Inmune Bio Inc. · NASDAQ:INMB
Inmune Bio — IPO Roadshow (September 2018)
36 slides from Inmune Bio's IPO roadshow presentation, Sep 6, 2018
Slide 1: Issuer Free Writing Prospectus
Issuer Free Writing Prospectus Filed Pursuant to Rule 433 Registration Statement No. 333-227122 Dated August 30, 2018 (To Preliminary Prospectus dated August 30, 2018) Free Writing Prospectus INmune Bio Inc. Company Presentation This free writing prospectus relates to the proposed initial public off
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 thes
Slide 3: INmune Bio: The Innate Immune Company
I INmune Bio: The Innate Immune Company oe + Clinical-stage company focused on reprogramming the innate immune system to fight cancer + Two therapeutic platforms + INBO3 — targets myeloid-derived suppressor cells (MDSC), which protect tumor from the immune system and immunotherapy + INKmune — improv
Slide 4: The Investment Opportunity
| The Investment Opportunity aioe + INMB platforms targets innate immune system + INMB platforms “universal” cancer therapies + INKmune targets residual disease to prevent cancer relapse + INBO3 expands market for checkpoint inhibitors (CPI) + CPI be largest class of cancer therapy by 2027* * Clinic
Slide 5: How is INmune Bio different?
| How is INmune Bio different? ® nunstie: + Most I/O companies focus ‘on the adaptive immune system (T cells) b 4 Innate Immune + INmune Bio focused on the _-—~ System innate immune system (NK Fr app and MDSC) > Immune System, + Most I/O therapy is focused yg on the effector cells that kill 7, “ can
Slide 6: Innate Immune Therapeutic Platforms
| Innate Immune Therapeutic Platforms ® Wenunedi INBO3 INKmune MDSC inhibitor Primes NK to kill cancer INBO3 decreases the number INKmune converts inert NK and function of MDSC to cells to cancer-killing NK cells improve sensitivity to immunotherapy Goal is to eliminate residual Goal is to dramatica
Slide 7: Slide 7
Slide 8: MDSCs Predicts Resistance to CPI
| Mpscs Predicts Resistance to CPI ° @ . Stage IV Melanoma treated with Ipilimumab — resistance to CPI seen in patients with MDSC in blood (woichok2016) C 10 =F MDSCs< 5.1% 3 «#* MDSCs < 9.5% TA Moscs 913% = 8 P=67 10) a 2 0.6 3 os 50 3 a 0.2 0.0 + ° 1 2 3 4 5 Years
Slide 9: INB03: CPI Potentiator
| 1nBo3: cPI Potentiator aioe + CPI promote patient’s T cells to attack their cancer; have become the backbone of cancer therapy + CPls expected to be best-selling class of cancer drugs by 2027 + <30% of patient's treated with currently approved CPls respond to therapy; that is, >70% are resistant t
Slide 10: INB03 targets soluble TNF
| INBOS targets soluble TNF* nn oap + INBO3 neutralizes soluble TNF (STNF) without affecting transmembrane TNF (tmTNF) or TNF receptors + Eliminates sTNF that promotes the growth and function of MDSC that protects the tumor from the patient's immune system and immunotherapy + Supports tmTNF that bol
Slide 11: Precision therapy: Targets sTNF not tmTNF
| Precision therapy: Targets sTNF not tmTNF ® Soluble TNF Trans-membrane TNF Inflammatory soluble TNF eliminated: 12 No paracrine signaling through receptors 2 ‘0 : = INBOS B os Deron e] 3 t) i Smet Y) vehicle os solTNF o INBO3 Exchange = © 02 Sebel No paracrine 00 signaling 32 3 0 «9 Log fant-TNF (
Slide 12: INB03 Development Program
® | INBO3 Development Program nemunetie Ongoing Phase 1 open- Phase 2 trial in Stage IV label, dose-escalation trial melanoma + CPI » Patients refractory to » Atleast 12 patients with CPI with 4 MDSC advanced solid tumors and 7 MDSC * Treatment: combo t therapy INBO3 + CPI * Treatment: INBO3 sub- ae
