Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — Investor Presentation (June 2019)
27 slides from Inmune Bio's investor presentation, Jun 26, 2019
Slide 1: INMB AD non-confidential
INMB AD non-confidential he ey Nasdaq Symbol: INMB Shares Outstanding: =10.7M Share Price 6/24/19: $9.20 Market Cap: =$100M Debt: $o Largest Shareholder: XNCR Insider Ownership: >50%
Slide 2: Forward-Looking Statements
l Forward-Looking Statements mols ‘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
Slide 3: Summary
| Summary , tte ¢ Clinical stage immunology company - programs in oncology and Alzheimer’s disease ¢ Platforms target “ignored” elements of immunology + Innate immune system + “Resistance” immunology of the Tumor Micro Environment (TME) + Neuroinflammation is a cause of Alzheimer's disease ¢ Large m
Slide 4: Our vision
l Our vision INmunesie Become the Leader in Reprograming the Innate Immune System for the Treatment of Disease Guiding principle: AD is a disease of innate immune dysfunction NMB. tial 6.26.19
Slide 5: INMB targets cells of innate immune system
| INMB targets cells of innate immune system > INmunesio NK MDSC Microglia
Slide 6: INMB pipeline
| INMB pipeline ® INmunskie Phase II Poc INBO3 for Checkpoint Inhibitor resistance (Melanoma and Renal Cell Cancer) INBO3 for trastuzumab resistance (breast eines INKmune for Relapse / Minimal Residual Disease (ovarian cancer) INKmune (High-risk MDS - Leukemia) XPro1595 for Alzheimer’s disease == Cu
Slide 7: AD: the problem
| AD: the problem.. INmunesio Nerve cell Synaptic Cognitive death dysfunction Decline INMB AD non-confidential 6.26.19
Slide 8: Three questions
| Three questions INmuneie Why inflammation? Why TNF? Why XPro1595? INMB AD non-confidential 6.26.19
Slide 9: Majority of genes associated with AD expressed in innate immune cells
] Majority of genes associated with AD expressed in innate immune cells INmungle Cell type Mico a | Hippocampal CA 1 pyramidal neurons | Endothelial cells H Prefrontal glutamergic neurons 2 Prefrontal glutamergic neurons 1 Oligodendrocytes Astrocytes 2 jodendrocyte precursor cells 1 GABAergic intern
Slide 10: Chronic inflammation: real disease, bad name
Chronic inflammation: ®) real disease....bad name INmUDS RE Acute inflammation fast and furious, coming and going quickly for the benefit of the patient. Chronic inflammation low, slow inflammatory response that doesn’t end and harms the patient. INMB AD non-confident
Slide 11: Inflammaging and cognitive decline
re decline nunenie | Inflammaging and cogn Atherosclerosis Risk in ‘i, Comeninies Aan! Honolulu-aging Study eepey : auartlesot “| hs-CRP Dement “ <0.34mg/L 1.0 cools mi 7 oe 0.34-0.56mg/L 29 i feet} apy TT TS fH } >1.00me/L aq] A hsCRP>0.57mg/dL had a increased risk of dementia over 25 years hsCRP>1
Slide 12: Pivotal role of TNF in AD
| Pivotal role of TNF in AD ryunene Microglia dysfunction/activation Synaptic Nerve cell dysfunction death INMB AD non-confidential 6.26.19
Slide 13: TNF in humans: the dark passenger of AD
TNE in humans: . the dark passenger of AD INmUDS RE * Elevated plasma TNF (Fillit et al. 1991) * TNF co-localized with 3 plaques (Dickson 1997) $ * * TNE levels correlate with © ° disease progression Sa (Paganelli et al. 2002) L Alzheimer Control * Elevated TNF in CSF Seattergram of TNE levels in Al
Slide 14: Does eliminating TNF prevent AD?
l Does eliminating TNF prevent AD? ® 800% 60% 1. Risk of AD in RA patients 8 times higher* 2. Risk of AD in RA patients treated with anti- TNF therapy is 0.4* * In RA patients compared to patients without RA from Chow et al. 2016 NMB A\ n-confidential 6.26.19
Slide 15: Why XPro1595?
vd | Why xPro15957 INmuneeie Difference between selective vs non-selective TNF inhibition XPro1595 Decreases inflammation YES Causes immunosuppression No Causes demyelination No Neuroprotective YES Enhances neuroplasticity YES INMB AD non-confidential 6.26.19 Ls |
Slide 16: XPro1595: selective inhibitor of soluble TNF (sTNF)
XPro1595: selective inhibitor of ® soluble TNF (sTNF) INmunseie 17kDal non-glycosylated protein attached Nea rly identical to to 10 kDal linear PEG with 18 hour half-life human TNF protein — 2 mutations produce MOA * Excellent CMC amd eee . binding site PK properties mutations — Qweek patient admini
Slide 17: Why is XPro1595 different?
