Inflarx N.v. · NASDAQ:IFRX
Inflarx — Investor Presentation (August 2025)
49 slides from Inflarx's investor presentation, August 2025
Slide 1: Corporate Presentation August 2025
CORPORATE PRESENTATION AUGUST 2025
Slide 2: Important Notice and Disclaimer
IMPORTANT NOTICE AND DISCLAIMER This presentation has been prepared by InflaRx N.V. (“InflaRx” or the “Company”). 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
Slide 3: Important Notice and Disclaimer
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 and InflaRx’s own internal estimates and research. While InflaRx believes these third-p
Slide 4: Harnessing C5a/C5aR for controlling inflammation in I&I
Harnessing C5a/C5aR for controlling inflammation in I&I InflaRx Highlights Uniquely targeting complement C5a/C5aR, a validated mechanism and critical part of the inflammation cascade with: • Best-in-class potential oral C5aR inhibitor INF904 – Addressing limitations of marketed comparator (clearly d
Slide 5: C5a/C5aR are validated targets promoting inflammation
C5a/C5aR are validated targets promoting inflammation Targeting strong pro-inflammatory mechanisms vilobelimab INF904 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 upregulate
Slide 6: C5a/C5aR1 signaling inhibition: importance of a C5a-targeted approach
C5a/C5aR1 signaling inhibition: importance of a C5a-targeted approach Complement Pathways Classical Lectin Alternative Antibody binding Mannose binding Foreign surfaces 1.) through C5 convertases C3 activation MG7 (complement mediated) C5-convertases domain 2.) through enzymatic cleavage at scissile
Slide 7: Pipeline targets multiple sizable markets
Pipeline targets multiple sizable markets INDICATION PRECLIN PHASE 1 PHASE 2 PHASE 3 MARKET STATUS & MILESTONES CRITICAL CARE critical COVID-19 US EUA granted vilobelimab SARS-CoV-2-induced ARDS Approved by European Commission* C5a inhibitor broader ARDS Phase 2 “Just Breathe” ASPR/BARDA clinical pl
Slide 8: Significant opportunity in immuno-dermatology
Significant opportunity in immuno-dermatology Why Immuno-Dermatology • Potential to target several attractive, billion-dollar+ commercial markets • InflaRx has identified unmet medical needs that INF904 could strongly address • Strong rationale for the role of C5a/C5aR based on mechanism of action,
Slide 9: C5a & C5aR inhibition: suggested medical utility in broader I&I
C5a & C5aR inhibition: Suggested medical utility in broader I&I by underlying pre- clinical and clinical research Infectious Autoimmune Immuno-derm • Initial focus on immuno-dermatology Cardiovascular • Vilobelimab with proven life-saving anti- inflammatory effect in critically ill COVID- C5a 19 pat
Slide 10: INF904: Oral Highly Selective C5aR Inhibitor With Best-in-Class Potential
INF904: Oral Highly Selective C5aR Inhibitor With Best-in-Class Potential
Slide 11: INF904: Oral C5aR antagonist with best-in-class potential
INF904: Oral C5aR antagonist with best-in-class potential 1,400 Avacopan 30mg ✓ Superior PK/PD profile in Phase 1 SAD and MAD studies compared to 1,200 INF904 3mg INF904 10mg INF904 30mg reported data from marketed comparator avacopan: 1,000 INF904 60mg INF904 120mg INF904 240mg − Plasma Conc. (ng/m
Slide 12: INF904 doubles inhibitory effect in vivo versus avacopan
INF904: Oral C5aR antagonist with best-in-class potential INF904 has double the inhibitory effect in vivo in a pre-clinical model compared to avacopan Inhibition of in vivo neutrophil activation by INF904 compared to avacopan-like molecule* ✱✱ Avacopan-like 120 (10mg/kg oral) 100 INF904 INF904 doubl
