Exhibit 99.1
Controlling inflammation LIFESCI CAPITAL ALPHA SERIES CONFERENCE 2020
Important Notice and DisclaimerThis presentation has been prepared by InflaRx N.V. (“InflaRx”), a
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presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, all of the market data included in this
presentation involves a number of assumptions and limitations, and there can be no guarantee as to the accuracy or reliability of such assumptions. Finally, while we believe our own internal research is reliable, such research has not been
verified by any independent source. InflaRx n.v. | Winzerlaer Str. 2, 07745 Jena, Germany, Email: info@inflarx.com, Tel: +49-3641-508180, www.inflarx.com
Investment Highlights 3 Complete and selective blockade of the biological activity of C5a in vitro and
in vivoStrong patent coverage on anti-C5a technology until end of 2030 / 2035 with extension Proven anti-inflammatory effect in multiple Phase II studies Statistically significant reduction of inflammatory lesions in Phase IIb Hidradenitis
Suppurativa study and impressive long-term efficacyFull data set analysis warrants continued development towards Phase III despite missing the primary endpoint (HiSCR) in Phase IIb studyFavorable safety profile and excellent tolerability (n
> 300 patients) Running phase II/III study in patients with COVID-19 Pneumonia in the EUOngoing Phase IIb studies in ANCA-associated vasculitis in the US and EUOngoing Phase IIa open label study in Pyoderma Gangraenosum in US and
CanadaFollow-on anti-C5a mAb IFX-2 in pipeline (pre-clinical stage) Pipeline extension of IFX-1 in other inflammatory diseases & oncology Leading Proprietary Anti-C5a Technology Established Clinical Efficacy for Lead Drug
IFX-1 Multiple ongoing studies and indication + Pipeline extension
Pipeline with Multiple Opportunities 4 Proposed Indications Prevalence Pre-Clinical Phase I Phase
II Phase III Update IFX-1C5a Inhibitor Hidradenitis Suppurativa (HS) Up to 200,000patients in the USOver 200,000 patients in Europe Phase IIb completedPlanning for next steps ANCA-Associated Vasculitis ~40,000 patients in the
US~75,000 patients in Europe Phase IIb enrollment ongoing in both Europe and US COVID-19 Pneumonia Currently Unknown Phase II/III ongoing in the EU Pyoderma Gangraenosum ~50,000 patients in the US and Europe are
affected Phase IIa open label enrollment ongoing in US and Canada Oncology Undisclosed Indication Development of TPP ongoing IFX-2C5a Inhibitor Undisclosed Chronic Inflammatory and Autoimmune Diseases Not
applicable Developing as injectable with optimized use for other chronic inflammatory indications
The Terminal Complement Pathway 5 Membrane Attack Complex (MAC)triggers lysis of pathogens strong
amplifierof inflammation C5aR C5b-9 = MAC C5L2 C5b C5a C5 cell activationcytokine generation Inflammation PKC-signaling HMGB-1 induction* (Inflammasome) C5a concentration in blood: 10 ~ 30 ng/ml (~1-2.5 nM) C5
concentration in blood: ~75 µg/ml (~400 nM) other ligands: C3a, ASP, C4a etc upregulated in many tissues during inflammation **Rittirsch et al. Nat Med. 2008 May ; 14(5): 551; Colley et al. MABS. 2018,10 (1), 104 Songlin et. al. J. Biol.
Chem. 2019; 294(21) 8384–839 Muenstermann et al.. Virulence, 2020; 10(1) 677-694 C5L2 has a different binding pocket for C5a compared to other ligands like C3a, ASP, etc. and this causes different cell signaling.* The C5a signaling has been
shown to be pro-inflammatory.** * Kalant D. et. al. J. Biol. Chem. 2003, 278 (13) 11123–11129 other signalling involved e.g. in triglyceride synthesis, etc.
