Exhibit 99.2

 CONTROLLING INFLAMMATION  CORPORATE PRESENTATIONJanuary 2021 

 IMPORTANT NOTICE AND DISCLAIMERThis presentation has been prepared by InflaRx N.V. (“InflaRx”), a US-Nasdaq publicly listed Dutch company having its principal 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 heading “Risk Factors” in InflaRx’s periodic 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  Page *  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; favorable safety profile & excellent tolerability in >300 patients Statistically significant reduction of inflammatory lesions and impressive long-term efficacy in Hidradenitis Suppurativa (HS)Encouraging Phase II data in patients with Severe COVID-19  Severe COVID-19: Phase III part of study is enrollingHS: Plan to submit Special Protocol Assessment (SPA) to the FDA for the Phase III in Q1 2021; positive scientific advice from European Medicines Agency (EMA) ANCA-associated vasculitis (AAV) & Pyoderma Gangraenosum (PG): clinical data readouts expected in 2021  LEADING PROPRIETARY ANTI-C5A TECHNOLOGY     ESTABLISHED CLINICAL EFFICACY FOR VILOBELIMAB (IFX-1):    MULTIPLE ONGOING STUDIES   

 Pipeline with Multiple Opportunities  Page *    PROPOSED INDICATIONS  PREVALENCE  PRE-CLINICAL  PHASE I  PHASE II  PHASE III  UPDATE    Severe COVID-19  Currently unknown          Phase II/III study: Phase II part: results published; Phase III part is enrolling  Vilobelimab(IFX-1)C5a Inhibitor  Hidradenitis Suppurativa   Up to 200,000patients in the USOver 200,000 patients in Europe          Phase IIb completedPositive EMA advice on pivotal program with new primary endpoint; SPA for the Phase III to be submitted to the FDA in Q1 ‘21    ANCA-Associated Vasculitis  ~40,000 patients in the US~75,000 patients in Europe          Phase II: treatment completed in US; fully enrolled in Europe    Pyoderma Gangraenosum  ~50,000 patients in the US and Europe are affected          Phase IIa open label; enrollment ongoing    Cutaneous Squamous Cell Carcinoma (cSCC)  PD-1 or PD-L1 Resistant/Refractory Locally Advanced or Metastatic           Phase II to be initiated in FH 2021  IFX-2C5a Inhibitor  Undisclosed Chronic Inflammatory and Autoimmune Diseases  Not applicable          Developing for optimized use for other chronic inflammatory indications               

 The Terminal Complement Pathway  Page *  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), 104Songlin 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.**    other signalling involved e.g. in triglyceride synthesis, etc.    * Kalant D. et. al. J. Biol. Chem. 2003, 278 (13) 11123–11129 

 VILOBELIMAB (IFX-1) FOR SEVERE COVID-19 

 A VIRAL PNEUMONIA WITH A BROAD SPECTRUM OF IMMUNE-MEDIATED INJURY    Coronavirus Disease 2019 (COVID-19)  Page *  Source: https://www.chinalawtranslate.com/en/coronavirus-treatment-plan-7/; Rapkiewicz et all, EclinicalMedicine (2020) 100434; Goshua et al., Lancet Haematol 2020 June 30; Cugno et al., J Allergy Clin Immunol July 2020:215;   CLINICAL & PATHOLOGY FEATURESDeath is typically caused by respiratory failure and viral sepsis in presence of immune-response induced multiple organ dysfunctionPathology LABORATORY FINDINGSSystemic inflammation: lymphocytopenia (>80%) + elevated CRP (>60%) at admissionModerately elevated levels of both Th1 cytokines (IL-6, TNF-α, IFN-Ƴ) and TH2 cytokines (IL-4 and IL-10); Other frequently increased markers: LDH, AST, ALT, troponin-I, ESR, serum ferritin et al.Coagulopathy markers: increased levels of D-dimer, fibrinogen, VWF, Factor VIII et al.Complement activation markers: C5a, sC5b-9  in lung: extensive inflammation, diffuse alveolar damage, marked microvascular thrombosisin kidney: thrombotic microangiopathy within the glomeruli; mild to moderate arteriolosclerosis in heart: scattered individual cell myocyte necrosis, not sufficient sign of viral myocarditis in liver: macro-vesicular steatosis, cirrhosis, platelet-fibrin microthrombi in hepatic sinusoids, hepatic vein thrombosis 

