InflaRx N.V 6-K, filed Jan 16, 2020
InflaRx N.V. (IFRX)
About this 6-K
InflaRx N.V filed this 6-K on January 16, 2020.
UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549
_____________________________
FORM 6-K
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REPORT OF FOREIGN PRIVATE ISSUER
PURSUANT TO RULE 13A-16 OR 15D-16 UNDER
THE SECURITIES EXCHANGE ACT OF 1934
For the month of January, 2020
Commission File Number: 001-38283
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InflaRx N.V.
(Translation of registrant's name into English)
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Winzerlaer Str. 2
07745 Jena, Germany
(Address of principal executive office)
_____________________________
Indicate by check mark whether the registrant files or will file annual reports under cover of Form 20-F or Form 40-F.
Form 20-F ☒ Form 40-F ☐
Indicate by check mark if the registrant is submitting the Form 6-K in paper as permitted by Regulation S-T Rule 101(b)(1): ☐
Indicate by check mark if the registrant is submitting the Form 6-K in paper as permitted by Regulation S-T Rule 101(b)(7): ☐
INFLARX N.V.
On January 16, 2020, in connection with a conference held by J.P. Morgan, InflaRx N.V. (the “Company”) updated and presented its corporate presentation (the “Corporate Deck”).
The Corporate Deck is attached hereto as Exhibit 99.1 and is incorporated by reference herein. The Corporate Deck is also available on the Company’s website located at www.inflarx.de, and the presentation will be available both live and in recorded form on the Company’s website, as well.
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SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned, thereunto duly authorized.
| INFLARX N.V. | ||
|---|---|---|
| Date: January 16, 2020 | By: | /s/ Niels Riedemann |
| Name: | Niels Riedemann | |
| Title: | Chief Executive Officer |
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EXHIBIT INDEX
| Exhibit | Description of Exhibit |
|---|---|
| 99.1 | InflaRx N.V. January 2020 Corporate Presentation titled “Controlling Inflammation” |
Exhibit 99.1
CONTROLLING INFLAMMATION JP Morgan Corporate Presentation January 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 Proven anti-inflammatory effect in multiple Phase II studiesStatistically 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) Ongoing 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 TECHNOLOGYComplete 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 ESTABLISHED CLINICAL EFFICACY FOR LEAD DRUG IFX-1 MULTIPLE ONGOING STUDIES AND INDICATION + PIPELINE EXTENSION Page 3
Pipeline with Multiple Opportunities We have multiple ongoing Phase II studies with potential to expand into further indications These compounds and/or uses of approved products are investigational and have not been approved by the FDA or any other regulatory agency for the uses under investigation. The safety and efficacy of these agents have not been established. PROPOSED INDICATIONS PREVALENCE PRE-CLINICAL PHASE I PHASE II PHASE III UPDATE IFX-1C5a Inhibitor HidradenitisSuppurativa (HS) Up to 200,000patients in the USOver 200,000 patients in Europe Phase IIb completedPlanning for next steps ANCA-AssociatedVasculitis ~40,000 patients inthe US~75,000 patients in Europe Phase IIb enrollment ongoing inboth Europe and US PyodermaGangraenosum ~50,000 patients in the US and Europe are affected Phase IIa open label enrollmentongoing 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 Page 3
The Terminal Complement Pathway Membrane Attack Complex (MAC) triggers lysis of pathogens strong amplifierof inflammation C5aR C5b-9 = MAC C5L2 C5b C5a C5 cell activationcytokine generation Inflammation 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 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 tobe pro-inflammatory.** * Kalant D. et. al. J. Biol. Chem. 2003, 278 (13) 11123–11129**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 other signalling involved e.g. in triglyceride synthesis, etc.PKC-signalingHMGB-1 induction* (Inflammasome) Page 3
