Adlai Nortye Group Ltd. · NASDAQ:ANL

Adlai Nortye — Investor Presentation (April 2026)

30 slides from Adlai Nortye's investor presentation, Apr 16, 2026

  1. Slide 1: April 2026 Corporate Presentation

    0 April 2026 Corporate Presentation NASDAQ: ANL

  2. Slide 2: Disclaimer

    1 Disclaimer This presentation has been prepared by Adlai Nortye Ltd. (the "Company") for informational purposes only and does not constitute an offer to sell or the solicitation of an offer to buy any securities. This presentation contains forward-looking statements within the meaning of the Privat

  3. Slide 3: Pipeline Chart

    2 Product MOA Indication Discovery IND Enabling Phase 1a Phase 1b Phase 2 Phase 3 Upcoming Milestone Worldwide Rights AN9025 pan- RAS(ON)i RAS-addicted tumors Ph1 dose escalation completion in H1 2027 Ex-China1 AN4035 CEACAM5 pan- RAS(ON)i ADC CEACAM5- enriched RAS- addicted solid tumors IND submiss

  4. Slide 4: AN9025: An Oral Small-Molecule Pan-RAS(ON) Inhibitor

    3 AN9025: An Oral Small-Molecule Pan-RAS(ON) Inhibitor

  5. Slide 5: Why Targeting Pan-RAS(ON)

    4 Why Targeting Pan-RAS(ON) KRAS (OFF)i KRAS (ON)i • RAS proteins cycle between an active GTP-bound ("ON") state and an inactive GDP-bound ("OFF") state to transmit signals from cell surface receptors. • Mutations in RAS result in constitutive activation and oncogenic signaling, with the GTP-bound (

  6. Slide 6: AN9025's Binding Affinity for CypA vs. RMC-6236

    5 AN9025's Binding Affinity for CypA Suggests It May Offer More Sustained RAS Inhibition vs. RMC-6236 KD1 = 3.2 nM Kinetic Analysis of AN9025 Binding to CypA on Octet Binary Affinity KD1 (nM) ka (1/[M*S]) kdis (1/s) AN9025 3.2 1.6 E+05 5.0 E-04 RMC-6236 12.4 2.8 E+05 3.4 E-03 AN9025 demonstrates a b

  7. Slide 7: AN9025 Shows Stronger Tri-Complex Binding Affinity vs. RMC-6236

    6 AN9025 Shows Stronger Tri-Complex Binding Affinity vs. RMC-6236 KD2 = 24.8 nM Mutant RAS(ON) Protein AN9025 RMC-6236 KD (nM) ka (1/[M*S]) kdis (1/s) KD (nM) ka (1/[M*S]) kdis (1/s) KRASG12D 8.8 4.9 E+05 4.3 E-03 24.8 5.4 E+05 1.3 E-02 KRASG12V 8.3 3.2 E+05 2.7 E-03 68.4 1.8 E+05 1.2 E-02 KRASG12C

  8. Slide 8: AN9025 Sensitivity Profile Across Cancer Cell Line Panel

    7 AN9025 Demonstrates a Sensitivity Profile Comparable to RMC-6236 Across a Cancer Cell Line Panel but with Significantly Higher Potency AN9025 demonstrates approximately 100-fold more potent inhibition of cell proliferation across RAS mutant cell lines than RMC-6236. AN9025 shares similar RAS mutan

  9. Slide 9: AN9025 Demonstrates More Sustained RAS Inhibition vs. RMC-6236

    8 AN9025 Demonstrates More Sustained RAS Inhibition vs. RMC-6236 Phospho-ERK(T202/Y204) inhibition (IC50, nM) in HPAC AN9025 RMC-6236 4 h incubation 0.048 0.27 4 h incubation + 48 h washout 0.18 4.3 IC50 Shift 3.7 X 16 X AN9025 enables prolonged inhibition of the RAS pathway, maintaining its effects

  10. Slide 10: AN9025 Deep Tumor Regression in HPAC CDX Model

    9 AN9025 Achieves Deep Tumor Regression and Provides More Sustained Anti-Tumor Effects vs. RMC-6236 in HPAC (KRASG12D) CDX Model AN9025 demonstrated comparable antitumor activity to RMC-6236; notably, AN9025 exhibited more sustained efficacy following drug withdrawal. Compounds HPAC CTG (IC50, nM) D

