Exhibit 99.1

I N M B IN V E S T O R PRES E NT A TIO N March 2023 H A R N E SS I N G T H E P O W E R O F T H E I NN A T E I MM U N E S Y S T E M Two Therapeutic Platforms: XPro Πand INKmune ΠHe l p Rep a ir Inn a te Immune D ysfunction

F O R W A R D L OO K I N G S T A T E M E N T S 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 expressions, as they relate to us or our management, identify forward - looking statements . Such statements, include, but are not limited to, statements contained in this presentation relating to our business strategy, our future operating results and liquidity and capital resources outlook . Forward - looking statements are based on our current expectations and assumptions regarding our business, the economy and other future conditions . Because forward – looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict . Our actual results may differ materially from those contemplated by the forward - looking statements . They are neither statements of historical fact nor guarantees of assurance of future performance . We caution you therefore against relying on any of these forward - looking statements . Important factors that could cause actual results to differ materially from those in the forward - looking statements include, without limitation, our ability to raise capital to fund continuing operations ; our ability to protect our intellectual property rights ; the impact of any infringement actions or other litigation brought against us ; competition from other providers and products ; our ability to develop and commercialize products and services ; changes in government regulation ; our ability to complete capital raising transactions ; and other factors relating to our industry, our operations and results of operations . There is no guarantee that any specific outcome will be achieved . Investment results are speculative and there is a risk of loss, potentially all loss of investments . Actual results may differ significantly from those anticipated, believed, estimated, expected, intended or planned . Factors or events that could cause our actual results to differ may emerge from time to time, and it is not possible for us to predict all of them . We cannot guarantee future results, levels of activity, performance or achievements . Except as required by applicable law, including the securities laws of the United States, we do not intend to update any of the forward - looking statements to conform these statements to actual results . INB 03 Œ , XPro 1595 , and INKmune Œ are still in clinical trials or preparing to start clinical trials and have not been approved by the US Food and Drug Administration (FDA) or any regulatory body and there cannot be any assurance that they will be approved by the FDA or any regulatory body or that any specific results will be achieved . 2 2

I N M B C o r p o r a t e F o c u s 3 x Disequilibrium of the innate immune system is a key driver of both cancer, neurodegenerative diseases and many other conditions x INmune Bio is developing two novel platform therapies that recalibrate the innate immune system XPro  DN - TNF selectively inhibits soluble TNF which suppresses destructive inflammation and improves neurologic function in Alzheimer ’s disease • X P r o Œ DN - TNF f or t r e a tme n t r esist a n t dep r ession and other CNS diseases • pSar DN - TNF for DMD, cancer and other indications INKmune  is a cell therapy that stimulates the anti - tumor activity of natural killer cells, which play a critical role in controlling the progression of many cancers • INKmune for liquid and solid tumors Chronic inflammatory diseases are the most significant cause of death in the world. The World Health Organization ranks chronic diseases as the greatest threat to human health. Worldwide, 3 of 5 people die due to chronic inflammatory diseases like stroke, chronic respiratory diseases, heart disorders, cancer, obesity, and diabetes. https://www.ncbi.nlm.nih.gov/books/NBK493173/

4 PIPELINE DEVELOPMENT D N - TNF PL A TFORM DI S E A S E FI E LD PRE - CLINICAL P H AS E I P H AS E I I ( POC) PIVOTAL ES T. N EX T MILESTONE E a rly A lzh e im e r’s P 2 D at a 2024 Treatment Resistant D epre s s i on P 2 S ta r t 2023 pSar D N - TNF DMD Cancer Other Future D evelopm ent and/or Partnership N K P RIMIN G P L A TF O R M Mye lo d ys pl a s t ic Syndrome ONCOLOGY P 1 D a ta 2 0 23 M e t a s t a t ic C a s t ra t io n - R e s i s t ant Pros t a t e Cancer P 1/ 2 S t ar t 2H 2023

MANAGEM E NT T EAM 5 Broad biotechnology background including legal, intellectual property, drug manufacturing, clinical trial management, FDA approval, drug marketing, finance, business development and operations.