Blocks C5a biological effects up to 100% in human bloodLeaves MAC formation intactBinds with high affinity to the discovered epitope IFX-1 is a First-in-Class Anti-C5a Monoclonal Antibody KEY FEATURES C5b C5 new epitope Cleavage of C5 through:Complement pathway activation orDirectly through enzymes via“extrinsic” pathway C5a conformational change IFX-1 MAC lysis ofinvading microorganisms C5b-9 = MAC Page 3
The C5a Blocking Potential of IFX-1 in Plasma of Patients Suffering from Hidradenitis Suppurativa Data source: InflaRx GmbH in-house data Control heparin plasma HS patient heparin plasma5 nM IFX-1 highly effectively blocks HS-plasma / C5a-induced neutrophil activation in human blood CD11b FITC [MFI] 100% 100% 5000 1500010000 0 Page 3
0 10 20 30 40 50 60 70 0h 24h
72h 8d concentration \[U/ml\] 5dTime placebolow dose medium dose high dose13d 28d 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 heat-inact. Plasma 0 µg/ml IFX-1 10 µg/ml IFX-120
µg/ml IFX-150 µg/ml IFX-1 0 30 40 50 60 70 80 90 100 110Plasma \(1:10 dilution\) \[µl\] OD \(542 nm\) IFX-1 Specificity In Vitro
and In Vivo IFX-1 impact on hemolytic activity \(CH50\)\* IFX-1 impact on CH50 analysis in patients\*\* IFX-1 does not influence the hemolytic activity and leaves C5 cleavage and formation of C5b-9 \(MAC\) intact.\* Riedemann NC et. Al., Clin.
Immunol. 2017 Mar 30;180:25-32 \*\* Data: InflaRx in house – Sepsis Clinical Trial Phase IIa Page 3 50% Iysis
Hidradenitis Suppurativa 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 folliclesMost commonly in the armpit, groin and genital regionsExtremely painful inflammatory nodules, boils or abscessesDraining fistulas leading to considerable scarring and functional disabilityHurley 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 requiredApproximately 50% of patients with moderate to severe HS do not respond and about 50% of responder patients lose response to Humira* PREVALENCEUp 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 10 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 RATIONALE FOR TARGETING C5A InflaRx established that HS patients have significant complement activation with elevated C5a levelsC5a is involved in several key pathophysiological mechanisms in HSNeutrophil activation is driven by C5aVarious C5a dependent players potentially involved (TNFa, IL-17, etc.)C5a is key neutrophil activator in HS patient plasmaHS patient plasma strongly provoked neutrophil activation in healthy donor blood; this effect could be completely blocked by the addition of IFX-1 11
IFX-1 in Hidradenitis Suppurativa Humira was approved based on HiSCR response – providing a potential pathway to approval HiSCR defines3 types of lesions: HiSCR response defined as:At least 50% reduction in total AN countNo increase in the number of abscesses from baselineNo increase in the number of draining fistulas from baseline HISCR – A VALIDATED ENDPOINT AN count AbscessesInflammatory nodules Draining fistulas 12
IFX-1 Phase IIa Promising Results in HS Clinical efficacy 0% 13 0% 50% 42% 67% 75% 83% 0% 40%20% 60% 80% HISCR response rate in HS patients100% Baseline Day 22 Day 50 Day 134 Day 29 Day 36 Day 43HiSCR response in HS patients DESIGN EFFICACY OUTCOME SAFETY / TOLERABILITY RESULTS Open label / single center / 12 patients / 1 dose group with weekly i.v. 800 mg until week 8 (plus one additional loading dose on day 4) 75% of patients HISCR responders at week 8 and 83% at end of trial (late-stage patients who previously failed to respond to SOC incl. TNF- alpha blockade) Repeated high dose i.v. administration of IFX-1 observed to be well tolerated with no detected safety issues