 Page *  COVID-19 induced Vascular Injury – Potential Role of C5aModel for Proposed Mode of Action of C5a in COVID-19 induced vascular injury  Endothelial damage is induced by SARS-CoV-2 infection which also activates the complement system leading to C5a generation. C5a activates neutrophils via C5aR leading to increased adherence to endothelial cells and damage through generation of oxidative radicals, granular enzyme release and neutrophil extracellular traps (NETs). C5a induces release of tissue factor from neutrophils as well as endothelial cells, which promotes coagulation leading to Fibrin formation. Thrombin, plasmin and other enzymes can further induce direct C5a activation (through direct cleavage of C5) which may establish a viscous circle leading to microangiopathy with thrombosis  Source: InflaRx GmbH 

 STUDY DESIGNCritically ill intubated* patients with COVID-19 induced pneumoniaPhase III primary endpoint: 28-day all-cause mortalityOther key endpoints include assessments of organ support, assessment of disease improvement on the ordinal scaleSTATUSPhase 2 part completed:Encouraging Topline Results publishedPhase 3 part ongoing:Blinded Interim Analysis after 180 patients Potential for an early stop for efficacy or futility  Design of Phase II/III study with Vilobelimab in Severe COVID-19  Page *  SOC: Standard of CareSOC includes venous thromboembolism prophylaxis at a minimum and may include other specific recommended treatments for COVID-19 per the locally adopted treatment recommendations.* in phase III part eligible patients must be early intubated, in the phase II part, patients were enrolled if either being early intubated or dependent on oxygen delivery           28 days  Vilobelimab + BSC(n=15)  Best supportive care(n=15)      Phase II Part       800mg i.v.   Dosing scheme:  Blinded Interim Analysis after 180 patients  Analysis  Phase III Part   Open-label  Vilobelimab + SOC(n=90 + 90)  placebo + SOC(n=90 + 90)  Double-blinded        Day:  1 2  4  15  8  11-13      22                  28 days                    28 days  COMPLETED  800mg i.v.   ONGOING      Continue to full enrollment of 180 +180 patients 

 Phase II Part Results: Overview  Page *  Primary endpoint: no difference detected in improvements between groups in PaO2/FiO2 ratio: high variability between patients: conclusion: endpoint not suitable as response parameterKey secondary and other endpoints: Observed effects in vilobelimab treatment arm compared to best standard of care arm:50% lower all-cause mortality rate (13% in vilobelimab group vs 27% for control group)Fewer patients experienced renal impairment assessed by estimated glomerular filtration ratesFaster reversal of blood lymphocytopeniaReduction in tissue damage: greater lowering of lactate dehydrogenase concentrations Temporary but statistically significant increase of D-dimer levels in first days after vilobelimab administration - potential signal of induction of blood clot lysis  PHASE II STUDY RESULTS*    * Vlaar, A et al. Lancet Rheumatol 2020. https://doi.org/10.1016/S2665-9913(20)30341-6 

 Phase II Part Results: Lymphocyte Count Normalization  Page *  * Shift Plot Lymphocytes – all randomized, n=15 per armVlaar, A et al. Lancet Rheumatol 2020. https://doi.org/10.1016/S2665-9913(20)30341-6  LYMPHOCYTES - BEST SUPPORTIVE CARE ONLY*  Normal (1.5 to 4.0 x 109 per L)  Low (0.75 to 1.5 x 109 per L)  Very low (<0.75 x 109 per L)  87% of vilobelimab treated patients showed normalized lymphocytes counts vs 47 % in control group (p=0.050)    LYMPHOCYTES - VILOBELIMAB+BEST SUPPORTIVE CARE*  vilobelimab  control  Time since randomization (days)  Patients (%)  Time since randomization (days)  Patients (%) 

