low) Presented at American Society of Hematology 2022 Annual Meeting ISB 1442 Clinical Development Corporate Presentation | Mar 2024 RPD2Phase 1 Dose Escalation in Triple-Class Refractory Multiple Myeloma Weekly SQ Dosing (on-going) Phase 2 Triple-Class Refractory Multiple Myeloma Monotherapy Phase 2 Multiple Myeloma Combination Studies (planned) Phase 1/2 Trial NCT05427812 BiologicallyActive Starting Dose Phase 1/2 Trial in Relapsed/Refractory Acute Myeloid Leukemia (planned start in 2024) • Australia, US, India • As of December 2023: 18 patients treated 43 ISB 1442-101 Clinical Trial Design Corporate Presentation | Mar 2024 Key Patient Eligibility Criteria: • R/R MM with measurable disease after a CD38 antibody, IMiDs, PIs, and who must not be candidates for regimens known to provide clinical benefit • Failed 3 or more prior lines of therapies Primary Objectives: • Assess safety, tolerability • Determine MTD/RP2D Secondary Objectives: • PK, immunogenicity • Assess preliminary clinical activity of ISB 1442 Exploratory Objectives: • Assess biomarkers and their correlation with clinical activity, safety, and other clinical endpoints of interest • Assess minimal residual disease (MRD) when indicated • a = the numerical value that leads to the next higher dose level in the standard titration design. n = number of subjects.. X = The dose level in the accelerated titration design at which the conversion criteria is met. DLT = dose-limiting toxicity; MFD = maximum feasible dose; MM = multiple myeloma; MTD = maximum tolerated dose; RP2D = recommended phase 2 dose; R/R = relapsed or refractory. • *According to Project Optimus, 2 putative recommended phase 2 doses will be tested.Dose levels to be determined. 44 Presented at American Society of Hematology 2023 Annual Meeting Biomarkers and Pharmacokinetics Corporate Presentation | Mar 2024 Dose-Dependence and Time Course of Soluble Biomarker Changes Following Treatment with ISB 1442 • Transient increases in soluble biomarkers were predominantly observed following the first dose of ISB 1442, with greater increases at dose level 4 (150 mg) compared to lower dose levels, and in patients exhibiting CRS-like symptoms (left panel). • The time course of biomarker changes during the first 48h after dosing is shown for one patient (DL4-ptatient 6), demonstrating the different timing of peak levels for several serum biomarkers after dosing within this patient (right panel). Pharmacokinetics • Mean ISB 1442 serum concentration versus time profile from Cohort 1 (6 mg SC), Cohort 2 (20 mg SC), Cohort 3 (60 mg SC) and Cohort 4 (150 mg SC) are shown. • Rich PK samples collected after C1D1 and C1D8 doses, followed by pre-dose samples for the remaining dose occasions. • Super-Proportional Increases in ISB 1442 Serum exposures (Cmax and AUC) most evident between cohorts 3 to 4. • Slow absorption of ISB 1442 after SC injection with Tmax achieved mostly on the 2nd day of dosing. Serum [Analyte] Days After First Dose Serum [MIP-1b] (pg/mL) Days After First Dose MIP-1b Time Course Time Course (DL4-6)Analyte 45 Presented at American Society of Hematology 2023 Annual Meeting Clinical Responses as of December 2023 Corporate Presentation | Mar 2024 Data extract update from 6th December, 2023 Best Overall Response DL1(6mg) N=2 DL2(20mg) N=1 DL3(60mg) N=5 DL4(150mg) N=9 DL5(300mg) N=1 Stable disease (SD) 0 0 1 (33%) 3 (33%) 0 Progressive Disease (PD) 1 (50%) 1 (100%) 1 (33%) 4 (44%) 0 Not Evaluable (NE) 1 (50%) 0 0 0 0 Missing 0 0 1 (33%) 2 (22%) 1 (100%) • Based on in-vitro modeling, current DL4 mean ISB 1442 concentration is in the EC50 range. EC90 range could potentially be achieved with DL 6 to 7 dose (450-600mg). 