Inflarx N.v. · NASDAQ:IFRX
Inflarx — Technical Presentation (June 2024)
87 slides from Inflarx's technical presentation, Jun 5, 2024
Slide 1: InflaRx - virtual R&D event
InflaRx - virtual R&D event INF904: oral C5aR inhibitor with best-in-class potential in the immuno-dermatology and broader I&I space June 5, 2024 – 12 p.m. EST (US) / 6pm CET (EU)
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. This presentation may not be relied up
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: Content
Content Presentation of today’s speakers and company introduction Current understanding of the C5a/C5aR1 biology Prof. Dr. med. Jörg Köhl The Role of C5aR in chronic spontaneous urticaria (CSU) Prof. Dr. med. Marcus Maurer The Role of C5aR in hidradenitis suppurativa (HS) Prof. Chris Sayed, MD Q&A N
Slide 5: Today's presenters
Today’s presenters Prof. Dr. med. Jörg Köhl Prof. Dr. med. Marcus Maurer Dr. Chris Sayed, MD Director, Institute for Systemic Managing Director, Institute for Prof. of Dermatology Inflammation Research (ISEF) Allergy Research, Charité University UNC School of Medicine, University of Lübeck, Germany
Slide 6: Late-stage pipeline targets multiple sizable markets
Late-stage pipeline targets multiple sizable markets INDICATIONS PRECLIN PHASE I PHASE II PHASE III MARKET STATUS & MILESTONES Enrollment ongoing vilobelimab pyoderma Interim analysis for adaptation and futility C5a Inhibitor gangrenosum anticipated in 2025 IMMUNO-DERMATOLOGY chronic spontaneous Pha
Slide 7: IFRX strategic focus: why immuno-dermatology
IFRX strategic focus: why immuno-dermatology • Strong rationale for the role of C5a/C5aR based on mechanism of action, pre-clinical and clinical data • Potential to target several attractive, billion-dollar+ commercial markets with an attractive new MoA which is not currently addressed by any other
Slide 8: INF904 – highly selective C5aR1 inhibitor with best in class potential
INF904 – highly selective C5aR1 inhibitor with “best in class” potential 1,400 Avacopan 30mg ✓ Superior PK/PD profile in Phase I SAD and MAD studies compared to reported INF904 3mg 1,200 INF904 10mg data from marketed comparator avacopan: INF904 30mg INF904 60mg 1,000 INF904 120mg o ~3-fold higher C
Slide 9: Current understanding of the C5a/C5aR1 biology
Current understanding of the C5a/C5aR1 biology Why target C5aR1 in the immuno-dermatologic space? Prof. Dr. Jörg Köhl
Slide 10: Complement translates danger signals into a broad range of cellular responses
Complement translates danger signals into a broad range of cellular responses Mast cell High/ Low Moderate Laumonnier et al Mol Immunol 2017 C5a C5adesArg C5aR1 C5L2/C5aR2 G-protein ßarrs G-protein ßarrs Zhang and Köhl Expert Rev Clin Immunol 2010 Page 10 Prof. Dr. Jörg Köhl – Current understanding
Slide 11: The multiple sources of C5 / C5a and its functions
The multiple sources of C5 / C5a and its systemic and cellular functions C5 Gosh and Rana Int. Immunopharmacol 2023 Local immune cell activation and function Singh and Kemper Eur. J. Immunol.2023 Page 11 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 12: Multi-functional roles of C5a in distinct myeloid cells via C5aR1
Multi-functional roles of C5a in distinct myeloid cells via C5aR1 activation C5aR1 drives NETosis Neutrophil Critical driver of inflammation in Neutrophilic Skin Diseases (Hidradenitis suppurativa, Pyoderma gangrenosum) Gosh and Rana Int. Immunopharmacol 2023 Silva et al J Clin Invest 2023 / Wang et
Slide 13: C5a/C5aR1 axis synergizes with other innate immune receptors
