Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — Investor Presentation (May 2020)
37 slides from Inmune Bio's investor presentation, May 18, 2020
Slide 1: Harnessing the Power of the Innate Immune System
HARNESSING THE POWER OF THE INNATE IMMUNE SYSTEM Modulating an Innate Immune Response Against Diseases IN MB CORPORATE PRESENTATION May 2020
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 the
Slide 3: Investment Summary
▪ Immunology company, advancing through Phase I and Phase II clinical trials ▪ Catalyst rich programs with multiple readouts in 2020 and 2021 ▪ Two platforms with novel approaches targeting the innate immune system First dominant - negative protein to enter clinic selectively targeting inflammation
Slide 4: Pipeline: Focused on Developing Therapies that Target the Innate Immune System
DN - TNF PLATFORM DISEASE FIELD PRE - CLINICAL PHASE I PHASE II (POC) PIVOTAL NEXT MILESTONE Trastuzumab Resistance ONCOLOGY NASH GI Alzheimer’s Disease CNS COVID - 19 1H - 21 Initiate p2 1H - 21 initiate p2 NK PRIMING PLATFORM DISEASE FIELD PRE - CLINICAL PHASE I PHASE II (POC) PIVOTAL NEXT MILESTO
Slide 5: DN-TNF Platform Technology
NEXT GENERATION TNF INHIBITOR - SAFER AND SELECTIVE TO TARGET MARKETS EXISTING TNF INHIBITORS MUST AVOID DN - TNF PLATFORM TECNOLOGY 5
Slide 6: Tumor Necrosis Factor (TNF): The Master Cytokine
TUMOR NECROSIS FACTOR (TNF) The “Master” Cytokine ▪ sTNF promotes translation of IL6, Lipocalin 2 and other downstream cytokines ▪ Block sTNF and downstream pro - inflammatory cytokines do not occur LCN2 IL 6 ANTI - INFLAMATORY Time Plasma Concentration sTNF 6 PRO - INFLAMATORY Adapted from Andrease
Slide 7: Negative effects of TNF are a result of sTNF
Negative effects of TNF are a result of sTNF WHEREAS tmTNF PROVIDES IMMUNOSUPPORTIVE AND NEUROPROTECTIVE FUNCTION IMPORTANT TO HOST SURVIVAL THE BIOLOGY OF CURRENT TNF INHIBITORS Current Inhibitors Are Not Selective and Block Both Forms of TNF Transmembrane - bound (‘tmTNF’) GOOD Soluble TNF (‘sTNF’
Slide 8: Selective vs. Non-Selective TNF Inhibition: How DN-TNF Works
Decreases inflammation Y Y Increased risk of infection Y N Increased risk of cancer Y N Causes demyelination Y N Neuroprotective N Y Enhances neuroplasticity N Y DIFFERENCES: Selective vs. Non - Selective TNF Inhibition Non - Selective DN TNF TNF BIOLOGY. HOW DN - TNF WORKS DN - TNF Neutralizes ONLY
Slide 9: Non-selective TNF Inhibition Causes Demyelination, DN-TNF Promotes Remyelination
9 Days Post - Infection % Survival FUNCTIONAL tmTNF PREVENTS IMMUNOSUPPRESSION SELECTIVE TARGETING PREVENTS DEMYLINATION Non - selective TNF Inhibition Causes Demyelination, DN - TNF Promotes Remyelination CUPRIZONE Model of Multiple Sclerosis REMYELINATION ETANERCEPT Anti - inflammatory AND immunos
Slide 10: Clinical Trial to Test Neuroinflammation in Alzheimer's Disease
Clinical Trial to Test Neuroinflammation as the Common Denominator of ALZHEIMER’S DISEASE 10
Slide 11: sTNF: A Validated Target in Alzheimer's Disease
RISK OF ALZHEIMER’S DISEASE IN MAN Risk of general population Adapted from Chou et al. 2016 8.5M claims Despite positive AD activity, non - selective TNF inhibitors increase the risk of cancer, infection, and MS AD risk is not reduced by other anti - inflammatory treatments 11 sTNF A VALIDATED TARGE
Slide 12: Phase 1 AD Trial: Phase IB in Patients with Biomarkers of Inflammation
IMMUNOLOGIC BIOMARKERS BEHAVIORAL BIOMARKERS OF INFLAMMATION SLEEP DISORDERS DEPRESSION PSYCHOSIS APATHY AGGRESSION Inflammation & Neurodegeneration ( Roche NeuroTool kit ) BIOLOGICAL BIOMARKERS OF INFLAMMATION DESIGN ▪ 18 patients in 3 cohorts ▪ Weekly XPro1595™ SubQ injections for 3 months ▪ Bioma
