INmune Bio Inc. · NASDAQ:INMB
INmune Bio — Investor Presentation (May 2022)
33 slides from INmune Bio's investor presentation, May 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 May 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 DISEASE FIELD PRE-CLINICAL PHASE I PHASE II (POC) PIVOTAL EST. NEXT DN-TNF PLATFORM 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 Disease as an Immunologic Disease
for AD Treating Alzheimer’s Disease as an Immunologic Disease …not A Neurologic Disease 5
Slide 6: Peripheral Inflammation Drives Central Inflammation
Peripheral Inflammation Drives Central Inflammation for AD
Slide 7: TNF Levels Increase Early in Life and Increase with Age
TNF Levels Increase Early in Life and Increase with Age for AD As Chronic Inflammation (sTNF) Pro-inflammatory cytokines are linearly and positively associated with age. Age alone accounts for the substantial portion (>80%) of explained variance for TNF, TNFR-I, TNFR-II. Parker et al. 2008 7
Slide 8: TNF is the Master Cytokine
TNF is the “Master Cytokine” for AD Cytokines drive immune dysfunction TNF is the master cytokine time time Aadapted from PMID: 27994591 PMID: 18673219 INMB AD Non-confidential 1.26.2021
Slide 9: Evidence of the role of sTNF in causing Alzheimer's
Evidence of the role of sTNF in causing Alzheimer’s for AD RISK OF ALZHEIMER’S ▪ Diseases with increased soluble TNF DISEASE IN MAN have an 8-fold increased risk of AD ▪ Blocking soluble TNF protect against AD & Dementia ▪ Current TNF inhibitors contraindicated in AD Risk of general population ▪ XPr
Slide 10: sTNF Drives Neuroinflammation that causes Glial Dysfunction
sTNF Drives Neuroinflammation that causes Glial Dysfunction for AD XPro™ removes sTNF thereby reducing neuroinflammation and glial dysfunction ▪ Neuroinflammation is a cause of AD ▪ Soluble TNF causes neuroinflammation ▪ XPro neutralizes soluble TNF to reduce neuroinflammation Cognitive Decline Amyl
Slide 11: XPro Decreases Neuroinflammation in AD
RESULT OF PHASE I TRIAL XPROTM DECREASES NEUROINFLAMMATION IN AD for AD Inflammatory Cytokines in CSF decrease after treatment with XProTM 11
Slide 12: XPro Decreases Neuroinflammation in AD
RESULT OF PHASE I TRIAL XPRO DECREASES NEUROINFLAMMATION IN AD for AD Decrease in Neuroinflammation for 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 -30 -40 -50 N=6 N=5 N=5 N
Slide 13: XPro Decreases Neurodegeneration, Promotes Synaptic Function
RESULT OF PHASE I TRIAL – DIRECT MEASUREMENT OF PROTEINS IN CSF XPRO™ DECREASES NEURODEGENERATION, PROMOTES for AD SYNAPTIC FUNCTION AND DECREASES NEUROINFLAMMATION Immune Inflammation Chitinase-3-like protein 1 (YKL-40) – 285% increase C-Reactive Protein (CRP) – 84% decrease Synaptic Proteins Conta
Slide 14: Consequences of reducing Neuroinflammation
RESULT OF PHASE I TRIAL – XPro1595 Proteomics in CSF Consequences of reducing Neuroinflammation unbiased proteomics for AD ▪ Conclusion: Markers of microglial activation, synaptic and axonal dysfunction were significantly regulated in CSF from AD patients treated with XPro1595 (1 mg/kg). ▪ Functiona
Slide 15: XPro Decreases Neurodegeneration, Promotes Regeneration and Remyelination
BENEFITS OF DECREASING NEUROINFLAMMATION IN ADi XPROTM DECREASES NEURODEGENERATION, for AD PROMOTES REGENERATION AND REMYELINATION ▪ XPRO improves axonal integrity in white matter tracts (increased AFD) ▪ XPRO promotes remyelination (RD) 12 month AFD improvement 1mg/kg 12 month RD improvement 1mg/kg
Slide 16: Assessing White Matter Pathology – pTau217/181
RESULT OF PHASE I TRIAL – p-tau217 as a biomarker of AD Assessing white Matter pathology – pTau217/181 CSF following 12 weeks of treatment with XPro1595 (1 mg/kg) for AD p<0.0001 p<0.01
Slide 17: 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 17
Slide 18: Improved Gray Matter Quality After XPro
IMPROVED GRAY MATTER QUALITY AFTER XPROTM for AD ▪ Metric: Cortical Disarray Measurement (CDM) ▪ Improvement (Green) within 3 months (Yellow – no change) Baseline 3 months ▪ Continued improvement over 9 months ▪ Improvement was observed in brain regions critically involved in Dementia - posterior an
Slide 19: XPro Phase 2 Program in AD with Biomarkers of Inflammation
XPROTM PHASE 2 PROGRAM IN AD WITH BIOMARKERS OF for AD INFLAMMATION All patients of both trials eligible for 12 month extension study Mild ADi MCI ADi Blinded randomized Blinded randomized placebo controlled placebo controlled ▪ 200 patients; 2:1 randomization ▪ 60 patients; 2:1 randomization ▪ 6 mo
Slide 20: Why is XPro the Ideal Drug for AD?
