InflaRx (Nasdaq: IFRX) details izicopan kidney strategy and funding through 2029

Rhea-AI Filing Summary

InflaRx N.V. is refocusing its pipeline around izicopan, an oral C5a receptor inhibitor, with Phase 2 planning underway in ANCA-associated vasculitis (AAV), a life-threatening kidney disease. The company aims to explore an expedited Phase 2/3 path to reach the commercial market faster.

InflaRx also plans open-label proof-of-concept studies for izicopan in complement‑mediated renal disorders, including atypical hemolytic uremic syndrome (aHUS), IgA nephropathy (IgAN) and C3 glomerulopathy (C3G), with clinical data expected next year and a pharmacokinetic bridging study in China this year.

The company believes izicopan’s pharmacology, safety and dosing profile could outperform the marketed comparator avacopan and estimates having sufficient funds to advance current development plans, including Phase 2 data in AAV and proof‑of‑concept readouts in aHUS, IgAN and C3G, and to support operations through 2029. Further hidradenitis suppurativa development, where market potential is projected above $1.5 billion annually, is currently envisaged only with a partner.

Insights

Biopharmaceutical equity analyst

InflaRx sharpens its izicopan kidney strategy and signals a long cash runway.

InflaRx is concentrating development around izicopan, moving into Phase 2 planning in ANCA-associated vasculitis and preparing open-label renal basket studies in aHUS, IgAN and C3G. The strategy leverages existing class validation from C5a/C5aR targeting and positions izicopan against the approved comparator avacopan.

The company highlights pharmacokinetic and safety data suggesting potentially higher C5aR blockade, cleaner drug–drug interaction profile and more convenient dosing than avacopan. It also describes possibilities for a seamless Phase 2–3 design in AAV, which, if accepted by regulators, could shorten time to a registrational data set.

Importantly, InflaRx estimates its current capital can fund development to key milestones, including AAV Phase 2 and renal proof‑of‑concept readouts, and support operations through 2029. That multi‑year runway reduces near‑term financing pressure while the company seeks a partner for hidradenitis suppurativa, a market it pegs at over $1.5 billion annually.

Key Figures

Cash runway: Through 2029 Avacopan peak sales estimate: ~$1.3B HS market potential for izicopan: >$1.5B per year +3 more

6 metrics

Cash runway Through 2029 Funds expected to cover planned izicopan programs and operations

Avacopan peak sales estimate ~$1.3B Estimated market for approved C5aR inhibitor in AAV

HS market potential for izicopan >$1.5B per year Company estimate for hidradenitis suppurativa opportunity

C5a blockade level ≥90% Blockade of C5a-induced neutrophil activation over 14 days

First-in-human single dose range 3–240 mg Izicopan single-dose safety evaluation with no safety signals of concern

Multiple dose range 30 mg QD to 90 mg BID 14‑day multiple dosing in human studies without safety signals of concern

Key Terms

ANCA-associated vasculitis (AAV), atypical hemolytic uremic syndrome (aHUS), C5a receptor (C5aR) inhibitor, pharmacokinetic bridging study, +2 more

6 terms

ANCA-associated vasculitis (AAV) medical

"develop izicopan, an oral C5a receptor (C5aR) inhibitor with potential best-in-class properties, in ANCA-associated vasculitis (AAV), a life-threatening kidney disorder"

atypical hemolytic uremic syndrome (aHUS) medical

"These additional renal disease targets include atypical hemolytic uremic syndrome (aHUS), IgA nephropathy (IgAN) and C3 glomerulopathy (C3G)"

Atypical hemolytic uremic syndrome (aHUS) is a rare, serious condition where the body’s immune system misfires and causes tiny blood clots that destroy red blood cells and block small blood vessels in the kidneys, often leading to sudden kidney failure. It matters to investors because aHUS drives demand for specialized treatments, influences clinical trial and regulatory outcomes, and can affect a company’s revenue, liability and pipeline valuation in the rare-disease market.