ifx-1 for COVID-19 Pneumonia
7 Source: cdc.gov; Zhou et al. 2020, Lancet Infectious Disease Cause: severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) which likely uses ACE2 receptors for cell entryFirst identified in Wuhan, Hubei Province, China in December 2019 Disease Background Clinical features Long latency: Incubation time prior to symptoms is estimated to
be between 2 and 14 days (data analysis from CDC, US)Symptoms: flu-like symptoms including fever or signs of lower respiratory tract illness including throat ache, dry cough and shortness of breath and HYPOXEMIA - typically no runny noseSlow
disease onset compared to SARS and MERSDeath is typically caused by respiratory failure in presence of sepsis and multiple organ dysfunction, similar to other viral pneumonia-induced sepsisRisk factors: Age, smoking, hypertension, diabetes,
COPD, immunodeficiency and others A viral pneumonia with immune-mediated injury Coronavirus Disease 2019 (COVID-19)
8 Source: https://www.chinalawtranslate.com/en/coronavirus-treatment-plan-7/ Source: cdc.gov Systemic
inflammation: lymphopenia (>80%) + elevated CRP (>60%) at admissionNeutrophil counts are positively correlated with disease severity and bad outcomePotential Prognostic Biomarker: NLR (neutrophil-to-lymphocyte ratio) – A patient with more
neutrophils and less lymphocytes has the worst outcome. Moderately elevated levels of both Th1 cytokines (IL-6, TNF-α, IFN-Ƴ) and TH2 cytokines (IL-4 and IL-10) Other frequently increased markers: D-dimer, LDH, AST, ALT, troponin-I, ESR, serum
ferritin et al. Laboratory findings Diagnosis & Pathological events (Health Commission of China Covid-19 guideline, version 7) Severe COVID-19 definition (at lease one): (1) Shortness of breath, RR≥30 times/min, (2) Oxygen saturation
(Resting state) ≤93%, or (3) PaO2 / FiO2 ≤300mmHgCT findings: Bilateral or unilateral pneumonia, multiple mottling and ground-glass opacityPathology in lung: Infiltration of monocytes and lymphocytes; hyaline thrombi in blood vessels; focal
pulmonary hemorrhage and thrombosis of small vessels, necrosis; pulmonary interstitial fibrosisPathology in heart: endothelial inflammation and thrombus formation; interstitial infiltration (monocytes, lymphocytes and/or neutrophils)Pathology
in liver: Hepatocyte degeneration and focal necrosis are accompanied by neutrophil infiltration A viral pneumonia with a broad spectrum of immune-mediated injury Coronavirus Disease 2019 (COVID-19)
Wang et al., Jama (2020) 1585 Gong et al., MedRXiv Preprint (2020) Feb.25 White blood cell counts and
neutrophil counts increase in non-survivors from day 9 on 9 Neutrophils are strongly activated by C5a– this can damage host tissue COVID-19: White Blood Cell and Neutrophil Counts
IFN-Ƴ
IP-10 IL-6 IL-1β IL-8 IL-14 IL-10TNF-α Tissue C5a DAMPs (e.g. O2-) NETosis Resolution:Lymphocyte recovery (IgG, IgM)Inflammation under controlEfferocytosis in lung Deterioration:Lymphocyte suppressionNeutrophil activation – tissue
inflammation Organ damages (e.g., lung > heart, liver, vessel)Coagulopathy (e.g., DIC) Blood vessel Initiation: viral inflammation Progression: Neutrophil-Mediated Injury Initiation:Type I IFN SignalingLocal inflammationLymphopenia
Dual Play of Viral Inflammation and Immune-mediated Injury 10 Neutrophil facts: 40-60% in WBCsHalf-life: 6-8h50-100 bn cells / dayOne neutrophil has approx. 200,000 binding sites for C5a Potential C5a effects:Neutrophil activation with
enzyme release and O2-radical productionTissue damageRelease of tissue factor from endothelial cells – induction of coagulation Viral-induced Immune Injury in COVID-19 – Potential Role of C5a
Overview of IFX-1 Phase II/III Study in COVID-19 Pneumonia - Study Design 11 Assessing safety and
efficacy of IFX-1 in COVID-19 PneumoniaPrimary endpoint: Relative change (%) from baseline in Oxygenation Index (PaO2 / FiO2) to day 5Key secondary endpoints: Number of patients (%) achieving an Early Response as defined by patients who
experience relief of symptoms and laboratory parameter normalization on day 7Number of patients (%) achieving a Late Response as defined by resolution of clinical symptoms or discharge on day 28Frequency, severity, and relatedness to study drug
of treatment-emergent adverse events and serious adverse events Adaptive, open-label, randomized, multi-center in EUTarget enrollment – 130 patientsFirst patient dosed – March 2020Phase II/III study consisting of two parts: In both study
parts, patients will be randomized to two treatment arms (Arm A: best supportive care [BSC] + IFX-1; Arm B: BSC alone).After all patients are treated in Phase II (approx. n = 30), an interim analysis will be performed to assess the clinical