f o r A D Treating Alzheimer’s as an Immunologic Disease … not a Neur o lo g ic Disease 6

’ Long duration of illness before death, as long as 20 years 121,499 deaths from Alzheimer’s disease in 2019 High burden and stress on family caregivers, especially spouses Total cost of care for Americans age 65 or older with AD: $321 billion

8 Q u e s t i o n s t o An s w e r a b o u t I N m u n e B i o ’ s a pp r o a c h t o A l z h e i m e r ’ s D i s e a s e ▪ Why neuroinflammation? ▪ What causes neuroinflammation? ▪ Why XPRO Œ ? ▪ XPRO results in patients with ADi ▪ Next steps in patients with Alzheimer’s Disease f o r A D

A wealth of evidence supports NEUROINFLAMMATION as a critical driver of the pathogenesis and progression of Alzheimer’s disease

10 Large genetic profile study of AD patients demonstrated strong association with immune dysfunction f o r A D A s t r o g lia MICROGLIA Genome - wide association study of 71,880 AD cases and 383,378 controls Jansen IE, et al. Nature Genetics . 2019;51:404 – 413 Genes associated with AD were strongly expressed in immune - related tissues and cell types, including microglia

11 Strong Evidence Supports Neuroinflammation in Alzheimer’s f o r A D Torres - Acosta N, et al. J Alzheimer’s Dis. 2020;78:619 – 626 R IS K O F A L Z H EIME R ’S DISEASE I N P A T EINTS W I T H Rheum a to id A r thritis Ri s k o f g e n e r a l p o p u lation Adap t ed fro m C h o u e t al . 2016 8.5M claims

f o r A D 12 An t i - T N F An t i b od i e s H a v e S e r i o u s L i m i t a t i o n s X P R O T M i m p r o v e s t h e b r a i n approved TNF Inhibitors “abuse” the brain Etanercept XPRO No n - s ele c t i v e T N F i nh i b i t o r s ( E t a n e r c e p t ) t h a t b lo c k b ot h t r a n sm em b r a n e T N F a n d s ol ub l e TNF cause demyelination (yellow arrow) and axonal degeneration (white arrows). Selective blocking of soluble TNF with XPRO TM promotes remyelination and axonal regeneration CuprizonemodelKaramita2017 PMID: 28422748 A x o n s M y elin

f o r A D 13 I N m u n e B i o ’ s A D P r o g r a m s i m p l i f i e d … s T NF Am ylo i d plaqu e s Neu r o f i b r ill a r y t an gles Behavioral, Environmental and G en e t i c f a c t o r s M IC R O GLIA N e r v e C e ll Death Synaptic Dy s f unc t i on Cogni t i v e Decline ▪ Neuroinflammation is a cause of AD ▪ Soluble TNF causes neuroinflammation ▪ XPro neutralizes soluble TNF to reduce neuroinflammation

f o r A D Summary of Successful Phase 1b trial: AD patients with biomarkers of inflammation (ADi) 14 DESIGN ▪ O pe n - l a b el Mul t i ple dosing c oh o r t s ( 0 . 3 , 0. 6 , 1.0 m g/kg) ▪ Weekly XPro1595 Œ SubQ injections for 3 months ▪ Biomarke r s a ssessed a t 0 a nd 12 we eks Inclusion ▪ AD Di a gn o sis ▪ At l e a st o n e b i omarke r s of i nflam m a t i on ▪ ( C RP, ESR, H g b A 1 c , APOE 4 ) STUDY G O A L S ▪ Demonstrate peripheral administration of XPro1595 reduces biomarkers of neuroinflammation and neurodegeneration, dose identification, did our ADi biomarkers identify patients with neuroinflammation

X P R O T M D E C R E A S E S N E U R O I N F L A M M A T I O N I N A D Inflammatory Cytokines in CSF after 3 months P h a se 1 b D a t a: T A R G E T ENG A G E MENT f o r A D 15