C5a receptor (C5aR) inhibitor medical

"izicopan, an oral C5a receptor (C5aR) inhibitor with potential best-in-class properties"

pharmacokinetic bridging study technical

"Toward these efforts, InflaRx anticipates conducting a pharmacokinetic bridging study in China this year"

hidradenitis suppurativa (HS) medical

"Izicopan for hidradenitis suppurativa (HS) InflaRx has largely concluded its interactions with FDA regarding an optimized clinical development program for izicopan in HS"

proof of concept financial

"goal of establishing rapid proof of concept for izicopan across a broader range of complement-mediated life-threatening kidney diseases"

A proof of concept is a demonstration that shows a new idea, product, or method is feasible and can work as intended. It serves as evidence that an approach has potential value before full development or investment begins. For investors, it helps assess the likelihood of success and reduces uncertainty about whether the concept can deliver its promised benefits.

Form 6-K: How Foreign Companies Report to the SEC →

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

FORM 6-K

Report of Foreign Private

Issuer Pursuant to Rule

13a-16 or 15d-16 of the

Securities Exchange Act

of 1934

For the month of May 2026

Commission File

Number: 001-38283

InflaRx N.V.

(Exact name of Registrant as Specified in Its Charter)

Winzerlaer Str. 2

07745 Jena,

Germany

(+49) 3641508180

(Address of principal executive offices)

Indicate by check mark whether the registrant files or will file annual reports under cover of Form 20-F or Form 40-F.

Form 20-F ☒ Form 40-F  ☐

EXPLANATORY NOTE

On May 6, 2026, InflaRx N.V. (the “Company”) issued a press release titled “InflaRx Announces Advancement of Izicopan in ANCA-Associated Vasculitis and Select Renal Diseases.”

The Company today announced that it intends to develop izicopan, an oral C5a receptor (C5aR) inhibitor with potential best-in-class properties, in ANCA-associated vasculitis (AAV), a life-threatening kidney disorder. The Company is conducting Phase 2 planning for izicopan in AAV and is evaluating the feasibility of multiple development approaches, including the potential for an expedited path to the commercial market, in an effort to best address the evolving regulatory environment surrounding the currently approved comparator, avacopan.

In addition, the Company announced its goal of establishing rapid proof of concept for izicopan across a broader range of complement-mediated life-threatening kidney diseases by conducting open-label studies that are expected to begin generating clinical data next year in certain indications. These additional renal disease targets include atypical hemolytic uremic syndrome (aHUS), IgA nephropathy (IgAN) and C3 glomerulopathy (C3G), where early evidence already exists for the role of C5a/C5aR inhibition and where izicopan’s favorable clinical profile could be a significant differentiator. Toward these efforts, the Company anticipates conducting a pharmacokinetic bridging study in China this year.

A copy of the press release and a copy of the Company’s presentation are attached as Exhibit 99.1 and Exhibit 99.2, respectively. Both Exhibit 99.1 and 99.2 shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act.

FORWARD-LOOKING STATEMENTS

This Report contains forward-looking statements. All statements other than statements of historical fact are forward-looking statements, which are often indicated by terms such as “may,” “will,” “should,” “expect,” “plan,” “anticipate,” “could,” “intend,” “target,” “project,” “estimate,” “believe,” “predict,” “potential” or “continue,” among others. Forward-looking statements appear in a number of places throughout this Report and may include statements regarding our intentions, beliefs, projections, outlook, analyses, current expectations and the risks, uncertainties and other factors described under the headings, “Risk factors” and “Cautionary statement regarding forward looking statements,” in our periodic filings with the U.S. Securities and Exchange Commission. These statements speak only as of the date of this Report and involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Given these risks, uncertainties and other factors, you should not place undue reliance on these forward-looking statements, and we assume no obligation to update these forward-looking statements, even if new information becomes available in the future, except as required by law.

EXHIBIT INDEX

Exhibit No.	Description
99.1	Press Release, dated May 6, 2026.
99.2	Corporate Presentation, dated May 6, 2026.

