Inflarx N.v. · NASDAQ:IFRX
Inflarx — Investor Day (November 2026)
77 slides from Inflarx's investor day presentation, Nov 3, 2026
Slide 1: Capital Markets Day November 3, 2026
Capital Markets Day November 3, 2026
Slide 2: Important notice and disclaimer
Important notice and disclaimer This presentation has been prepared by InflaRx N.V. (“InflaRx” or “we”). 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 in any jurisdiction in which such offer or solic
Slide 3: Today's agenda
Today’s agenda 01 Welcome Niels Riedemann 04 AAV clinical development and commercial opportunity Niels Riedemann, Thomas Taapken 05 Closing remarks 06 Q&A session InflaRx team, Jörg Köhl, Peter Merkel PROF. DR. NIELS RIEDEMANN Chief Executive Officer & Founder DR. THOMAS TAAPKEN Chief Financial Offi
Slide 4: Izicopan: Next-generation oral C5aR inhibitor
Izicopan Next-generation oral C5aR inhibitor
Slide 5: Izicopan's triple threat for a potential best-in-class agent
Izicopan’s “triple threat” for a potential best-in-class agent 5 Sources: InflaRx data on file; for TAVNEOS (avacopan) US prescribing information, EU SmPC, NDA filing documents for ANCA-associated vasculitis. No head-to-head clinical studies performed with izicopan vs avacopan. Abbreviations: AUC [A
Slide 6: Today's takeaways
Today’s takeaways Izicopan has potential to expand the AAV market, with multiple differentiating features that could drive a $1.5B – $2B peak sales potential Izicopan AAV development program is primed for generating differentiated efficacy and safety data placebo-controlled study in patients with re
Slide 7: Targeting C5aR1-driven inflammation in ANCA vasculitis and beyond
Prof. Dr. Jörg Köhl Targeting C5aR1-driven inflammation in ANCA vasculitis and beyond
Slide 8: ANCA-associated vasculitis
ANCA-associated vasculitis A group of rare, systemic small-vessel vasculitides AAV WHAT IT IS Necrotizing inflammation damages predominantly small blood vessels, with few or no immune deposits. Antineutrophil cytoplasmic antibodies usually target proteinase 3 (PR3) or myeloperoxidase (MPO). Some pat
Slide 9: Pathways driving the pathogenesis of ANCA-associated vasculitis
Nakazawa et al Nat Rev Rheumatol 2019 Pathways driving the pathogenesis of ANCA-associated vasculitis Infectious stimuli active DCs to drive Th17 TNF/IL-1ß TNF/IL-1ß prime neutrophils MPO/PR3 surface transition Complement AP activation C5a –> neutrophil priming ANCAs bind and activate FcgRs on
Slide 10: Activation of complement and the C5/C5a/C5aR1 axis in PMN priming
A Nakazawa et al Nat Rev Rheumatol 2019 Activation of complement and importance of the C5/C5a/C5aR1 axis in PMN priming Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 10
Slide 11: C5-deficient mice are protected from anti-MPO-induced crescent GN
C5-deficient mice are protected from anti-MPO-induced crescent GN Xiao et al. AJP 2007 Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 11 Gou et al. Clin J Am Soc Nephrol 2013
Slide 12: C5aR1-deficient mice are protected from anti-MPO-induced crescent GN
Schreiber et al. JASN 2009 C5aR1-deficient mice are protected from anti-MPO-induced crescent GN C5ar1-/- Wildtype Wildtype C5ar1-/- Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 12 Brilland et al. Kidney Int Rep 2026
Slide 13: C5aR1-deficient but not C6-deficient mice are protected
Xiao et al. JASN 2014 C5aR1-deficient but not C6-deficient mice are protected from anti-MPO-induced GN Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 13
Slide 14: FcgR activation on neutrophils drives ROS release
B Falk et al. Proc Natl Acad Sci 1990 Activation of FcgRs on neutrophils by ANCA-speficic IgG drives ROS release from neutrophils Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 14
Slide 15: C5a/C5aR1 axis synergizes with FcgRs
The C5a/C5aR1 axis synergizes with FcgRs to promote a pro-inflammatory environment Synergistic effects on Inflammation Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 15
Slide 16: Cross-talk between C5aR1 and activating FcgRs
Amplification of neutrophil activation through cross-talk between C5aR1 and activating FcgRs Heller et al. JI 1999 Shushakova et al. JCI 2002 Godau et al. JI 2004 Skokowa et al. JI 2005 Kumar et al. JCI 2006 Karsten and Köhl Immunobiol 2012 Schreiber et al. JASN 2009 Prof. Dr. Jörg Köhl – Role of C5
Slide 17: Activation of FcgRs on neutrophils drives NET formation
