Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — Investor Presentation (August 2024)
30 slides from Inmune Bio's investor presentation, August 2024
Slide 1: Inflammation and Immunology Repair
Inflammation and Immunology Repair Two Platforms in the Clinic: XPro and INKmune INMB August 2024 Nasdaq
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: Two Novel Platforms with Near Term Data
Two Novel Platforms with Near Term Data ➢ Two platforms targeting CNS and Oncology ➢ Treating Alzheimer's as an Immunologic Disease without immunosuppression a ➢ Creating memory-like NK cells for solid tumors ➢ Phase 2 Alzheimer's top-line expected in early 2025; Phase 1 metastatic prostate cancer r
Slide 4: Development Timeline
Development Timeline EST.NEXT DN-TNF PLATFORM DESEASE FIELD PRE-CLINICAL PHASE 1 PHASE II (POC) PIVOTAL MILESTONE Early Alzheimer’s Full Enrollment Q3-2024 Disease Topline Data ~ 6m Later Treatment Resistant P2 Start 2024 Depression NK PRIMING PLATFORM Metastatic Castrate Open Label Trial Resistant
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: Chronic Inflammation: the Match that Lights the Fire
Chronic Inflammation: the Match that Lights the Fire 6 6
Slide 7: The Doom Loop of Neuroinflammation and Cognitive Decline
The "Doom Loop" of Neuroinflammation and Cognitive Decline Essential Pathologies NeuroInflammation of Cognitive Decline • Synaptic Cytokines Dysfunction Released Activated • Demyelination Microglia • Nerve Cell Death Targeting neuroinflammation with XPRO should stop 1. 2. Chang R, et al. J Cent Nerv
Slide 8: Targeting the Root Cause of Neuroinflammation
Targeting the Root Cause of Neuroinflammation Why sTNF? sTNF is the "Master Cytokine" that drives neuroinflammation Soluble TNF (sTNF) drives Inflammatory cytokines drive neuroinflammation immune dysfunction • Glial cells, the immune cells of the brain, cause neuroinflammation • Glial cells are more
Slide 9: Targeting sTNF in Man Makes a Difference
Targeting sTNF in Man Makes a Difference Prevention of chronic inflammation with anti-TNF therapy lowers risk of AD TNF Inhibitors Reduce Risk of Developing AD +800% Rheumatoid Arthritis a Risk of General Population Rheumatoid Arthritis -60% + Anti-TNF treatment Epidemiological studies including a m
Slide 10: Soluble TNF Promotes Deposition of the Biomarkers of AD
Soluble TNF Promotes Deposition of the Biomarkers of AD sTNF drives neuroinflammation that promotes amyloid plaque deposition • TNF potently induces the expression and accumulation of Ab via a number of mechanisms • Targeting sTNF should stop amyloid deposition Amyloid plaque Aβ 3 APP Blasko et al.1
Slide 11: Phase 1 Results: XPro Decreases Neuroinflammation
Phase 1 Results: Neutralizing sTNF with XPro Decreases Neuroinflammation Dose-dependent reduction of CSF biomarkers of neuroinflammation CSF *1 mg/kg group (N=6) Olink® Target 48 Cytokine 11
Slide 12: Phase 1 Results: XPro Decreases Neurodegeneration
Phase 1 Results: XPro Decreases Neurodegeneration pTau217 is best biomarker for neurodegeneration in patients with AD* Phase I data: XPro 1mg/kg subQ once a week for 12 weeks decrease pTau is CSF in patients with AD p<0.0001 p<0.01 *https://jamanetwork.com/journals/jamaneurology/fullarticle/2813751
Slide 13: Phase 1 Results: XPro Improves Synaptic Function
Phase 1 Results: XPro Improves Synaptic Function Studies have demonstrated both changes in synaptic proteins and improvements in synaptic function as measured by EEG Alpha waves Synaptic Proteins Contactin-2 +222% increase Neurogranin -56% decrease Above: CSF synaptic proteins improved after treatme
Slide 14: Remodeling of White Matter Tracts After XPro
Remodeling of White Matter Tracts After XPro Phase 1b Data: CHANGES IN AFD IN AD WHITE MATTER TRACTS – CASE STUDY 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 quali
Slide 15: A TNF Inhibitor Designed to Treat Neurologic Disease
A TNF Inhibitor Designed to Treat Neurologic Disease XPro : a dominant-Negative selective inhibitor of ONLY soluble TNF XPro 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 muta
Slide 16: TNF Biology: Two Ligands with Opposite Effects
TNF Biology: Two Ligands with Opposite Effects Neurodegenerative Neuroprotective Adapted from (MacEwan et al. 2002) Current TNF inhibitors block both TNF ligands 16
Slide 17: XPro Mechanism of Action
XPro Mechanism of Action XPro freely exchanges with soITNF TmTNF homotrimers are anchored to monomers to form inactive heterotrimers the cell membrane; XPro cannot exchange Inflammatory soluble TNF eliminated: No paracrine signaling through receptors Dominant-Negative in genetics: "A mutation produc