 Phase II Part Results: eGFR Level Stability  Page *  eGFR*  control  At day 15, mean eGFR showed a 3% change from baseline in the vilobelimab group versus -14% in the best supportive care groupOnly 1 patient developed a kidney injury in the vilobelimab group vs 4 patients in the control group developed acute renal failure with moderately to severely decreased eGFR (7% vs. 27%)eGFR higher and mean unchanged in vilobelimab-treated patients while a trend to worsening could be detected in the best supportive care group  Kidney function in vilobelimab treated patients remained mostly within normal limits or declined only mildly     eGFR LEVEL    eGFR: estimated glomerular filtration rateVlaar, A et al. Lancet Rheumatol 2020. https://doi.org/10.1016/S2665-9913(20)30341-6  Time since randomization (days)  Vilobelimab + Best supportive care  Best supportive care only  Least squares mean percentage change 

 Phase II Part Results: Vilobelimab Treatment Associated Significant Increase in D-dimer Levels   Page *  D-DIMER*  control    Vilobelimab treatment was associated with significant increase of D-dimer levels, suggesting potential pro-fibrinolytic activity of anti-C5a treatment    Significant temporary D-dimer increase observed directly upon initiation of vilobelimab therapy (day 2)Possible sign of induction of a direct or indirect pro-fibrinolytic effectIn line with observed 3-fold lower rate in pulmonary embolisms reported as SAE´s in vilobelimab treatment arm and may be mechanistically linked to observed lower death rateHypothesis: Inhibition of C5a by vilobelimab may lead to a decrease in C5a-induced coagulation and directly or indirectly fostered thrombolysis  LEVELS OF D-DIMER    Vlaar, A et al. Lancet Rheumatol 2020. https://doi.org/10.1016/S2665-9913(20)30341-6  Time since randomization (days)  Vilobelimab + Best supportive care  Best supportive care only  Least squares mean percentage change 

 VILOBELIMAB (IFX-1) FOR HIDRADENITIS SUPPURATIVA 

   Hidradenitis Suppurativa (HS)Phase IIb SHINE Study Details  Page *  Important Note: Patients entering the OLE were not unblinded to their initial therapy  Test a dose-dependent effect of vilobelimab on HiSCR* response at week 16 (primary endpoint) Assess long-term safety of vilobelimabTest durability of response with lower maintenance therapy in open label extension period  MAIN GOALS  Placebo  Vilobelimab minimal dose  Vilobelimab low dose  Vilobelimab medium dose  Vilobelimab 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: Vilobelimab low dose  Week 16 HiSCR Non-Responders: Vilobelimab 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   HS: A chronic severely debilitating C5a-driven inflammatory skin condition with high unmet need 

 SHINE Study: Outcome at Week 16  Page *  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 group:  DRAINING FISTULA CHANGE (MEAN %)**  IHS-4 SCORE CHANGE (MEAN %)**  ** Full analysis set – baseline adjusted  IHS-4 Points = Sum of the number of inflammatory nodules (x1), number of abscesses (x2) and number of draining fistulas (x4)AN Count = Total number of combined inflammatory nodules and abscesses   p= 0.0359  p= 0.0202  Primary Endpoint HiSCR Dose Response Signal not met but Signal towards Improved AN countStatistically significant change in DF and in IHS-4 scores detected   

 SHINE Study and Next Steps in HS Development  Page *  * Serious adverse events ** including aspects of the Ph III design, vilobelimab dosing, target study population, nonclinical & clinical pharmacology packages   HiSCR is burdened by high variability (driven by AN count variability) and by a lack of capturing reduction of draining fistulasEvidence for a high C5a turnover rate in HS, leading to increased dose requirements of vilobelimabVilobelimab leads to a marked reduction of all inflammatory lesions in HS with a durable long-term effect detected even at non-optimal dosesVilobelimab long-term treatment was well tolerated, no drug related SAEs* in the open label extension phase  Scientific Advice received from EMA in July 2020EMA agreed to key proposals for pivotal program** including change of primary endpoint to support MAA submission Acknowledged that HiSCR response does not account for the clinical relevance of a reduction in draining fistulas. Agreed that IHS4 could be an appropriate tool to evaluate the efficacy of a novel compound in HS as primary endpointEnd-of-Phase II meeting with FDA held in June 2020FDA agreed to key proposals** to support BLA submissionFDA did not agree that IHS4 score is fit for purpose as a primary efficacy endpoint tool to support labeling Recommended that IFRX obtain HS patient input to help determine validityPlan to submit Special Protocol Assessment (SPA) to the FDA for the Phase III in Q1 2021  OUR CONCLUSIONS    CURRENT STATUS & NEXT STEPS   

