Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — Investor Presentation (August 2019)
77 slides from Inmune Bio's investor presentation, Aug 15, 2019
Slide 1: INMB non - confidential3Q19.v2
INMB non - confidential3Q19.v2
Slide 2: 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 terms and similar expres
Slide 3: Building a Next Generation immunology company
3 Building a Next Generation immunology company • Immunology focused - platforms in immuno - oncology and neurodegenerative diseases • Target “ignored” elements of immune system • Innate immune system • TME (tumor microenvironment) • Neuroinflammation is a cause of neurodegenerative disease • Multip
Slide 4: Financial Highlights
4 Financial Highlights • Nasdaq: INMB • Pro Forma Cash 6/30/19 ~$9.4 million • Debt $0 • Common Shares outstanding 10.8 million Insider ownership: ~50% Notable Shareholder: Xencor (XNCR) XNCR outstanding licensing fee: buy 10% of INMB at $100m pre INMB non - confidential3Q19.v2
Slide 5: INmune Bio = Innate Immunity
5 INmune Bio = Innate Immunity Our Vision: Become the Leader in Reprograming the Innate Immune System for the Treatment of Diseases INMB non - confidential3Q19.v2
Slide 6: INMB Pipeline & Clinical Status
6 INMB Pipeline & Clinical Status Pre - clinical Phase I Phase II POC Pivotal INB03 for resistance to immunotherapy INKmune to eliminate Minimal Residual Disease (ovarian cancer) XPro1595 for Neuro - inflammation (Alzheimer’s disease) INMB non - confidential3Q19.v2
Slide 7: Pipeline Market Opportunity
Pipeline Market Opportunity 7 • XPro1595 - Alzheimer’s/dementia market* – 5.8 M patients in US – 2019 est cost to care for US AD patients $280B • INKmune - Cancer residual disease market ** – 1,735,350 new cases and 609,640 people will die – Initial targets: Ovarian Cancer and High Risk MDS • INB03
Slide 8: INB03 for treatment of cancers resistance to immunotherapy
INB03 for treatment of cancers resistance to immunotherapy INMB non - confidential3Q19.v2
Slide 9: Resistance to immunotherapy case study: CPI
• Small cell Lung • Melanoma • RCC • Bladder • Ureothelial • Merkel Cell • NSCLC • Gastric • HNC • HCC • Microsatellite instability INMB non - confidential3Q19.v2 Resistance to immunotherapy case study: CPI 9 Eligible Benefit 10% 30% 20% 40% 60% JAMA Hasim2019 Eligibility vs Benefit CPI US patients
Slide 10: INB03: novel inhibitor of soluble TNF
• 17 kDal mutated protein +10 kDal linear PEG • Identical to human TNF except for 6 amino acid substitutions • Once a week dosing by subQ injection INMB non - confidential3Q19.v2 Receptor binding, "DE loop" domain (subunit A) Receptor binding , "small" domain (subunit A) Mutation A145R Receptor bind
Slide 11: Targeting sTNF: fibrosarcoma model
INMB non - confidential3Q19.v2 0 2 4 6 8 10 12 14 16 ↓MDSC in tumor Decreased sTNF decreases differentiation and proliferation of MDSC 0 2 4 6 8 10 etanercept INB03 ↑CD8+ lymphocytes in tumor + tmTNF promotes NK/DC crosstalk that recruits CD+8 TILs 0 1 2 3 4 5 6 7 8 9 10 control INB03 ↑112 day survi
Slide 12: INB03 reverses trastuzumab resistance
JIMT - 1 breast cancer into nude mouse I g G T D N T + D N 0 20 40 60 % C D 1 1 b / C D 4 5 + * * Fewer Myeloid Cells from Schillaci 2018 T =trastuzumab DN =INB03 INMB non - confidential3Q19.v2 More activated NK INB03 reverses trastuzumab resistance 12
Slide 13: INB03: on-going Phase I
• Open label, biomarker directed, dose - escalation trial in patients with advanced solid tumors and elevated markers of inflammation • Enrollment criteria: – Advanced solid tumors – hsCRP > 4 mg/L – Treatment: INB03 subQ once a week – 3 cohorts of 3: 0.3, 1.0, 3.0 mg/kg INMB non - confidential3Q19.