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned, thereunto duly authorized.

	INFLARX N.V.
Date: May 6, 2026	By:	/s/ Niels Riedemann
		Name: Niels Riedemann
		Title: Chief Executive Officer

Exhibit 99.1

InflaRx Announces Advancement of Izicopan in ANCA-Associated Vasculitis and Select Renal Diseases

• InflaRx intends to develop izicopan in ANCA-associated vasculitis (AAV), with a secondary goal of establishing rapid proof of concept in additional life-threatening renal diseases

• Capital Markets Day highlighting the promise and potential of izicopan in AAV and broader renal disorders now planned for summer 2026

• The Company estimates it will have sufficient funds for currently planned clinical development activities and ongoing operations through 2029

• InflaRx will continue to engage in dialog with potential collaborators to advance its development goals with izicopan across all geographies

• The Company will host a webcast to discuss its new strategy in AAV and renal disease on Friday, May 8, at 8:30 AM ET / 2:30 PM CET

Jena, Germany, May 6, 2026 – InflaRx N.V. (Nasdaq: IFRX), a biopharmaceutical company pioneering anti-inflammatory therapeutics by targeting the complement system, today announced that it intends to develop izicopan, an oral C5a receptor (C5aR) inhibitor with potential best-in-class properties, in AAV, a life-threatening kidney disorder. InflaRx is conducting Phase 2 planning for izicopan in AAV and is evaluating the feasibility of multiple development approaches, including the potential for an expedited path to the commercial market, in an effort to best address the evolving regulatory environment surrounding the currently approved comparator, avacopan.

In addition, the Company has announced its goal of establishing rapid proof of concept for izicopan across a broader range of complement-mediated life-threatening kidney diseases by conducting open-label studies that are expected to begin generating clinical data next year in certain indications. These additional renal disease targets include atypical hemolytic uremic syndrome (aHUS), IgA nephropathy (IgAN) and C3 glomerulopathy (C3G), where early evidence already exists for the role of C5a/C5aR inhibition and where izicopan’s favorable clinical profile could be a significant differentiator. Toward these efforts, InflaRx anticipates conducting a pharmacokinetic bridging study in China this year.

Prof. Niels C. Riedemann, Chief Executive Officer and Founder of InflaRx, said: “We have elected to pursue development in ANCA-associated vasculitis following our thorough evaluation of the high unmet need in this life-threatening disease and izicopan’s promise as a significantly differentiated inhibitor of C5aR, with potential advantages in efficacy, safety and convenience. Furthermore, with a strong body of evidence supporting the role of the C5a/C5aR axis in multiple kidney diseases, our additional goal is to establish proof of concept in other renal disorders, such as atypical hemolytic uremic syndrome, IgA nephropathy and C3 glomerulopathy.”

InflaRx estimates it will have sufficient funds to execute currently planned development programs through meaningful milestones, including proof-of-concept data readouts in aHUS, IgAN and C3G, the Phase 2 data readout in AAV, as well as ongoing operations, through 2029.

Capital Markets Day

InflaRx expects to host a Capital Markets Day to further detail the potential of izicopan’s best-in-class properties in AAV, aHUS, IgAN and C3G this summer.

Webcast

InflaRx will host a webcast/conference call on Friday, May 8, at 8:30 AM ET / 2:30 PM CET. To participate in the call, participants may pre-register here to receive an invite link and dial-in details.

The live webcast and audio archive of the presentation can be accessed on the InflaRx website at https://www.inflarx.de/Home/Investors/Events.html.

Izicopan for hidradenitis suppurativa (HS)

InflaRx has largely concluded its interactions with FDA regarding an optimized clinical development program for izicopan in HS, and believes a viable path forward exists. The Company believes HS remains a significant  opportunity for izicopan, with a market potential that could exceed $1.5 billion per year, with further development currently envisioned only in collaboration with a partner.

