Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — Investor Presentation (March 2026)
58 slides from Inmune Bio's investor presentation, March 2026
Slide 1: Modulating the Innate Immune System to Transform Inflammation-Driven Disease
Modulating the Innate Immune System to Transform Inflammation- Driven Disease Corporate Presentation March 2026 NASDAQ: INMB 1
Slide 2: Disclaimer
Disclaimer This presentation has been prepared by INmune Bio. Inc. (“INmune Bio” or the “Company”) solely for information purposes and does not constitute investment, legal, or medical advice. The Company makes no representation or warranty, express or implied, as to the accuracy, completeness, or t
Slide 3: Forward-Looking Statements
FORWARD-LOOKING STATEMENTS This presentation contains “forward-looking statements” Forward-looking statements reflect our current view about future events. When used in this presentation, the words “anticipate,” “believe,” “estimate,” “expect,” “future,” “intend,” “plan,” or the negative of these te
Slide 4: Late-Stage Pipeline Across Inflammation & Immunology
Late-Stage Pipeline Across Inflammation & Immunology • Two Late - Stage Assets: Leading with CORDStrom (RDEB) and XPro1595 (Alzheimer’s), both entering regulatory/pivotal phases. • Near - Term Commercialization: CORDStrom targeting MAA filing (UK/EU) in mid - 2026 and BLA (US) in late 2026 .* • Regu
Slide 5: Key Patents & Exclusivity Position
Key Patents & Exclusivity Position CORDStromTM XPro1595TM International PCT Stage International PCT Stage USPTO (ISA) USPTO (ISA) Favorable Written Favorable Written Opinion on Patentability Opinion on Patentability (all claims) (all claims) -CoM -CoM -Formulation -Formulation -MoT -MoT Nominal Pate
Slide 6: CORDStrom (pobistrocel) for EB
CORDStrom ( pobistrocel ) for EB Beyond Topical Care: Disease - Modifying Systemic Therapy 6
Slide 7: Summary: A De-Risked, Scalable Asset for an Ultra-Rare Disease
Summary: A De-Risked, Scalable Asset for an Ultra-Rare Disease The Asset The Market Opportunity The Innovation CORDStrom (Pooled Allogeneic RDEB is devastating and costly Proprietary Pooled Donor Umbilical Cord MSCs). A systemic ( $90k /year/patient for bandages manufacturing yields > 300,000 doses
Slide 8: The Burden of RDEB is Systemic and Life-Limiting
The Burden of RDEB is Systemic and Life-Limiting Aligning with the FDA’s Patient - Focused Guidance Regulatory Insight Corneal erosions Esophageal strictures The FDA acknowledges & Malnutrition that reduction in Itch and Pain are valid clinical endpoints for RDEB, Severe Anemia moving away from 'wou
Slide 9: CORDStrom: A Systemic Disease Requires a Systemic Solution
CORDStrom : A Systemic Disease Requires a Systemic Solution (Source: FDA PFDD Meeting) 9 https://www.youtube.com/live/Ids1WAe5Czo
Slide 10: The Unmet Need: The Itch-Pain Cycle Drives Disease Progression
The Unmet Need: The “Itch-Pain” Cycle Drives Disease Progression Patients identify Pruritus (Itch) as their #1 or #2 concern, driving disease progression. "I don't sleep because of the itch. "The itch is a monster... an itch that I just wait for the sun to come up." feels like it's inside my bones."
Slide 11: The Progressive Nature of RDEB
The Progressive Nature of RDEB 18 Months to 10 Years: The Critical Therapeutic Window 0-18 18 months-10 10-20 Over 20 Squamous cell months years years years carcinoma 11
Slide 12: What Treatments do People Living with DEB Want Right Now?