The C5a/C5aR1 axis synergizes with other innate immune receptors to promote a pro-inflammatory environment TLR Autoimmunity Infection Synergistic effects on Inflammation Page 13 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 14: C5aR1 signaling induces pro-inflammatory patterns in myeloid cells
C5aR1 signaling induces pro-inflammatory patterns in myeloid immune cells Monocyte C5aR1 C5aR1 LPS PGE2 IL-6, TNF-, IFN- Myeloid cell Page 14 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 15: C5a/C5aR1 axis activation in macrophages drives Th17 development
C5a/C5aR1 axis activation in macrophages drives Th17 development • Th17 responses are frequently found in neutrophilic skin diseases such as HS and PG. • IL-17 promotes neutrophil migration into affected skin areas. Hashimoto et al. J. Exp. Med. 2010 HS = Hidradenitis suppurativa; PG = Pyoderma gang
Slide 16: C5a/C5aR1 in disease areas
Infectious Diseases Autoimmune Diseases Cardiovascular Diseases C5a Neurodegenerative Neoplastic Diseases Diseases C5aR1 Allergic Diseases Kidney Disease Page 16 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 17: C5aR1 As a Target in the Complement System
C5aR1 As a Target in the Complement System Prof. Dr. Jörg Köhl
Slide 18: C5a/C5aR1 signaling inhibition: the importance of a targeted approach
C5a/C5aR1 signaling inhibition: the importance of a 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 19: Allergic Diseases
C5a C5aR1 Allergic Diseases Page 19 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 20: C5ar1-/- mice are protected from the development of anaphylaxis
C5ar1-/- mice are protected from the development of anaphylaxis Ovalbumin induced allergic / anaphylactic gut permeability increase leading to diarrhea Percent incidence of diarrhea 100 wt (m) 80 C5aR1-/-(m) 60 p< 0.0001 40 Ahrens et al., Am J Pathol 2012 20 0 0 1 2 3 4 5 6 7 Challenge Kordowski et
Slide 21: 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 22: Mast cell activation and its role in CSU
Mast cell activation and its role in chronic spontaneous urticaria (CSU) addressed by Prof. Maurer Yanase et al. Cells 2021 Page 22 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 23: Autoimmune Diseases
Autoimmune Diseases C5a C5aR1 Page 23 Prof. Dr. Jörg Köhl – Current understanding of the C5a/C5aR1 biology
Slide 24: Neutrophilic skin diseases are associated with activation of C5aR1
Neutrophilic skin diseases are associated with activation of C5aR1 • Increased systemic C5a levels Addressed by • Hidradenitis suppurativa* • Increased local C5aR1 expression Prof. Sayed • Skin microbiota expressing C5-cleaving enzyme * Grand et al. Exp. Dermatol. 2019 ** Flora et al. Exp. Dermatol.
Slide 25: Bacterial-induced C5aR1 / TLR cross-talk driving skin inflammation
The hypothesis of bacterial-induced C5aR1 / TLR cross-talk driving skin inflammation • The bacterium Porphyromonas in the oral cavity cleaves C5 into C5a and activates TLR2 to subvert complement/TLR-driven anti-microbial responses. • This leads to a dysbiotic microbial community activating complemen
Slide 26: Neutrophilic skin diseases are associated with activation of C5aR1
Neutrophilic skin diseases are associated with activation of C5aR1 • Increased systemic C5a levels Addressed by • Hidradenitis suppurativa* • Increased local C5aR1 expression Prof. Sayed • Skin microbiota expressing C5-cleaving enzyme • High levels of local C5a in wound fluid • Pyoderma gangraenosum
Slide 27: Neutrophilic skin diseases are associated with activation of C5aR1
Neutrophilic skin diseases are associated with activation of C5aR1 • Increased systemic C5a levels Addressed by • Hidradenitis suppurativa* • Increased local C5aR1 expression Prof. Sayed • Skin microbiota expressing C5-cleaving enzyme • High levels of local C5a in wound fluid • Pyoderma gangraenosum