Slide 14: Preliminary data: INB03 Phase I
• Goals: 1. Determine safety 2. Determine Phase II dose 3. Demonstrate PD effect 4. Determine Phase II strategy • “Top - Line” Results 1. Safe and well tolerated 2. Phase II dose: 1mg/kg 3. Pharmacodynamic effect confirmed 4. Planning Phase II study • 11 of 12 patients treated – Demographics : age (
Slide 15: Determining INB03 dose
[ wtTNF ] = 50 g/ml; [DN - TNF] = 50 g/ml Exchange at equilibrium in PBS + 0.1 mg/ml BSA Separation & quantitation by native PAGE Flag His Flag + His 1 to 1 ratio DN - TNF to TNF 4 DNs + 4 TNFs = Theory Experiment 0.1 1 10 0.0 0.2 0.4 0.6 0.8 1.0 Fraction DN-TNF added vs native TNF Relative abun
Slide 16: INB03 dose for Phase II: 1mg/kg SQ QW
• Goal: blood trough level at least 2 logs greater than blood TNF level • Conclusion: – 1mg/kg dose provides adequate drug level – Above 3 log target 8 hours after first dose 0.3mg 1.0mg day 8 2 of 3 0 of 3 day 15 2 of 3 1* of 3 day 22 2 of 3 0 of 3 day 29 1 of 2 0 of 3 day 43 1 of 2 0 of 2 day 57 0
Slide 17: INB03: moving to Phase II in cancer
Phase I summary • Safe at all doses tested – No SAE, No DLT, Well tolerated • 1mg/kg once a week will be carried into Phase II – Dose provides robust trough drug levels • Pharmacologically active at all dose levels – >50% decreases IL6 Phase II combination trial • Design variables: 1. Combination wi
Slide 18: XPro1595 (for the treatment of Alzheimer's Disease/dementia)
XPro1595 (for the treatment of Alzheimer's Disease/dementia) INMB non - confidential3Q19.v2
Slide 19: AD: the problem
19 AD: the problem.. Nerve cell death Synaptic dysfunction Cognitive Decline INMB non - confidential3Q19.v2
Slide 20: 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* (60% lower) * In RA patients compared to patients without RA 1 2 20 Does eliminating TNF prevent AD? from Chou et al. 2016 INMB non - confidential3Q19.v2
Slide 21: Long term inhibition of TNF: the good and the bad
The good: confirmation of findings from database of 63M patients INMB non - confidential3Q19.v2 21 TNF inhibitor Odds Ratio Cases Enbrel 0.31 21,280 Humira 0.35 20,130 Remicade 0.54 10,320 Adapted from Xu, Zhu and Gurney AAIC 2019 Long term inhibition of TNF: the good and the bad The bad: ↑ risk of
Slide 22: XPro1595 Clinical Development Supported by the Alzheimer's Association
22 XPro1595 Clinical Development Supported by the Alzheimer’s Association Alzheimer’s Association awards INmune Bio Part the Cloud Grant - $1M USD translational funding to study XPro1595 in Alzheimer's disease INMB non - confidential3Q19.v2
Slide 23: XPro1595 AD Development Program
XPro1595 AD Development Program 18 patients in 3 cohorts • Weekly XPro1595 subQ for 3 months • Biomarkers of inflammation at 0, 6 and 12 weeks • Endpoints: – Safety – ↓ neuro - inflammation measured in: blood, cerebrospinal fluid, brain, breath and behavior – Measures of cognition, neuro - psychiatr
Slide 24: Immunologic biomarkers: AD
24 Immunologic biomarkers: AD MRI CSF Breath Blood Free Water content of white matter Volatile Organic Compounds Inflammation & Neurodegeneration Inflammation & Neurodegeneration Behavioral biomarkers of inflammation • Sleep disorders • Depression • Psychosis • Apathy • Aggression INMB non - confide
Slide 25: INKmune (for the treatment of Ovarian Cancer and high risk MDS)
INKmune (for the treatment of Ovarian Cancer and high risk MDS) INMB non - confidential3Q19.v2
Slide 26: Problem: Minimal Residual Disease (MRD) causes relapse
Problem: Minimal Residual Disease (MRD) causes relapse 26 Difference between survivors and relapsers is MRD INMB non - confidential3Q19.v2
Slide 27: INKmune Primed NK Cells Kill Cancer
