Inflarx N.v. · NASDAQ:IFRX
Inflarx — Investor Presentation (May 2026)
38 slides from Inflarx's investor presentation, May 6, 2026
Slide 1: AAV + Renal Strategy
AAV + RENAL STRATEGY = May 2026 — - 7 = _ a a
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
Slide 3: Important Notice and Disclaimer: Information and sources
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
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 has been validated from a clinical, regulatory and commercial perspective in AAV – Further validation in AAV provided by promising cl
Slide 5: InflaRx Pipeline: Targeting the C5a–C5aR1 axis to control inflammation
InflaRx Pipeline: Targeting the C5a–C5aR1 axis to control inflammation INDICATION PRECLIN PHASE 1 PHASE 2 PHASE 3 MARKET STATUS & MILESTONES ANCA-associated vasculitis Phase 2b planning ongoing Additional renal indications such as aHUS, IgAN, C3G, other renal indications and others izicopan Oral C5a
Slide 6: Izicopan prevents binding of C5a to C5aR1
Izicopan prevents binding of C5a to C5aR1 Complement Pathways Classical Lectin Alternative Antibody binding Mannose binding Foreign surfaces through C5 convertases C3 activation 1 (complement mediated) MG7 domain C5-convertases C5 2 through enzymatic cleavage at scissile bond (thrombin, scissile try
Slide 7: 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
Slide 8: 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
Slide 9: 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
Slide 10: ANCA-associated vasculitis (AAV)
CONTROLLING INFLAMMATION ANCA-associated vasculitis (AAV)
Slide 11: 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
Slide 12: 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
Slide 13: 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
Slide 14: 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 – Avacopan label does not state steroid-sparing Increase signal delta to placebo especially during early major flare phase while demonstrating a
Slide 15: Izicopan AAV Phase 2 trial – Base case / current planning stage
Izicopan AAV Phase 2 trial – Base case / current planning stage Screening Remission Induction Remission Maintenance w 52 w 26 GC Arm 1: Placebo + Standard GC Taper + RTX Placebo + RTX indiv. 0 2 4 6 8 10 12 14 16 18 20 GC Arm 2: IZI dose 1 BID + Standard GC Taper + RTX Izi dose 1 BID + RTX indiv. 0
Slide 16: 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/QD + Rapid GC Taper + RTX IZI dose X BD/QD + SOC indiv.
Slide 17: 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 an expedited clinical and regulatory path for izicopan in AAV Options for expedited clinical and
Slide 18: Additional renal indications
CONTROLLING INFLAMMATION Additional renal indications Development opportunities
Slide 19: 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
Slide 20: Potential izicopan renal disease PoC basket studies
Potential izicopan renal disease PoC basket 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 exper
Slide 21: Renal indications: aHUS
CONTROLLING INFLAMMATION Renal indications aHUS (atypical hemolytic uremic syndrome)
Slide 22: 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
Slide 23: 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
Slide 24: Renal indications: IgA nephropathy (IgAN)
CONTROLLING INFLAMMATION Renal indications IgA nephropathy (IgAN)
Slide 25: 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
Slide 26: 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
Slide 27: Renal indications: C3 glomerulopathy (C3G)
CONTROLLING INFLAMMATION Renal indications C3 glomerulopathy (C3G)
Slide 28: 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
Slide 29: 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
Slide 30: 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
Slide 31: Hidradenitis suppurativa (HS)
CONTROLLING INFLAMMATION Hidradenitis suppurativa (HS)
Slide 32: 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
Slide 33: Appendix
CONTROLLING INFLAMMATION Appendix
Slide 34: 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
Slide 35: Izicopan design: Optimized avacopan backbone structure
Izicopan design: Optimized avacopan backbone structure avacopan Strong IP positions in INF904 Markush Structure Li et al. US patent No. 11,149,009 (2021.10) Among ~100 compounds synthesized with modifications to avacopan core izicopan structure in positions C3, R8 and/or R9, izicopan was selected an
Slide 36: 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 AUCinf h.ng/ml 10 mg 1264 130 30 mg 5956 628 3 mg 254 23 AUClast h.ng/ml 10 mg 1117 122 30 mg 5197 557 3 mg 21.5 9 Cmax 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 5.01 1
Slide 37: 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 ( ) * + , # * 6 ! ! 7 - ; 4 < = R L < 4 > - ? " - @ 3 -A B C B > - ! % -C R < 4 < ( ) * + , # * 6 ! ! 7 -; 4 < = R L < 4 > - ? " -@ 3 - 7 ABA C A > - $ a -C R < 4 < ( ) * + , # * 6 ! ! 7 -;
Slide 38: 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