Slide 13: White Matter Free Water: A Biomarker for Neuroinflammation
WHITE MATTER FREE WATER: 13 From Dumont 2019 White Matter Free Water A Biomarker For Neuroinflammation WMFW - sex and age matched NC and AD subjects AD Normal aging
Slide 14: Clinical Trial in COVID-19 Targeting Soluble TNF
14 Clinical Trial to Determine if Targeting Soluble TNF (sTNF) may Prevent Catastrophic Complications of COVID - 19
Slide 15: Blunting Cytokine Storm and Hyperinflammation
▪ Cytokine storm caused by increase expression of sTNF, IL1, and IL6 ▪ sTNF significantly elevated in blood of patients ▪ Neutralizing sTNF should decrease expression of IL1 and IL6 ▪ Ideal therapy has 5 characteristics: ▪ Safe and well tolerated ▪ Not immunosuppressive ▪ Easy to use ▪ Rapid onset ▪
Slide 16: Why sTNF and Why Quellor? Not Immunosuppressive
▪ Stops inflammation ▪ Not immunosuppressive ▪ Rapid onset ▪ No contra - indications ▪ Easy to use ▪ Safe and well tolerated ▪ Crosses BBB (Blood Brain Barrier) 16 WHY s TNF AND WHY ? IS NOT IMMUNOSUPPRESSIVE Approved cytokine inhibitors (anti - TNF/IL6/IL1) are immunosuppressive ▪ QUELLOR does not
Slide 17: Phase II Trial: Treating Pulmonary Complications of COVID-19
PHASE II TRIAL: Treating Pulmonary Complications of COVID - 19 Goal : Prevent progression to catastrophic complications ▪ Enrollment criteria: COVID - 19 infection with room air SaO2<94% ▪ One or more medical/demographic comorbidities: age ≥ 60; hypertension, cardiovascular disease, BMI ≥ 30; diabet
Slide 18: DN-TNF Options in Immuno-Oncology
DN - TNF Options in Immuno - Oncology for Treatment of Resistance to Immunotherapies 18
Slide 19: Trastuzumab Resistance in Breast Cancer
▪ ~20% of women with breast cancer are HER2+ ▪ ~25% have metastatic disease ▪ ~30% will develop brain metastasis ▪ MUC4 expression predicts trastuzumab resistance PROBABILITY OF DISEASE - FREE SURVIVAL 19 TRASTUZUMAB RESISTANCE IN BREAST CANCER FEWER MYELOID CELLS JIMT - 1 BREAST CANCER INTO NUDE MO
Slide 20: INB03 Reverses Trastuzumab Resistance
INB03 REVERSES TRASTUZUMAB RESISTANCE 1 st – It Modifies immunology of TME and DECREASES MYELOID CELLS, INCREASES NK CELLS IN VIVO 2 nd – It Decreases MUC4 Expression – MUC4 Expression resistance to Trastuzumab and promotes metastasis T - trastuzumab DN - INB03 Schillaci - NYAS2020 MUC4 BLOCKS TRAST
Slide 21: Conclusions from INB03 Phase I Data
SAMPLE 11 patients treated DEMOGRAPHIC Age (median): 54 Gender: 6M/5F DISEASE Ovary, Mesothelioma; RCC, Lung; Prostate; Colon, Cholangial, other PREVIOUS LINES OF THERAPY 3 (range:2 - 5) INB03 DURATION 74 days (21 - 119d) • No drug related SAE • All discontinuation due to disease progression PHASE I
Slide 22: Phase II in HER2+ Metastatic Breast Cancer
22 Twofer1: PHASE II IN HER2+ METASTATIC BREAST CANCER Step 1: eliminating MUC4 and modifying the TME GOAL: IMPROVE RESPONSE TO IMMUNOTHERAPY Modifying the TME To Reverse Resistance To Immunotherapy ▪ Metastatic HER2+ breast cancer resistant to immunotherapy ▪ Trastuzumab resistant ▪ Immune checkpoi
Slide 23: Liver Fibrosis, Innate Immune Cells and Inflammation
Addressing the Link Between Liver Fibrosis, the Innate Immune Cells of the Liver and Inflammation, a Pleiotropic Approach 23
Slide 24: Three Cycles of Inflammation Lead to NASH
THREE CYCLES OF INFLAMMATION LEAD TO NASH LIVNate™ REDUCES INSULIN RESISTANCE 25 27 29 31 33 35 37 39 41 43 B a s e l i n e W e e k 1 W e e k 2 W e e k 3 W e e k 4 W e e k 5 W e e k 6 W e e k 7 W e e k 8 W e e k 9 W e e k 1 0 w e e k 1 1 w e e k 1 2 w e e k 1 3 B o d y W e i g h t ( g ) Control/Sali
Slide 25: LIVNate Reduces Hepatocyte Death and Fibrosis In Vivo