Slide 28: Neutrophilic skin diseases are associated with activation of C5aR1
Neutrophilic skin diseases are associated with activation of C5aR1 • Increased systemic C5a levels Addressed by • Hidradenitis suppurativa* • Increased local C5aR1 expression Prof. Sayed • Skin microbiota expressing C5-cleaving enzyme • High levels of local C5a in wound fluid • Pyoderma gangraenosum
Slide 29: Role of the C5a/C5aR1 axis in pemphigoid disease
Pathophysiologic role of the C5a/C5aR1 axis in pemphigoid disease Epidermolysis Bullosa Acquisita (EBA) Miyamoto et al., An Bras Dermatol., 2022 Role of C5a/C5aR1 in blister formation and skin inflammation Schmidt and Zillikens, Lancet, 2013 Structural proteins of the dermal/epidermal junction (DEJ)
Slide 30: The C5a/C5aR1 axis controls neutrophil migration into the skin
The C5a/C5aR1 axis controls neutrophil migration into the skin 20 Immunization-induced „active“ model of EBA B6.s (n=21) B6s. C5ar1-/- (n=18) Body affected area (%) 15 10 5 0 2 4 6 8 10 12 Weeks after immunization Week-2 Week-4 Week-6 Week-8 B6.s B6.s Ly6G C5ar1-/- C5ar1-/- C5aR1 controls neutrophil
Slide 31: C5aR1 controls early generation of auto-antigen-specific IgG Abs
C5aR1 controls the early generation of auto-antigen-specific IgG Abs and their inflammatory potential Auto-antibody (AAb) formation IgG AAb-driven ROS release from 1.0 1.0 neutrophils 0.8 IgM AAbs 0.8 IgG1 AAbs 500 B6.s Chemiluminascence OD450 0.6 OD450 0.6 400 C5ar1-/- 0.4 0.4 300 0.2 0.2 0.0 200 0
Slide 32: C5aR1 drives disease development in experimental EBA
C5aR1 drives disease development in experimental EBA at several levels 1. The recruitment of neutrophils into the skin. 2. The early generation of Type VII collagen-specific IgG Aabs. 3. The inflammatory potential (ROS) of Type VII collagen-specific IgG Aabs. Page 32 Prof. Dr. Jörg Köhl – Current un
Slide 33: Summary
Summary
Slide 34: Why target C5aR1 in the immuno-dermatologic space? Key Messages
Why target C5aR1 in the immuno-dermatologic space? Key Message 1 Key Message 2 C5aR1 activates and controls key Evidence for local C5a and effector cells (neutrophils, C5aR1 expression in disease eosinophils, basophils, MCs), the B cell response and Th17 development Key Message 3 Key Message 4 Key T
Slide 35: Thank you for your attention
Thank you for your attention 35
Slide 36: The role of C5aR in chronic spontaneous urticaria (CSU)
The role of C5aR in chronic spontaneous urticaria (CSU) Prof. Dr. Marcus Maurer
Slide 37: Objectives for CSU session
Objectives for CSU session 1. Introduction to CSU disease, epidemiology and current unmet medical needs 2. Pathophysiology of the disease : Type I & IIb endotypes 3. The role of C5a/C5aR signaling : IgE dependent and independent pathways 4. The potential role of INF904 in the future treatment landsc
Slide 38: 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 39: 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 1 Type I autoallergens (IgE mediated) Close contact of two Fc regions of the IgG anti-FcERI or
Slide 40: C5aR is upregulated in the skin of CSU patients
C5aR is upregulated in the skin of CSU patients CSU 20 ** C5aR+ cell/5 fields 15 10 5 healthy controls 0 CSU Healthy Munoz M. Charite Berlin Data on file Page 40 Prof. Dr. Marcus Maurer – The role of C5aR in chronic spontaneous urticaria (CSU)
Slide 41: C5a levels are increased in CSU
C5a levels are increased in CSU: an important new mechanism for histamine releases CSU patients show evidence of C5a induces histamine release from CSU patients have elevated C5a levels complement activation in the skin basophils in a dose-dependent manner C4d staining in skin biopsy 46.9 ng/ml p =
Slide 42: INF904 can effectively block C5a-mediated histamine release