XPRO DECREASES NEUROINFLAMMATION IN AD D e cr e ase in N eu r oinflam m ation in whit e matter tra c ts over 12 months RE S U L T OF P H A S E I TRIAL XPro decreases neuroinflammation over 12 months in patients with AD - 60 - 30 - 40 - 50 - 20 - 10 30 20 10 0 Fr e e - w a te r i n A D bun d l es ( % c h a n ge ) XPro1595 1 mg/kg ADNI database N = 36 N = 6 N = 5 N = 5 N = 3 0 3 6 9 12 15 18 21 24 Visit (months) White Matter Free Water is a non - invasive measure of neuroinflammation measured by MRI f o r A D 16

W H I T E M A TT E R M E T R I C S f o r A D Hea l th Whi t e matter 17 AD wh i te matter

D O W N S T R E A M B E N E F I T S OF X P R O Ρ T R E A T M E N T : D E C R E A S E S NEURODEGENERATION AND IMPROVES SYNAPTIC FUNCTION Phase 1b Data: CSF PROTEOMICS f o r A D Synaptic Proteins Contactin - 2 – 222% increase Neurogranin – 56% decrease Neuronal Injury Visinin - like protein 1 (VILIP - 1) – 91% decrease Neurofilament light (NFL) – 84% decrease 18

f o r A D RESULT OF PHASE I TRIAL – p - tau217 as a biomarker of AD A “ t r a d i t i on a l ” b i o m a r k e r o f A D – p T a u 2 1 7 / 1 8 1 CSF following 12 weeks of treatment with XPro1595 (1 mg/kg) p<0.0001 p<0.01 Phospho - tau is a biomarker of neurodegeneration Phospho - tau217 correlates best with cognitive dysfunction 19

0 3 6 18 21 24 - 10 0 - 5 5 20 15 10 9 12 15 V i s i t ( m on t hs ) Fiber Density in AD bundles (% change) XPro1595 1 mg/kg ADNI database N = 36 N = 6 N = 5 N = 5 N = 3 12 month AFD improvement 1mg/kg 12 month RD improvement 1mg/kg T H E “ D O W N S T R E A M ” B E N E F I T S O F X P R O T M I N P A T I E N T S W I T H A D I Phase 1b Data ▪ XPRO improves axonal integrity in white matter tracts (increased AFD) ▪ XPRO promotes remyelination/myelin repair (RD) f o r A D 20

XPR O ΠINCREASED WHITE MATTER VOLUME 0 1 2 5 00 0 5 50 0 6 00 0 6 50 0 3 6 9 Visit (months) Left Inferior Temporal volume (mm 3 ) 0.0839 0.0381 0.1226 INMB AD Non - confidential 1.5.22 f o r A D 21 Phase 1b Data

R E M O D E L I N G O F W H I T E M A TT E R T R A C T S A F T E R X P R O TM Phase 1b Data: CHANGES IN AFD IN AD WHITE MATTER TRACTS IN MAN Baseline 3 months 6 months 9 months ▪ 65 - year - old white male retired due to AD ▪ Returned to work after 6 months of XPro therapy ▪ Increasing green/blue shows improvement in axonal quality f o r A D 22

Clinical Benefit in Pha s e I t rial Disclaimer: small N, disease status heterogeneity, short time period ▪ Assessments administered: ▪ Cognitive: MMSE, Verbal Fluency Test, Digit Symbol Coding ▪ Neuropsychiatric Inventory ▪ Bristol Activities of Daily Living Scale ▪ To compare across patients of different disease states, Dr . Judith Jaeger issued each patient a qualitative score of ( - 2 , - 1 , 0 , 1 , 2 ) based on her assessment of the overall change over 3 months . - 2 - 1 0 1 2 M ea n i n g f u l p r og r e ssi on Minor p r og r ession Stable Disease Minor Imp r o v em e n t Meaningful Imp r o v em e n t Patients with the greatest improvement in cognition had the largest reduction in neuroinflammation INMB AD Non - confidential 1.5.22 f o r A D 23

Correlation bet w een decreased neuroinflam m ation and i m proved cognition R 2 = 0.4 to 0.6 CSF cytokines by OLINK platform INMB AD Non - confidential 1.5.22 f o r A D 24