Slide 13: INKmune
INKmune NK Cell Therapeutic
Slide 14: INKmune: Primes NK Cells to Kill Cancer
lon | INKmune: Primes NK Cells to Kill Cancer Wmune! Residual disease cannot be eliminated without activated NK cells survivors -& >12% NK operational a <12% NK operational ®. 0=0,007 “relapsers” 1-7 + 1 1 1-7 0 12 24 36 48 60 72 S& 96 108 Months inCR
Slide 15: How Cancer Evades NK Killing
| How Cancer Evades NK Killing... nnose Innate Immune System Cancer NK cell “tumor primed” (TpNK) with INKmune aNKCel —-Pre-Cancer Cell TpNK Cell Pre-Cancer Cell Pre-cancerous INKmune binds cells express to the NK prime ‘both priming and receptor... ligands, allowing , al NK cell killing J A ‘NK Cel
Slide 16: INKmune: "universal" Cancer Therapy
® | INKmune: “universal” Cancer Therapy pee INKmune TpNK are active against many types of cancers: » Blood cancers: AML, MM, lymphoma * Solid tumors: breast, ovary, prostate, renal, lung 8 ss 8 % specific lysis % Specific lysis: Bess aa a a we og
Slide 17: Results with 1st-Generation TpNK Therapy
| Results with 15t-Generation TpNK Therapy = AML Phase 1 Remunszie 2 Phase 1 clinical trials performed in 20 patients with high-risk AML using a 1-generation, ex vivo, personalized TpNK therapy Clinical Results Tp N K — Produced projonged remissions with excellent quality of life th era py mad e D>
Slide 18: INKmune Development Program
| INKmune Development Program on ay 2°4_generation TpNK allows in vivo priming Stimulates patient's NK cells to kill their cancer Targets naturally occurring tumor antigens Phase 1/2 study in relapsed/ Phase 1/2 dose-finding study refractory CaOva in high-risk MDS » Patients with low burden, » Patie
Slide 19: INKmune Market: CaOva and High-Risk MDS
| INKmune Market: CaOva and High-Risk MDS ® Patients U.S. EU + ROW Market Op Ovary 14,080 15,488 29,568 High-risk MDS 5,000 5,500 10,500 Total 19,080 20,988 40,068 Assumptions — U.S. market, NCI data with deaths used as proxy for advanced disease ~— ROW market is 10% of EU/U.S. market Significant op
Slide 20: Intellectual Property
| Intellectual Property ® INBO3 INKmune * 2021 — composition-of- » 2035 — use for treatment matter (licensed from of cancer Xencor) » Multiple filings in process » 2035 — use for treatment of cancer (licensed from University of Pittsburgh) » Multiple filings in process Continuing to expand patent po
Slide 21: Accomplished Leadership
| Accomplished Leadership ® Management RJ Tesi, MD coronado Chief Executive Officer & Chief Medical Officer SANGSTAT “Wwerensce @ Mark Lowdell, PhD Chief Scientific Officer be | ne TONIX. () petentrseg Chief Financial Officer Board of Directors J. Kelly Ganjei CEO of Cognate Timothy Schroeder CEO an
Slide 22: Summary of the Offering
| Summary of the Offering INmunesio Listing NASDAQ Ticker INMB Proposed offering price $8 Minimum offering amount $8,000,000 Maximum offering amount $20,000,000 Shares to be outstanding after offering Minimum 9,719,441 Maximum 11,219,411 iF w appe
Slide 23: Use of Proceeds - $20M raise
P ® I Use of Proceeds - $20M raise INmunesio INKmune Phase 1 & 2 ovarian cancer $4M INBO3 Phase 1 elevated MDSC $1.5M INBO3 Phase 2 CPI combo $2.5M INKmune high-risk MDS $4M Manufacturing scale-up $3M R&D, working capital and general corporate $3.1M Maximum offering proceeds expected to be $18.1 mil
Slide 24: The Investment Opportunity
l The Investment Opportunity ® + The immunotherapy market is growing at 13% annually* + INmune’s platforms target the innate immune system + INKmune can treat both hematologic and solid malignancies + INBO3 should improve efficacy of CPI in resistant patients * CPI market in infancy - is expected to