INKmune Primed NK Cells Kill Cancer 27 rN Human ovarian cancer cells plus patient’s own NK cells cancer cell NK cell Human ovarian cancer cells with patient’s NK cells after INKmune treatment TpNK cancer cell INMB non - confidential3Q19.v2
Slide 28: INKmune Clinical Trial
INKmune Clinical Trial Phase 1/2 study in relapsed/ refractory CaOva Platinum resistant/refractory patients with residual disease • Treatment: INKmune - 6 doses • Endpoints: – Safety – ↑ NK activation and tumor killing – ↓ tumor burden* 28 INKmune causes in vivo priming so patient’s NK cells can kil
Slide 29: INmune Bio = Innate Immunity
INmune Bio = Innate Immunity INMB non - confidential3Q19.v2
Slide 30: Milestones
Milestones 30 February 1, 2019 – IPO closed Feb19 – Part the Cloud award – Alzheimer’ Assoc 3Q19 – initial data on INB03 Phase I 4Q19 – first patient enrolled INKmune CaOva 1H20 – initiate INB03 combination Phase II trial 3Q19 – first patient enrolled XPro1595 AD trial 1H20 – initial data from INKmu
Slide 31: Experienced Leadership
Experienced Leadership 31 RJ Tesi, MD Chief Executive Officer & Chief Medical Officer Mark Lowdell, PhD Chief Scientific Officer David Moss Chief Financial Officer Management Board of Directors J. Kelly Ganjei CEO of Cognate Timothy Schroeder CEO and Founder of CTI David Szymkowski, PhD VP of Cell B
Slide 32: Intellectual Property
Intellectual Property • 2021 – composition - of - matter (licensed from Xencor) • 2032 – Methods for treatment of neurologic disease • 2035 – use for treatment of cancer (licensed from University of Pittsburgh) INB03/XPro1595 INKmune Continuing to expand patent portfolio for both platforms 32 • 2035
Slide 33: INB03/XPro1595 MOA Appendix
INB03/XPro1595 MOA Appendix INMB non - confidential3Q19.v2
Slide 34: How XPro1595/INB03 Neutralizes sTNF
Active TNF + Inflammation Normal sTNF activity TNFR sTNF bind TNFR XPro1595 Active TNF + Inactive heterotrimers or NO Inflammation Heterotrimers cannot bind TNFR No sTNF activity How XPro159/INB03 Neutralizes sTNF 34 INMB non - confidential3Q19.v2
Slide 35: Why is Xpro1595/INB03 Different?
35 Why is Xpro1595/INB03 Different? TNFR1 TNFR2 tmTNF (good) sTNF (bad) Normal TNF Biology 35 tmTNF INB03 INB03 does not neutralize tmTNF X tmTNF binds TNFR with normal function TNFR1 TNFR2 tmTNF (good) sTNF (bad) Approved TNF inhibitors X X TNFR1 TNFR2 tmTNF (good) sTNF (bad) XPro1595/INB03 X Preve
Slide 36: Precision Therapy: Targets sTNF not tmTNF
Precision Therapy: Targets sTNF not tmTNF Inflammatory soluble TNF eliminated: No paracrine signaling through receptors Immunoprotective transmembrane TNF unaffected: Allows juxtacrine cell - cell signaling solTNF (recombinant or physiological) Exchange = No paracrine signaling Normal juxtacrine sig
Slide 37: Repeat Dose Modeling of XENP1595 in Humans
0.1 1 10 0 5 10 15 20 25 30 Time (day) 10d 5d 7d Repeat Dose Modeling of XENP1595 in Humans 1mg/kg Administered SC Every 5, 7, or 10 Days 0.5 g/ml 2.4 g/ml 1.3 g/ml V = 494.9 ml k 01 = 3.552/day k 10 = 0.25/day Allometric scaling of cyno PK data suggests weekly dosing of 1 mg/kg SC in humans w
Slide 38: Manufacturing
Pegylated [92 - 94% main peak] unpegylated Receptor binding, Subunit C Subunit B Receptor binding, "DE loop" domain (subunit A) "large" domain (subunit C) Receptor binding, "small" domain (subunit A) Subunit C Subunit B Mutation R31C (for 10kD pegylation) Subunit A RP - HPLC of INB03 • INB03 was eng
Slide 39: MDSC Appendix
MDSC Appendix INMB non - confidential3Q19.v2
Slide 40: Eligibility vs Response to CPI - US
Eligibility vs Response to CPI - US • 44% US cancer patients eligible for CPI • 29% of cancer patients who receive CPI respond INMB non - confidential3Q19.v2 JAMA2019
Slide 41: Resistance to Immunotherapy: CPI
INMB non - confidential3Q19.v2 12% 47% 41 from Haslam 2019 Resistance to Immunotherapy: CPI 41