| Why is XPro1595 different? ® WamURERIe Normal TNF Biology XPro1595 does not neutralize tmTNF TNFR1 TNFR2 2) ®> vy @ insos at, ay aod ‘tmTNF ole 2 tmTNF binds TNFR with normal function Approved TNF inhibitors XPro1595 TNFR1 TNFR2 TNFR1 TNFR2 sT, tm)NF sTQF tmTNF (bad) (good) (bad) (good) Prevent fu
Slide 18: How XPro1595 neutralizes sTNF
l How XPro159 neutralizes sTNF Inmuneeie Normal sTNF activity oo+ Y% =) de > Inflammation bed VV vVov Active TNF TNFR STNF bind XPr01595, TNFR Po gs 8 No sTNF activity Vv > Vv =e — ga Heterotrimers Pind TNE Inactive cannot bind TNFR heterotrimers INMB AD non-confidential 6.26.19
Slide 19: Bad history of non-selective TNF therapy in neurologic disease
l Bad history of non-selective TNF ) therapy in neurologic disease Imunerie Non-selective TNF inhibitors exacerbates RMS 19 * Lenercept made RRMS worse * Non-selective TNF inhibitors contra- indicated in neurologic disease 08 Freo Patients placebo Proportion of Exacerbat ‘Suay Day Neurology 1999 nfi
Slide 20: In retrospect: XPro1595 improves, etanercept worsens
| In retrospect.... INmunesie XPro1595 improves, etanercept worsens MOG-EAE: Clinical Score Vehicle Etan £ 20: s 15 § XPro. é g 10 0s. 00 : ° 5 10 “| n 6 » 6 © & 8 85 Daysatfter immunization Treament (Grambrilaetal.2011) INMB AD non-confidential 6.26.19 | 20 |
Slide 21: What happened?
l What happened? INmunesio XPro1595 promotes remyelination, etanercept promotes demyelination CP25+saline CPZ5+XPro CPZ5+etanercept Ss x Myelin density “CES Probert et al. 2017 INMB AD non-confidential 6.26.19
Slide 22: XPro1595 attenuates AD pathology and restores normal function
| XPro1595 attenuates AD pathology and restores normal function INmunEeIe Synapse dysfunction Cognitive Impairment Saline xProts% Nte ‘Ty Ws ‘sm austance ‘Pofist block) g # Pe: THT z Tetning block Immune dysfunction " Amyloid pathology Saline XProi895 Activated Myeloid.cells Brain T cell ifitration
Slide 23: XPro1595 clinical development supported by the Alzheimer's Association
XPro1595 clinical development supported by the Alzheimer’s Association PART THE CLOUD Hone + About rumune! More than $30 Million Raised and Invested in Alzheimer’s Translational Research (ur Mission: To fund Alzheimer's research with the highest probability of slowing, stopping or ultimately curing
Slide 24: XPro1595 AD development program: two step process
| XPro1595 AD development program: ® two step process Step1: demonstrate XPro1595 reverses neuroinflammation in AD patients (short open label study) Step 2: decrease of neuroinflammation in AD patients treated with XPro1595 decreases cognitive decline (longer placebo controlled study)
Slide 25: Phase 1b biomarker directed immunology study in Mild to Moderate AD
| Phase 1 biomarker directed immunology ® study in Mild to Moderate AD Inmunsele Phase 1b Open-Label, Dose-Escalation Study of XPro1595 in Patients with Mild to Moderate AD with Elevated hsCRP in Blood Primary endpoint: Safety Dose for Phase Seconclary endpoints: Inflammatory & AD biomarkers blood&C
Slide 26: Immunologic biomarkers
l Immunologic biomarkers ® INmUnERIE Behavioral biomarkers of inflammation Sleep disorders * Depression Psychosis Apathy * Aggression Inflammation & eurodegeneration Neurodegeneyation Volatile Organic Cg non-confidenti
Slide 27: INMB: treating AD as an immunologic disease
| INMB: treating AD as an ® immunologic disease INUAERIE ¢ Problem: synaptic dysfunction and nerve cell death causes cognitive decline ¢ Pathophysiology: sTNF causes microglial activation that drives chronic neuroinflammation * Solution: neutralize sTNF without affecting tmTNF ¢ Drug: XPro1595 * Str