25 f o r A D All patients canenroll in a 12 - month open - label extension A randomized, placebo - controlled, double - blind study of XPro1595 in patients with Early Alzheimer's Disease with biomarkers of inflammation − A t l e a s t o n e n i f l a m m a t o ry b i o m a r k e r : − CRP > 1.5 − E S R > 1 0 mm / h − H b A 1 C >6 D C CT % − A t l e a s t o n e A P O E 4 all e l e − ( 2 : 1 ) X P r o 159 5 ( 1 m g/ k g) , p la c e b o − W ee k l y S ub Q i n j e c t i on s Inclusion − E a r l y AD − C l i n c i a l D ia g n o s i s o f M C I o r M il d AD − C D R g l o b a r l a t i n g o f 0 . 5 o r 1 Treatment ~ 210 Number of patients 6 months Duration Early/mild Alzheimer’s Cognitive Composite (EMACC)*: − I n t e r n a t i o n a l S h o pp i n g s L t i T e s t − I mm e d a i t e r e c al l − D i g i t S p a n F o r w a r d a n d B a c k w a r d − C a t e g o ry f l u e n c y T e s t ( D K E F S ) − L e t t e r f l u e n c y T e s t ( D K E F S ) − TrailmakingTest Part A & B − D i g i t S y m b o l C o d i n g T e s t International L o c a t i o n S e c o n da r y E n dp o i n t s E x pl o r a t o r y E n dp o i n t s − GoalAttainment Scale (GAS) Small a n d F a s t Enrichment Se n s i t i ve Endpoint W H A T I S D I FF E R E N T A B O U T X P R O T M P H A S E 2 P R O G R A M I N E A R L Y A D ?

f o r A D S t a t i s t i c a l P o w e r : w h y X P R O c l i n i c a l t r i a l s a r e d e s i g n e d t o b e s h o r t a n d s m a l l • Patients with neuroinflammation have faster cognitive decline that patients without neuroinflammation • Enrichment strategy selects patients with neuroinflammation • Goal of XPRO therapy is to prevent cognitive decline not slow cognitive decline CDR - SB Lecanemab Phase III trial Adapted from NEJM 2022 Stable cognition is the goal 26

Targeting Neuroinflammation for the Treatment of TREATM E NT RESISTANT DEPR E SSION (TRD) 27

TREATMENT RESI S TA N T DEPRE S SI O N ( T R D ) ▪ There are 200+ symptom combinations that will lead to a depression diag n os i s ▪ No Biomarker s ▪ High p l a c e b o res ponse ▪ Drug development failure rate in psychiatry i n Pha se II: 35% i n Phas e III: 6 5 % ▪ Effect i veness of approv ed d r ugs ▪ 50% do not a c h i eve rem i ss i o n ▪ 33 % have no response (tr eatmen t res i st a nt) F r u s t r a t i o n s o f p s y c h i a t r i c d r u g d e v e l o p m e n t ▪ Drug development in psychiatry is a “one size fits all” approach ▪ 2 00 + ways to b e diagnos ed w i th depres sion T H E P R O B L E M M DD , T R D a n d I n f l a mm a t i o n f o r T R D 28

TREATMENT RESI S TA N T DEPRE S SI O N ( T R D ) Why sTNF is the right Tar g et f o r T R D 1 H a r oo n e t a l . , P syc honeu r oendo cr inology , 2018 2 Raison CL, et al. JAMA Psychiatry. 2013;70(1):31 - 41 P l asm a TN F l e v e l s a r e i nc r ease d i n TR D p at i e n ts 1 c o m bined < 5mg/L > 5mg/L Baseline CRP Responders (%) 0 20 40 60 80 A n t i - TN F t r ea t me n t r educe s d e p r ess i v e s y m p t o m s in patients with elevated biomarkers of inflammation 2 Infliximab (TNF inhibitor) Placebo 29

A biomarker of neuroinflammatory depression f o r T R D Felger et al., Mol Psychiatry, 2016 Patients with higher levels of blood CRP (>3mg/L) had lower Functional Connectivity between the ventral striatum (VS) and a cluster in ventromedial prefrontal cortex (vmPFC) compared to those with CRP <1 mg/L; a region of the brain that subserves an h edon i a a nd mot i va t io n . V mP F C 30