What Treatments do People Living with DEB Want Right Now? Prioritisation survey 865 members EB global community 1. Pain relief 2024-Top 5 issues 2. Itch relief 3. Mental health children/YP 4. Impact of inflammation 5. GI issues e.g., dysphagia 12
Slide 13: Mission EB Phase III: Randomized, Placebo-Controlled Crossover Trial
Mission EB Phase III: Randomized, Placebo-Controlled Crossover Trial 13
Slide 14: Comprehensive Organ System Improvements
Comprehensive Organ System Improvements ISCOREB Improvement Scores Period 1 at 3 and 6 months Pain indicies Pain Scores 20 CS 3m Placebo 3m 15 CS 6m Placebo - 10) Improvement Score Placebo 6m 10 Pain Score (e.g., 0 5 CORDStrom 0 -5 Weeks O 2 4 6 8 10 12 Skin Mouth Eye Joint Site CORDStrom is potenti
Slide 15: Comprehensive Organ System Improvements
Comprehensive Organ System Improvements Itch Man Itch Man Categorical mITT 40 CORDStrom Placebo Patients affected % 30 20 10 0 Se ity vel Pre e Se ity vel Pre e -P t t -P t t s os s os Pr Pr v e - Po v e - Po ve y le 2 - ve lev 3 - ve y le 2 - ve lev 3 - 2 l3 2 l3 el el el el ve lev ve lev le le y S
Slide 16: Comprehensive Organ System Improvements
Comprehensive Organ System Improvements iscorEB Improvement Scores Gastrointestinal symptoms Wellbeing 20 30 Pain indicies 20 15 20 CS 3m Improvement Score Placebo 3m Improvement Score 10 15 CS 6m 10 Improvement Score Placebo 6m 5 0 10 0 -10 5 -5 -20 Eating Bowel General Sleep 0 Hands Leisure School
Slide 17: Comprehensive Skin Quality Improvements
Comprehensive Skin Quality Improvements iscoreEB & EBDASI Improvement Scores Period 1 at 3 and 6 months Clinician EBDASI Skin Score Incidence of improvement vs worsened Pain indicies Wellbeing Placebo 3m iscorEB Skin Score 30 20 Placebo 6m 100 CS 3m Change from baseline (%) 30 Number of patients 20
Slide 18: CORDStrom Mechanisms of Action – IDO/PGE2 to M1 to M2 Differentiation
CORDStrom Mechanisms of Action – IDO/PGE2 to M1 to M2 Differentiation Itch & Pain REDUCTION Th2/17 Effect of CPD on cytokine synthesis 25000 200 FGF1 20000 FGF2 IL-6 150 HGF 15000 pg/ml pg/ml 100 VEGF 10000 IL-8 50 5000 M1 0 0 CORDStrom 0 D PD 0 D PD 0 D PD 0 D PD 0 D PD PGE2 >2 CP >2 CP >2 P >2 CP
Slide 19: CORDStrom Mechanisms of Action – IL-31 Reduction
CORDStrom Mechanisms of Action – IL-31 Reduction Itch & Pain REDUCTION Th2/17 Effect of CPD on cytokine synthesis 25000 200 FGF1 20000 FGF2 IL-6 150 HGF 15000 pg/ml pg/ml 100 VEGF 10000 IL-8 50 5000 M1 0 0 CORDStrom 0 D PD 0 D PD 0 D PD 0 D PD 0 D PD PGE2 >2 CP >2 CP >2 P >2 CP >2 CP C C C C C C 0 0
Slide 20: CORDStrom Mechanisms of Action – IL-31 & TNF reduction
CORDStrom Mechanisms of Action – IL-31 & TNF reduction – Itch and Pain Improved TNF-a In vivo Itch & Pain 20 REDUCTION Th2/17 Effect of CPD on cytokine synthesis IscorEB Pain 3 months 25000 200 10 FGF1 40 20000 FGF2 IL-6 150 HGF Delta preRx 15000 pg/ml pg/ml 0 100 VEGF Improvement Score 20 10000 IL-
Slide 21: The Problem of Heterogeneity
Why Historical MSC Development Failed: The Problem of Heterogeneity The Heterogeneity issue The Consequence Inconsistent Identity: Donor Variation: Clinically Naive Lots of subsets (with unknown High heterogeneity from donor - to- donor and source - to- source Assumptions. potency or MOA. (Bone marr
Slide 22: The CORDStrom Solution: Engineered Homogeneity Through Identity Selection and Pooling
The CORDStrom Solution: Engineered Homogeneity Through Identity Selection and Pooling Minimum Proprietary High Potency 4 “ selected” UC Donors High Reproducibility Pooling Process Master Cell Stock Source Identity Advantage Umbilical Cord Tissues Characterized by standard markers Pooling minimizes d