INF904 can effectively block C5a-mediated histamine releases (IgE-independent) C5a-mediated histamine release from human basophils can be effectively inhibited by INF904 C5a (100 nM) 80 IC50=140.3 nM D1 Histamine release (%) D2 60 40 20 IC50=88.74 nM 0 0.1 1 10 100 1000 10000 100000 INF904 (nM) Infl
Slide 43: 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 44: Current treatment landscape including Phase 3 clinical compounds
Current treatment landscape including Phase 3 clinical compounds Therapy MoA Efficacy: 12 weeks Limitations 300 mg Q4w Placebo Black box warning 1 Xolair® (omalizumab) UAS7 (CFB) ~-21 ~-8 SC injection Anti-IgE mAb marketed UAS7=0 36% 9% > 30 % remain symptomatic 5 Dupixent® (dupilumab) 300 mg Q2w Pl
Slide 45: Opportunities for another novel MoA such as anti-C5aR with INF904
There are opportunities for another novel MoA such as anti-C5aR with INF-904 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 a
Slide 46: Predictor of efficacy from Phase 2 UAS7 data at 4 weeks
Predictor of efficacy from Phase 2 UAS7 data change from baseline (CFB) at 4 weeks • Historical UAS7 placebo rates at 4 weeks have ranged from -5.4 to – 9.6 (with an average of -7) • UAS7 efficacy results at 4 weeks show that those who did not achieve a min. CFB vs placebo of -9 have not succeeded i
Slide 47: A strong rationale for developing INF904 in CSU
A strong rationale for developing INF904 in CSU Conclusion: • C5aR signaling is involved in histamine release and mast cell/basophil activation 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 inhibiti
Slide 48: Charité Berlin Team
Charité Berlin Team Page 48 Prof. Dr. Marcus Maurer – The role of C5aR in chronic spontaneous urticaria (CSU)
Slide 49: The Role of C5aR in Hidradenitis Suppurativa
The Role of C5aR in Hidradenitis Suppurativa Dr. Chris Sayed, MD Prof. of Dermatology
Slide 50: Disease background
Disease background Dr. Chris Sayed, MD Prof. of Dermatology
Slide 51: Hidradenitis Suppurativa (HS)
Hidradenitis Suppurativa (HS) HS Overview and Unmet Need Clinical features • A chronic inflammatory disease characterized by abscesses, nodules and draining tunnels (dTs) with purulent and bloody drainage in sites such as axillae, groin, buttocks, and breasts • Flares are unpredictable and cause per
Slide 52: Pathophysiology – what's new
PATHOPHYSIOLOGY – what’s new Chris Sayed, MD Prof. of Dermatology
Slide 53: C5a is elevated in HS and has a role in HS pathogenesis
C5a is elevated in HS and has a role in HS pathogenesis Mechanism in HS development: • Follicular inflammation and an altered microbiome trigger complement activation including C5a/C5aR engagement • Inflammation and dysregulated wound healing lead to chronically inflamed and draining tunnels • This
Slide 54: 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 55: What have we learned from C5a/C5aR signaling inhibition in HS
What have we learned from C5a/C5aR signaling inhibition in HS Dr. Chris Sayed, MD Prof. of Dermatology
Slide 56: Phase 2a open label study vilobelimab in HS: HiSCR results
Phase 2a open label study vilobelimab in HS : HiSCR results 8 Male (66.7%) 83% 48 ± 15 Age [y] 75% 50 (22; 69) 80% 67% Hurley Stage III 12 (100%) 60% 50% 27.3 ± 4.9 BMI 42% 26.6 (19.6; 34.5) 40% 82.2 ± 14.7 Weight [kg] 78.0 (63.0; 105.0) 20% 20 ± 9 Duration of HS [y] 0% 20 (3; 35) 0% 0% 6.4 ± 2.5 AN
Slide 57: Phase 2a vilobelimab in HS: visual result examples
Phase 2a open label study vilobelimab in HS: visual result examples DAY 1 DAY 22 Hypogastrium DAY 1 DAY 22 Left axilla InflaRx data on file Page 57 Dr. Chris Sayed, M.D. Prof. of Dermatology – The Role of C5aR in Hidradenitis Suppurativa
Slide 58: Phase 2a vilobelimab in HS: visual result examples