About izicopan

Izicopan is an orally administered, small molecule inhibitor of the C5a receptor (C5aR) that has shown anti-inflammatory therapeutic effects in several pre-clinical disease models and in human studies. Further, in contrast to the marketed C5aR inhibitor, in vitro experiments demonstrated that izicopan does not exhibit time-dependent inhibition of cytochrome P450 3A4 (CYP3A4), which plays an important role in the metabolism of a variety of metabolites and drugs, including glucocorticoids. Izicopan has also demonstrated a favorable reactive metabolite profile in human liver microsomes. Reported results from a first-in-human study demonstrated that izicopan was well tolerated in treated subjects and exhibited no safety signals of concern in single doses ranging from 3 mg to 240 mg or multiple doses ranging from 30 mg once per day to 90 mg twice per day for 14 days. Pharmacokinetic / pharmacodynamic data support the best-in-class potential of izicopan, with a ≥90% blockade of C5a-induced neutrophil activation achieved over the 14-day dosing period. Topline Phase 2a data further support the safety profile of izicopan, with no reported safety signals of concern. In patients with hidradenitis suppurativa, over 4 weeks of therapy, izicopan provided rapid and clinically meaningful reductions in abscesses and nodules (ANs) and draining tunnels (dTs), robust HiSCR responses that continued to deepen four weeks after the treatment period, and substantial reductions in patient-reported pain scores, overall demonstrating the potential for biologic-like efficacy. In chronic spontaneous urticaria, InflaRx observed substantial reductions in the 7-day Urticaria Activity Score (UAS7) broadly across patients and particularly in those with severe disease, as well as improved disease control as measured by the Urticaria Control Test (UCT7). In addition, InflaRx has begun planning for development of izicopan in AAV and additional renal indications.

About InflaRx N.V.

InflaRx (Nasdaq: IFRX) is a biopharmaceutical company pioneering anti-inflammatory therapeutics by applying its proprietary anti-C5a and anti-C5aR technologies to discover, develop and commercialize highly potent and specific inhibitors of the complement activation factor C5a and its receptor, C5aR. C5a is a powerful inflammatory mediator involved in the progression of a wide variety of inflammatory diseases. InflaRx‘s lead program is izicopan, an orally administered small molecule inhibitor of C5a-induced signaling via the C5a receptor, which has shown promising PK/PD characteristics as well as therapeutic potential in Phase 1 and Phase 2a clinical studies. The Company is developing izicopan for the treatment of AAV and additional renal diseases. InflaRx also has developed vilobelimab, a novel, intravenously delivered, first-in-class, anti-C5a monoclonal antibody that selectively binds to free C5a and has demonstrated disease-modifying clinical activity and tolerability in multiple clinical studies.

InflaRx was founded in 2007, and the group has offices and subsidiaries in Jena and Munich, Germany, as well as Ann Arbor, MI, USA. For further information, please visit www.inflarx.de. InflaRx GmbH (Germany) and InflaRx Pharmaceuticals Inc. (USA) are wholly owned subsidiaries of InflaRx N.V. (together, InflaRx).

Contacts:

	InflaRx N.V.		MC Services AG
	Jan Medina, CFA Vice President, Head of Investor Relations Email: IR@inflarx.de		Katja Arnold, Laurie Doyle, Dr. Regina Lutz Email: inflarx@mc-services.eu Europe: +49 89-210 2280 U.S.: +1-339-832-0752