Slide 13: PK results from single ascending dose Phase 1
INF904: Oral C5aR antagonist with best-in-class potential PK results from single ascending dose (SAD) Phase 1 1,400 Parameter Unit Dose INF904 Avacopan* Avacopan 30mg INF904 3mg AUCinf h.ng/ml 3 mg 285 25 1,200 INF904 10mg INF904 30mg 10 mg 1264 130 INF904 60mg 1,000 INF904 120mg 30 mg 5956 628 INF9
Slide 14: C5a-mediated CD11b upregulation on neutrophils ex vivo
INF904: Oral C5aR antagonist with best-in-class potential C5a-mediated CD11b upregulation on neutrophils ex vivo up to 14-day dosing INF904: 30 MG QD INF904: 30 MG BID INF904: 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
Slide 15: INF904: Phase 2a trial
INF904: Phase 2a trial
Slide 16: Phase 2a open-label basket study
Phase 2a open-label basket study Primary and Secondary Endpoints Include Safety and PK CSU [n = 45 patients in three cohorts] HS [n = 30 patients in three cohorts] 4-week treatment period − 4-week follow-up 4-week treatment period 3 study arms with 15 patients per arm − 4-week follow-up − 45 patient
Slide 17: INF904 for Chronic Spontaneous Urticaria (CSU)
INF904 for Chronic Spontaneous Urticaria (CSU)
Slide 18: Chronic spontaneous urticaria (CSU)
Chronic spontaneous urticaria (CSU) CSU Overview and Unmet Need Clinical features • An immune-mediated chronic inflammatory skin disorder, with dysregulated inflammatory cascades that leave patients predisposed to symptom development: debilitating and intensely itchy hives / wheals for > 6 weeks and
Slide 19: A strong rationale for developing INF904 in CSU
A strong rationale for developing INF904 in CSU C5aR Signaling is Involved in Histamine Release in an IgE Independent Manner • Increasing scientific evidence suggests that C5aR signaling is involved in histamine release from mast cells and basophils in CSU in an IgE independent manner. This mechanis
Slide 20: CSU endotypes: Type I auto-allergens and type IIb autoimmunity
CSU endotypes: Type I auto-allergens and type IIb autoimmunity C5aR Signaling is Suggested to be Involved in Both Type I and Type IIb Endotypes Activated Coagulation Factors II and X generate C5a from C5 Type I autoimmune (IgE mediated) 1 Also known as autoallergic CSU, is characterized by the prese
Slide 21: C5a drives mast cell attraction, activation and degranulation
C5a drives mast cell attraction, activation and degranulation ▪ The chemoattractant nature of C5a for mast cells explains their accumulation at inflammation sites ▪ Mast cells amplify this cross talk by producing complement proteins and activating them via their released tryptase ▪ C5a is also produ
Slide 22: C5a in CSU and its role in IgE-independent histamine release
C5a in CSU and its role in IgE-independent histamine release CSU patients have elevated C5a levels C5a induces histamine release from basophils C5a mediated histamine release is in a dose-dependent manner independent of the IgE pathway 46.9 ng/ml p = 0.004 20.1 ng/ml N=95 N=42 CSU patients show evid
Slide 23: C5aR1-mediated induction of anaphylaxis via mast cell activation
C5aR1-mediated induction of anaphylaxis via mast cell activation 3 2 1 Kordowski et al. Allergy 2019 Activation of the C5a/C5aR1 axis drives the development of anaphylaxis at several levels 1. The regulation of the B cell response in male mice that leads to the production of antigen-specific IgE. 2.