Phase 2a open label study vilobelimab in HS: visual result examples DAY 1 DAY 134 DAY 1 DAY 134 DAY 1 DAY 134 GLUTEAL FOLD RIGHT INGUIINAL SCROTUM InflaRx data on file Page 58 Dr. Chris Sayed, M.D. Prof. of Dermatology – The Role of C5aR in Hidradenitis Suppurativa
Slide 59: Vilobelimab in HS: Phase 2b SHINE study details
Vilobelimab in HS: Phase 2b SHINE study details Main Period: n = 179 enrolled, 177 treated Open Label Extension Period (OLE): n = 156 Placebo n=36 Week 16 HiSCR Responders: (800 mg q4w) Vilobelimab minimal dose (400 mg q4w) n=34 Vilobelimab low dose 67/72(93%) finished Vilobelimab low dose (800 mg q
Slide 60: SHINE study: primary endpoint not achieved, high placebo response
SHINE STUDY: primary endpoint HiSCR response not achieved with unusually high placebo response rate (week 16) HiSCR 50 (week 16) HiSCR 50 – reported placebo data week 16 80 80 60 60 % HiSCR response % HiSCR response 51,5 47,1 45,5 47,1 40,0 38,9 41,5 38,7 40 40 32,5 30,5 28,8 20 20 0 0 Placebo 400 Q
Slide 61: HiSCR50 comparison from reported positive studies to vilobelimab
HiSCR50 comparison from reported positive studies (week 16 or week 12) to vilobelimab outcome HiSCR 50 – reported for primary endpoint (w12/16) 100 80 Secukinumab (anti-IL17A) phase 3 Sunshine n=180 / Kimball et al, Lancet 2023 66 % HiSCR response Secukinumab (anti-IL17A) phase 3 Sunrise n=180 / Kim
Slide 62: HiSCR 50% response in the OLE
HiSCR 50% response in the OLE suggests that non-responders gain response (42%) on vilo and that 71% keep response on low dose vilo maintenance treatment HiSCR response rate (%) per visit* (OLE) – with 95% CI All OLE patients 100 100 100 90 90 80 80 70 70,6 Responders 70 56,3 60 (n = 72) 60 50 50 40
Slide 63: SHINE: inflammatory lesion reductions after OLE phase
SHINE STUDY: Patients who completed the OLE phase (w 40) showed substantial inflammatory lesion reductions when compared to observed placebo count reductions from the double-blind main period (w 16) Relative reduction (% mean) of counts / scores compared to respective baseline (Day1)* Placebo patien
Slide 64: SHINE study: ANdT count and IHS4 score outcome
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 -51,5 -60 -60
Slide 65: SHINE: evidence of inflammatory lesion reduction under C5a inhibition
SHINE STUDY: evidence of inflammatory lesion reduction under C5a inhibition (w 16) 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 absolute del
Slide 66: 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 67: What have we learned from C5a/C5aR inhibition in HS
What have we learned from C5a/C5aR inhibition in HS Dr. Chris Sayed, MD Prof. of Dermatology
Slide 68: Rationale for developing INF904 as oral C5aR inhibitor in HS
Summary and rationale for developing INF904 as 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 69: Q&A Experts panel
Q&A Experts panel iinflaRx
Slide 70: Next clinical development steps for INF904
Next clinical development steps for INF904 Dr. Camilla Chong, MD CMO
Slide 71: Phase 2a open label basket study in CSU and HS
Phase 2a open label basket study in CSU and HS Clinical development strategy • To determine the appropriate dosing regimen in CSU & HS with safety, PK and efficacy measurements in order to progress to a larger placebo-controlled Phase 2b clinical program. • Basket study approach has been agreed with
Slide 72: Phase 2a open label basket study concept
Phase 2a open label basket study concept Primary and Secondary endpoints are the same in determination of safety and PK measurements in CSU and HS study population CSU 4 weeks treatment (n=15 per arm) HS 4 weeks treatment (n=10 per arm) arm Baseline Baseline Arm 1 INF904 30 mg BID Arm 1 INF904 30 mg