  11. Slide 11: PK-PD Analysis Supports More Durable RAS Inhibition

    10 PK-PD Analysis Further Supports More Durable RAS Inhibition by AN9025 vs. RMC-6236 in HPAC (KRASG12D) CDX Model This study evaluated the PK–PD correlation at the end of 7 days of continuous oral dosing and also assessed PK after the first dose for comparison The results indicate that AN9025 has t

  12. Slide 12: AN9025 More Prolonged Anti-Tumor Effects in KP-4 CDX Model

    11 AN9025 Achieves More Prolonged Anti-Tumor Effects Compared to RMC-6236 and RMC-9805 in KP-4 (KRASG12D) CDX Model Compounds Dose (mg/kg) RTV1 (%) on the day of best tumor regression RTV1 (%) on Day 42 AN9025 0.2 26.6% 41.0% 0.1 41.6% 58.2% RMC-6236 25 81.0% (D14) 1331% RMC-9805 100 25.7% (D14) 658

  13. Slide 13: AN9025 Demonstrates Overall Favorable PK Properties

    12 AN9025 Demonstrates Overall Favorable PK Properties Mouse Rat Dog Monkey IV Dose (mpk) 0.25 0.03 0.005 0.1 T1/2 (h) 39 21 49 18 Vdss (L/Kg) 1.9 2.4 1.7 0.92 CL (mL/Kg/min) 1.2 1.6 0.44 0.7 AUC0-inf (ng/mL*h) 3350 324 203 2373 PO Dose (mpk) 0.50 0.10 0.02 0.5 Cmax (ng/mL) 46 16 9.5 100 T1/2 (h) 37

  14. Slide 14: Therapeutic Index and Human PK Simulation of AN9025

    13 Therapeutic Index (TI) and Human PK Stimulation of AN9025 for Once-Daily Dosing Drug Species TSC 1 nM MED 1 MTD (Observed in 4-week in-vivo efficacy study in mice and 2-week DRF toxicology studies in rats) TI b (MTD/MED) Dose mpk AUC nM*hour Cmax nM Dose mpk AUC nM*hour Cmax nM AN9025 Mouse 6.9 0

  15. Slide 15: Lower Tumor Stasis Concentration with QW Dosing

    14 A potentially lower tumor stasis concentration (TSC) was observed with QW dosing compared to QD dosing, supported by durable PD inhibition 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 0 200 400 600 800 1000 1200 1400 Days after the start of treatment Tumor volume(mm3) Vehicle (P.O.,QD) AN9025 (0.04

  16. Slide 16: Widening of Therapeutic Window with Intermittent Dosing

    15 Widening of AN025 Therapeutic Window with Intermittent Dosing Species Dosing Regimen TSC 1 nM (95% CI) MED 1 MTD(Observed in 4-week in-vivo efficacy model in mice and 2-week DRF toxicology study in rats) TI (MTD/MED) Dose mpk Weekly AUC nM*hour Cmax nM Dose mpk AUC nM*hour Cmax nM Mouse QD 6.2 0.

  17. Slide 17: Summary of AN9025

    16 Summary of AN9025 AN9025 holds best-in-class potential within the Pan-RAS(ON) inhibitor category: • Exhibited a binding affinity for cyclophilin A (CypA) that is 4-folder stronger than that of RMC-6236, driven by a slower dissociation rate from CypA, which may enable more sustained RAS inhibition

  18. Slide 18: AN4035: A Novel CEACAM5 Pan-RAS(ON)i ADC

    17 AN4035: A Novel CEACAM5 Pan-RAS(ON)i ADC

  19. Slide 19: RAS Inhibitor Conjugated Antibodies (RASiCA) Platform

    18 RAS Inhibitor Conjugated Antibodies (RASiCATM) - Diversifying ADC Payloads to Overcome Clinical Resistance References: 1. Abelman et al. Clin Cancer Res 2025; 2. Peng et al. Breast, 2025; 3. Tarantino et al. Clin Cancer Res 2025 (abstr P1-08-08) RASiCATM platform is designed to overcome TWO major

  20. Slide 20: Pan-RAS(ON) Inhibitor as a Next-Generation ADC Payload

    19 Pan-RAS(ON) Inhibitor as a Next-Generation ADC Payload • Cyclophilin A, an abundant intracellular protein (μM levels), is the target engaged by pan- RAS(ON) inhibitors, much like MMAE targeting tubulin • ADCs leveraging pan-RAS(ON) inhibitors could further enhance the therapeutic index MOA of Pan

  21. Slide 21: Payload Is a Proprietary Highly Potent Pan-RAS(ON) Inhibitor

    20 Payload Is a Proprietary Highly Potent Pan-RAS(ON) Inhibitor Binary (CYPA) KD1 (nM) Tri-complex (KRAS) KD2 (nM) G12C G12D G12V WT Payload 14.9 4.7 30.5 14.0 18.6 RMC-6236 12.5 19.1 174 45.9 52.8 Cancer Cell Indication RAS mutation type Payload 72h CTG IC50 (nM) Imax % NCI-H2009 NSCLC Kras G12A 0.