benefit of the treatment using the assessed clinical parameters in order to potentially adapt and determine the confirmatory second part of the study Study Objective Study Design
ifx-1 for Hidradenitis Suppurativa
Hidradenitis Suppurativa 13 A chronic severely debilitating C5a-driven inflammatory skin condition with
high unmet need * Combined Phase III trial data for Humira: response measured by HiSCR 50 and KOL quotes in LifeSci Capital initiation report 12/2018 Hurley staging for hs Clinical features Chronic, inflammatory, recurrent, debilitating
skin disease of the hair follicles Most commonly in the armpit, groin and genital regionsExtremely painful inflammatory nodules, boils or abscessesDraining fistulas leading to considerable scarring and functional disability Hurley staging
system used to classify progression / chronicity (Stage I – III) Current Treatment – Medical Need Adalimumab (TNF-alpha inhibitor) from AbbVie is the only approved biological in US and EuropeAccepted (but not approved) SOC includes topical,
oral or i.v. antibioticsIn some instances, surgery is required Approximately 50% of patients with moderate to severe HS do not respond and about 50% of responder patients lose response to Humira* Prevalence Up to 200,000 moderate to severe
(Hurley II+III) HS patients in USHigher prevalence in Europe with reports > 1% total HS prevalence Stage ISingle / multiple abscesses but no sinus tracts or scarring Stage IISingle or multiple separated, recurrent abscesses with tract
formation and scarring Stage IIIMultiple interconnected tracts and abscesses involving an entire anatomic region
IFX-1 in Hidradenitis Suppurativa 14 InflaRx established that HS patients have significant complement
activation with elevated C5a levels C5a is key neutrophil activator in HS patient plasma HS patient plasma strongly provoked neutrophil activation in healthy donor blood; this effect could be completely blocked by the addition of
IFX-1 Rationale for targeting C5a C5a is involved in several key pathophysiological mechanisms in HSNeutrophil activation is driven by C5aVarious C5a dependent players potentially involved (TNFa, IL-17, etc.)
IFX-1 in HS: SHINE Study Details 15 Important Note: Patients entering the OLE were not unblinded to
their initial therapy Test a dose-dependent effect of IFX-1 on HiSCR* response at week 16 (primary endpoint) Assess long-term safety of IFX-1Test durability of response with lower maintenance therapy in open label extension period Main
Goals Placebo IFX-1 minimal dose IFX-1 low dose IFX-1 medium dose IFX-1 high dose Screening 28 weeks (24 weeks treatment + 4 weeks observation) 16 weeks (double blind) Total treatment time: 9 months (week 40) + 1 month observation
(week 44) Open Label Extension Period (OLE): n = 156 Main Period: n = 177 treated (400 mg q4w) (800 mg q4w) (800 mg q2w) (1200 mg q2w) Week 16 HiSCR Responders: IFX-1 low dose Week 16 HiSCR Non-Responders: IFX-1 medium dose (800 mg
q4w) (800 mg q2w) *HiSCR response defined as: At least 50% reduction in total AN count (abscesses & inflammatory nodules) with no increase in the number of abscesses from baseline and no increase in the number of draining fistulas from
baseline
SHINE Study: Primary Outcome HiSCR at Week 16 versus AN Count Reduction 16 HiSCR response rate (%)
week 16* * Full analysis set AN count score change (mean %) week 16* n = approx. 35/ group placebo minimum low medium high Treatment groups: Primary endpoint: HiSCR dose response signal not met but signal towards improved AN count
SHINE Study: Outcome on Draining Fistula and IHS-4* Score Reduction – Week 16 17 Draining fistula
change (mean %)** IHS-4 score change (mean %)*** placebo minimum low medium high Treatment groups: Statistically significant change in DF and in IHS-4 scores detected ** Full analysis set for patients with at least 1 DF at baseline,
baseline adjusted *** Full analysis set – baseline adjusted p= 0.0202 p= 0.0359 *IHS-4 Points = Sum of the number of inflammatory nodules (x1), number of abscesses (x2) and number of draining fistulas (x4)
Inflammatory Lesion Reductions in All OLE Patients at End of Treatment (Week 40) Compared to Placebo
Group Performance in Main Period (Week 16) 19 of all OLE patients at week 40 (n=116) of placebo patients at week 16 Marked improvement of all inflammatory lesions over time – not explainable by placebo effect * Full analysis set
(unadjusted) Relative reduction (% mean) of counts / scores compared to respective baseline (Day 1)* placebo group week 16 OLE patients week 40
