INmune Bio Inc. · NASDAQ:INMB
INmune Bio — Investor Presentation (September 2022)
33 slides from INmune Bio's investor presentation, September 2022
Slide 1: Harnessing the Power of the Innate Immune System
HARNESSING THE POWER OF THE INNATE IMMUNE SYSTEM XPro™ and INKmune™ Modulate Innate Immune Dysfunction into Innate Immune Function INMB INVESTOR PRESENTATION Sept 2022
Slide 2: 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 3: Investment Highlights
INVESTMENT HIGHLIGHTS Targeting Innate Immune Dysfunction ▪ Two platforms INMB ▪ XPro™ for CNS ▪ INKmune™ for CANCER PRICE(5/19/22) COMMON S/O $7.43 ~17.9 M ▪ Cap structure ▪ Large insider ownership MARKET CAP CASH/DEBT ( 3 /3 1 /2 1 ) ~$135M ~$66M/$15M ▪ All common stock, no warrants 52-WEEK RANGE
Slide 4: An Active Pipeline
DEVELOPMENT AN ACTIVE PIPELINE PATENTS PENDING DN-TNF PLATFORM EST. NEXT DN-TNF PLATFORM DISEASE FIELD PRE-CLINICAL PHASE I PHASE II (POC) PIVOTAL MILESTONE 2032 Methods for treatment of neurologic disease 2035 Use for treatment of cancer (issued in US) Mild Alzheimer’s 2039 Disease CNS P2 Data 2023
Slide 5: Treating Alzheimer's as an Immunologic Disease, not a Neurologic Disease
for AD Treating Alzheimer’s as an Immunologic Disease …not a Neurologic Disease 5
Slide 6: Questions to Answer about INmune Bio's approach to Alzheimer's Disease
Questions to Answer about INmune Bio’s approach to for AD Alzheimer’s Disease ▪ Why neuroinflammation? ▪ What causes neuroinflammation? ▪ Why XPRO™? ▪ XPRO results in patients with ADi ▪ Next steps in patients with Alzheimer’s Disease 6
Slide 7: Why Neuroinflammation? Genetics Paints AD as an Immunologic Disease
WHY NEUROINFLAMMATION? Genetics (GWAS) Paints AD as an Immunologic Disease for AD MICROGLIA Astroglia 7
Slide 8: Why soluble TNF? Elevated TNF causes Alzheimer's Disease
WHY soluble TNF? Elevated TNF causes Alzheimer’s for AD Disease RISK OF ALZHEIMER’S DISEASE IN PATEINTS WITH RA Risk of general population Adapted from Chou et al. 2016 8.5M claims 8
Slide 9: Why XPro? XPro improves the brain
Why XPRO? - XPRO improves the brain – current TNF for AD Inhibitors “abuse” the brain Cuprizone model ETANERCEPT XPRO DEMYELINATION REMYELINATION Cuprizone model of demyelination in mice: Prober 2017 https://inmunebio.com/index.php/en/science/xpro1595/references 9
Slide 10: INmune Bio's AD Program simplified
INmune Bio’s AD Program simplified… for AD ▪ Neuroinflammation is a cause of AD ▪ Soluble TNF causes neuroinflammation ▪ XPro neutralizes soluble TNF to reduce neuroinflammation Cognitive Decline Amyloid plaques Nerve Cell Neurofibrillary tangles Death Behavioral, MICROGLIA Environmental Synaptic an
Slide 11: XPro Decreases Neuroinflammation in AD
TARGET ENGAGEMENT XPROTM DECREASES NEUROINFLAMMATION IN AD for AD Inflammatory Cytokines in CSF after 3 months 11
Slide 12: XPro Decreases Neuroinflammation in AD: Phase I Result
RESULT OF PHASE I TRIAL XPRO DECREASES NEUROINFLAMMATION IN AD for AD Decrease in Neuroinflammation in white matter tracts over 12 months XPro decreases neuroinflammation over 12 months in patients with AD 30 Free-water in AD bundles (% change) 20 10 0 -10 XPro1595 1 mg/kg -20 ADNI database N = 36 -
Slide 13: Downstream Benefits of XPro Treatment
