Exhibit 99.1
IFX-1 C5a Controlling inflammation Developing the First in Class Anti-C5a Antibody IFX-1: Lessons
Learned from Clinical Trials Niels C. Riedemann
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verified by any independent source. InflaRx n.v. - Winzerlaer Str. 2, 07745 Jena, Germany, Email: info@inflarx.com, Tel: +49-3641-508180, www.inflarx.com
The anti-inflammatory and tissue saving potential of IFX-1 Discussing the potential IFX-1 holds for
various inflammatory disease indications
The Complement Pathways Classical Lectin Alternative Complement Pathways Extrinsic
“Pathway” Enzymatic C5 Cleavage Membrane Attack Complex (MAC)triggers lysis of pathogens strong amplifierof inflammation Antibody binding Mannose binding Foreign surfaces C3 activation C5aR C5b-9 =
MAC C5-convertases C5L2 C5b C5a Terminalcomplementactivation C5 Thrombin, Trypsin, Elastase, etc. The extrinsic pathway represents an additional route, outside of the well-known complement pathways, to activate
C5 Arg751/Leu752 Scissile bonds other ligands: C3a, ASP, C4a etc
The Terminal Complement Pathway Membrane Attack Complex (MAC)triggers lysis of pathogens strong
amplifierof inflammation C5aR C5b-9 = MAC C5L2 C5b C5a C5 cell activationcytokine generation Inflammation PKC-signalling HMGB-1 induction* (Inflammasome) C5a concentration in blood: 10 ~ 30 ng/ml (~1-2.5 nM) C5
concentration in blood: ~75 µg/ml (~400 nM) other ligands: C3a, ASP, C4a etc upregulated in many tissues during inflammation * Rittirsch et al. Nat Med. 2008 May ; 14(5): 551; Colley et al. MABS. 2018,10 (1), 104 Songlin et. al. J. Biol.
Chem. 2019; 294(21) 8384–839 C5L2 has a different binding pocket for C5a compared to other ligands like C3a, ASP etc. and this causes different cell signaling**. The C5a signaling has been shown to be pro-inflammatory* ** Kalant D. et. al.
J. Biol. Chem. 2003, 278 (13) 11123–11129 other signalling involved e.g. in triglyceride synthesis etc.
The InflaRx anti-C5a Technology MAC lysis invading microorganisms C5b-9 = MAC C5b KEY
FEATURES Blocks C5a biological effects up to 100% in human blood Leaves MAC formation intactBinds with high affinity to the discovered epitope C5 newepitope Cleavage of C5 through:Complement pathway activation, orDirectly through
enzymes via “extrinsic” pathway C5a conformational change IFX-1 MAC lysis invading microorganisms C5b-9 = MAC
The C5a Blocking Potential of IFX-1 in Plasma of Patients suffering from Hidradenitis Suppurativa 5 nM
IFX-1 highly effectively blocks HS-plasma / C5a-induced neutrophil activation in human blood Data source: InflaRx GmbH in-house data
IFX-1 Specificity in Vitro and In Vivo * Riedemann NC et. Al., Clin. Immunol. 2017 Mar
30;180:25-32 IFX-1 does not influence the hemolytic activity and leaves C5 cleavage and formation of C5b-9 (MAC) intact. Plasma (1:10 dilution) [µl] OD (542 nm) 50%
Iysis IFX-1 impact on Hemolytic Activity (CH50)* IFX-1 impact on CH50 Analysis in Septic Patients** * Data: InflaRx – Sepsis
Clinical Trial Phase IIa
Neutrophil Activation Potential of C5a Data Source: Prof. Peter Ward, University of
Michigan Neutrophils , (4’600x enlarged) + C5a control C5a Mode of Action on Neutrophils:chemotaxis of neutrophils (Shin et al 1968, Science 162,361-3)enzyme release (Goldstein et al 1974, J. Immunol. 113, 1583-8)production of
O2-radicals in neutrophils (Sacks et al 1978, J Clin Invest 161, 1161-7)
Potential of IFX-1 to Prevent Tissue damage in H7N9 induced Lung Inflammation non-treated monkey lung -
H7N9 infection IFX-1-treated monkey lung - H7N9 infection IFX-1 treatment markedly improved the lung injury score in H7N9 infected lungsIFX-1 treatment strongly decreased viral load in H7N9 infected lungs Sun et al., Clin Infect Diseases,
2014, Sept.