Slide 42: Different Approach to Immuno-oncology
Different Approach to Immuno - oncology 42 MDSC NK cells T & NK cells Innate Immunity Protector cells Effector cells Adaptive Immunity Most I/O companies • Effector cells: T and NK cells • Protector cells: MDSC, TAM, TAN, Treg, CAF INMB INKmune INB03
Slide 43: MDSC Predict Resistance to CPI
Stage IV Melanoma treated with Ipilimumab (Wolchok2016) MDSC Predict Resistance to CPI 43 (n=209) • INB03 targets MDSC • CPI + INB03 should overcome MDSC based resistance by eliminating MDSC so CPI become effective INMB non - confidential3Q19.v2
Slide 44: INB03 decreases MDSC by starvation
tmTNF required for NK/DC crosstalk ↓ MDSC causes ↓ TAM and Treg No pSTAT3 stops differentiation and proliferation of myeloid cells to MDSC ↑NK/DC recruits CD8+ TIL to tumor INMB non - confidential3Q19.v2 44 INB03 decreases MDSC by “starvation” 44
Slide 45: INB03 HER2/MUC4 Appendix
INB03 HER2/MUC4 Appendix INMB non - confidential3Q19.v2
Slide 46: Trastuzumab Resistance in Breast Cancer
Trastuzumab Resistance in Breast Cancer 46 • ~30% of women with breast cancer are HER2+ • 30% - 50% patients have 1 ◦ or 2 ◦ resistance to trastuzumab • MUC4 expression predicts trastuzumab resistance 0 2 0 4 0 6 0 0 2 5 5 0 7 5 10 0 M U C 4 n e g a t i ve n = 3 1 M U C 4 po s i t i ve n = 4 7 P = 0
Slide 47: INB03 Reverses Trastuzumab Resistance
INB03 Reverses Trastuzumab Resistance 47 INB03 overcomes trastuzumab resistance in JIMT - 1 tumors T - trastuzumab DN - INB03 Schillaci - SABCS2018 MUC4 blocks trastuzumab binding INB03 decreases MUC4 expression INMB non - confidential3Q19.v2
Slide 48: Alzheimer's Disease Appendix
Alzheimer’s Disease Appendix INMB non - confidential3Q19.v2
Slide 49: Cancer vs. Alzheimer's disease/Dementia
Cancer vs. Alzheimer’s disease/Dementia 49 http://go.bio.org/rs/490 - EHZ - 999/images/BIO_HPCD4_ALZHEIMERS.pdf?_ga=2.221439256.1049474662.1560812904 - 160068109.1560812904 INMB non - confidential3Q19.v2
Slide 50: XPro1595 to Treat Alzheimer's Disease
XPro1595 to Treat Alzheimer’s Disease 50 AD is an expanding, expensive and intractable disease that defies a therapeutic solution • Problem: synaptic pruning and nerve cell death • Solution: reduce neuroinflammation • Drug: XPro1595 • Target: activated glial cells in the brain • Status: entering Pha
Slide 51: Majority of genes associated with AD expressed in innate immune cells
51 INMB non - confidential3Q19.v2 Jansen2019 Majority of genes associated with AD expressed in innate immune cells
Slide 52: Genetics implicates every aspect of the immune cell is dysfunctional
52 Genetics implicates every aspect of the immune cell is dysfunctional INMB non - confidential 7.3.19
Slide 53: Chronic inflammation: real disease, bad name
53 Chronic inflammation: real disease….bad name 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 non - confidential3Q19.v2
Slide 54: Inflammaging and cognitive decline
Inflammaging and cognitive decline 54 INMB non - confidential3Q19.v2 Quartiles of hs - CRP Risk of Dementia <0.34mg/L 1.0 0.34 - 0.56mg/L 2.9 0.57 - 1.0mg/L 3.8 >1.00mg/L 2.7 Atherosclerosis Risk in Communities Study (ARIC) hsCRP>1.05 mg/L had greater cognitive decline over a 20 year period Honolulu
Slide 55: Pivotal role of TNF in AD
55 Pivotal role of TNF in AD TNF Microglia dysfunction/activation Nerve cell death Synaptic dysfunction INMB non - confidential3Q19.v2
Slide 56: TNF in humans: the dark passenger of AD
56 TNF in humans: the dark passenger of AD • Elevated plasma TNF (Fillit et al. 1991) • TNF co - localized with plaques (Dickson 1997) • TNF levels correlate with disease progression ( Paganelli et al. 2002) • Elevated TNF in CSF ( Tarkowski et al. 2003) INMB non - confidential3Q19.v2
Slide 57: Why XPro1595?