SHINE Study and Next Steps in HS Development 20 HiSCR is burdened by high variability (driven by AN
count variability) and by a lack of capturing reduction of draining fistula Our conclusions Evidence for a high C5a turnover rate in HS, leading to increased dose requirements of IFX-1 IFX-1 leads to a marked reduction of all inflammatory
lesions in HS with a durable long-term effect detected even at non-optimal doses IFX-1 long-term treatment was well tolerated, no drug related SAEs* in the open label extension phase * Serious adverse events Requested End-of-Phase II
FDA Meeting in Q1 2020 Next steps Discuss with FDA the path forward for regulatory approval towards a Phase III pivotal program Depending on meeting timing and feedback: define path forward by 2H 2020
ifx-1 for ANCA-associated vasculitis
ANCA-Associated Vasculitis (AAV) 22 A life-threatening autoimmune condition Source: Chen, Jayne and
Zhao. Complement in ANCA-associated vasculitis: mechanism and implication for management Rare, life-threatening autoimmune disease, characterized by necrotizing vasculitisLife-threatening flare phases affect organs, leading to potentially
fatal organ dysfunction and failure Predominantly affecting small vessels associated with anti-neutrophil cytoplasmic antibodies, or ANCADisease activity is assessed using Birmingham Vasculitis Activity Score v3 (BVAS) Clinical
features Current Treatment – Medical Need Induction of remission critical during flare phases – induction treatment differs from maintenance therapy and consists of high dose corticosteroids plus either cyclophosphamide or rituximabInduction
of remission therapy has significant side effects Prevalence Approx. 40,000 AAV patients in the USApprox. 75,000 AAV patients in EuropeOrphan drug market
IFX-1 in AAVClinical PoC established for Role of C5a / C5aR Pathway in AAV 23 C5a is essential for
development of MPA-ANCA crescentic glomerulonephritis in a mouse model Complement activation in active AAV patients is significant Evidence for role of C5a / C5aR pathway through recent Phase III success of an oral C5aR
inhibitor* Rationale Rapid onset of action: intravenous administration with fast onset of action, inhibiting C5a signaling completely protecting from C5a induced priming and activation of neutrophils → potentially quicker induction of
remission compared to the SOCPotential potency difference: by blocking upstream ligand C5a, which inhibits signaling through both receptors, C5aR and C5L2; C5a pro-inflammatory MoA through both C5aR and C5L2 has been shown to be important for
ANCA-primed and C5a-induced neutrophil degranulation as key disease-driving mechanism in AAV.** Potential advantages of IFX-1 for AAV * Chemocentryx. (25 November 2019). ChemoCentryx and VFMCRP Announce Positive Topline Data from
Pivotal Phase III ADVOCATE Trial Demonstrating Avacopan’s Superiority Over Standard of Care in ANCA-Associated Vasculitis** Hao & Wang et al 2013, PLoS ONE, 8(6)
IFX-1 – P2.6 Phase II Study in AAV in the US (IXPLORE)Study Design 24 Treatment: 16 weeks Follow
up: 8 Weeks Remission Induction Phase Maintenance Phase Maintenance Therapy:remain on SOC or transition to guideline maintenance therapy* IFX-1 low dose + SOC(n=12) IFX-1 high dose + SOC(n=12) Placebo +
SOC(n=12) A Groups: B C SOC = Rituximab or Cyclophosphamide + glucocorticoids Randomization 1:1:1 Study objective (target: n=36)Assessing safety and efficacy of IFX-1 in AAV – First Patient Dosed in October 2018Primary endpoint:
SafetySecondary endpoint: Response rate based on the Birmingham Vasculitis Score (BVAS), various other secondary endpoints Day 1 Week 16 Week 24 * Guideline maintenance allows for: azathioprin / methotrexate / mycophenolate mofetil / low
dose corticosteroids
IFX-1 – P2.5 Phase II study in AAV in Europe (IXCHANGE)Study Design 25 Study objective (target:
n=81)First patient dosed: May 2019Primary objective: Efficacy of IFX-1 treatment as replacement for glucocorticoid (GC) therapy in GPA and MPA Secondary objectives: To assess safety and tolerability of IFX-1 & compare toxicity of
standard-dose GC with IFX-1 * Guideline maintenance allows for: azathioprin / methotrexate / mycophenolate mofetil / low dose corticosteroids Treatment: 16 weeks Follow up: 8 Weeks Remission Induction Phase Maintenance
Phase IFX-1 + SOC with reduced GC (n=15) placebo + SOC incl. GC (n=15) A B Week 24 Week: Part 1 Treatment: 16 weeks Follow up: 8 Weeks Remission Induction Phase Maintenance Phase IFX-1 + SOC w/o
GC (n=33) placebo + SOC incl. GC (n=18) C B Dosing scheme: Dosing scheme: 2 4 6 8 10 12 14 16 SOC = rituximab or cyclophosphamideGC = glucocorticoids Maintenance Therapy:remain on SOC or transition to