C Activation of FcgRs on neutrophils drives NET formation Kessenbrock et al. Nat Med 2009 Healthy Ctrl Serum MPO AAV Serum Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 17
Slide 18: C5aR1 drives NETosis
C C5aR1 drives NETosis Neutrophil Critical driver of of inflammation in Neutrophils Silva et al J Clin Invest 2023 / Byrd et al. Sci. Immunol. 2019 C5aR1 on neutrophils drives NETosis Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 18
Slide 19: Cross-talk between FcgRs and C5aR1 drives NET formation
C Kessenbrock et al Nat Med 2009 Huang et al. Arthr Rheumatol 2015 Healthy Ctrl Serum MPO AAV Serum MPO AAV Serum Anti-C5ar1 mAb + Cross-talk between FcgRs and C5aR1 on neutrophils drives NET formation Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 19
Slide 20: Pathways driving the pathogenesis of ANCA-associated vasculitis
Nakazawa et al Nat Rev Rheumatol 2019 Pathways driving the pathogenesis of ANCA-associated vasculitis Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis D Page 20
Slide 21: Autocrine C5/C5a/C5aR1 loop controls Germinal Center B cells
An autocrine C5/C5a/C5aR1 loop controls Germinal Center B cell differentiation and IgG1/IgE class switch WT C5ar1-/- Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Created in Page 21 Einwohlt et al (unpublished)
Slide 22: Key Messages: Why targeting C5aR1 in ANCA-associated vasculitis?
Key Messages Why targeting C5aR1 in ANCA-associated vasculitis ? Key Message 2 C5aR1 primes and activates neutrophils as the key effector cell. It is intertwined with FcgR-mediated neutrophil activation by ANCA Key Message 4 Tailored targeting effect: Blocking C5aR1 leaves upstream and downstream co
Slide 23: Outlook: C5a/C5aR1 axis in AKI to CKD transition
Outlook – role of the C5a/C5aR1axis in the AKI to CKD transition Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis
Slide 24: C5aR1 signaling in tubular epithelial cells drives AKI-CKD transition
Ma. et al. Nephrol. Dial. Transplant. 2026 Created in C5aR1 signaling in tubular epithelial cells drives AKI-CKD transition by enhancing autophagy in ischemia reperfusion injury Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 24
Slide 25: Myeloid and pericyte C5aR1 signaling drives AKI-CKD transition
Sahu et al. Am. J. Physiol. Renal Physiol. 2022 Created in Myeloid and pericyte C5aR1 signaling drives AKI-CKD transition in a folic-acid injury model Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Page 25
Slide 26: References
Page 26 Schreiber, A. et al. J. Am. Soc. Nephrol. 2009. Ma, J. et al. Nephrol. Dial. Transplant. 2026. Sahu, R. K. et al. Am. J. Physiol. Renal Physiol. 2022. Yu, S. M.-W. et al. Am. J. Pathol. 2025. McGraw, M. et al. Physiol. 2026. Brilland, B. et al. J. Am. Soc. 2026. Brilland, B. et al. Kidney In
Slide 27: Thank you for your attention
Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis https://isef-luebeck.de/ Page 27 Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis Thank you for your attention
Slide 28: Appendix
Appendix
Slide 29: Page Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis
Page 29 Prof. Dr. Jörg Köhl – Role of C5aR1 in ANCA-associated vasculitis
Slide 30: Peter Merkel, MD, MPH
Peter Merkel, MD, MPH Chief, Division of Rheumatology; Professor of Medicine (Rheumatology); Professor of Epidemiology in Biostatistics and Epidemiology; University of Pennsylvania
Slide 31: Standard of Care and Unmet Medical Needs in ANCA-Associated Vasculitis
Standard of Care and Unmet Medical Needs in ANCA-Associated Vasculitis Peter A. Merkel, M.D., M.P.H.Chief, Division of RheumatologyPI, Vasculitis Clinical Research Consortium Director, Penn Vasculitis Center Professor of Medicine and EpidemiologyUniversity of Pennsylvania Philadelphia, PA, USA pmerk
Slide 32: Presentation Outline
Presentation Outline Brief introduction to the clinical spectrum of ANCA-associated vasculitis (AAV), specifically, granulomatosis with polyangiitis (GPA) / microscopic polyangiitis (MPA) Outline unmet needs for the treatment of AAV Based on current sets of consensus guidelines and key clinical tria
Slide 33: Variable vessel vasculitis classification
Adapted from A&R 2013 Variable Vessel Vasculitis Behçet's Disease Cogan’s Syndrome Single-Organ Vasculitis CNS Vasculitis Other Organs Drug-Induced Vasculitis Relapsing Polychondritis IgG4-Related Disease Vasculitis in CTD SLE, SSc, SjS, RA, etc.