The tissue damaging effect of C5a
C5a as Key Player in Inflammation C5a Neutrophils & Monocytes proinflam. Cytokines > 5000
publications since the 1970th Endothelials/vascular Macrophages Epithelial cells Strong Amplifier Chemotaxis & ActivationAdhesionO2 RadicalsEnzyme release Upregulation of C5aRANGIOGENESISIncreased vascular permeabilityAdhesion
moleculesCoagulation, e.g. TF Upregulation of C5aRTissue inflmmation Promote Th1/Th17Inhibition of Treg TNF-α, IL-1β, IL-6, IL-17Chemokines, e.g. IL-8HMGB-1others ROS production Release of granular enzymes Coagulation increasing tissue
factor Blood Numerous publicationsWell understood MoA T-cells
Summary IFX anti-C5a Technology: IFX-1 Strong IP on discovered conformational epitope on C5a with
protection until late in 2030 and with potential extension until late in 2035IFX-1 shows a superior performance:up to 100% biological blocking activity towards its target C5a in a 1:1 ratioleaves MAC formation intact – is highly selectiveIFX-1
has shown its anti-inflammatory potential in various settingsIFX-1 and IFX-2 are based on the IFRX technology and are believed to be multi-applicable in various disease indications
Hearing clinical trials results and examining lessons learned
Hidradenitis Suppurativa Clinical features Chronic, inflammatory, recurrent, debilitating skin
disease of the hair follicles Most commonly in the armpit, groin and genital regionsExtremely painful inflammatory nodules, boils or abscessesDraining fistulas leading to considerable scarring and functional disability Hurley staging system
used to classify severity (stage I – III) Current Treatment – Medical Need Adalimumab (TNF-alpha inhibitor) from AbbVie is the only approved biological in US and EuropeAccepted (but not approved) SOC includes topical, oral or i.v.
antibioticsIn some instances, surgery is required Approximately 50 - 55% of patients with moderate to severe HS do not respond or lose response to Humira1 Prevalence Up to 200,000 moderate to severe (Hurley II+III) HS patients in USHigher
prevalence in Europe with reports > 1% total HS prevalence Stage ISingle / multiple abscesses but no sinus tracts or scarring Stage IISingle or multiple separated, recurrent abscesses with tract formation and scarring Stage IIIMultiple
interconnected tracts and abscesses involving an entire anatomic region Hurley staging for hs 1 combined phase III trial data for Humira: response measured by HiSCR 50 and KOL quotes in LifeSci Capital initiation report 112/2018
The HiSCR as Endpoint Used for Approval in HS HISCR – a validated endpoint Humira was approved
based on HiSCR response – providing a potential pathway to approvalHiSCR defines 3 types of lesions:AbscessesInflammatory nodules Draining fistulasHiSCR response defined as:At least 50% reduction in total abscess and inflammatory nodule count
(AN count)No increase in the number of abscesses from baselineNo increase in the number of draining fistulas from baseline
IFX-1 Open Label Phase IIa Study in Hidradenitis Suppurativa 1 dose groupWeekly i.v. 800 mg until week 8
(plus one additional loading dose on day 4) Open labelSingle-center12 patients Assessing safety and efficacy of IFX-1 in HSPrimary endpoint: safetySecondary endpoint:HiSCR response at different time points, Study
design design Male 8 (66.7%) Age [y] 48 ± 1550 (22; 69) Hurley Stage III 12 (100%) BMI 27.3 ± 4.926.6 (19.6; 34.5) Weight [kg] 82.2 ± 14.778.0 (63.0; 105.0) Duration of HS [y] 20 ± 920 (3; 35) AN count 6.4 ± 2.56 (3;
11) Failure to TNF-alpha blockade 9/12 objective Treatments Patient characteristics
IFX-1 Open Label Phase IIa Study in Hidradenitis Suppurativa: HiSCR Response 83% HiSCR response rate in
a severe patient population – with long effect durationStrong effect on draining fistula reduction detected (not captured with the HiSCR) – data not shown HiSCR response: Treatment period day 1 – day 50
Efficacy of IFX-1: Skin Response Example, Phase IIa Trial in HS DAY 1 DAY 134 Peri-rectal IFX-1
demonstrated a long lasting effect on the inflammatory lesions after only 8 weeks of 800mg qw dosing
IFX-1 in HD: SHINE Study Details Important Note: Patients entering the OLE were not unblinded to their
initial therapy Test a dose dependent effect of IFX-1 on HiSCR responds at week 16 (primary endpoint) Assess long term safety of IFX-1Test durability of response with lower maintenance therapy in open label extension period MAIN
GOALs Placebo IFX-1 minimal dose IFX-1 low dose IFX-1 medium dose IFX-1 high dose Week 16 HiSCR Responders: IFX-1 low dose Week 16 HiSCR Non-Responders: IFX-1 medium dose Screening 28 weeks (24 weeks treatment + 4 weeks