57 Why XPro1595? Non - selective TNF inhibitor XPro1595 Decreases inflammation YES YES Causes immunosuppression YES No Causes demyelination YES No Neuroprotective NO YES Enhances neuroplasticity NO YES Difference between selective vs non - selective TNF inhibition INMB non - confidential3Q19.v2
Slide 58: Bad history of non-selective TNF therapy in neurologic disease
• Lenercept made RRMS worse • Non - selective TNF inhibitors contra - indicated in neurologic disease 58 Bad history of non - selective TNF therapy in neurologic disease placebo lenercept Non - selective TNF inhibitors exacerbates RRMS Neurology 1999 INMB non - confidential3Q19.v2
Slide 59: In retrospect: XPro1595 improves, etanercept worsens
59 In retrospect…. XPro1595 improves, etanercept worsens ( Brambrilla et al. 2011) INMB non - confidential3Q19.v2 XPro Etan Veh
Slide 60: What happened?
60 What happened? XPro1595 promotes remyelination, etanercept promotes demyelination Probert et al. 2017 INMB non - confidential3Q19.v2
Slide 61: XPro1595 attenuates AD pathology and restores normal function
XPro1595 attenuates AD pathology and restores normal function Efficacy has been shown in 3xTgAD, 5xFAD, TgCRND8 and aged mice Hippocampus Saline XPro 1595 Activated Myeloid cells Saline XPro 1595 Brain T cell infiltration Saline XPro 1595 Saline XPro 1595 Vehicle XPro 1595 Microglia Cognitive Impair
Slide 62: Problem XPro1595 Addresses: Neuroinflammation
62 Problem XPro1595 Addresses: Neuroinflammation, Linked to Every Aspect of Alzheimer’s Disease Pathology Microgliosis and Astrogliosis Excitotoxicit y Suppression of growth factors Neuronal cell death Synaptic loss sTNF Abnormal Ab and Tau processing XPro1595 is a protein biologic that targets solu
Slide 63: Phase 1b Biomarker Directed, Proof of Biology Study
Phase 1b Biomarker Directed, Proof of Biology Study in Mild to Moderate AD Patients 63
Slide 64: INKmune Appendix
INKmune Appendix INMB non - confidential3Q19.v2
Slide 65: INKmune to Treat Residual Disease
INKmune to Treat Residual Disease 65 Residual disease is the cause of relapse and death in a majority of patients • Problem: cancer remains after treatment • Solution: eliminate residual disease • Drug: INKmune • Target: patient’s NK cells • Status: entering Phase I/II trial in women with relapse/re
Slide 66: What is MRD?
