Nkgen Biotech Inc. · OTC:NKGN
Nkgen Biotech — Investor Presentation (January 2026)
29 slides from Nkgen Biotech's investor presentation, January 2026
Slide 1: Transformative Therapy for Neurodegenerative Diseases
Transformative Therapy for Neurodegenerative Diseases Corporate Overview January 2026
Slide 2: Disclaimer: Forward-Looking Statements
Disclaimer Forward-Looking Statements This Presentation may contain "forward-looking statements" within the meaning of Section 27A of the Securities Act and, to the extent applicable, Section 21E of the Exchange Act. NKGen Biotech, Inc.'s ("NKGen" or "the Company") forward-looking statements include
Slide 3: Disclaimer: Forward-Looking Statements
Disclaimer Forward-Looking Statements Important factors that may affect actual results or outcomes include, among others, the risk that regulatory approvals for the Company’s product development are not obtained, are delayed or are subject to unanticipated conditions that could adversely affect NKGe
Slide 4: Corporate Summary – Strategic Pivot from Oncology to Alzheimer's Disease
Corporate Summary – Strategic Pivot from Oncology to Alzheimer’s Disease due to Serendipitous Human Data in Advanced AD Unprecedented Troculeucel (SNK01), improvement in autologous “Super” Investment-to-date advanced AD NK cells in early patient positions NKGen’s pivot to AD Phase 2a for moderate AD
Slide 5: Different Populations of NK Cells Play Critical Roles in Modulating Inflammation
Different Populations of NK Cells Play Critical Roles in Modulating Inflammation NK cells can recognize harmful foreign cells via 40+ receptors, migrating to target region to mediate immune defense NK cell dysregulation typically “bright” NK cell Regulates immune occurs with immune (high CD56+) syst
Slide 6: Super NK Autologous Cells: Dual-Function NK Power to Maximize Immune Integrity
Super NK Autologous Cells: Dual-Function NK Power to Maximize Immune Integrity We uniquely combine the functional strengths of both bright and dim NK cell subtypes into one “dim” NK cell “bright” NK cell Super NK cell (SNKTM) CD56dim CD16+ CD56bright CD16low/- CD56bright CD16+ Cytotoxic activity Imm
Slide 7: A Serendipitous Discovery Guides NKGen's Pivot
A Serendipitous Discovery Guides NKGen’s Pivot: Remarkable Symptom Improvement in Advanced AD Patient Cultural context: SNK01 infusion shows boosting notable improvement immunity with in family member AD cell therapy symptoms Compassionate case study: family member of In Japan, physician-led, non-GM
Slide 8: Compassionate Case Study: Daniel, Korean Man with PSEN1 Mutation + Advanced AD
Compassionate Case Study: Daniel, 38 Y.O. Korean Man with PSEN1 Mutation + Advanced AD Pre-Treatment Advanced AD with strikingly decreased parietal activity with moderate diffuse temporal, occipital and posterior fossa activity Treatment: 19 doses SNK01, 4~8B cells per dose (once every 2 weeks), ove
Slide 9: Compassionate Case Study: Janice, Woman with Advanced Alzheimer's
Compassionate Case Study: Janice, 70 Y.O. Woman with Advanced Alzheimer’s Improvement after resuming treatment even after 2y pause Pre-treatment 2020 2021 2022 2023 2024 treatment paused treatment treatment • Difficulty naming Initial treatment: No treatment for nearly 2 Subsequent treatment: family
Slide 10: These Three Advanced AD Patients Demonstrate Unprecedented Improvement in Symptoms
These Three Advanced AD Patients Demonstrate Unprecedented Improvement in Symptoms 2021 2025 Anti-amyloids Super NK cells Prior to 2021, no disease- Paradigm shift: Next-generation: modifying therapies existed Anti-amyloids NKGen Biotech’s SNKTM (e.g., lecanemab) autologous cell therapy Drugs only o
Slide 11: Advancing from Remarkable Anecdotal Data to Small Ph1 in Mexico
Advancing from Remarkable Anecdotal Data to Small Ph1 in Mexico Serendipitous observation of improved How could we convince the FDA to allow a symptoms in advanced AD (NKGen Phase 1/2a study in AD with SNK01? executive's family member) • Needed to provide scientific justification Compassionate use i
Slide 12: SNK01-MX04 Phase 1: Study Design to Support IND in US
SNK01-MX04 Phase 1: Study Design to Support IND in US Phase I Dose Escalation: 3+3 Design Single Site in MX • Location: Angeles Tijuana Hospital, 10 patients (11 enrolled), all AD: Cohort 3 4.0x109 cells • 5 mild, 3 moderate, and 2 severe AD I/E Criteria • Age 55 to 85 years old, Stage 3,4,5, and 6
Slide 13: SNK01-MX04 Phase 1: Efficacy in Dose Escalation Study by Dose