46 Presented at American Society of Hematology 2023 Annual Meeting Preliminary Results of the Ongoing Phase I Study Corporate Presentation | Mar 2024 • Overall, treatment with ISB 1442 is well tolerated. • CRS events observed at DL4 (150mg) were of low grade (1 or 2) and mostly resolved within one day. • No risk of neurotoxicity, hemolytic anemia or infections have been observed to date. • Soluble biomarker changes, with increased macrophage-related markers, are among the first changes observed supporting proof of mechanism. • Dose escalation is ongoing with participants enrolling in DL5 (300 mg). • Phase 1 dose-finding study in relapsed/refractory AML planned in late 2024/early 2025. 47 Presented at American Society of Hematology 2023 Annual Meeting ISB 2001 48 ISB 2001 - Executive Summary Corporate Presentation | Mar 2024 • Phase I, first-in-class trispecific BCMAxCD38xCD3 antibody, developed in RRMM • Pre-clinical data show potential for ISB 2001 to induce enhanced cytotoxicity relative to clinical benchmarks against MM expressingvariable levels of BCMA and CD38, mimicking naturaltumor heterogeneity. + Increased killing of tumor cells compared to teclistamab and alnuctamab + Higher potency when compared to the combination of daratumumab and teclistamab + Superior cytotoxicity over teclistamab in ex vivo assays in patient bone marrow aspirates + Superior efficacy over teclistamab in in vivo models demonstrating 100% complete response • An innovative quantitative systems pharmacology model supports an optimal first-in-human dose, eliminating useof primates and reducing patient exposure to sub-efficacious doses of therapies. • Phase 1 first-in-human study of ISB 2001 for the treatment of relapsed/refractorymultiple myeloma is currently ongoing in the US and Australia (Clinicaltrials.gov identifier: NCT05862012). • Granted orphan drug designation (ODD) by the U.S. Food and Drug Administration (FDA) 49 ISB 2001 is First TREAT TM Trispecific Antibody For Relapsed/Refractory Multiple Myeloma • BCMA and CD38 are expressed on the surface of multiple myeloma cells and are clinically validated targets. • ISB 2001 combines three proprietary Fab arms binding to CD3e on T-cells, and to BCMA and CD38 on myeloma cells. • In vitro studies showed increased tumor killing potency of ISB 2001 compared to all tested antibodies, including currently approved and investigational multiple myeloma therapies. • In vivo studies in multiple myeloma models also show superior potency of ISB 2001 relative to antibodies for the treatment of multiple myeloma. • ISB 2001 redirects CD3+ T lymphocytes to kill tumor cells expressing from low to high levels of both BCMA and CD38. • With two different tumor-associated antigens, ISB 2001 is expected to be more resistant to antigen escape associated with treatment of MM patients. • Ichnos received authorizations from HREC in Australia and the U.S. FDA to initiate a Phase 1 first-in-human study of ISB 2001 for the treatment of MM and was granted ODD by the U.S. FDA for the same indication. Corporate Presentation | Mar 2024 KEY ATTRIBUTESISB 2001 (BCMA x CD38 x CD3) trispecific antibody 50 TREAT : Trispecific Engagement by Antibodies based on the TCR MHC: Major histocompatibility complex, CDC: Complement-Dependent Cytotoxicity ADCC: Antibody-Dependent Cell-mediated