Slide 24: Comparator data for UAS7 change from baseline
Comparator data for Urticaria Activity Score 7 (UAS7) change from baseline for “successful drug candidates” = phase 2 progressed into - or completed phase 3 Change from baseline (CFB) in UAS7, week 4 Change from baseline (CFB) in UAS7, week 12 UAS7 CFB Placebo w4 UAS7 CFB Treatment w4 UAS7 CFB Treat
Slide 25: Opportunity for a novel MoA such as anti-C5aR
Opportunity for a novel MoA such as anti-C5aR Opportunities Ease of administration to address patient preference and adherence ▪ Oral capsules (BD or QD dosing) New mechanism of action to treat all affected CSU patient populations ▪ Type I IgE mediated and Type IIb autoimmune non-IgE mediated ▪ Anti
Slide 26: INF904 development in CSU
INF904 development in CSU Conclusion • C5aR signaling is involved in histamine release from mast cells / basophils in CSU • This C5a-mediated histamine release is independent of the IgE pathway and has been suggested to play a role in both subtypes of CSU • C5aR inhibition represents a novel mechani
Slide 27: INF904 for Hidradenitis Suppurativa (HS)
INF904 for Hidradenitis Suppurativa (HS)
Slide 28: Hidradenitis suppurativa (HS)
Hidradenitis suppurativa (HS) HS Overview and Unmet Need Clinical features • A chronic, recurring, debilitating neutrophil-driven inflammatory disease, that can persist for years • Characterized by abscesses, nodules and draining tunnels (dTs) with purulent or bloodstained discharge, that can flare
Slide 29: A strong rationale for developing INF904 in HS
A strong rationale for developing INF904 in HS New Mechanisms are Needed • New mechanisms are needed to address the disease more completely – Moderate to severe patients with active draining disease have limited approved treatment options proven to be effective – Response to treatment with approved
Slide 30: An important role for C5a/C5aR is recognized in HS pathogenesis
An important role for C5a/C5aR is recognized in HS pathogenesis Mechanism in HS development Follicular occlusion of the folliculo-pilosebaceous unit, followed by follicular rupture, leading to immune responses which involve complement activation including C5a/C5aR engagement, resulting in the develo
Slide 31: Strong rationale for developing an anti-C5a/C5aR in HS
Strong rationale for developing an anti-C5a/C5aR in HS HS Patients Have Elevated C5a, a Major Neutrophil Activator That Can Be Blocked by an Anti-C5a/C5aR HS patients have significant complement C5a/C5aR activation is a key neutrophil activator in HS patient activation with elevated C5a levels plasm
Slide 32: Neutrophils play a critical role in HS pathogenesis
Neutrophils play a critical role in HS pathogenesis especially in draining tunnels (DTs) Hurley stage III patient with tunnel formation T: Tunnel and surrounding granulomatous G: Granuloma F: Fibrosis inflammation with foreign body giant cells. C5aR1 staining positive – neutrophils, histiocytes and
Slide 33: Clinical evidence for the role of C5a/C5aR signaling in HS
Clinical evidence for the role of C5a/C5aR signaling in HS Vilobelimab (anti-C5a mAb) • SHINE Phase 2b study in moderate-severe HS patients resulted in various signals of efficacy for high dose treatment group (1200mg EOW) including an overall inflammatory lesion reduction * • In SHINE, dT reduction
Slide 34: Vilobelimab SHINE study: ANdT count and IHS4 score
Vilobelimab - SHINE STUDY: outcome of ANdT count and IHS4 score (week 16) ANdT Count Change (LS means)* IHS-4 Score Change (LS means)* 0 0 -10 -10 placebo Relative Change % Relative Change % -20 minimum -20 -19,8 low -25,3 -24,6 medium -30 -30 -29,4 high -40 -40 -38,4 -41,0 -41,1 -50 -50 -48,3 -50,4
Slide 35: Vilobelimab SHINE study: inflammatory lesion reduction
Vilobelimab - SHINE STUDY: Evidence of inflammatory lesion reduction under C5a inhibition DT Count Change Week 16 (LS means)* Complete resolution of DT (DT100) ** Placebo 400 Q4W 800 Q4W 800 Q2W 1200 Q2W % Reduction in Number of Draining Tunnels 0 45 40,9 % patients with DT 100 response -10 40 absol
Slide 36: Summary and rationale for developing INF904 in HS