SNK01-MX04 Phase 1: Efficacy in Dose Escalation Study by Dose ADCOMS 1×109 cells (n=4) 2×109 cells (n=3) 4×109 cells (n=3) Improved Improved Improved Stable Stable Stable Declined Declined Declined SNK01 Q3W SNK01 Q3W SNK01 Q3W Mild AD Moderate AD Severe AD At Week 11, 90% of participants showed eit
Slide 14: SNK01-MX04 Phase 1: CSF Biomarkers Data
SNK01-MX04 Phase 1: CSF Biomarkers Data pTau 181 α-Synuclein Aβ42/40 ratio Abnormal proteins Improved Improved Improved SNK01 Q3W GFAP YKL-40 N=4 Neuroinflammatory N=3 N=3 markers CSF biomarker changes correlated with Improved Improved improvement in both abnormal proteins and neuroinflammatory mark
Slide 15: SNK01-AD01 Study: Abbreviated Phase 1 in Moderate AD Patients in the US
SNK01-AD01 Study: Abbreviated Phase 1 in Moderate AD Patients in the US • MX04 Mexico dose ranging study supported FDA IND SNK01-AD01 filing Abbreviated Phase 1 • NKGen wanted to move to higher dose for 1 year of • 3 Moderate AD patients dosing Q3W of 6B cell/dose and needed to bridge • Dose 6B cell
Slide 16: SNK01-AD01 Study Phase 1: 2/3 Moderate AD Patients Show Improvement in Cognition
SNK01-AD01 Study Phase 1: 2/3 Moderate AD Patients Show Improvement in Cognition SNK01 6x109 cells Q3W (17 doses); n = 3 moderate AD patients: extraordinary improvement in moderate AD No drug-related adverse events. CDR-SB ADCOMS * Mild AD Mild AD * * * Moderate AD Moderate AD CDR-SB = Clinical Deme
Slide 17: SNK01-AD01 Study Phase 1: Preliminary Biomarker Data
SNK01-AD01 Study Phase 1: Preliminary Biomarker Data 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 17
Slide 18: 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.,
Slide 19: Therapeutic Mechanism-of-Action Hypothesis: SNK Cells Reduce AD Pathogenesis
Therapeutic Mechanism-of-Action Hypothesis: SNK Cells Reduce AD Pathogenesis via Anti-Neuroinflammation Abnormal protein and Neuroinflammation plaque accumulation and BBB leakage Inflammatory T- Amyloid β plaque cells (CD4+/CD8+) Activated microglia Super NK cell (SNKTM) ↑ Inflammatory CD56bright CD
Slide 20: Autologous Next Generation Low-Cost Manufacturing
Autologous Next Generation Low-Cost Manufacturing NKGen’s “Off-the-Shelf” SNKTM Cell Therapy 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 Tes
Slide 21: NKGen's Strong, Multi-layered IP Strategy
NKGen’s Strong, Multi-layered IP Strategy Major/original technology Manufacturing technology Therapeutic applications Core NK cell activation and Manufacturing process of Invention of the product expansion technology with the product candidate and candidate for Parkinson’s feeder cells formulation f
Slide 22: Thank you!
Thank you! Contact: investors@nkgenbiotech.com
Slide 23: Appendix
Appendix
Slide 24: SNK01 MOA (Expanded)
SNK01 MOA (Expanded) Abnormal protein aggregation (Aβ / Tau /α-Synuclein), leading to inflammation Activated microglia 1, 2.) Disruption of immune homeostasis ↑Inflammation (astrocytes, microglia) chronically activated by proteinopathy ↑ CXCL10 Autoreactive ↑ Inflammation Activated T-cell astrocyte
Slide 25: Mechanistic Investigation of SNK01: Functional Activity
Mechanistic Investigation of SNK01: Functional Activity SNK01 kill activated inflammatory T SNK01 secrete anti-inflammatory SNK01 internalizes and degrade cells through engagement of cytokines protein aggregates highly expressed NKG2D & DNAM-1 amyloid β α-synuclein Activated T cells γ Resting T cell
Slide 26: 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 migration Relative CD56 Specific chemokines lin
Slide 27: NKGen's Value and IP Position is Driven by Manufacturing Process
NKGen’s Value and IP Position is Driven by Manufacturing Process NKGen’s proprietary manufacturing process can produce multiple doses of highly pure SNK cells from a single collection of patient’s whole blood (WB) or leukapheresis product (LP), even when derived from patients that present with low N
Slide 28: NKGen Can Reliably Produce Homogenous, Robust, Pure SNK Product
NKGen Can Reliably Produce Homogenous, Robust, Pure SNK Product NKGen can increase activating receptor expression NKGen can produce high purity (≥95%) NK cell that are markers of NK cell effector Function product Pure NK cells 98.74±0.90 63.31±21.52 Other populations 0.66±0.79 0.003±0.007 0.08±0.05
Slide 29: Preserved Cell Viability and Cytotoxic Function Following Cryopreservation
Preserved Cell Viability and Cytotoxic Function Following Cryopreservation Cell Viability Cytotoxicity Function 100.0 94.5 89.8 90.9 98.0 94.6 98.0 94.7 96.5 100.0 89.8 80.0 74.4 Viability (%) 67.3 62.9 80.0 Lysis(%) 60.0 52.0 60.0 42.1 44.5 40.0 40.0 20.0 20.0 0.0 0.0 after thawing in infusion afte