BIOMA RKERS OF I N F L A MM A T I O N D E S I G N ▪ S i x - w ee k d o u b l e b l i n d p l a c e b o - c o n t r o ll e d s t u d y o f X P r o 1 5 9 5 ▪ 4 5 p a t i e n t s i n X P r o 1 5 9 5 a t 1 m g / k g ▪ 4 5 p a t i e n t s i n p l a c e b o c o n t r o l gr o u p ▪ B i o m a r k e r s o f i n fl a mm a t i o n a t 0, 2, 6 w ee k s INCLUSION ▪ Failed 2 courses of antidepressants ▪ C - r e a c t i v e p r o t e i n ( C R P ) l e v e l s > 3 m g / L ▪ Anhedonia ENDPOINTS ▪ Primary: Improve functional connectivity Secondary: Improve clinical measures of motivation and anhedonia P H A S E 2 T R D T R I A L Supported by Small Business Innovation Research (SBIR) grant from the National Institutes of Health MRI 31 WM F W a s m ea s u re o f neuroinflammation B L OO D Inflammation ( R o che N e u r o T oo l ki t ) fMRI F u nc t i o n a l connectivity between m o t i va t i o n a nd rewa rd cen t ers in b ra i n B E H A V I O R AL Motivation Clinical s ca l es

Off - th e - Shelf NK Th erapy Conver t s Patien t ’s Resting NK cells in t o Cancer Kill i ng me m ory like NK cells f o r Oncolo g y 32

33 N a t u r a l K i ll e r ( N K ) c e ll s p l a y a c r i t i c a l r o l e i n e l i m i n a t i n g c a n c e r c e ll s i n Onco l o g y i n Onco l o g y A n t i - T u m or Cytotoxic Immunity x NK cells are principal anti - tumor cells in innate immune system x 5 - 15% of the circulating lymphocytes x Primed NK cells are capable of high cytotoxicity against tumors without prior sensitization x Capable of triggering and expanding adaptive immune responses against targeted tumor cells NK c e ll s T c e l l s Karvouni M, et al. Front Immunol. 2022;13:825979

34 NK cell cytotoxicity is a predictor of survival in m y e l o d y s p l a s t i c s y n d r o m e i n Onco l o g y i n Onco l o g y Alive >2yrs % K562 Lysis NO YES Tsirogianni M, et al. Leukemia & Lymphoma. 2019;60(10):2457 - 2463. Greater NK - mediated cell function in long - term survivors Better NK cytotoxicity correlates with increased survival

35 Why don’t NK cel s kil cancer cells more effectively? i n Onco l o g y i n Onco l o g y Karvouni M, et al. Front Immunol. 2022;13:825979 resting NK (rNK) tumor primed NK (tpNK) 1. INSUFFICIENT ACTIVATION Resting NK cells are not sufficiently activated by NK - resistant cancer cells 2. TUMOR - MEDIATED INHIBITION Tumors release factors that inhibit NK cell activity Activated NK cells can kill cancer cells effectively NK activators

36 Many NK cell - based immunotherapy approaches are being tested i n Onco l o g y i n Onco l o g y 1. Adoptive NK cellular therapy 2. Cytokine activation ex - vivo and in - vivo 3. Chimeric antigen receptor (CAR - NK) 4. mAb inhibition of NK inhibitor receptors 5. Checkpoint inhibitors Paul S, Lal G. Front Immunol. 2017;8:1124

Several NK cell - based immunotherapies have serious limitations i n Onco l o g y i n Onco l o g y 37 ᤵ Poor activation of NK cells by single cytokine signal  suboptimal efficacy ᤵ Toxic side effects ( in vivo cytokine therapy) ᤵ Requirement for lymphopenia  risk of infection (adoptive transfer) ᤵ Short - lived therapeutic persistence  requires frequent dosing ᤵ Complex and expensive manufacturing