guideline maintenance therapy* 20 Safety analysis Part 2
ifx-1 for Pyoderma Gangraenosum
Pyoderma Gangraenosum (PG) 27 Source: Demis.net PG is a rare ulcerative skin disorder that can lead to
chronic painful and difficult-to-treat wounds / ulcers occurring predominantly in people in their 40s and 50sMany PG patients also suffer from other autoimmune disorders, including inflammatory bowel diseases like ulcerative colitis, rheumatoid
arthritis, and hematological diseases Patients suffer from severe pain, long healing times, and frequent relapsesDiagnosis is based on the exclusion of other conditions and typical ulcers Clinical features Current Treatment – Medical Need No
drugs currently approved in the US or EUCurrent treatment options include the use of systemic immunosuppression in rapidly progressing cases or, for less severe cases, topical or intralesional treatments can be used, including topical
steroids INCIDENCE Rare - Estimated that up to 50,000 patients in the US and Europe are affectedOrphan drug market An autoimmune condition with high unmet need
Overview of IFX-1 Phase IIa Study in PG - Study Design 28 Assessing safety and efficacy of IFX-1 in
PGRationale: PG is associated with a neutrophilic leukocytosis, which is likely to be triggered by C5a. Pyoderma Gangraenosum lesions have pronounced neutrophilic infiltration and the expression of interleukin (IL)-1β, IL-17, tumor necrosis
factor (TNF)-alpha, and their receptors are significantly elevated, indicating auto-inflammatory conditions.Primary endpoint: SafetyKey secondary endpoints:Responder rate defined as Physicians Global Assessment ≤3 of target ulcer at visits V4,
V6, V10, and V16 (end of treatment); Time to complete closure of Pyoderma Gangraenosum target ulcer (investigator assessment) Open labelMulti-center in US and CanadaTarget enrollment – 18 patientsFirst patient dosed – June 2019 Trial started
with 1 dose group: amendment approved to introduce a dose escalation to test 3 dose groupsSubjects receive IFX-1 dosing every other weekDose: 800 mg biweekly first 5 patients Study Objective Study Design Treatments
29 5 patients have been treated 2 out of the first 5 patients showed complete closure of the target
ulcer with both patients in full disease remission. Both remained healed even after finishing the studyIn one additional patient, initial wound healing activity was detected in the first 2-3 weeks of treatment – but no wound size decrease or
closure detected2 additional patients with extensive disease (very large ulceration / ulcer reaching the entire circumference of the leg) did not heal the target ulcer and are still under treatmentThe “responders” have higher baseline C5a
levelsPD analysis (C5a levels) warrants higher dosingDose escalation recently approved by relevant authorities STUDY UPDATE C5a Levels at Baseline responder responder Pyoderma Gangraenosum (PG)Autoimmune Condition with High Unmet
Need
Female patient with extensive genital PG disease and target ulcer on lower extremity (no concomitant
IBD)Various failed treatment attempts including high dose corticosteroids, etc.Significantly elevated baseline C5a levelsPatient completely healed of all PG lesions at the end of treatment and remained healed after the end of the study 30 day
1 day 18 Male patient with treatment resistant PG disease and Addison´s disease from high-dose GC (no concomitant IBD)Significantly elevated baseline C5a levelsPatient completely healed of all PG lesions at the end of treatment and remained
healed after the end of the study day 43 Patient Example 1 day 1 day 30 day 131 Patient Example 2 Pyoderma Gangreaosum (PG)Two Patients show Complete Wound Closure with IFX-1 Treatment
Our Strategy 31 Advance our lead program IFX-1 for HS towards Phase III / approval based on regulatory
guidanceExplore application of IFX-1 for AAV, COVID-19, PG and oncology in clinical developmentExtend pipeline with initiation of clinical development of IFX-1 in other complement-mediated autoimmune / inflammatory diseasesPursue the
development of IFX-2 and continue to expand the breadth of our anti-C5a technologyContinue to explore broadening the R&D pipeline beyond anti-C5a technology as part of diversification strategy goalS and strategy We have a strong cash
balance to pursue these activities (End of Q3 2019: US$151 million)
Winzerlaer Str. 207745 Jena, GermanyEmail: info@inflarx.comTel: +49-3641-508180Fax:
+49-3641-508181www.inflarx.com Jordan ZwickGlobal Head of Business Development & Corporate StrategyEmail: jordan.zwick@inflarx.de InflaRx N.V. Investor Relations InflaRx N.V.