Slide 34: Clinical Features of ANCA-Associated Vasculitis: GPA/MPA
Clinical Features of ANCA-Associated Vasculitis: GPA/MPA Upper airway disease Nasal septum Sinuses Subglottic stenosis Mastoiditis/OM/ Conductive hearing loss Pulmonary disease Nodules Alveolitis/capillaritis ILD-fibrosis Other Glomerulonephritis Neuropathy Sensory Motor CNS Sensorineural hearing lo
Slide 35: Treatment of AAV: Unmet Needs
Treatment of AAV: Unmet Needs Less toxic regimens Glucocorticoid-sparing CYC-sparing/avoiding Non-sterilizing & non-teratogenic drugs Reduction in infections More rapid induction of remission Prevention of relapse/remission-maintenance Relapse rates are still high, even on treatment Prevention/rever
Slide 36: Treatment of AAV: Unmet Needs
Treatment of AAV: Unmet Needs Less toxic regimens Glucocorticoid-sparing CYC-sparing/avoiding Non-sterilizing & non-teratogenic drugs Reduction in infections More rapid induction of remission Prevention of relapse/remission-maintenance Relapse rates are still high, even on treatment Prevention/rever
Slide 37: Glucocorticoid Toxicity
Glucocorticoid Toxicity Psychosis Insomnia Anxiety/depression Hyperactivity Cataracts Glaucoma Weight gain Cushingoid appearance Diabetes mellitus Adrenal suppression Myopathy Hypertension Heart failure Edema Skin fragility/ecchymoses Osteoporosis Osteonecrosis Infections Reduced vaccine response Mo
Slide 38: Treatment of AAV: Unmet Needs
Treatment of AAV: Unmet Needs Less toxic regimens Glucocorticoid-sparing CYC-sparing/avoiding Non-sterilizing & non-teratogenic drugs Reduction in infections More rapid induction of remission Prevention of relapse/remission-maintenance Relapse rates are still high, even on treatment Prevention/rever
Slide 39: Renal (Kidney) Disease in AAV
Renal (Kidney) Disease in AAV Major source of morbidity and mortality in AAV Residual kidney function after initial disease or a relapse is highly predictive of mortality Rates of end-stage kidney disease (ESKD, dialysis) in AAV remain high ESKD is associated with marked reductions in function, HRQo
Slide 40: Standard of Care Treatment for AAV
Standard of Care Treatment for AAV Based on data from >25 years of high-quality, large, multi-center, randomized, controlled, clinical trails
Slide 41: International Guidelines for Treatment of AAV
International Guidelines for Treatment of AAV
Slide 42: Treatment of ANCA-Associated Vasculitis
TREATMENT OF ANCA-ASSOCIATED VASCULITIS rag i {Remission Induction \ Remission Maintenance ; \ (6-48 Months-Indefinite) ( Rituximab ==» Rituximab + SSS observe off Treatment
Slide 43: Rituximab is the current mainstay of treatment for AAV
Rituximab is the current mainstay of treatment for AAV Rituximab was a major advance in the treatment of AAV Repeated use (every 6 months) with continuous B cell depletion is now the usual treatment for AAV Once rituximab is discontinued high rate of relapse However Still only 70% of patients ente
Slide 44: Retracted NEJM avacopan article
‘i rt ha be acted: Wg Jad. 0 8186 NE MK Th NEW ENGLAND JOURNAL o MEDICINE RETRACTED: Avacopan for the Treatm of ANCA-Associated Vasculitis onan RecA Mee 0, MP ea Su gv ; Srnaittecom peanut indian fa ers mam or ‘eck 52. ll he paint eee eyoposphamide or ritsimab, The safety and linia ffs of avcopan be
Slide 45: NEJM Retraction of Avacopan article
The NEW ENGLAND JOURNAL of MEDICINE EDITORIAL Retraction: Jayne DRW et al. Avacopan for the Treatment of ANCA-Associated Vasculitis, N Engl J Med 2021;384:599-609. Eric J. Rubin, The two academic authors of the article by Jayne et al., Avacopan for the Treatment of ANCA- Associated Vasculitis, N Eng
Slide 46: Post-ADVOCATE NEJM Retraction Actions
Post-ADVOCATE NEJM Retraction Actions Amgen sponsored an independent full readjudication of the primary outcome data for all study patients and re-analyzed the results using the original statistical analysis plan A new report focusing on primary outcome at 26 and 52 weeks was published on August 14,
Slide 47: ADVOCATE Report with Readjudicated Data
