Inflarx N.v. · NASDAQ:IFRX

Inflarx — Investor Presentation (August 2026)

37 slides from Inflarx's investor presentation, August 2026

  1. Slide 1: Corporate Presentation August 2026

    CORPORATE PRESENTATION August 2026

  2. Slide 2: Important Notice and Disclaimer

    CONTROLLING INFLAMMATION 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

  3. Slide 3: Important Notice and Disclaimer

    CONTROLLING INFLAMMATION Important Notice and Disclaimer Information and sources Certain information contained in this presentation relates to or is based on studies, publications, surveys and other data obtained from third-party sources, as well as InflaRx’s own internal estimates and research. Whi

  4. Slide 4: Izicopan: A next-generation C5aR inhibitor for AAV and broader renal

    Izicopan: A next-generation C5aR inhibitor for AAV and broader renal ▪ Izicopan is an oral inhibitor of C5a/C5aR, a critical driver of the inflammatory cascade – C5aR validated from a clinical, regulatory and commercial perspective in AAV – Further validation and option value in AAV provided by prom

  5. Slide 5: InflaRx Pipeline: Targeting the C5a–C5aR axis to control inflammation

    InflaRx Pipeline: Targeting the C5a–C5aR axis to control inflammation INDICATION PRECLIN PHASE 1 PHASE 2 PHASE 3 MARKET STATUS & MILESTONES ANCA-associated vasculitis Phase 2b planning ongoing izicopan other renal indications aHUS, IgAN, C3G, and others I&I Oral C5aR inhibitor HS + CSU Topline Phase

  6. Slide 6: C5a/C5aR are validated targets promoting inflammation

    C5a/C5aR are validated targets promoting inflammation Targeting strong pro-inflammatory mechanisms vilobelimab izicopan intravenous mAb oral small molecule C5 C5a C5aR Cleavage of C5a through complement pathway or enzymatic strong amplifier expressed on many immune cells of inflammation and upregula

  7. Slide 7: Izicopan prevents binding of C5a to C5aR

    Izicopan prevents binding of C5a to C5aR Complement Pathways Classical Lectin Alternative Antibody binding Mannose binding Foreign surfaces through C5 convertases C3 activation 1 [complement mediated] MG7 domain C5-convertases C5 through enzymatic cleavage 2 at scissile bond scissile [thrombin, tryp

  8. Slide 8: Izicopan's “triple threat” for a potential best-in-class agent in AAV

    Izicopan’s “triple threat” for a potential best-in-class agent in AAV Superior PK/PD profile in Phase 1 and Phase 2 studies compared to reported data from marketed comparator avacopan * ▪ ~10-fold higher AUClast and ~3-fold higher Cmax (Phase 1) ▪ Significantly increased blocking activity >90% block

  9. Slide 9: Izicopan's improved chemistry, metabolic & safety features

    Izicopan’s improved chemistry, metabolic & safety features Feature Avacopan Izicopan Key differentiation for izicopan Used as a lead compound series for Further structure-activity optimization Izicopan has improved PK/PD profiling in humans and improved Medicinal chemistry the development of izicopa

  10. Slide 10: Izicopan design: Optimized avacopan backbone structure

    Izicopan design: Optimized avacopan backbone structure Cyan cartoon: CYP3A4; Wheat sticks: HEM Purple sticks: Avacopan; Green sticks: Izicopan Yellow dash lines: hydrogen bonds; Blue dash line: pi-pi stacking; Docking Score: -8.19 (avacopan); -7.13 (izicopan) Experimental data demonstrate that izico

  11. Slide 11: Izicopan shows ~2x the inhibitory effect in vivo compared to avacopan

    Izicopan shows ~2x the inhibitory effect in vivo compared to avacopan Inhibition of in vivo neutrophil activation by izicopan compared to avacopan* 2X APPROXIMATELY izicopan doubled the in vivo inhibitory effect at comparable dose when tested head-to-head with avacopan. + Plasma concentration The st

  12. Slide 12: PK results from single ascending dose (SAD) Phase 1

    PK results from single ascending dose (SAD) Phase 1 Parameter Unit Dose INF904 Avacopan* 3 mg 285 25 AUC inf h.ng/ml 10 mg 1264 130 30 mg 5956 628 3 mg 254 23 AUC last h.ng/ml 10 mg 1117 122 30 mg 5197 557 3 mg 21.5 9 C max ng/ml 10 mg 74.8 25 30 mg 289 79 3 mg 3.5 1.2 t max hr 10 mg 4 1.7 30 mg 5.0

