Nkgen Biotech Inc. · OTC:NKGN

Nkgen Biotech — AD/PD 2026

21 slides from Nkgen Biotech's conference presentation, March 2026

  1. Slide 1: First-in-class NK Cell Therapy Troculeucel Shows Cognitive Benefit in Moderate Alzheimer's

    First-in-class NK Cell Therapy Troculeucel Shows Cognitive Benefit in Moderate Alzheimer’s: Dose- Dependent Phase 1 Findings Paul Y. Song, MD NKGen Biotech March 2026, Copenhagen, Denmark

  2. Slide 2: Disclosure of conflicts of interest

    No, Nothing to disclose X Yes, please specify Company / Honoraria / Consulting / Funded Royalties Stock Ownership Employee Other Name Expense Advisory Research / Patent Options / Equity (Please Board Position specify) NKGen Biotech x x x

  3. Slide 3: Natural Killer Cells

    Natural Killer Cells Innate Lymphoid Cells: 5-20% of circulating lymphocytes (CD3- CD56+) Can Distinguish Healthy Cells (self) From Dangerous Cells (non-self): Ability to identify and eliminate “dangerous” cells Mediate antibody-dependent cellular cytotoxicity (ADCC) Immune regulatory capabilities,

  4. Slide 4: NK cell manufacturing process

    Collection D0 ~D18 ~D30 Manufacturing of all doses for 1-year treatment 1 2 3 4 5 6 7 Collection PBMC Isolation Activation Ex-vivo Harvesting, Drug Product Administration /NK Cell Expansion Packaging, QC Testing Selection Cryo- preservation Leukapheresis CD3-CD56+ NK cell Co-cultivation & High purif

  5. Slide 5: Autoreactive T cells Cause Neuroinflammation And Damage

    Autoreactive T cells Cause Neuroinflammation And Damage Chronic protein deposition leads to an autoinflammatory cascade and damage Removing proteins only addresses one aspect of the underlying pathology Activation of Autoreactive CD4+ and CD8+ T cells1-5 which migrate to the brain via CXCR36 is a ve

  6. Slide 6: Mechanistic Investigation of SNK01: Brain Migration

    Mechanistic Investigation of SNK01: Brain Migration SNK01 expresses high level of SNK01 migrates toward CSF SNK01 has migratory potential CXCR3, also found in AD patients and plasma of AD patients toward chemokine ligands CSF CX3CL1 CXCL9 CXCL10 CXCL11 Relative migration Specific chemokines linked t

  7. Slide 7: Mechanistic Investigation of SNK01: Functional Activity

    Mechanistic Investigation of SNK01: Functional Activity SNK01 kill activated inflammatory SNK01 secrete anti-inflammatory SNK01 internalizes and degrades T-cells through engagement of cytokines protein aggregates highly expressed NKG2D & DNAM-1 amyloid β α-synuclein Activated T cells γ Resting T cel

  8. Slide 8: Troculeucel reduces AD pathogenesis via anti-neuroinflammation

    Troculeucel reduces AD pathogenesis via anti-neuroinflammation Super NK cell (SNKTM) Abnormal protein and Neuroinflammation CD56bright CD16+ plaque accumulation and BBB leakage Inflammatory T- Amyloid β plaque cells (CD4+/CD8+) Activated microglia ↑ Inflammatory cytokines Reactive astrocytes Tau neu

  9. Slide 9: Objectives

    Objectives • To evaluate preliminary dose-response to troculeucel, an autologous, non-genetically modified NK cell therapy with enhanced cytotoxicity and activating receptor expression, in moderate Alzheimer’s disease (AD) patients across two Phase 1 studies.

  10. Slide 10: Methods

    Methods Study SNK0-MX04 (NCT04678453) • Phase 1 dose-escalation study (n=10) • AD patients – Median MMSE score of 14 • Troculeucel 4 doses (1B, 2B or 4B) IV every three weeks for 3 months Study SNK01-AD01 (NCT06189963) • Phase 1 part of 1/2a study (n=3) • Moderate AD patients – Median MMSE score of

  11. Slide 11: Results - Safety

    Results - Safety • Troculeucel was very well tolerated. • No drug related adverse reactions reported.