Re - equilibrating the immune system in cancer i n Onco l o g y i n Onco l o g y INKmune  • Is a proprietary cell line that when given directly to patients delivers essential priming signals to ”turn on” NK cells to become tumor killing memory - like NK cells. 38

How does INKmune Œ prime NK cells to kill cancer cells? i n Onco l o g y i n Onco l o g y 39 1. Robustly activates resting NK to tpNK cells via multiple signals similar to using a combination of at least 3 cytokines in combination (IL - 12, IL - 15, IL - 18) 2. Increases avidity of binding of tpNK cells to tumor target cells to overcome inhibition 3. Prolongs therapeutic persistence by concomitant activation of resting NK cells 4. Enhances NK cell survival by upregulating nutrient receptors and mitochondrial survival proteins INKmu n e  :

40 INKmune Πstimulates differentiation of resting NK cells to m e m o r y - l i k e N K c e ll s i n Onco l o g y i n Onco l o g y INKmune - primed NK cells (TpNK) are phenotypically comparable to cytokine - induced memory - like NK cells 0 5000 10000 NK G 2 C I F e M 0 10000 20000 30000 40000 NK G 2 D M e F I 0 10000 20000 30000 15000 N K G 2 A M eF I 0 20000 40000 60000 80000 C D9 4 I F e M ) ) ) ) 0 N K 0 N K 0 ) y 0 K y 0 N K a y T p a y T p a y N K d a p N d a T p ( d ( d ( d T p K ( T K ( K N K K r N r N r N r r N 0 5000 10000 15000 20000 C D1 6 I F e M INKmune Generates Memory - Like NK Cells Without Use of IL - 12, IL - 15 and IL - 18 CD 16 CD 94 N K G 2 A N K G 2 D N K G 2 C r N K t p NK r N K t p NK r N K t p NK r N K t p NK M eF I r N K t p NK Cytokine Cocktail (IL - 12 + IL - 15 IL - 18) Generates Memory - Like NK Cells Romee R, et al. Scientifica . 2014;205796

41 INKmune Œ Increases Avidity of NK Cell Binding to Tumor Cells i n Onco l o g y i n Onco l o g y 0 20 0 80 0 100 0 400 600 rForce (pN) 0 2 0 4 0 6 0 8 0 % N K C e l l s B ou n d A v i d ity of tu m or ce ll b i n d i n g by re s ti n g a nd pri m e d NK ce l ls SK - OV - 3 (n=3) 5 min 100 resting NK TpNK - INKmune primed NK NK IL - 2 N K - I L - 1 5 ▪ Appropriate priming permits NK cells to kill otherwise NK - resistant tumor cells • rNK bind weakly to NK - resistant SKOV - 3 ovarian cancer cells and do not lyse them. • IL - 2 primed NK bind more strongly but do not lyse SKOV - 3 • IL - 15 priming and INKmune priming generates NK able to bind with high avidity and lyse SKOV - 3 cells

i n Onco l o g y INKmune Œ priming allows NK to kill NK - resistant tumor cells e v e n i n t h e h y p o x i a o f t h e T M E • SKOV - 3 tumor cells establish active growth in 1% O2 for 24h before addition of rNK cells • 12h later, INKmune is added to 50% of cultures (light green) • RNK cells do not lyse SKOV - 3 • The SKOV - 3 cells are killed by TpNK during dynamic growth in hypoxia ▪ Appropriate priming permits NK cells to kill otherwise NK - resistant tumor cells, even in hypoxia

I N K m u n e Πi m p r o v e s N K f i t n e s s by activating critical genes and pathways for enhanced NK function / survival i n Onco l o g y i n Onco l o g y INB16 upregulates 522 genes distinct from IL2 Рincluding CD70, CXCL10, Stat5 INB16 upregulates 1461 proteins distinct from IL15 Рincluding TIMM29, USP20 43 Target cell lysis proteins INB16 upregulates the same proteins as IL15 Mitochondrial survival proteins INB16 upregulates significantly more than IL15

INKmune ΠPhase 1 study: First patient to have completed treatment i n Onco l o g y Persistence of activated tumor - killing memory - like NK cells in blood at 119 days 44