What is MRD? 66 • Residual disease is the cancer that is left behind after treatment • Two types: – Overt: visible by imaging studies – Minimal (MRD): invisible by imaging studies • Natural Killer (NK) cells are responsible for eliminating MRD • Problem: patient’s NK cells are inert • Solution: INKm
Slide 67: Tumor not Immune System Cause of Relapse
Survivor AML Survivor NK cells Kills Relapser AML Relapser NK cells Does not kill • Relapser NK cells kill survivors AML. • Survivor NK cells can not kill relapser AML. Conclusion: AML mutates to evade NK cell killing. 67 67 Tumor not Immune System Cause of Relapse INMB non - confidential3Q19.v2
Slide 68: INKmune primes NK cells to eliminate MRD
S1 Relapse due to Minimal Residual Disease 68 S2 S2 aNK Cell = Activated NK Cell rNK Cell = Resting NK Cell INKmune INKmune artificially replaces S1 allowing the NK to engage and kill cancer cells TpNK Cell Dead - Cancer Cell Priming Triggering S2 INKmune primes NK cells to eliminate MRD S2 Cancer d
Slide 69: INKmune: universal Cancer Therapy
INKmune: “universal” Cancer Therapy INKmune TpNK are active against many types of cancers: • Blood cancers: AML, MM, lymphoma • Solid tumors: breast, ovary, prostate, renal, lung modified from Lowdell2007 and 2011 69 TpNK
Slide 70: Results with 1st-Generation TpNK Therapy
Results with 1 st - Generation TpNK Therapy AML Phase 1 TpNK therapy made a difference 70 2 Phase 1 clinical trials; 20 patients with high - risk AML using ex vivo , personalized TpNK therapy Clinical Results ‒ Prolonged remissions with excellent quality of life ‒ Put chemo - resistant disease into
Slide 71: Biomarker – Patient Selection
AML CLL MCF-7 0 10 20 30 40 50 60 70 % Specific lysis Autologous INKmune pNK cells lyse primary MM cells irrespective of prior treatment INKmune Normal B cells Myeloma B cells INKmune pNK target tumor and NOT normal cells Am J Hematology; 86:967 - 973 71 71 Biomarker – Patient Selection INMB non - c
Slide 72: INKmune Development Program
INKmune Development Program Phase 1/2 study in relapsed/ refractory CaOva Platinum resistant/refractory patients with residual disease • Treatment: INKmune IP • Endpoints: – Safety – ↑ NK activation and tumor killing – ↓ tumor burden* Phase 1/2 dose - finding study in high - risk MDS Patients with h
Slide 73: NK cells and INKmune in Ovarian Cancer
SKOV3 killing by NK cells from healthy donor (HD) or CaOva patient ascites SKOV-3 ALONEHD NK+SKOV3HD TpNK+SKOV3HD LAK+SKOV3PT08 ASC NK+SKOV3PT08 ASC TpNK+SKOV3PT08 ASC LAK+SKOV3 0 20 40 60 80 100 % Viable SKOV3 Cells * * NK cells and INKmune in Ovarian Cancer 73 IL2 primed NK cells do not kill SKOV3
Slide 74: INKmune MOA
INB16 INB16 vs cytokine priming – Differential protein expression @16h • Paradoxical decrease (not loss) in ligand expression associated with increased function • INKmune priming fundamentally different than cytokine or antibody priming INKmune MOA 74 INMB non - confidential3Q19.v2
Slide 75: INKmune Primed NK Cell Killing Assay
0.0 5.0 10.0 15.0 20.0 25.0 30.0 35.0 40.0 24.0 36.0 48.0 60.0 72.0 84.0 % Cytolysis Time (hr Post - Treatment) Real - Time Cytolysis Plot NK 1:1 NK 2:1 NK 5:1 NK 20:1 TP-NK 1:1 TP-NK 2:1 TP-NK 5:1 NK added INKmune added 75 INKmune Primed NK Cell Killing Assay INMB non - confidential3Q19.v2
Slide 76: INKmune MOA
TaNK alone TaNK +CD15TaNK+OKT11TaNK+CD15+OKT11TaNK+ W632 0 5 10 15 20 25 30 35 %CD25 Expression TaNK alone TaNK +CD15TaNK+OKT11TaNK+CD15+OKT11TaNK+ W632 0 10 20 30 %RAJI Lysis CD2 CD16 CD3 z SS CD2L CD15 epitope INB16 NK rNK TpNK 4h NK signalling upon co-culture with CTV-1 0 10 20 30 40 50 60 70 0 1
Slide 77: INB16 vs LAK Priming – 412 Gene Expression Profiles
INB16 IL - 2 LAK ALCAM – NK cell migration and adhesion STAT5 – “molecular switch” essential for NK killing CD70 – CD27L and NCR for B cell tumours VEGFA – survival signal for NK CXCL10 – chemoattractant for NK cells 77 INB16 vs LAK Priming – 412 Gene Expression Profiles INMB non - confidential3Q19.