  12. Slide 12: Anti-Aβ Drugs Still Showed Decline, Most SNK01 Patients Stabilized or Improved

    Anti-Aβ Drugs (Mild AD) Still Showed Decline, Most SNK01 Patients (Moderate AD) Stabilized or Improved CDR-SB, Anti-Aβ Drugs CDR-SB, SNK01 EMERGE CLARITY AD TRAILBLAZER- MX04 dose escalation AD-01 (in US) at AL 2 below RP2D 6x109 Cells (RP2D) cf1 cf1 cf1 cf1 cf1 cf2 cf2 cf2 cf2 Raket, L. L. et al.,

  13. Slide 13: CDR-SB change from baseline

    CDR-SB -6 Improved -5 -4 Change from baseline -3 At 3 months, 50% (one at 4B, MCID two at 6B) improved from -1 Stable moderate to a mild AD rating 0 on CDR-SB 1 MCID Declined 3 4 0 SNK01 Q3W 11/14 Time after baseline (weeks) 1 x 109cells 4 x 109cells 6 x 109cells

  14. Slide 14: Two patients at 6B completing one year

    Two patients at 6B completing one year showed maintained improvement. ** emphasizes baseline moderate AD patient improving to mild AD and continually improving or stabilizing at week 14 and 50

  15. Slide 15: ADCOMS change from baseline

    ADCOMS -0.30 Improved -0.25 -0.20 Change from baseline -0.15 MCID -0.05 Stable 0.00 0.05 MCID Declined 0.15 0.20 0 SNK01 Q3W 11/14 Time after baseline (weeks) 1 x 109cells 4 x 109cells 6 x 109cells

  16. Slide 16: ADAS-Cog change from baseline

    ADAS-Cog Improved -10 -8 Change from baseline -6 MCID -2 Stable 0 2 MCID Declined 6 8 0 SNK01 Q3W 11/14 Time after baseline (weeks) 1 x 109cells 4 x 109cells 6 x 109cells

  17. Slide 17: CSF biomarkers

    AD/PD% Q a-Synucleins A im: _ 2 yne Ap42/40 ratio 3 3 3 Sl mmc) v 9 8g i 3 ; a ie: : i ; r] £ E 0.001 a — ie 3 : 5 ia : & < 6 é a S Ss ® e Car sw : ie 2 - 2 3 go _ 3 Eo ie i Es 5 £ ox 2.» E 10° cells N=4 st ie 5 “noone |S c . D 4xl0° cells N=3 sé ay FE: =~ en cota nng —-[SN=Ee ] = -20 vvyy So * weok

  18. Slide 18: CSF GFAP change from baseline

    Change from baseline 10000004 -1000000 -20000004 CSF GFAP @ ADO01-105-001 # ADO1-105-003 & ADO01-105-004 -3000000: T T Baseline Week 26 (6 months) Aw.NKGEN

  19. Slide 19: Biomarkers

    SNK01 6x109 cells Q3W (17 doses); n = 3 moderate AD patients: improvement in biomarkers observed as well Biomarkers Plasma GFAP Plasma Aβ42/40 Improved Improved 19

  20. Slide 20: Results - Efficacy

    Results - Efficacy • Despite over half of all AD patients in both studies receiving low doses (< 2 B), 12/13 (92%) showed stable or improved cognitive function at 3 months. • Among all six moderate AD patients, 100% were stable or improved using MCIDs of ±2 for CDR-SB, ±4 for ADAS-Cog, and ±0.1 for

  21. Slide 21: Conclusion

    Conclusion Troculeucel demonstrated excellent tolerance and early signs of dose- dependent meaningful cognitive benefit in moderate AD patients. Troculeucel also demonstrated improvements in CSF levels of AB42/40, pTau, and α-synuclein as well as GFAP and YLK-40 largely in a dose responsive manner.

NKGen Biotech — AD/PD 2026 on 6ix