Slide 23: CMC Process in Place
CMC Process in Place Test/select/pool MCB Scale up WCB Scale out ~ 40 x 200M WCB Bags CORDStrom DP ~ 200 Doses (30 patients’ annual treatment) 23
Slide 24: CORDStrom: The Path To Commercial Approval
CORDStrom: The Path To Commercial Approval Complete technology RPDD approved transfer to commercial F-2-F pre MAA Submit MAA to by FDA manufacture (Catapult UK) meeting MHRA MHRA and EMA PIP Type B meeting (pre-IND) ODD approved by FDA response for “open label” trial Submit BLA MHRA to FDA Submit fo
Slide 25: CORDStrom: Rare Disease Therapy with Systemic Treatment Needs
CORDStrom : Rare Disease Therapy with Systemic Treatment Needs Anticipated treatment schedule • One treatment (2 doses over 14 days) every 4 months: 3 Rx (6 doses)/yr • Anticipated Annual COG per treatment: $120 -180K (scale dependent) Anticipated reimbursement per treatment: • CORDStrom as the only
Slide 26: CORDStrom RDEB Summary
CORDStrom RDEB Summary • Beyond topical care: First-in-class systemic therapy addressing multi-organ pathology of RDEB • CORDStrom i.v. infusions significantly improve multiple SYSTEMIC symptoms of RDEB and improve clinical skin scores in a randomised, double blind, placebo-controlled trial • EBDASI
Slide 27: Parent Quotes
Parent Quotes When she has been getting ill she has just been recovering in the same time as her brother, normally illness affects her much more because it causes inflammation. We have just been able to cope with everything so much better and have lots of energy and I suppose life has felt normal I
Slide 28: Children's Quotes
Children’s Quotes It was less painful, when I itch it’s painful so obviously that’s not comfortable but I had less pain, my skin was less itchy, my hands were less hot and when they are hot I itch. That was not happening that much Normally it would hurt when I have a bath but lately it hasn’t been h
Slide 29: MISSION EB Team 2024 – Parent Quote
MISSION EB Team 2024 Quote from a parent: “If it makes only one per cent difference, then I’m happy to come whenever they call us for the trial because that one per cent isn’t a lot I know, maybe it’s nothing for somebody, but it’s a lot for him, one per cent less pain for him is one per cent more r
Slide 30: Approaching Alzheimer's as an Immunologic Disease
Approaching Alzheimer’s as an Immunologic Disease 30
Slide 31: Strong Evidence for anti-TNF to Treat Alzheimer's Disease
Strong Evidence for anti-TNF to Treat Alzheimer’s Disease Evidence linking TNF to AD TNF increases TNF levels increase beginning the 3rd or 4th with Age decade of life and correlate with age6 TNF increased in Plasma and CSF TNF levels increased in AD AD Patients patients2,3 TNF co-localizes with amy
Slide 32: Biomarker Enrichment Rationale
Biomarker Enrichment Rationale Matching drug biology to patient · Predictive enrichment using downstream indicators of TNF-driven biology Enrichment is predictive — identifying patients with TNF-driven disease biology most likely to benefit from XPro1595. hypothesis-driven precision medicine. ADi =
Slide 33: MINDFuL Phase 2: Consistent Signal in ADi
MINDFuL Phase 2: Consistent Signal in ADi 6-month RCT · N = 206 (mITT: XPro n=139, placebo n=67) · ADi enrichment: ≥2 of 4 biomarkers AND amyloid positive (n=100) Key Findings: ADi Enriched Population Overall Population (mITT) Endpoint Effect Size Signal 72 yrs median age · 51% female · 45% MCI Clin
Slide 34: Differentiated Safety Profile
