Controlling inflammation LIFESCI CAPITAL ALPHA SERIES CONFERENCE 2020 Important Notice and DisclaimerThis presentation has been prepared by InflaRx N.V. ("InflaRx"), a US-Nasdaq publicly listed Dutch company having its p

Controlling inflammation LIFESCI CAPITAL ALPHA SERIES CONFERENCE 2020

Important Notice and DisclaimerThis presentation has been prepared by InflaRx N.V. ("InflaRx"), a

US-Nasdaq publicly listed Dutch company having its principle place of business in Germany. This presentation is made for informational purposes only and does not constitute an offer to sell or a solicitation of an offer to buy securities. The

information set forth herein does not purport to be complete or to contain all of the information you may desire. Statements contained herein are made as of the date of this presentation unless stated otherwise, and neither the delivery of this

presentation at any time, nor any sale of securities, shall under any circumstances create an implication that the information contained herein is correct as of any time after such date or that information will be updated or revised to reflect

information that subsequently becomes available or changes occurring after the date hereof.This presentation may contain forward-looking statements. Forward-looking statements are neither historical facts nor assurances of future performance.

Instead, they are based on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, our clinical results and other future conditions. All statements other than statements of historical

facts contained in this presentation, including statements regarding future results of operations and financial position, business strategy, current and prospective product candidates, planned clinical trials and preclinical activities, product

approvals, research and development costs, current and prospective collaborations, timing and likelihood of success, expectations regarding market acceptance and size, plans and objectives of management for future operations, and future results

of anticipated product candidates, are forward-looking statements. These risks and uncertainties include those described under the caption "Risk Factors" in InflaRx's Registration Statement on Form F-1 and the accompanying prospectus filed with

the Securities and Exchange Commission in connection with the company's initial public offering and other filings with the Securities and Exchange Commission. New risks and uncertainties may emerge from time to time, and it is not possible to

predict all risks and uncertainties. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed

circumstances or otherwise. Although we believe the expectations reflected in such forward-looking statements are reasonable, we can give no assurance that such expectations will prove to be correct. Accordingly, readers are cautioned not to

place undue reliance on these forward-looking statements. No representations or warranties (expressed or implied) are made about the accuracy of any such forward-looking statements.Certain information contained in this presentation relates to

or is based on studies, publications, surveys and other data obtained from third-party sources and InflaRx's own internal estimates and research. While InflaRx believes these third-party sources to be reliable as of the date of this

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 g/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- , IFN- ) 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

IP-10 IL-6 IL-1 IL-8 IL-14 IL-10TNF- 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

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