  13. Slide 13: C5a-mediated CD11b upregulation on neutrophils ex vivo

    C5a-mediated CD11b upregulation on neutrophils ex vivo IZICOPAN 30 MG QD IZICOPAN 30 MG BID IZICOPAN 90 MG BID rh C 5 a -C D 1 1 b R e s p o n s e , 3 0 m g q .d ., 1 4 d o s e s r h C 5 a - C D 1 1 b R e s p o n s e , 3 0 m g b .i. d . , 2 7 d o s e s r h C 5 a - C D 1 1 b R e s p o n s e , 9 0 m g

  14. Slide 14: ANCA-associated vasculitis (AAV)

    CONTROLLING INFLAMMATION ANCA-associated vasculitis (AAV)

  15. Slide 15: ANCA-associated vasculitis (AAV)

    ANCA-associated vasculitis (AAV) A LIFE-THREATENING AUTOIMMUNE CONDITION Clinical features ▪ Rare, life-threatening autoimmune disease, characterized by necrotizing vasculitis ▪ Life-threatening flare phases affect organs, leading to potentially fatal organ dysfunction and failure ▪ Predominantly af

  16. Slide 16: The key role of C5a/C5aR in AAV pathophysiology

    The key role of C5a/C5aR in AAV pathophysiology C5a-driven vicious cycle in ANCA Proposed model for the interaction of ANCA, neutrophils and complement activation in the pathogenesis of AAV ▪ ANCAs trigger complement activation/C5a generation, leading to neutrophil activation ▪ ANCAs can activate pr

  17. Slide 17: Izicopan in AAV – A proven large market opportunity

    Izicopan in AAV – A proven large market opportunity ▪ Market for C5aR inhibitor avacopan (marketed as Tavneos) estimated to be Tavneos Global Sales ($M) Estimates ~$1.3B* $1.400 ▪ MoA has been established and accepted to drive organ dysfunction in AAV $1,270 US ex-US ▪ With avacopan under regulatory

  18. Slide 18: Izicopan in AAV – Capturing the opportunity

    Izicopan in AAV – Capturing the opportunity Goal: ‘Rock the Boat’ Scenario Key Development Improvements ▪ Steroid-reducing / rapid taper label Overall Goal Increase signal delta to placebo especially during early major – Avacopan label does not state steroid-sparing flare phase while demonstrating a

  19. Slide 19: Izicopan AAV Phase 2 trial – Base case / current planning stage

    Izicopan AAV Phase 2 trial – Base case / current planning stage Screening Remission Induction w 26 Remission Maintenance w 52 GC Arm 1: Placebo BID + Standard GC Taper (modified PEXIVAS) + RTX Safety Placebo QD + RTX indiv. FU 0 2 4 6 8 10 12 14 16 18 20 GC Arm 2: IZI 60 mg BID + Standard GC Taper (

  20. Slide 20: Izicopan AAV Phase 3 trial – Base case / current planning stage

    Izicopan AAV Phase 3 trial – Base case / current planning stage Screening Remission Induction w 26 Remission Maintenance w 52 GC Arm 1: Placebo + Standard GC Taper + RTX Placebo + SOC indiv. 0 2 4 6 8 10 12 14 16 18 20 GC Arm 2: IZI dose X BID + Rapid GC Taper + RTX IZI dose X QD + SOC indiv. 0 2 4

  21. Slide 21: Izicopan in AAV – Exploring potential for expedited development

    Izicopan in AAV – Exploring potential for expedited development Concurrent with AAV planning and in accordance with the fluid regulatory environment for avacopan, InflaRx is evaluating the feasibility of expedited clinical and regulatory paths for izicopan and potentially vilobelimab in AAV in the U

  22. Slide 22: Development opportunities in additional renal disorders

    CONTROLLING INFLAMMATION Development opportunities in additional renal disorders

  23. Slide 23: C5aR proof-of-concept in AAV, other renal diseases, and broader I&I

    C5aR proof-of-concept in AAV, other renal diseases, and broader I&I Clinical POC for C5aR inhibitor • ANCA-associated vasculitis (AAV) AAV: Approved nephrology • Atypical hemolytic uremic syndrome (aHUS) C3G: Phase 2 (n=22) avacopan • Immunoglobulin A nephropathy (IgAN) • Anti-C3 glomerulopathy (C3G