CSF PROTEOMICS DOWNSTREAM BENEFITS OF XPRO™ TREATMENT: DECREASES for AD NEURODEGENERATION AND IMPROVES SYNAPTIC FUNCTION Synaptic Proteins Contactin-2 – 222% increase Neurogranin – 56% decrease Neuronal Injury Visinin-like protein 1 (VILIP-1) – 91% decrease Neurofilament light (NFL) – 84% decrease 1
Slide 14: Remodeling of White Matter Tracts After XPro
CHANGES IN AFD IN AD WHITE MATTER TRACTS IN MAN REMODELING OF WHITE MATTER TRACTS AFTER XPROTM for AD Baseline 3 months ▪ 65-year-old white male retired due to AD ▪ Returned to work after 6 months of XPro therapy ▪ Increasing 6 months 9 months green/blue shows improvement in axonal quality 14
Slide 15: Clinical Benefit in Phase I trial
Clinical Benefit in Phase I trial Disclaimer: small N, disease status heterogeneity, short time period for AD ▪ Assessments administered: ▪ Cognitive: MMSE, Verbal Fluency Test, Digit Symbol Coding ▪ Neuropsychiatric Inventory ▪ Bristol Activities of Daily Living Scale ▪ To compare across patients o
Slide 16: Correlation between decreased neuroinflammation and improved cognition
Correlation between decreased for AD neuroinflammation and improved cognition R2 = 0.4 to 0.6 CSF cytokines by OLINK platform INMB AD Non-confidential 1.5.22
Slide 17: What is Different About XPro Phase 2 Programs in ADi?
WHAT IS DIFFERENT ABOUT XPROTM PHASE 2 PROGRAMS for AD IN ADI? Mild ADi Two trials MCI ADi Blinded randomized Blinded randomized placebo controlled placebo controlled ▪ 200 patients; 2:1 ▪ 60 patients; 2:1 randomization Small and Fast randomization ▪ 6 months of therapy; ▪ 3 months of therapy – 1mg/
Slide 18: Statistical Power: why XPro clinical trials are short and small
Statistical Power: why XPRO clinical trials are short for AD and small Cognitive Decline • Patients with neuroinflammation have “Flatline” faster cognitive decline that patients without neuroinflammation Cognition anti-amyloid • Enrichment strategy selects patients with neuroinflammation Placebo • G
Slide 19: Off-the-Shelf NK Therapy for Oncology
for Oncology Off-the-Shelf NK Therapy Converts Patient’s Resting NK cells into Cancer Killing memory like NK cells 19
Slide 20: Why INKmune?
INKmune for treatment of cancer WHY INKmune? in Oncology On-going Phase I enrolling high-risk MDS patients with a pivot to treatment of solid tumors • INKmune converts patient’s resting NK cells into cancer killing memory like NK cells without the use of cytokines • Effects of a single course of the
Slide 21: INKmune the Pseudokine is More Powerful than Cytokines
INKMUNE THE "PSEUDOKINE" IS MORE POWERFUL THAN CYTOKINES in Oncology MoA #1 – INKmune™ Increases Avidity of NK Cell Binding to Tumor Cells Avidity of tumor cell binding by resting and primed NK cells SK-OV-3 (n=3) 5 min 100 % NK Cells Bound resting NK 80 INKmune primed NK cells TpNK NK IL-2 60 NK-IL
Slide 22: INKmune Produces NK Cells That Kill Cancer in the TME of Solid Tumors
INKMUNE PRODUCES NK CELLS THAT KILL in Oncology CANCER IN THE TME OF SOLID TUMORS Unique MOA – hypoxia and immunosuppressive TME is hostile to immune cells • The TME is hypoxic (low oxygen level) • Normal immune cells and engineered immune cells do not function in hypoxic TME • INKmune primed ml NK
Slide 23: INKmune the Pseudokine Improves NK Fitness