 VILOBELIMAB (IFX-1) FOR ANCA-ASSOCIATED VASCULITIS 

 AAV, Life-threatening Autoimmune ConditionClinical PoC established for Role of C5a / C5aR Pathway in AAV  Page *  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 VILOBELIMAB (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; (9 July 2020) ChemoCentryx Submits New Drug Application to the U.S. FDA for Avacopan in ANCA-Associated Vasculitis** Hao & Wang et al 2013, PLoS ONE, 8(6)  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*  LEADING PROPRIETARY ANTI-C5A TECHNOLOGY    

 Phase II Study in AAV in the US (IXPLORE)Study Design  Page *        TREATMENT: 16 WEEKS  FOLLOW UP: 8 WEEKS      Remission Induction Phase      Maintenance Phase  Maintenance Therapy:remain on SOC or transition to guideline maintenance therapy*  Vilobelimab low dose + SOC  Vilobelimab high dose + SOC  Placebo + SOC  A  GROUPS:  B  C  SOC = Rituximab or Cyclophosphamide + glucocorticoids  Randomization 1:1:1  Day 1  Week 16  Week 24  * Guideline maintenance allows for: azathioprin / methotrexate / mycophenolate mofetil / low dose corticosteroids 

 Phase II study in AAV in Europe (IXCHANGE)Study Design  Page *  Study (total enrolled: n=57**)Primary objective: Proof of Concept for efficacy of vilobelimab as replacement for glucocorticoid (GC) therapy in GPA and MPA Secondary objectives: To assess safety and tolerability of vilobelimab & compare toxicity of standard-dose GC with vilobelimabStatus: Blinded interim analysis of Part 1 completed. Part 2: enrollment finalized. Final results expected in 2021        TREATMENT: 16 WEEKS  FOLLOW UP: 8 WEEKS      Remission Induction Phase      Maintenance Phase  Vilobelimab + 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  Vilobelimab + SOC w/o GC (goal: n=16)  placebo + SOC incl. GC (goal: n=9)  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  Guideline maintenance allows for: azathioprin / methotrexate / mycophenolate mofetil / low dose corticosteroids** Enrolled two more patients on Part 2 over the goal 

 VILOBELIMAB (IFX-1) FOR PYODERMA GANGRAENOSUM  

 Pyoderma Gangraenosum (PG)Rationale and Phase IIa Study Overview  Page *  Assessing safety and efficacy of vilobelimab in PGRationale: Pyoderma Gangraenosum (PG) is a rare ulcerative skin disease with a high unmet medical need. 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 labelMulticenterTarget enrollment – 18 patientsFirst patient dosed – June 2019  The first 5 patients were dosed at 800mg biweekly and have finished treatmentTwo additional biweekly higher dose groups have been added; enrollment is ongoing, and patients are under treatmentAdditional data in the higher dose groups expected in 2021  STUDY OBJECTIVE    STUDY DESIGN    TREATMENT   

 Status and Next Steps  Page *  PHASE IIA STUDY UPDATE  C5A LEVELS AT BASELINE  TREATMENTS  Data reported on first 5 patients treated in Feb 20202 of 5 pts: complete closure of target ulcer; full disease remission; remained healed even after finishing the studyAdditional patient: initial wound healing activity in first 2-3 weeks of treatment; no wound size decrease or closure detectedRemaining 2 pts had extensive disease*: target ulcer did not heal, were still under treatmentThe “responders” showed higher baseline C5a levelsPD analysis (C5a levels) warranted higher dosingTwo additional higher dose groups are enrolling, and patients are undergoing treatmentAdditional data with higher doses expected in 2021      day 1  day 18  day 43  day 1  day 30  day 131    Two Patients Show Complete Wound Closure with Vilobelimab Treatment  responder  * very large ulceration / ulcer reaching entire circumference of leg            Healthy  Patients 