Differentiated Safety Profile No ARIA · Immune Function Preserved · SAEs Lower on Drug 0 ARIA Events Placebo infection rates 2× higher Despite a high-risk population: XPro1595 preserves systemic immune function 68.5% APOE4+ · 34% with microbleeds — selectively inhibiting inflammatory TNF (sTNF) 27%
Slide 35: FDA Alignment: Phase 2b/3 Adaptive Trial Design
Phase 2b/3 Adaptive Trial Design — FDA Aligned End-of-Phase 2 Meeting Completed Q1 2026 FDA Alignment Enrichment Design Endpoint Exploratory ADi biomarker strategy endorsed Adaptive 2b/3 with decision CDR-SB as sole Phase 3 primary Non-enriched cohort gate accepted recommended Summary represents spo
Slide 36: CDR-SB Confidence: Why 18 Months Will Work
CDR-SB Confidence: Why 18 Months Will Work EMACC detects subtle cognitive changes- CDR-SB measures the consequences. The Confidence Bridge: In external AD cohorts, correlation between cognitive composites and CDR-SB strengthens over time: r = 0.41 (early) → r = 0.65 (18 months). Cognition precedes f
Slide 37: Why CDR-SB Requires More Time: Evidence from External AD Cohorts
Why CDR-SB Requires More Time: Evidence from External AD Cohorts Conceptual Framework — Not Derived from Trial Data EMACC captures subtle cognitive change early — the leading indicator. CDR-SB captures cognitive and functional consequences later – lagging indicator and registrational endpoint Concep
Slide 38: XPro Summary: A Targeted Approach to Early AD and Inflammation
XPro Summary: A Targeted Approach to Early AD and Inflammation Phase 2 MINDFuL Trial Outcomes Strategic Roadmap: Phase 2b/3 Design Consistent Efficacy Across All Modalities - Cognitive FDA Alignment on Dual - Phase De - risked Staged - Neuropsychiatric Target Population Efficacy Endpoints Investment
Slide 39: XPro1595 Path to Execution
XPro1595 Path to Execution o Staged Investment: The Phase 2b/3 design stages the capital commitment. The Phase 2b serves as a de-risking milestone with a built-in go/no-go decision before full Phase 3 expenditure. o Partnership Strategy: With all this data in hand, we will run a structured global pr
Slide 40: INmune Bio Strategy
The Anchor CORDStrom Approvals Expected (2027) * US, UK, & EU Markets * Transition to Revenue Generation « PRV Asset Realization The Upside XPro Phase 3 Readiness * De-risked Protocol * Biomarker-Driven Precision * Massive Alzheimer’s Opportunity
Slide 41: Appendix
Appendix INmune Bio Inc. 225 NE Mizner Blvd. Ste. 640 Boca Raton, FL 33432 (561) 710-0512 info@inmunebio.com INMB (Nasdaq) 41
Slide 42: Milestones in 2026–2027
Milestones in 2026–2027* Clear regulatory pathway and late - stage execution across rare disease and Alzheimer’s Q1 2026 Mid - 2026 Late - 2026 2027 Pre-MAA Doc MAA Submission BLA & MAA Approval Expected Submitted (UK) (UK) Submission (UK,EU,US) CORDStrom / (US/EU) Rare Disease XPro1595 / Neuro End-
Slide 43: Phase 1: 0 to 18 months
Phase 1: 0 to 18 months • Cutis aplasia-months to heal • Wounds heal • Weight gain satisfactory • Relatively stable period
Slide 44: Phase 2: 18 months to 10 years
Phase 2: 18 months to 10 years • Wound burden & skin colonization advances • Wounds heal within 21 days • They are recurrent & reoccurring wounds but not chronic • First signs of internal involvement • inflammatory markers elevated • weight faltering • the onset of anemia • first signs of esophageal
Slide 45: Phase 1 and 2
Phase 1 and 2 • Window of opportunity for anti-inflammatory therapy such as CORDStrom for systemic disease pathology Therapeutic Requirements: Anti-inflammatory cytokines Reprogramming pro-inflammatory macrophages (M1) to anti-inflammatory (M2)
Slide 46: Phase 3: 10 to 20 years