Cytotoxicity ISB 2001 is Designed to Mediate Potent MM Cell Killing via Dual Targeting Avidity-Driven Tumor Binding Corporate Presentation | Mar 2024 IgG1 IgG3 TCR constant alpha TCR constant beta Fc silencing (L234A, L235A, P329A) KMS-12-BM (BCMAlow CD38low) NCI-H929 (BCMAint CD38int) MOLP-8 (BCMAlow CD38high) Potency LO HI 0.1 1 10 100 1000 10000EC 50 (pM) ✱✱✱✱ ✱✱✱✱ NQ 0.1 1 10 100 1000 10000EC 50 (pM) ✱✱✱✱ ✱✱✱✱ NQ 0.1 1 10 100 1000 10000EC 50 (pM) ✱✱✱✱ ✱✱✱✱ Expression sABC CD38 mean BCMA mean KMS-12-BM 28,000 9,000 NCI-H929 85,000 52,000 MOLP-8 512,000 3,200 ****= p <0.0001 CD38 BCMA CD3 ✱✱✱✱ 51 NQ: Not Quantifiable. DU: Dummy (irrelevant binder) Presented at American Society of Hematology 2022 Annual Meeting and American Association for Cancer Research 2023 Annual Meeting ISB 2001 Potency is Superior to the Combination of Teclistamab + Daratumumab Corporate Presentation | Mar 2024 0 20 40 60 80 100 ISB 2001 or Teclistamab at 10 pM Daratumumab at 100 nM % Cytotoxicity ✱✱✱✱ ✱✱✱✱ ✱✱✱✱ ✱✱✱✱ ISB 2001 or Teclistamab at 100 pM Daratumumab at 100 nM % Cytotoxicity ✱✱✱✱ ✱✱✱✱ ✱✱ *=p <0.05 **=p <0.01 ****= p <0.0001 • Multiple Mode of Action Killing assay of tumor cell line KMS-12-BM • The tumor cells were incubated for 48 hours with human PBMCs from healthy donors at a 5:1 effector to target ratio • 10 pM or 100 pM of ISB2001, teclistamab in the presence or absence of 100 nM of daratumumab were added to the culture • The percentage of cytotoxicity is displayed 0 20 40 60 80 100 ✱ 52 Paired one-way ANOVA followed by Tukey’s multiple comparisons test Presented at American Society of Hematology 2022 Annual Meeting and American Association for Cancer Research 2023 Annual Meeting ISB 2001 Exhibits Desirable PK and shows 100% Complete Responses In Vivo in a BCMAlow CD38low MM Model Corporate Presentation | Mar 2024 **=p <0.01 ***= p <0.001 ****= p <0.0001 0 7 21 28 Days 1 10 100 1000 Molecule (mg/ml) Pharmacokinetic 5 mg/kg single dose i.v. ISB 2001 -10 -8 -6 -4 -2 0 2 4 6 8 10 12 14 16 18 20 1400 1200 1000 800 600 400 200 0 Treatmentdays Tumorvolume(mm3) Vehicle 0.1 mg/kg Teclistamab 0.1 mg/kg ISB 2001 ✱✱✱✱ ✱✱✱✱ Efficacy in NSG-PBMC transfer Mouse Model (KMS-12-BM)ISB 2001 Half-Life in Tg32 (huFcRn Tg) Mice Molecule Half-Life (days) Cmax (µg/ml) AUC (µg.days/ml) ISB 2001 7.6 ± 0.9 95 ± 26 417 ± 75 Treatment Complete Response Teclistamab 0% (0/8 mice) ISB 2001 100% (8/8 mice) 14 53 Presented at American Society of Hematology 2022 Annual Meeting and American Association for Cancer Research 2023 Annual Meeting ISB 2001 Exhibits Higher Cytotoxic Potency Ex Vivo Compared to Teclistamab on MM Patient Samples Corporate Presentation | Mar 2024 + Treatment Myeloma Patient samples: sMM, NDMM, r/r MM, PCL Myeloma cells 1 0.1 0.01 Antibody Concentration (nM) -20 0 60 40 20 80 100 % Killingof CD138+ cells ISB 2001 Teclistamab * *** ** Plasma Cell Leukemia r/r MM Newly Diagnosed MMSmoldering MM 0 25 50 75 100 Antibody Concentration [nM] % Killing of CD138+ cells Antibody Concentration [nM] % Killing of CD138+ cells Antibody Concentration [nM] % Killing of CD138+ cells ISB 2001 EC50 = 9.1 pM TeclistamabEC50 = 351.7 pM Antibody Concentration [nM] % Killing of CD138+cells ISB 2001 EC50 = 7.2pM Teclistamab EC50 = 829 pM *=p <0.05 **=p <0.01 ***= p <0.001 0 25 50 75 100 0 25 50 75 100 0 25 50 75 100 54 sMM: Smoldering Multiple Myeloma NDMM: Newly Diagnosed Multiple Myeloma r/r MM: Relapsed Refractory Multiple Myeloma PCL: Plasma Cell Leukemia Presented at American Society of Hematology 2022 