ADVOCATE Report with Readjudicated Data Note: This paper has not been peer-reviewed
Slide 48: ADVOCATE Report with Readjudicated Data: Weeks
ADVOCATE Report with Readjudicated Data: 26 Weeks
Slide 49: ADVOCATE Report with Readjudicated Data: Weeks
ADVOCATE Report with Readjudicated Data: 52 Weeks
Slide 50: ADVOCATE with Readjudicated Data Secondary Outcomes
ADVOCATE with Readjudicated Data Secondary Outcomes None of the key secondary outcomes were impacted by the issue of adjudication or readjudication The raw data was unaffected by the issue of readjudication, including eGFR, glucocorticoid toxicity, HRQoL Avacopan vs. Prednisone Taper Less glucocorti
Slide 51: Detailed kidney outcomes in ADVOCATE
Detailed kidney outcomes in ADVOCATE These analyses are not impacted by the readjudication issues in ADVOCATE
Slide 52: Kidney outcomes among patients with kidney disease at baseline
Report of kidney outcomes among the 268/330 (81%) of patients in ADVOCATE with kidney disease at baseline
Slide 53: Change in UACR from baseline in patients with kidney involvement
Change in UACR from baseline in patients with kidney involvement andbaseline UACR > 300 mg/g. Kidney Int Rep 2025
Slide 54: Kidney outcome in ADVOCATE among patients with eGFR ≤20
Analysis of kidney outcome in ADVOCATE among patients with eGFR ≤20 ml/min per 1.73 m2 N=50 patients 2025
Slide 55: Change in kidney function with baseline eGFR ≤20
Change in kidney function among patients in the ADVOCATE trial with baseline eGFR ≤20 ml/min per 1.73 m2. *P < 0.05 **P < 0.01 Kidney Int Rep 2023
Slide 56: Treatment of AAV: Unmet Needs
Treatment of AAV: Unmet Needs Less toxic regimens Glucocorticoid-sparing CYC-sparing/avoiding Non-sterilizing & non-teratogenic drugs Reduction in infections More rapid induction of remission Prevention of relapse/remission-maintenance Relapse rates are still high, even on treatment Prevention/rever
Slide 57: Benefits of More Rapid Induction of Remission of AAV
Benefits of More Rapid Induction of Remission of AAV Prevent progression to organ- or life-threatening status Preserve kidney function predictor of long-term outcome Prevent damage to other organs; e.g. nerves, airways Allow for more rapid reduction or elimination of glucocorticoids Reduce hospita
Slide 58: Treatment of AAV: Unmet Needs
Treatment of AAV: Unmet Needs Less toxic regimens Glucocorticoid-sparing CYC-sparing/avoiding Non-sterilizing & non-teratogenic drugs Reduction in infections More rapid induction of remission Prevention of relapse/remission-maintenance Relapse rates are still high, even on treatment Prevention/rever
Slide 59: The Potential of Enhanced Complement Inhibition for the Treatment of AAV
The Potential of Enhanced Complement Inhibition for the Treatment of AAV Stronger/better complement inhibition could result Overall better outcomes Faster remission Faster and greater recovery of kidney function Less permanent damage to kidneys and other organs An alternativee to rituximab for maint
Slide 60: Summary
Summary Treatment of patients with AAV has improved markedly over the past 25 years However, the rates of remission, relapse-free remission, and prevention of organ damage, especially kidney function, remain unacceptably low Strong inhibition of complement C5a/C5aR offers the potential for substanti
Slide 61: Izicopan: Next-generation oral C5aR inhibitor
Izicopan Next-generation oral C5aR inhibitor
Slide 62: Potential for better efficacy: fast onset with deep C5aR blockade
Potential for better efficacy: fast onset with deep C5aR blockade 62 FAST ONSET OF ACTION Week 1 Izicopan exceeds avacopan’s steady state exposure within first week* Izicopan ≤1 week Avacopan ~13 weeks Izicopan Avacopan ~10× higher exposure AUC (h·ng/mL) after a single 30 mg dose, Phase 1** 5,197 55
Slide 63: Potential for better safety: lower liver and drug-drug interaction risk
Potential for better safety: lower liver and drug-drug interaction risk 63 REACTIVE METABOLITES* >100-fold lower reactive-metabolite signal than avacopan in the early reaction phase (GSH trapping, 5–10 min) GSH-conjugate signal, avacopan relative to izicopan (log scale) 5–10 min >100× 20–40 min >10×