IFX-1 in HS:SHINE Study Details 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 periodImportant Note: Patients entering the OLE were not unblinded to their initial therapy MAIN GOALS Placebo Screening 16 weeks (double blind) 28 weeks (24 weeks treatment + 4 weeks observation)TOTAL TREATMENT TIME: 9 months (week 40) + 1 month observation (week 44) Open Label Extension Period (OLE) – n = 156 Main Period – n = 177 treated IFX-1 minimal dose (400 mg q4w) IFX-1 low dose (800 mg q4w) IFX-1 medium dose (800 mg q2w) IFX-1 high dose (1200 mg q2w) Week 16 HiSCR Responders:IFX-1 low dose Week 16 HiSCR Non-Responders:IFX-1 medium dose 15 (800 mg q4w) (800 mg q2w)
SHINE Study:Primary Outcome HiSCR at Week 16 versus AN Count Reduction * Full analysis set HiSCR response rate (%) week 16* AN count score change (mean %) week 16*n = approx. 35/ group 100 0 90 -10 80 -20 70 -30 -26.5 605040 47.1 40.0 51.5 38.7 45.5 -40-50-60 -32.7 -54.6 -44.9 -47.7 30 -70 20 -80 10 -90 0 -100 placebo minimum low medium high Treatment
groups: Primary endpoint: HiSCR dose response signal not met but signal towards improved AN count 16
-19.8 -24.6 -41.1 -38.4 -51.5 -80 -70 -60 -50 -40 -30 -20 -10 0 -18 -14.5 -15 -28 -63.2 -80 -70 -60 -50 -40 -30 -20 -10 0 SHINE
Study:Outcome on Draining Fistula and IHS-4 Score Reduction – Week 16 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 17
IHS-4 Score:Includes and Weights All Inflammatory Lesions Developed by KOLs / physicians to establish a new severity scoring system, suitable for tracking treatment responseCaptures reduction of draining fistulas (unlike HiSCR)Weighs the most fluctuating lesions (infl. nodules) less than abscesses or fistula – lower variabilityInternal validation work shows correlation with DLQI, Pain Scores, Drainage etc. in SHINE data set IHS-4 POINTS = SUM OF HS STAGE number of inflammatory nodules X 1 number of abscesses X 2 number of draining fistulas X 4 Mild: Moderate: Severe: ≤ 3 points4-10 points≥ 11 points 18
Comparison of HiSCR for Week 16 Responder versus Non-responder Groups (OLE) Over Time HiSCR response rate (%) per visit* (OLE) – with 95% CI All OLE patients Responders: 71% maintain HiSCR response with low dose IFX-1Non-responders: 42% become HiSCR responders with medium dose IFX-1 * Full analysis set 1009080706050403020100 week 16 week 20 week 36 week 40 week 24800 mg IFX-1 q4w week 28 week 32 800 mg IFX-1 q2w Responders(n = 72) Non-responders(n = 84) 56.3 19 HiSCR responders9 months
Inflammatory Lesion Reductions in All OLE Patients at End of Treatment(Week 40) Compared to Placebo Group Performance in Main Period (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)*of all OLE patients at week 40 (n=116) of placebo patients at week 16 -66.9 -46.0 -54.5 -60.9 0-10-20-30-40-50-60-70-80-90-100 placebo group week 16 OLE patients week 40 -26.5 -17.7 -21.4 -26.3 0-10-20-30-40-50-60-70-80-90-100 AN count DF count IHS-4 score ANF count AN count DF count IHS-4 score ANF count 20
IHS-4 Scores Over Time in OLE: Non-responders versus Responders Non-responders improve under medium dose IFX-1 treatment during OLEResponders are relatively “stable” with their IHS-4 scores on low dose IFX-1 * Full analysis set 0 5 10 15 20 Change in IHS-4 scores between week 16 and week 40 in week 16 HiSCRresponders versus non-responders*3025 week 16 week 20 week 38 week 40 week 24 week 28 800 mg IFX-1 q4w week 32 800 mg IFX-1 q2w Responders(n = 72) Non-responders (n = 84) 21 IHS4 score
IHS-4 Scores in OLE Patients: Relative Change from Baseline (Day 1) HiSCR Non-responder Group (Week 16) Main period placebo and minimal dose patients show strongest improvement in IHS-4 scores when being treatedwith medium IFX-1 dose (for week 16 HiSCR non-responders) * Last observation carried forward analysis set 100-10-20-30-40 20 IHS-4 scores: Relative change from baseline (mean) in OLE patients week 16 + week 40 inHiSCR non-responder patients (week 16) – displayed per main period treatment group*30 week 16 IFX-1 800 mg q2w week 40placebo minimum low medium high 22 Treatment group in main period: IHS4 score