Annual Meeting and American Association for Cancer Research 2023 Annual Meeting Corporate Presentation | Mar 2024 RPD2 Part 1 Dose Escalation in Triple-Class Refractory Multiple Myeloma Weekly SQ Dosing (on-going) Accelerated Titration followed by 3+3 Part 2 Dose Expansion Putative RP2D #1 Part 2 Dose Expansion Putative RP2D #2 • Phase 1, First-in-Human, Multicenter, Open-Label, Dose Escalation and Dose-Expansion Study of Single-Agent ISB 2001 in Subjects with Relapsed/Refractory Multiple Myeloma (R/R, MM) • Approved by the U.S. FDA on 12 April 2023, Australian HREC on 5 April 2023 and granted Orphan Drug Designation for the treatment of multiple myeloma by the U.S. FDA on 28 June 2023. • Study is open to accrual, First patient dosed on November 1, 2023 Innovative QSP-based Starting Dose ISB 2001 Clinical Development 55 QSP: Quantitative Systems Pharmacology (in-silico) RP2D: Recommended Phase 2 Dose ISB 2001-101 Clinical Trial Design Corporate Presentation | Mar 2024 • a = the numerical value that leads to the next higher dose level in the standard titration design. n = number of subjects.. X = The dose level in the accelerated titration design at which the conversion criteria is met. DLT = dose-limiting toxicity; MFD = maximum feasible dose; MM = multiple myeloma; MTD = maximum tolerated dose; RP2D = recommended phase 2 dose; R/R = relapsed or refractory. • *According to Project Optimus, 2 putative recommended phase 2 doses will be tested. Dose levels to be determined. Key Patient Eligibility Criteria: • R/R MM with measurable disease after a CD38 antibody, IMiDs, PIs, and who must not be candidates for regimens known to provide clinical benefit • Failed 3 or more prior lines of therapies Primary Objectives: • Assess safety, tolerability • Determine MTD/RP2D Secondary Objectives: • PK, immunogenicity • Assess preliminary clinical activity of ISB 2001 Exploratory Objectives: • Assess biomarkers and their correlation with clinical activity, safety, and other clinical endpoints of interest • Assess minimal residual disease (MRD) when indicated 56 Presented at American Society of Hematology 2023 Annual Meeting 1Cohen, A. D. et al. J. Clin. Invest. 129, 2210–2221 (2019). 2 Nijhof, I. S. et al. Blood 128, 12 (2016). Preliminary Results of the Ongoing Phase I Study Corporate Presentation | Mar 2024 • Overall, treatment with ISB 2001 is well tolerated. No DLT observed. • Low grade CRS events observed in 2/6 subjects (one Gr1 and one gr2). Injection site reactions observed in 3/6 subjects (all gr 1). • No risk of neurotoxicity, cytopenias, or infections have been observed to date. • All 6 subjects are ongoing on treatment (longest is 7 cycles). • Dose escalation is ongoing with participants enrolling in DL5 (300 mg/kg). • High interest from investigators/recruitment. 57 Company Summary Corporate Presentation | Mar 2024 • 3 Phase 1 Assets in Multiple Myeloma • Phase 1 Trial in R/R AML with ISB 1442 Planned in mid-2024 • Phase 1 Trial in Solid Tumors with Cbl-b Inhibitor GRC 65327 planned in early 2025 • Out-licensing of All Non-Oncology Assets Completed • Divestiture of the process development and manufacturing plant in progress • Standardized Process Development and Manufacturing Operations Achieving High-Titer Yield for BEAT® Multispecifics. • Privately-Held Biotech Company with Plan for IPO in the medium-term 58 Corporate Presentation | Mar 2024 Thank you! Let’s collaborate to accelerate cancer cure

The release as fetched from its publisher. iginnovate.com ↗