  24. Slide 24: Potential izicopan renal disease PoC studies

    Potential izicopan renal disease PoC studies • A strategy to conduct studies in regions where InflaRx can rapidly generate data, including China, for a strategic advantage in indications such as IgAN, aHUS, and C3G • Large patient populations, centralized nephrology networks, and strong expertise in

  25. Slide 25: aHUS (atypical hemolytic uremic syndrome)

    CONTROLLING INFLAMMATION aHUS (atypical hemolytic uremic syndrome)

  26. Slide 26: A new paradigm for aHUS: C5a likely a key driver for TMA

    A new paradigm for aHUS: C5a likely a key driver for TMA aHUS is a potentially life-threatening condition that aHUS is a systemic TMA that affects multiple organs causes small blood clots and organ damage o Caused by genetic abnormalities that result in chronic uncontrolled complement activation, le

  27. Slide 27: aHUS: Ex vivo PoC with avacopan

    aHUS: Ex vivo PoC with avacopan Ex vivo findings in aHUS patients treated with avacopan (CCX168, n = 5) • Serum from Day 0: Lead to strong platelet aggregates and C5b- 9 deposition • Serum from Day 14 after CCX168 treatment: Platelet aggregates were almost reduced to baseline level, while C5b-9 depo

  28. Slide 28: IgA nephropathy (IgAN)

    CONTROLLING INFLAMMATION IgA nephropathy (IgAN)

  29. Slide 29: IgAN: An autoimmune condition with complement activation

    IgAN: An autoimmune condition with complement activation IgAN is an autoimmune condition in which IgA deposits in the glomeruli of the kidneys, impacting filtration • Prevalence5: US: ~85k; EU5: ~180k; China: ~800K; Japan: ~85k • IgAN is the most common cause of primary glomerulonephritis (GN)3 • It

  30. Slide 30: Avacopan – Blockade of C5aR1 “PoC” in Patients with IgAN

    Avacopan – Blockade of C5aR1 “PoC” in Patients with IgAN Avacopan treatment - Attenuated kidney injury Urinary Proteinuria – uPCR ↓ - Reduced inflammation Urinary MCP-1/creatine ↓ Proposed MOA Inhibition of C5a/neutrophil– mediated endothelial injury and downstream inflammatory activation in the kid

  31. Slide 31: C3 glomerulopathy (C3G)

    CONTROLLING INFLAMMATION C3 glomerulopathy (C3G)

  32. Slide 32: Complement activation in C3G

    Complement activation in C3G C3G is a rare immune disease characterized by complement dysregulation that undermines the ability of the kidneys to perform many vital functions • A life-threatening kidney disease; half of all patients with C3G ultimately have kidney failure; Kidney transplant does not

  33. Slide 33: Avacopan Phase 2 data in C3G

    Avacopan Phase 2 data in C3G Promising results from the avacopan Accolade Phase 2 trial Improvement from Baseline in UPCR N = 22 for each group Safety • Adverse event incidence similar between the two groups Efficacy • Rapid and sustained reduction of proteinuria • Improved kidney function (eGFR) at

  34. Slide 34: Potential izicopan renal disease PoC basket studies

    Potential izicopan renal disease PoC basket studies Izicopan has a differentiated safety and convenience profile versus other complement inhibitors, including fast onset, oral administration, no vaccination requirement, and no increased infection risk, with potential to drive improved physician adop

  35. Slide 35: Hidradenitis suppurativa (HS)

    CONTROLLING INFLAMMATION Hidradenitis suppurativa (HS)

  36. Slide 36: FDA interactions indicate a viable path forward for izicopan in HS

    FDA interactions indicate a viable path forward for izicopan in HS Phase 2a data indicate izicopan has biologic-like activity within just 4 weeks of treatment, with AN count reduction and HiSCR in line with successful Phase 3 comparators, fast and deep reduction in dT, and significant improvement in

  37. Slide 37: InflaRx N.V.

    CONTROLLING INFLAMMATION InflaRx N.V. Winzerlaer Str. 2 07745 Jena, Germany Email: IR@inflarx.com Tel: +49-3641-508180 Fax: +49-3641-508181 www.inflarx.com

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