INKMUNE THE “PSEUDOKINE” IMPROVES NK FITNESS MOA - INKmune™ activates critical genes and pathways for enhanced NK function / survival in Oncology INB16 upregulates 522 genes distinct from IL2 – including CD70, CXCL10, Stat5 INB16 upregulates 1461 proteins distinct from IL15 – including TIMM29, USP20
Slide 24: INKmune First in Man Trial – MDS/AML
INKMUNE FIRST IN MAN TRIAL – MDS/AML Day 119 data - First Patient treated with INKmune IV in Oncology CD69+ of NKG2D+ BM Blasts 20 In vitro Tumor Killing assay % Activated NKG2D NK 100 100 PB NK+K562 15 % BM blasts 80 PB NK+Raji % specific lysis 10 60 50 40 5 20 0 0 0 D15 D43 D73 D119 D15 D43 D73D11
Slide 25: INKmune Compassionate Use: AML Patients with No Options
INKMUNE COMPASSIONATE USE: AML 2 Patients with No Options in Oncology #1 Refractory AML relapsed post unrelated donor BMT AML M2 – VUD HSCT 2020 Relapsed 2/21 Hospitalized 3/21 Treated 9/8/21 – 3x108, 1x108, 1x108 7 Months in Hospital and Discharged post INKmune - home 11/2/21 Currently well – parti
Slide 26: NK Competitive Landscape
NK COMPETITIVE LANDSCAPE in Oncology 18 Programs and Counting… Why is INKmune different? ▪ Not giving NK cells! INKmune makes patient’s NK cells cancer killers ▪ Converts patient’s own NK cells into the cancer killing NK cells ▪ LONG Therapeutic Persistence exceeds 4 months ▪ Short persistence is th
Slide 27: XPro and INKmune: Tip of the Iceberg
TIP OF THE ICEBERG XPROTM AND INKMUNE ▪ Visible programs ✓ AD, TRD, ALS ▪ “Out-of-Sight” ✓ Parkinson’s Disease, MS, dementia, traumatic brain injury ✓ PTSD, autism, bi-polar disease ✓ Much, much, more…. ▪ Visible programs ✓ High risk MDS; solid tumor program ▪ “Out-of-Sight” ✓ Leukemia, myeloma and
Slide 28: Thank you
Thank you 28
Slide 29: The Downstream Benefits of XPro in Patients with ADi
BENEFITS OF DECREASING NEUROINFLAMMATION IN ADi THE “DOWNSTREAM” BENEFITS OF XPROTM IN PATIENTS for AD WITH ADI ▪ XPRO improves axonal integrity in white matter tracts (increased AFD) ▪ XPRO promotes remyelination/myelin repair (RD) 12 month AFD improvement 1mg/kg 12 month RD improvement 1mg/kg 20 F
Slide 30: A Traditional Biomarker of AD – pTau217/181
RESULT OF PHASE I TRIAL – p-tau217 as a biomarker of AD A “traditional” biomarker of AD – pTau217/181 CSF following 12 weeks of treatment with XPro1595 (1 mg/kg) for AD p<0.0001 p<0.01 Phospho-tau is a biomarker of neurodegeneration Phospho-tau217 correlates best with cognitive dysfunction
Slide 31: XPro Increased White Matter Volume
White Matter volumetric analysisWhite Matter volum XPRO™ INCREASED WHITE 460000 0.1469 1000 460000 0.1469 1 Total White Matter volume (mm3) 0.1084 (mm3)) 3 Left Entorhinal volume (mm3) volume(mm MATTER VOLUME 440000 440000 900 for AD Mattervolume 420000 420000 800 Entorhinal 400000 400000 LeftWhite
Slide 32: cGMP Manufacturing – Doable vs Practical
cGMP MANUFACTURING – DOABLE VS PRACTICAL…. in Oncology Competing NK Companies MFG Process 1 or MFG Process 2 INKmune 500 liter bioreactor 500 liter bioreactor 1 batch = 15,000 patient doses Billions of iPSC CLP + differentiating cytokines DRUG PRODUCT Billions of iPSC-NK + gene editing (x1 x2 x3 x4?
Slide 33: Management Team
MANAGEMENT TEAM TEAM PEDIGREE Raymond J. Tesi, MD, CEO/CMO & Chairman of the Board Dr. Tesi has been our President, Chief Executive Officer and acting Chief Medical Officer since the formation of the Company in September 2015. From November 2011 to May 2015, Dr. Tesi was CEO, President and Acting Ch