WHY IS XPROTM THE IDEAL DRUG FOR AD? for AD Precision Therapy for AD The Benefits of INMB’s Selective vs. Non- Selective sTNF Inhibition • Decreases neuroinflammation in man NON- Selective Selective DN TNF • Safe in elderly patients with AD Decreases Y Y • Simple self administration at home inflamma
Slide 21: How XPro Works and Why It Is Different
HOW XPRO WORKS AND WHY IT IS DIFFERENT for AD XPro Not Competing with Currently Approved TNF Inhibitors or Biosimilars Dominant-Negative Technology Neutralizes soluble TNF DN-TNF Can Not Neutralize trans-membrane TNF 21
Slide 22: XPro Is Unique: Promotes Remyelination While Approved TNF Inhibitors Cause Demyelination
XPROTM IS UNIQUE: XPROTM PROMOTES REMYELINATION WHILE for AD APPROVED TNF INHIBITORS CAUSE DEMYELINATION Demyelination - an Off-Target Safety Side Effect of Currently Approved TNF Therapies NORMAL CUPRIZONE ETANERCEPT XPRO Model of Multiple Sclerosis Worsens demyelination Promotes remyelination WORS
Slide 23: Off-the-Shelf NK Therapy Converts Patient's Resting NK Cells
for Oncology Off-the-Shelf NK Therapy Converts Patient’s Resting NK cells into Cancer Killing memory like NK cells 23
Slide 24: Why INKmune?
INKmune for treatment of cancer WHY INKmune? in Oncology On-going Phase I enrolling high-risk MDS patients in open label dose escalation trial • Cancer patients have lots of NK cells…but they ignore the cancer • INKmune converts patient’s resting NK cells into cancer killing memory like NK cells • E
Slide 25: INKmune More Powerful Than Cytokines
INKMUNE MORE POWERFUL THAN CYTOKINES in Oncology MoA #1 – INKmune™ Increases Avidity of NK Cell Binding to Tumor Cells ▪ AVIDITY is a measure of how Avidity of tumor cell binding by resting and primed NK cells firmly an NK cell attaches to a SK-OV-3 (n=3) 5 min tumor cell target 100 % NK Cells Bound
Slide 26: 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 INKmune activates tumor killing NK cells and is associated with reduction in BM blast count CD69+ of NKG2D+ BM Blasts 20 Laurel Subject 03 % Activated NKG2D NK 100 50 15 40 % BM blasts INKmune x3 Az
Slide 27: 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 28: 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 ▪ Only memory like NK cells are relevant to cancer therapy. ▪ Therapeutic
Slide 29: 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 30: INKmune Phase 1 Study
INKMUNE™ PHASE 1 STUDY in Oncology Phase I Trial in High-Risk MDS DESIGN GOAL Evaluate Safety and Open-label dose escalation study of Tolerability of INKmune™ in intravenous INKmune enrolling 9 High-Risk MDS patients FIRST IN HUMAN TRIAL OF INKMUNE™ INCLUSION Patients with MDS with excess blasts Ass
Slide 31: 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; Ovarian Cancer ▪ “Out-of-Sight” ✓ Leukemia, myeloma and lymph
Slide 32: 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
Slide 33: Thank you
Thank you 33