Slide 64: Better convenience: simpler dosing and fewer drug-drug interactions
Better convenience: potential for simpler dosing and fewer drug-drug interactions 64 PILL BURDEN at equivalent dose, 1 pill twice per day vs 3 pills twice per day for avacopan Capsules per day, by regimen Avacopan 30 mg BID (label) – 6 pills total Izicopan 60 mg BID (Ph2a) – 4 pills total Izicopan 3
Slide 65: Izicopan differentiation driven by optimized molecular structure
Izicopan differentiation driven by optimized molecular structure Modelling indicates that the additional trifluoromethyl group in izicopan introduces steric interactions (clashes) within the CYP3A4/5 binding pocket ...thereby providing a molecular basis for three key experimental findings: absence o
Slide 66: Izicopan AAV market considerations
Izicopan AAV market considerations
Slide 67: Market research: Physicians back izicopan as next-generation C5aR inhibitor
67 Market research: Physicians back izicopan as the next-generation C5aR inhibitor C5a/C5aR blockade remains a key target – physicians see izicopan’s profile as a potentially safer, more convenient successor with added potential kidney upside What drives appeal Complement-class MoA 11 Kidney / eGFR
Slide 68: Izicopan in AAV: ~$1.5-2B global peak net sales potential
Izicopan in AAV: ~$1.5-2B global peak net sales potential1 68 Base-case izicopan global peak net sales $1.65bn US $1.160M Japan $255M EU4 + UK $241M Sensitivity analysis: Peak izicopan sales by scenario, $M (ONLY in US + EU4/UK, excl. ROW) With additional GC data available 25.1k eligible patients/yr
Slide 69: AAV clinical development program
AAV clinical development program
Slide 70: Izicopan in AAV: capturing the opportunity
Izicopan in AAV – capturing the opportunity 70 (A) Demonstrate superiority with focus on renal endpoints in randomized placebo-controlled Phase 2 Randomized, placebo-controlled Phase 2 trial optimized to increase signal delta to placebo by allowing severely ill AAV patients with renal vasculitis and
Slide 71: Randomized, placebo-controlled Ph2 trial design
Randomized, placebo-controlled Ph2 trial design Abbreviations: BID [twice daily]. BVAS [Birmingham Vasculitis Assessment Score]. eGFR [estimated Glomerular Filtration Rate]. FU [follow-up]. GC [glucocorticoids]. IZI [izicopan]. N [number]. Ph [Phase]. RTX [rituximab]. SOC [Standard of Care]. Wk [wee
Slide 72: Open-label AAV Ph2 trial design planning
Open-label AAV Ph2 trial design planning Highlights open-label two-stage Phase 2 trial key safety / efficacy endpoints at wk 16 / 24 / 48 safety assessment prior start of stage 2 n ~ 30 patients data in 2028 Endpoint analysis Primary safety including BVAS-0 assessment Secondary sustained remission w
Slide 73: Development opportunities in additional renal disorders
Development opportunities in additional renal disorders
Slide 74: Planned izicopan pilot study in IgAN / RPGN
Planned izicopan pilot study in IgAN / RPGN in IgAN – signal searching 74 IZI 60 mg BID on top of SOC Safety FU Open label study to assess safety and explore efficacy in patients with IgAN and IgAN RPGN (rapidly progressive glomerulonephritis) Cohort may be expanded based on interim signals Wk 12 Wk
Slide 75: IIT in patients with atypical hemolytic uremic syndrome (aHUS)
IIT in patients with atypical hemolytic uremic syndrome (aHUS) 75 IZI 60mg BID Safety FU Key efficacy focus is TMA response (platelet count normalization, LDH normalization, kidney function improvement ≥ 25% creatinine drop from baseline) until week 24 Study participants may receive izicopan up to 1
Slide 76: Today's takeaways
Today’s takeaways Izicopan has potential to expand the AAV market, with multiple differentiating features that could drive a $1.5B – $2B peak sales potential Izicopan AAV development program is primed for generating differentiated efficacy and safety data placebo-controlled study in patients with re
Slide 77: InflaRx N.V. (IFRX)
inflaRx InflaRx N.V. (IFRX) Winzerlaer Str. 2 \ il: [email protected]—— -508180