Summary and rationale for developing INF904 as a potent oral C5aR inhibitor in HS Learnings • Both C5a as well as C5aR signaling inhibition have resulted in clear signals of efficacy (reduction of inflammatory lesions + established scores) in moderate to severe HS patients • Both treatment attempts
Slide 37: Gohibic (vilobelimab) Critical COVID-19 & ARDS
Gohibic (vilobelimab) Critical COVID-19 & ARDS
Slide 38: Emergency Use Authorization (EUA) granted for Gohibic
Emergency Use Authorization (EUA) granted for Gohibic (vilobelimab) Gohibic (vilobelimab) has not been approved, but has been authorized for emergency use by FDA under an EUA*, for the treatment of COVID-19 in hospitalized adults when initiated within 48 hours of receiving IMV**, or ECMO** Authoriza
Slide 39: COVID-19: Disease progression and therapeutic interventions
COVID-19: Disease progression and therapeutic interventions Vaccines Antiviral Treatments Anti-inflammatorische Anti-inflammatory Behandlung Treatments Versterben oder Death Heilung or Recovery Healthy Early Stage Intermediate to Severe Stage Critical Stage Recovery (pre- Incubation / asymptomatic o
Slide 40: PANAMO Phase 3 primary endpoint: 28-day all-cause mortality
PANAMO Phase 3 primary endpoint: 28-day all-cause mortality Placebo + SOC PANAMO Phase 3 trial 1:1 randomized, double-blind, placebo-controlled, multi-national trial in (n=369) invasive mechanically ventilated COVID-19 patients Day 28: 23.9 % relative reduction Kaplan-Meier point estimate: Placebo:
Slide 41: InflaRx N.V. contact
InflaRx N.V. Winzerlaer Str. 2 07745 Jena, Germany Email: IR@inflarx.com Tel: +49-3641-508180 Fax: +49-3641-508181 www.inflarx.com
Slide 42: Appendix
APPENDIX
Slide 43: Main inclusion criteria for CSU
Main inclusion criteria for CSU Patients diagnosed with moderate to severe CSU and inadequately controlled by second generation H1-antihistamines at the time of randomization as defined in the following: 1. The presence of itch and hives for ≥6 consecutive weeks prior to screening in spite of use of
Slide 44: Main inclusion criteria for HS
Main inclusion criteria for HS Moderate or severe hidradenitis suppurativa (with Hurley Stage II or III), and an Abscess and Nodule (AN) count ≥ 5. Inflammatory lesions should affect at least 2 distinct anatomic areas Diagnosis of HS based on clinical history and physical examination for at least 6
Slide 45: INF904 development in the immuno-dermatology field
INF904 development in the immuno-dermatology field Phase 2a Study Ongoing Initial Phase 2a – demonstrating pipeline-in-a-drug potential of INF904 • Open-label PK / PD “basket study” to explore initial efficacy signals • 4-week treatment period in 2 immuno-derm indications CSU and HS with established
Slide 46: Evidence for efficacy of C5aR inhibition in HS: Avacopan data
Evidence for efficacy of C5aR inhibition in HS: Avacopan data Efficacy Evidence in Total Data Set* AN count reduction (w12)* 0 Primary outcome** Absolute change -2 -4 -3,1 -3,4 -6 -5,1 -8 Spalte4 IHS-4 count change (w12)* 0 Absolute change -2 -4 -6 -8 -6,4 -7,9 -10 -9,4 -12 placebo Spalte4 Avacopan
Slide 47: Avacopan data in Phase 2 showed efficacy emerging only at week 12
Avacopan data in Phase 2 showed efficacy emerging only at week 12 Results From Avacopan in HS Patients (Hurley III)* • Avacopan’s efficacy (separation from placebo group) in HS only starts to emerge at W12 – please note: steady state reported from ANCA patients was only reached at approx. 3 months d
Slide 48: Avacopan data in ANCA patients show steady state reached by 13 weeks
Avacopan data in ANCA patients show steady state reached by 13 weeks • Steady state plasma levels of avacopan 30mg BID are reached by 13 weeks and the accumulation is approximately 4-fold • Mean steady state plasma exposure estimates of Avacopan reported plasma trough avacopan are: 3466 h*ng/mL for
Slide 49: Vilobelimab SHINE study patients who completed OLE phase
Vilobelimab – SHINE study patients who completed OLE phase (w 40) Substantial inflammatory lesion reductions when compared to placebo from the double-blind main period (w 16) Relative reduction (% mean) of counts / scores compared to respective baseline (Day1)* Placebo patients on week 16 All OLE pa