SHINE Study – Our Conclusions OUR CONCLUSIONS HiSCR is burdened by high variability (driven by AN count variability) and by a lack of capturing reduction of draining fistulaEvidence for a high C5a turnover rate in HS, leading to increased dose requirements of IFX-1IFX-1 leads to a marked reduction of all inflammatory lesions in HS with a durable long-term effectdetected even at non-optimal dosesIFX-1 long-term treatment was well tolerated, no drug related SAEs* in the open label extension phase * Serious adverse events 23
HS – Next Steps NEXT STEPS Request End-of-Phase II FDA Meeting in Q1 2020Discuss with FDA the path forward for regulatory approval towards a Phase III pivotal programDepending on meeting timing and feedback: define path forward by 2H 2020 24
ANCA-Associated Vasculitis (AAV) 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 failurePredominantly 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 NEEDInduction of remission critical during flare phases – induction treatment differs from maintenance therapyand 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 26
IFX-1 in AAVClinical PoC established for Role of C5a / C5aR Pathway in AAV C5a is essential for development of MPA-ANCA crescentic glomerulonephritis in a mouse modelComplement activation in active AAV patients is significantEvidence 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) 27
IFX-1 – P2.6 Phase II study in AAV in the US (IXPLORE) Study Design 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) GROUPS: TREATMENT: 16 WEEKS A B C Randomization 1:1:1 Day 1 Week 16SOC = Rituximab or Cyclophosphamide + glucocorticoids Week 24 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* Guideline maintenance allows for: azathioprin / methotrexate / mycophenolate mofetil / low dose corticosteroids 28
IFX-1 – P2.5 Phase II study in AAV in Europe (IXCHANGE) Study Design Study objective (target: n=81) May 2019 First patient dosed:Primary objective:Secondary objectives: Efficacy of IFX-1 treatment as replacement for glucocorticoid (GC) therapy in GPA and MPA 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 FOLLOW UP: 8 WEEKSMaintenance Phase IFX-1 + SOC with reduced GC (n=15)placebo + SOC incl. GC (n=15) A B Week: Part1 TREATMENT: 16 WEEKSRemission Induction Phase FOLLOW UP: 8 WEEKSMaintenance Phase placebo + SOC incl. GC (n=18)IFX-1 + SOC w/o GC(n=33) B C TREATMENT: 16 WEEKSRemission Induction PhaseDosing scheme: Dosing scheme: 12 14 16 2 4 6 8 10SOC = rituximab or cyclophosphamideGC = glucocorticoids 20 Week 24Maintenance Therapy:remain on SOC or transition toguideline maintenance therapy* Safetyanalysis Part 2 29
Pyoderma Gangraenosum (PG) Source: Demis.net An autoimmune condition with high unmet needCLINICAL FEATURESPG 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 diseasesPatients suffer from severe pain, long healing times, and frequent relapsesDiagnosis is based on the exclusion of other conditions and typical ulcersINCIDENCERare - Estimated that up to 50,000 patients in the US and Europe are affectedOrphan drug marketCURRENT TREATMENT – MEDICAL NEEDNo drugs currently approvedCurrent 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 31
Overview of IFX-1 Phase IIa Study in PG Study Design 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 ≤3of 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 submitted to introduce a dose escalation to test 3 dose groupsSubjects will receive IFX-1 dosing every other week STUDY OBJECTIVE STUDY DESIGN TREATMENTS 32
Our Strategy Advance our lead program IFX-1 for HS towards Phase III / approval based on regulatory guidanceExplore application of IFX-1 for AAV, PG and within the oncology field in Phase II 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 technologyBroaden R&D pipeline beyond anti-C5a technology as part of diversification strategy GOALS AND STRATEGY As of Q3 2019, we have a strong cash balance of US$151 million to pursue these activities Page 34
Winzerlaer Str. 207745 Jena, Germany Email: info@inflarx.com Tel: +49-3641-508180Fax: +49-3641-508181www.inflarx.com Jordan ZwickGlobal Head of Business Development & Corporate Strategy Email: jordan.zwick@inflarx.de INFLARX N.V. INVESTOR RELATIONS INFLARX N.V.