Slide 25: Appendix
Appendix
Slide 26: INB03 engineered human protein
INBO3 engineered human protein + 17kDal non- glycosylated protein Subunit B * 6 amino acid substitutions + 10kDal PEG + 71/2-18h (subunit A) + Expressed in E.coli Subunit C Mutation A145R Receptor binding, “DE loop” domain (subunit A) + VIM (better expression) Mutation Y87H M + CBOVIEIOTA pec (for 1
Slide 27: Precision therapy: neutralizes sTNF without affecting tmTNF
Soluble TNF Trans-membrane TNF Precision therapy: neutralizes sTNF without affecting tmTNF Inflammatory soluble TNF eliminated: 42 ‘No paracrine signaling through 19 = = wwe003 ‘: —, ~ Oo. oe ee c) ie. 7s solTNF 6 (recombinant or — os 7 . = 2 4 0 Log [anti-TNF (g/m) Immunoprotective transmembrane TN
Slide 28: Anti-inflammatory MOA: simple and elegant
Anti-inflammatory MOA: simple and elegant Normal sTNF activity wv 4 23 + Yv v c> wer Inflammation Active TNF TNFR TNF bind INMBOO3 — INMB0OO3 neutralizes sTNF es 2 + <> c> => Ne 4 Vv Inflammation nd se Heterotrimers Active TNF Inactive cannot bind ® heterotrimers Le INURE To roadshow appendix draft
Slide 29: TNF biology: complicated
TNF biology: complicated ... 4 elements — 2 cytokines: sTNF and tmTNF Normal TNF Biology — 2 TNF receptors: TNFR1 and TNFR2 a TNFRO Bad TNF: sTNF/TNFR1 — Causes inflammation and/or cell death INS] Good TNF: tmTNF/TNFR2 and TNFR1 — Cytoprotective, promotes proliferation, STNF tmTNF promotes immune fu
Slide 30: CaOva lysis assay by xCELLigence
CaOva lysis assay by xCELLigence ~ To INKmune Real-Time Cytolysis Plot ; ~y added CLAS sso NK added a ® IPO roadshow appendix draft 8.13.18 INmuneBio
Slide 31: Biomarker — patient selection
Biomarker — patient selection H INKmune pNK target tumor and NOT normal celts ye 1| - | sa \ecr 6) Mo ‘Am J Hematology, 86:967-973 PO roadshow append cra 8.13.18 INmuneBio
Slide 32: The surprise: the tumor, NOT the immune system is the cause of relapse
The surprise: the tumor, NOT the immune system is the cause of relapse! Relapser Survivor NK cells NK cells Ww you sa0oq * Relapser NK cells kill survivors AML. * Survivor NK cells can not kill relapser AML. Conclusion: AML mutates to evade NK cell killing. ®) fink. $3.18 IURERIE IPO ow append
Slide 33: Leukemic Priming of Resting NK Cells Is Killer Ig-like Receptor Independent
Leukemic Priming of Resting NK Cells Is Killer Ig-like Receptor Independent but Requires CD15-Mediated CD2 Ligation and Natural Cytotoxicity Receptors. tie jan of tnoumiogy TOTPTTTTTTTT erveerenererererereerere COU INB16 CD16
Slide 34: INB16 vs alternative priming — Differential protein expression @16h
INB16 vs alternative priming — Differential protein expression @16h C16 Colour Key CD54 (ICAM-1) cD62L $ 75% Decrease D184 (CXCR4) D226 (DNAM-1), D244 (284) No change C314 (NKG2D) D335 (NKp46) D337 — $75% Increase Paradoxical decrease (not loss) in ligand expression associated with increased functio
Slide 35: INB16 vs IL-2 priming — Differential gene expression profiles
INB16 vs IL-2 priming — 412 Differential gene expression profiles INB16 2 ALCAM — NK cell migration and adhesion STATS — “molecular switch” essential for NK killing CD70 — CD27L and NCR for B cell tumours VEGFA — survival signal for NK CXCL10 — chemoattractant for NK cells ® IPO roadshow append
Slide 36: TpNK best for Ovarian Cancer
TpNK best for Ovarian Cancer INKmune SKOV3 killing by NK cells from healthy donor (HD) or CaOva patient ascites td 8 & SI19D EAOMS MGA %