observation) 16 weeks (double blind) Total treatment time: 9 months + 1 month observation Open Label Extension Period (OLE) Main Period (400mg q4w) (800mg q4w) (800mg q2w) (1200mg q2w) (800mg q4w) (800mg q2w)
SHINE Study Patient Disposition for Open Label Extension (OLE) Completed OLEn = 122
(69%) Discontinuedn = 34 (19%) visit at EOT at wk 40n = 116 completed wk 44n = 122 Patients Enrolledn = 179 Patients Dosed n = 177 (100%) Entered Extensionn =156 (88%) MAIN PERIOD OLE Period week 16 week 40 + 4 End of Treatment
(EOT) - week 40: Sept. 6th 2019 (completed at snapshot: n = 116)Last patient last visit (week 44): Oct. 4th 2019 Final Data will be available early 2020 Snapshot Analysis end of Sep. 2019
SHINE STUDY: Primary Outcome HiSCR at Week 16 versus AN Count Reduction Primary Endpoint: HiSCR dose
response signal not met but signal towards improved AN count n = approx. 35/ group * Full analysis set Treatment Group
SHINE STUDY: Outcome on Draining Fistula and IHS-4 Score Reduction – week 16 stat. significant change in
DF and in IHS-4 scores detected * Full analysis set Treatment Group ** Full analysis set – baseline adjusted p= 0.0202
IHS-4 Score: Includes and Weights All Inflammatory Lesions number of inflammatory nodules IHS-4
points = sum of number of abscesses number of draining fistulas x 1 x 2 x 4 Developed by KOL´s / Physicians to establish a new severity scoring system, suitable for tracking treatment response Captures reduction of draining
fistulas (unlike HiSCR) Internal validation work shows correlation with DLQI and Pain Scores in SHINE data set Weights the most fluctuating lesions (infl. nodules) less than abscesses or fistula – lower variability Mild: ≤ 3
pointsModerate: 4-10 pointsSevere: ≥ 11 points HS Stage
Inflammatory Lesion Reductions in all OLE Patients at End of Treatment (week 40) Compared to Placebo
Group Performance in Main Period Marked improvement of all inflammatory lesions over time – not explainable by placebo effect Relative Reduction (% mean) of Counts / Scores compared to Respective Baseline (Day1)* of Placebo patients on week
16 placebo group week 16 OLE patients week 40 of all OLE patients on week 40 (n=116) * full analysis set (unadjusted)
IHS-4 Scores Over Time in OLE: Non-responders versus Responders Non-responders improve under medium dose
IFX-1 treatment during OLE Responders are relatively “stable” with their IHS-4 scores on low dose IFX-1 Change in IHS-4 scores between week 16 and week 40 in week 16 HiSCR responders versus non-responders* Responders(n = 72) Non-Responders(n
= 84) * full analysis set
IHS-4 Scores in OLE Patients: Relative Change from Baseline (Day 1) HiSCR Non-responder Group (week
16) IFX-1 800 mg q2w Treatment Group in Main period: IHS-4 scores: Relative change from baseline (mean) in OLE patients at week 16 and week 40 in HiSCR non-responder patients (week 16) – displayed per Main Period Treatment group* Main
period placebo and minimal dose patients show strongest improvement in IHS-4 scores when being treated with medium IFX-1 dose (for week 16 HiSCR Non-Responders) * Last observation carried forward analysis set
IHS-4 Scores in OLE Patients: Relative Change from Baseline (Day 1) HiSCR Responder Group (week
16) IHS-4 Scores relative change to baseline (mean) in OLE patients at week 16 and week 40 in week 16 HiSCR responders - displayed per Main Period Treatment group* IFX-1 800 mg q4w Treatment Group in Main period: Main period HiSCR
responders maintain or slightly lose their IHS-4 score improvements when treated with the low dose IFX-1 * Last observation carried forward analysis set
SHINE Study – Insights into Pharmacokinetics/Pharmacodynamics LEARNINGS from SHINE study PK/PD and
Related modeling Results indicate that IFX-1 consumption in HS is much higher than in other diseases (trough levels are a multiple lower at same dose) Results further indicate that this consumption in HS is likely driven by a very
high C5a turnover rate Models suggest that IFX-1 achieves a good tissue penetration rate, especially for higher dose groups Models suggest a target mediated drug clearance: this means, the higher the generation rate of C5a the higher the
IFX-1 clearance
Key Takeaways of SHINE Study: HiSCR is burdened by high variability (driven by AN
count variability) and by a lack of capturing reduction of draining fistula Evidence for a very high C5a turnover rate in HS, leading to IFX-1 consumption IFX-1 leads to a market reduction of all inflammatory lesions in this disease with a
durable long term effect detected even at non-optimal doses IFX-1 long term treatment was well tolerated, no drug related SAE´s in the open label extension phase
InflaRx N.V.Winzerlaer Str. 207745 Jena, GermanyEmail: info@inflarx.comTel:
+49-3641-508180Fax: +49-3641-508181www.inflarx.com Thank you for your attention