  22. Slide 22: Overview of AN4035

    21 Overview of AN4035 CEACAM5: overexpressed in CRC, PDAC, & NSCLC where RAS is frequently mutated Conjugator: homogenous DAR 8 with high stability; no retro-Michael reaction Linker: highly hydrophilic; excellent circulation stability and efficient payload release Payload: highly potent pan-RAS(ON)

  23. Slide 23: CEACAM5 as a Compelling Target for Pan-RAS(ON) ADC

    22 CEACAM5 as a Compelling Target for Pan-RAS(ON) Inhibitor-Based ADC RAS-Mutant Cancer–Enriched, Skin-Sparing Expression Differential Expression in Normal Epithelium Adapted from ASCO 2024 Discussant on Abs #3000, 3001, 3002 Expression data are derived from TCGA, GTEx datasets HER2 mRNA-IHC thresho

  24. Slide 24: AN4035 Superior Target-Mediated Intracellular Payload Retention

    23 AN4035 Achieved Superior Target-Mediated Intracellular Payload Retention Incubation Time AN4035 (10 μg/mL) Isotype-payload (10 μg/mL) CEACAM5C (10 μg/mL) Cell supernatant payload conc. (nM) Cell lysate payload conc. (nM) lysate/ supernatant payload ratio Cell supernatant payload conc. (nM) Cell l

  25. Slide 25: AN4035 Potent Cytotoxicity and Bystander Effect

    24 AN4035 Demonstrated Potent Cytotoxicity and a Robust Bystander Effect in CEACAM5- Positive, RAS-Addicted Cancer Cell Models Cancer Cell Line Cancer Type CEACAM5 mRNA nTPM RAS mutation type 6-day CTG AN4035 Isotype ADC IC50 (nM) Imax % IC50 (nM) CL-40 CRC 1821 Kras G12D 0.77 98 SK-CO-1 784 Kras G1

  26. Slide 26: AN4035 Robust Anti-Tumor Activity in CDX Models

    25 AN4035 Demonstrated Robust Anti-Tumor Activity in CDX Models Compound CTG1 (IC50, nM) Dose (mg/kg) ΔRTV2 (%) on Day 25 AN4035 0.10 3.0, single dose -78% 10, single dose -85% (1) CTG = cell-titer glow in vitro assay (2). ΔRTV = relative tumor volume; relative to the tumor volume at the start of tr

  27. Slide 27: AN4035 Enhanced Tumor Retention and Tumor Selectivity

    26 AN4035 shows enhanced target-mediated tumor retention versus payload alone, with significantly improved tumor selectivity over normal tissues (1) Ratio of tumor/tissue concentration (or AUC exposure) over blood concentration; (2) Concentrations in these tissues were below the limit of quantificat

  28. Slide 28: AN4035 Activity in Single-Mouse PDX Trials

    27 AN4035 Exhibited Compelling Activity in Single-Mouse PDX Trials 27 The response was determined by comparing tumor volume change at time t to its baseline with ΔRTV = (Vt-V0) / V0 × 100; Criteria for response were adapted from RECIST clinical criteria; Complete Response (CR): at least an 85% decre

  29. Slide 29: AN4035 Favorable PK and Tolerability in Monkeys

    28 0 7 14 21 28 0.1 1 10 100 1000 CB17-SCID mouse Time after drug injection(day) Plasma Conc. (ug/mL) CEACAM5 mAb AN4035 AN4035 Demonstrated Favorable PK and Tolerability in Monkeys AN4035 showed an antibody-like PK profile, comparable to CEACAM5 mAb in mice1 Compound Dose C0 (μg/mL) AUC (h*μg/mL) T

  30. Slide 30: Summary of AN4035

    29 Summary of AN4035 AN4035 is a potential first-in-class CEACAM5-targeting ADC armed with a highly potent pan-RAS(ON) inhibitor payload: • Favorable thermal and plasma stability with desirable pharmacokinetic properties • Strong intracellular payload retention, driving nanomolar to picomolar cytoto

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