Slide 73: Study design for CSU
Study design for CSU CSU 4 weeks treatment (n=15 per arm) 4 weeks follow-up Baseline EOT EOS Arm 1 INF904 30 mg BID R 1:1 Arm 2 INF904 INF904 60 mg BID n=10 90 mg BID Arm 3 Anti-IgE non responders INF904 90 mg BID Exploratory Endpoints Primary Endpoint: • Change of the weekly Urticaria Activity Scor
Slide 74: 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 75: Study design for HS
Study design for HS HS 4 weeks treatment (n=10 per arm) 4 weeks follow-up Baseline EOT EOS Arm 1 INF904 30 mg BID R Arm 2 INF904 60 mg BID 1:1:1 Arm 3 INF904 90 mg BID Exploratory Endpoints (all change from baseline, CFB): • Total Abscess (A), Inflammatory Nodule (N) and draining tunnels (dT) Count
Slide 76: 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 77: Commercial Opportunity
Commercial Opportunity Dr. Thomas Taapken CFO
Slide 78: Focus on immuno-dermatology – rapidly growing market opportunity
Focus on immuno-dermatology – attractive and rapidly growing market opportunity The immuno-dermatology market is witnessing robust growth, driven by the increased incidence of disease, emerging targeted therapeutics and improved diagnostic capabilities Market growth rates are attracting several phar
Slide 79: Strong commercial potential based on differentiated profile of INF904
Strong commercial potential based on differentiated profile of INF904 • Oral availability provides for ease of administration and patient acceptance • Favorable drug metabolism, PK and toxicology profile positions INF904 as a potential strong alternative to other drug classes • INF904 could address
Slide 80: CSU market dynamic and INF904 commercial opportunity
CSU market dynamic and INF904 commercial opportunity • Overall CSU US market size* estimated to be US$ 1.1 Bn in 2024 and growing at 10% CAGR to US$ 3.1 Bn by 2035, POTENTIAL DRIVERS mainly driven by new therapies for severe disease entering the market strong efficacy − incidence approx. 400k patien
Slide 81: HS market dynamic and INF904 commercial opportunity
HS market dynamic and INF904 commercial opportunity • Overall HS US market size* estimated to be US$ 1.3 Bn in 2024 and growing at 15% CAGR to US$ 6 Bn by 2035, POTENTIAL DRIVERS mainly driven by new therapies for severe disease entering the market strong efficacy − incidence approx. 320k patients p
Slide 82: Role of C5aR inhibition spans well beyond immuno-dermatology
Role of C5aR inhibition spans well beyond immuno-dermatology Possible disease areas in which C5aR has relevance • “Pipeline in a drug” potential of INF904 • C5aR inhibition could be developed broadly in different I&I indications • Initial focus on HS and CSU but other indications (e.g., renal diseas
Slide 83: Conclusions and next steps
Conclusions and next steps InflaRx has sufficient resources to complete Phase 2a basket study in HS and CSU • Cash position as of Q1 2024 was EUR 85.8M (~$93M) – a runway into 2026 Expected start of Phase 2a open label study by year-end 2024, with data in summer 2025 • Goal is to generate additional
Slide 84: Summary
Summary Prof. Dr. Niels C. Riedemann CEO
Slide 85: Summary and conclusions from today's presentation
Summary and conclusions from today’s presentation The new oral C5aR inhibitor INF904 has best-in-class potential and has been developed to become a pipeline-in- a-drug in the immuno-dermatology space and broader I&I space Supported by cutting-edge science, there is significant market potential for I
Slide 86: Q&A all presenters
Q&A all presenters iinflaRx
Slide 87: www.inflarx.com
InflaRx N.V. Winzerlaer Str. 2 07745 Jena, Germany Email: [email protected] Tel: +49-3641-508180 Fax: +49-3641-508181 www.inflarx.com