Slide 18: XPro is the only TNF inhibitor that is safe for the Brain
XPro is the only TNF inhibitor that is safe for the Brain Etanercept XPro • Currently approved TNF inhibitors are contraindicated in treatment of neurologic disease such as AD Myelin • promote demyelination (yellow arrow) • promote axon degeneration (white arrows) Axons • XPro promotes remyelination
Slide 19: Benefits of Selective Versus Non-Selective TNF Inhibition
Benefits of Selective Versus Non-Selective TNF Inhibition Non-Selective TNF Inhibitor XPro Decreases Inflammation yes yes Immunosuppression yes No Demyelination yes No Neuroprotective no yes Enhances Neuroplasticity no yes 19
Slide 20: Phase 2 Trial of XPro in Early Alzheimer's Disease
Phase 2 Trial of XPro in Patients with Early Alzheimer's Disease Top-Line Data Expected in Early 2025 8 Countries ➢ 6-Month Trial Powered Off CDR 35 Sites ➢ 201 Patients ➢ 2:1 XPro / Placebo ➢ Primary Endpoint: EMACC ➢ Secondary Treatment Endpoint: CDR ➢ Patient Pool Enriched for Biomarkers of Infla
Slide 21: Clinically Proven Cognitive Endpoints of EMACC and CDR
Clinically Proven Cognitive Endpoints of EMACC and CDR Study designed around these primary and key secondary endpoints EMACC CDR ➢ EMACC was empirically derived by ➢ Approvable endpoint for AD in pharma to measure change in Early AD registration studies ➢ Clinically validated measurements ➢ Used to
Slide 22: Phase 2 Trial Summary
Phase 2 Trial Summary ▪ Enriching for patients that have AD with elevated neuroinflammation (ADi) ▪ ADi patients have faster progressing disease with less variance which allows for smaller trial size and shorter trial duration ▪ Cognitive and functional measures that are meaningful and relevant for
Slide 23: Off-the-Shelf NK Therapy Converts Resting NK Cells into Memory-Like NK Cells
Off-the-Shelf NK Therapy Converts Patient’s Resting NK cells into Cancer Killing memory like NK cells 23
Slide 24: Problem: New mCRPC Treatments Have Little Impact on Survival
Problem: New Treatments for Metastatic Castration Resistant Prostate Cancer (mCRPC) Have Little Impact on Survival • Incidence of prostate cancer increasing • New therapies for mCRPC give <6 month survival benefit • Immune check-point inhibitors have failed in mCPRC Sipuleuc Enzalutami Docetax Cabaz
Slide 25: Solution: Use INKmune to Target NK Cells in mCRPC
Solution: Use INKmune to Target NK Cells in mCRPC in vitro* - INKmune induced changes needed to promote NK function in Tumor MicroEnvironment (TME) Normal vs Tumor • Prostate cancer immune infiltrate cells are resting NK cells NOT T cells • Is lack of T cell infiltrate why PDL1 and TIGIT fail in mCR
Slide 26: INKmune Primed NK Cells Fitter Than Cytokine Primed NK Cells
INKmune Primed NK Cells “Fitter” Than Cytokine Primed NK Cells rNK LAK-15 CIML-NK INKMUNE-TpNK Change in mitochondrial survival proteins following priming 3 TpNK Log change from rNK (Average Log ratio) 2 CIML IL15 1 0 proteomics -1 -2 GATB GATC GFM2 HARS1 HARS2 LARS2 MRPL10 MRPL16 MRPL2 MRPL23 MRPL4
Slide 27: INKmune Primed NK Cells Present in Circulation Longer
INKmune Primed NK Cells Present in Circulation Longer Than Cytokine Primed NK Cells Most important elements of INKmune therapy: • INKmune primed NK cells seen in patient blood for months • INKmune primed NK cells kill NK resistant targets in vitro INKmune induces memory-like NK cells with enhanced N
Slide 28: INKmune mBION12 mCRPC Trial Design
INKmune mBION12 mCRPC Trial Design Step 1: Step 2: Short term safety Long term safety Confirmatory group Immunologic Immunologic efficacy In this example: SRC choses efficacy Anti-tumor effects middle dose for pivotal trial Low-dose 1 1 1 6 patients Middle-dose 1 1 1 6 patients 6 patients High-dose
Slide 29: Anticipated Milestones in 2024 and 2025
Anticipated Milestones in 2024 and 2025 Key Upcoming Clinical & Regulatory Milestones EXPECTED EVENT TIMING Complete Phase 2 AD Enrollment Q3 2024 ~6m From Last Topline Phase 2 AD Data Patient Enrolled Mid 2025 End of Phase 2 FDA Meeting AD Pre-clinical Anti-AB and XPro Data 2H 2024 Initiate Phase 2
Slide 30: Contact Us
Contact Us: INmune Bio Inc. 225 NE Mizner Blvd.Suite 640 Boca Raton, FL 33432 Inflammation and (858) 964-3720 info@inmunebio.com Immunology Repair Investor Relations: Daniel Carlson (415) 509-4590 daniel@inmunebio.com Mike Moyer Symbol: INMB (Nasdaq) (617) 308-4306 mmoyer@lifesciadvisors.com 30