Phase 3: 10 to 20 years • Skin involvement continues to increase • chronic wounds over 21 days • bacterial colonisation • multiple co morbidities • Dramatic reduction in the ability to heal Therapeutic Requirements: Wound healing cytokines Increased innate immune activity against bacteria/fungi
Slide 47: Phase 3: 10 to 20 years
Phase 3: 10 to 20 years • Massive levels of chronic inflammation • affects 4 major pathways Therapeutic Requirements: Wound healing cytokines Increased innate immune activity against bacteria/fungi
Slide 48: Phase 4: From 20 years onwards
Phase 4: From 20 years onwards • Steady progression of the severity • Chronic wounds very rarely heal Therapeutic Requirements: Symptom control
Slide 49: Phase 4: From 20 years onwards
Phase 4: From 20 years onwards • Patients are at high risk for developing squamous cell carcinoma, a life threatening complication of severe RDEB • Tumors are usually well differentiated and rapidly-growing, often on the extremities with a median survival of 2.4 years for this EB subtype • Anti-infl
Slide 50: XPro1595 Peer-Reviewed Publications: Breadth of Scientific Validation
XPro1595 Peer-Reviewed Publications: Breadth of Scientific Validation More Than A Decade of Research Excellence XPro1595's therapeutic potential has been rigorously validated across more than 90 peer-reviewed publications spanning 24 therapeutic areas, 2 dozen independent laboratories, and 3 contine
Slide 51: Cytokines are not informative biomarkers of chronic inflammation
Cytokines are not informative biomarkers of chronic inflammation (Immune Dysfunction) Adapted from PMID: 27994591 and 18673219 51
Slide 52: Capturing Stability: from Minutes to Lifelong Predisposition
Capturing Stability: from Minutes to Lifelong Predisposition Xu et al., 2020; Resi et al., 2021 52
Slide 53: Mechanistic Links Between TNF and Downstream Biomarkers
Mechanistic Links Between TNF and Downstream Biomarkers Macrophage Amplifies TNF Production Argi12 Arg158 Astrocyte Microglial cell Genetic variants Arg112/Arg158 trigger lifelong glial inflammation, increasing TNF production in microglia and astrocytes. Inflammatory cell ™ = Hepatocyte TNF-activate
Slide 54: The ≥2 of 4 Composite Design: Identification of a TNF-Driven Phenotype
The "≥2 of 4" Composite Design: High-Confidence Identification of a TNF-Driven Phenotype Requiring positivity on at least two independent biomarkers substantially increases specificity for TNF-driven biology and reduces misclassification arising from single-marker noise or non-TNF-related inflammato
Slide 55: XPro1595: Dominant-negative proteins
XPro1595: Dominant-negative proteins XPro1595 is identical to the human soluble TNF monomer with the exception of mutations in the receptor binding domain and another for pegylation. Dominant-Negative in genetics: "A mutation producing a rogue protein that interferes with the function of the native
Slide 56: Normal Soluble TNF activity
Normal Soluble TNF activity solTNF monomers form active heterotrimers that bind to TNF receptor. Each monomer in the trimer contacts one TNFR subunit 56
Slide 57: XPro1595 MOA
XPro1595 MOA Xpro7595treely exchanges with solINF monomers = tmTNF homotrimers are anchored to the cell to form inactive heterotrimers membrane, XPro/595 cannot exchange Inflammatory soluble TNF eliminated: No paracrine signaling through receptors ae. 2 XProtg95 soit NF Immunoprotective transmembran
Slide 58: XPro1595 is neuroprotective
XPro1595 is neuroprotective Normal Cuprizone Etanercept XPro1595 (Model of Multiple Sclerosis) Anti-inflammatory AND Anti-inflammatory NOT immunosuppressive immunosuppressive Exacerbated demyelination Remyelination Adapted from: Karamita et al., 2017 58