0 1 2 3 0 1 2 3 0 1 2 Control 2 4 1 - - - 1 6 3 3 1 LIVNate™ 4 4 - - - - 5 3 8 - - HEPATOCYTE BALLOONING LOBULAR INFLAMMATION STEATOSIS Control 4.4 ц 0.8 LIVNate™ 2.9 ц 0.8 NAS (mean ц SD) Parameter (mean ц SD) Control LIVNate™ Sirus Red positive area (%) 0.96 ц 0.29 0.69 ц 0.23 FIBROSIS SCORE N 7 8
Slide 26: NASH Trial Design
NASH TRIAL DESIGN Phase IIa Biomarker Directed Trial Phase IIa open label trial ▪ Patients with F2/3 NASH by non - invasive studies with >10% fat in liver with LIVNate™ 1mg/kg SQ treatment with for 12 weeks ▪ PIFF and non - invasive biomarkers at 0, 6 and 12 weeks ▪ Open label so biomarkers “visible
Slide 27: Natural Killer Cells Clear Residual Disease
Natural Killer cells are responsible for clearing residual disease 27
Slide 28: NK Cells Determine Relapse or Survival
NK CELLS DETERMINE RELAPSE OR SURVIVAL THROUGH THEIR ABILITY TO TARGET RESIDUAL DISEASE ▪ Patients who relapse have NK cells that do not target the MRD which survives chemotherapy ▪ Patients who survive have NK cells that can see and target MRD and provide long lasting remissions ▪ Circulating resti
Slide 29: INKmune Cells Prime NK Cells to Eliminate MRD
S1 S2 rNK Cell = Resting NK Cell TpNK Cell = tumor - primed NK Cell INKmune™ provides missing signals to the NK cells to initiate NK killing of tumor cells INKmune™ CELLS PRIME NK CELLS TO ELIMINATE MRD S2 Tumor cells down - regulate surface molecules which prime NK cell activity, “evading” NK cell
Slide 30: INKmune Primed NK Active Against Many Types of Cancers
INKmune™ PRIMED NK CELLS Human ovarian cancer cells plus patient’s own NK cells Human ovarian cancer cells with patient’s NK cells after INKmune treatment Modified from Lowdell et al 2007 & 2011 BROAD THERAPEUTIC PLATFORM x Blood cancers: AML, MM, lymphoma x Solid tumors: breast, ovary, prostate, re
Slide 31: High-Risk MDS Clinical Study
HIGH - RISK MDS CLINICAL STUDY A Phase I Open - Label Dose Escalation Study of Intravenous INKmune™ in Patients with Myelodysplastic Syndrome with Excess Blasts (MDS - EB - 1/2 - MDS - CMML 1/2) Primary 1. To evaluate the safety and tolerability of INKmune when given intravenously 31 Exploratory 1.
Slide 32: Refractory Ovarian Cancer Clinical Study
REFRACTORY OVARIAN CANCER CLINICAL Phase 1 Open - label Study of Intraperitoneal INKmune™ in Patients with Relapsed Platinum - resistant, Platinum - refractory, or Platinum - Intolerant Ovarian Cancer Primary 1. To evaluate the safety and tolerability of INKmune when given intraperitoneally 32 Explo
Slide 33: DN-TNF and NK Patents
DN - TNF PATENTS* 2021 composition - of - matter (licensed from Xencor) 2032 Methods for treatment of neurologic disease 2035 use for treatment of cancer (issued in US) 2039 use for treatment of NASH 2040 use for immune mediated complications from COVID - 19/CRS 33 NK PATENTS* 2035 use for treatment
Slide 34: Future Catalysts
34 Q1 Q2 2019 Q3 Q4 Q1 Q2 2020 2H 1H 2021 2H NASDAQ Listing $1 Million Park the Cloud Award – Alzheimer’s Association Initial Data on INB03 Phase 1 $1 Million Park the Cloud Award – Alzheimer’s Association INB03 Phase 1 Readout XPro1595 First Patient Enrolled in Phase 1 AD Trial $500,000 ALS Associa
Slide 35: Management Team
MANAGEMENT TEAM 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 Chief Medic
Slide 36: Non-Employee Board of Directors
NON - EMPLOYEE BOARD OF DIRECTORS David Szymkowski, PhD David E . Szymkowski leads the immunology group as Vice President of Cell Biology at Xencor Inc where he is focused on translational development of Fc - engineered and bispecific antibodies for the treatment of autoimmune diseases, allergic dis
Slide 37: Contact Us
CONTACT US 37 HARNESSING THE POWER OFTHE INNATE IMMUNE SYSTEM INMB INmune Bio Inc. 1200 Prospect Str. Suite 525 La Jolla, CA 92037 (858) 964 - 3720 www.inmunebio.com