 VILOBELIMAB (IFX-1) IN ONCOLOGY 

 Cutaneous Squamous Cell Carcinoma (cSCC)PD-1 or PD-L1 Inhibitor Resistant/Refractory Locally Advanced or Metastatic Patients  Page *  Inhibition of C5a signaling in the tumor microenvironment may decrease tumor growthCombination of C5a with PD-1 checkpoint inhibition could reverse resistance to PD-1 or PD-L1 inhibitor therapy    POTENTIAL ROLE OF C5A IN ONCOLOGY & cSCC    DISEASE INFORMATION cSCC    C5a induces an immunosuppressive tumor microenvironment Accumulation of immunosuppressive MDSC and M2 macrophages1Induction of PD-L1 expression on tumor-associated macrophages (TAM)1,2PD-L1+ TAM are predictive for worse outcome of PD-1 inhibitor treatment3C5a promotes metastasesIncrease of EMT, tumor cell motility and vascular permeability4C5a is readily available in the tumor environment and may promote tumor growth directly Tumor cells, immune cells and coagulation pathway generate C5a5Tumor cells inhibit complement deactivation2C5aR expression increased in many epithelial tumors, incl. cSCC1  Risk factors include Hidradenitis Suppurativa, cumulative UV radiation, irradiation, chronic inflammatory processes, immunosuppression, β-HPV infection, BRAF-inhibitor treatment (e.g., vemurafinib, dabrafenib)6Incidence is estimated at 15-35 per 100,000 people; expected to increase 2-4% per year; Metastasizes in approximately 2-5% of cases overall7,8,10Advanced SCC 10-year survival rates are less than 20% with regional lymph node involvement and less than 10% with distant metastases; Distant metastases have median survival of less than 2 years7,9PD-1 checkpoint inhibitors are FDA approved for recurrent or metastatic cSCC in defined patient populationsNo treatment is available for PD-1 or PD-L1 resistant or refractory patients  EMT: epithelial–mesenchymal transition; MDSC: myeloid-derived suppressor cell  1. Medler et al., 2018; 2. Bonavita, 2015; 3. Liu, et al., 2019 ; 4. Hu et al., 2016; 5. Corrales et al., 2012; 6. Que et al., 2018; 7. Stratigos et al., 2015; 8. Burton et al., 2016; 9. Hillen et al., 2018; 10. Li et al, 2015 

     Study in Cutaneous Squamous Cell Carcinoma (cSCC)  Page *    ARM A: VILOBELIMAB ALONE    ARM B: VILOBELIMAB + PEMBROLIZUMAB       N=7  Safety Analysis    Safety run-in      N=3      N=3 (+3) Regimen 1      N=3 (+3) Regimen 2      N=3 (+3) Regimen 3      N=4 or 7 Regimen 1,2 or 3  DLT Analysis  DLT: Dose limiting toxicity; CR: complete response; PR: partial response  DLT Analysis  DLT Analysis      N=19       N=19    Stage 2  Analysis: CR or PR 1/10  Analysis: CR or PR 1/10    Stage 1    Stage 2    Stage 1  Locally advanced or metastatic cSCCRefractory or resistant to PD-1 or PD-L1 inhibitor Locally advanced cSCC not amenable for curative treatmentMetastatic cSCC resistant to all approved therapies  INCLUSION CRITERIA    Arm A: Assess antitumor activity of vilobelimabArm B: Determine the maximum tolerated dose (MTD) or recommended Phase II dose (RP2D)Assess the antitumor activity and safety profile of vilobelimab + pembrolizumab  Primary Endpoints   

 STRATEGY AND OUTLOOK 

 Medium Term Deliverables and Strategic Objectives  Page *  Complete Phase III development of lead program vilobelimab in Severe COVID-19; submit for approval if results positiveAdvance vilobelimab in HS towards Phase III and ultimate approval based on regulatory guidanceExplore application of vilobelimab for AAV, PG and oncology in clinical developmentExplore extension of pipeline with initiation of clinical development of vilobelimab in other complement-mediated autoimmune / inflammatory diseasesPursue development of early-stage pipeline 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 (€95.7 million as of September 30, 2020)   

 Winzerlaer Str. 207745 Jena, GermanyEmail: info@inflarx.comTel: +49-3641-508180Fax: +49-3641-508181www.inflarx.com  Jordan ZwickChief Strategy OfficerEmail: jordan.zwick@inflarx.de          INFLARX N.V.  INVESTOR RELATIONS INFLARX N.V.