B u t i s I N K m u n e Πs a f e ? i n Onco l o g y i n Onco l o g y 45 1. Does not require lymphopenia be induced first unlike adoptive transfer of NK cells 2. Does not have side effects associated with cytokine therapy since it does not contain cytokines 3. Activation of NK cells has been very well tolerated 4. No SAE/R reported despite heavily pre - treated patients 5. INKmune is replication incompetent and does not engraft

cGMP MANUFACTURING – DOABLE VS PRACTICAL…. i n Onco l o g y IN K mu n e Ρ 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???) MFG Process 2 500 liter bioreactor DRUG PRODUCT Many NK Manufacturing Approaches DRUG PRODUCT Development Plan – US site in 2023/4: 4 x bioreactors in 4000 sqft ISO7 facility inc QC 15 staff in manufacture & QC 46

Thank you H A R N E SS I N G T H E P O W E R O F T H E I NN A T E I MM U N E S Y S T E M 47

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49 T N F b i o l o g y i s c o m p l i c a t e d : t w o l i g a n d s w i t h o pp o s i t e e ff e c t s 49

Adapted from MacEwan et al 2002 XPRO is very different from currently available drugs Precise neutralization of the TNF ligand that drives disease Approved TNF inhibitors block both cytokines ▪ So l uble TNF ( s T N F ): “ba d ” TNF th a t is k n o w n t o c a u s e acu t e a n d chronic inflammation and cell death ▪ Transmembrane TNF (tmTNF): “ goo d ” TNF im p r o v es the immu ne r es p on s e , is n e u r op r o t ecti v e a n d p r om o t es r em y el i n a tion S o l ub l e T N F ( ‘ s T N F ’ ) BAD T N F R 1 T N F R 2 Internalization Transmembrane - bound ( ‘ t m T N F ’ ) GOOD X X C 5 ONFIDENTIAL

51 Safety side effects of non - selective TNF blockade are all from b l o c k i n g t m T N F Co n seq u enc e s of b l ocking tmTNF: ▪ Infection ▪ Cancer ▪ Demyelination 51

Adapted from MacEwan et al 2002 XPRO is very different from currently available drugs Precise neutralization of the TNF ligand that drives disease ▪ So l uble TNF ( s T N F ): “ba d ” TNF th a t is k n o w n t o c a u s e acu t e a n d chronic inflammation and cell death ▪ Transmembrane TNF (tmTNF): “ goo d ” TNF im p r o v es the immu ne r es p on s e , is n e u r op r o t ecti v e a n d p r om o t es r em y el i n a tion S o l ub l e T N F ( ‘ s T N F ’ ) BAD T N F R 1 T N F R 2 Internalization Transmembrane - bound ( ‘ t m T N F ’ ) GOOD X XPro blocks solTNF C 5 ONFIDENTIAL

St e e d e t a l 20 0 3 XPro1595 is id e n t ical to t h e h u man so l uble TNF mono m er wi t h the exce p t i on of mu t a t io n s in the recep t or bindi n g do m ain a n d ano t h e r for p e gyla tio n . 53 XPro1595: a selective inhibitor of ONLY soluble TNF XPRO: a TNF inhibitor designed to treat neurologic disease

XPRO unique M e c h a n i s m o f A c t i o n 54

Suc c essful Phase 1b trial: AD p a tients with biomarkers of inf l ammat i on ( A Di) DESIGN ▪ O pe n - l a b el Mul t i ple dosing c oh o r t s ( 0 . 3 , 0. 6 , 1.0 m g/kg) ▪ Weekly XPro1595 Œ SubQ injections for 3 months ▪ B i o marke r s a sses s ed a t 0 a nd 12 w e eks Inclusion ▪ AD Di a gn o sis ▪ Biomarke r s of i nflam m a ti o n ▪ ( C RP, ESR, H g bA 1 c , A P O E 4 ) STUDY G OALS ▪ Demonstrate peripheral administration of XPro1595 reduces biomarkers of neuroinflammation and neurodegeneration, dose identification, did our ADi biomarkers identify patients with neuroinflammation 55