FORWARD-LOOKING STATEMENTS

This press release contains forward-looking statements. All statements other than statements of historical fact are forward-looking statements, which are often indicated by terms such as “may,” “will,” “should,” “expect,” “plan,” “anticipate,” “could,” “intend,” “target,” “project,” “estimate,” “believe,” “predict,” “potential” or “continue,” among others. Forward-looking statements appear in a number of places throughout this release and may include statements regarding our intentions, beliefs, projections, outlook, analyses and current expectations concerning, among other things, the success of our future clinical trials for izicopan’s treatment of anti-neutrophil cytoplasmic AAV and other renal diseases, including aHUS, IgAN and C3G, and our ability to establish proof-of-concept for izicopan across such indications; the success of our future clinical trials for vilobelimab's treatment of other debilitating or life-threatening inflammatory indications, including acute respiratory distress syndrome; potential strategic transactions or collaborations, including a potential partnership of izicopan, or vilobelimab for PG; the success of our future clinical trials for  izicopan, and whether such clinical results will reflect results seen in previously conducted pre-clinical studies and clinical trials; the timing, progress and results of pre-clinical studies and clinical trials of vilobelimab, izicopan and any other of our product candidates and statements regarding the timing of initiation and completion of studies or trials and related preparatory work, the period during which the results of the trials will become available, the costs of such trials and our research and development programs generally; our interactions with regulators regarding the results of clinical trials and potential regulatory approval pathways, including related to our biologics license application submission for GOHIBIC (vilobelimab), and our ability to obtain and maintain full regulatory approval of vilobelimab or GOHIBIC (vilobelimab) for any indication; whether the FDA, or any comparable foreign regulatory authority will accept or agree with the number, design, size, conduct or implementation of our clinical trials, including any proposed primary or secondary endpoints for such trials; our ability to leverage our proprietary anti-C5a and anti-C5aR technologies to discover and develop therapies to treat complement-mediated immunological and inflammatory diseases; our ability to protect, maintain and enforce our intellectual property protection for vilobelimab, izicopan and any other product candidates, and the scope of such protection; our manufacturing capabilities and strategy, including the scalability and cost of our manufacturing methods and processes and the optimization of our manufacturing methods and processes, and our ability to continue to rely on our existing third-party manufacturers and our ability to engage additional third-party manufacturers for our planned future clinical trials and for commercial supply of vilobelimab and for the finished product GOHIBIC (vilobelimab); our estimates of our expenses, ongoing losses, future revenue, capital requirements and our needs for or ability to obtain additional financing; our ability to defend against liability claims resulting from the testing of our product candidates in the clinic or, if approved, any commercial sales; if any of our product candidates obtain regulatory approval, our ability to comply with and satisfy ongoing obligations and continued regulatory overview; our ability to comply with enacted and future legislation in seeking marketing approval or commercialization; our future growth and ability to compete, which depends on our retaining key personnel and recruiting additional qualified personnel; and our competitive position and the development of and projections relating to our competitors in the development of C5a and C5aR inhibitors or our industry; and the risks, uncertainties and other factors described under the heading “Risk Factors” in our periodic filings with the SEC. These statements speak only as of the date of this press release and involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Given these risks, uncertainties and other factors, you should not place undue reliance on these forward-looking statements, and we assume no obligation to update these forward-looking statements, even if new information becomes available in the future, except as required by law.

Exhibit 99.2

 CORPORATE PRESENTATION  AAV + RENAL STRATEGY  May 2026 

 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 which such offer or solicitation would be unlawful prior to the registration or qualification of such securities under the securities law of any such jurisdiction.  Cautionary statement regarding forward looking statements  This presentation contains forward-looking statements that involve substantial risks and uncertainties. In some cases, you can identify forward-looking statements by terms such as “may,” “will,” “should,” “expect,” “plan,” “anticipate,” “could,” “intend,” “target,” “project,” “estimate,” “believe,” “predict,” “potential” or “continue” or the negative of these terms or other similar expressions intended to identify statements about the future. These statements speak only as of the date of this presentation and involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. We based these forward-looking statements largely on our current expectations and projections about future events and financial trends that we believe may affect our business, financial condition and results of operations. These forward-looking statements include, without limitation, statements about the following: the success of our future clinical trials for vilobelimab’s treatment of other debilitating or life-threatening inflammatory indications, including ARDS; the potential strategic transactions or collaborations, including a potential partnership of izicopan, or vilobelimab for PG; the success of our future clinical trials for izicopan, and whether such clinical results will reflect results seen in previously conducted preclinical studies and clinical trials; the timing, progress and results of preclinical studies and clinical trials of vilobelimab, izicopan and any other product candidates, including for the development of vilobelimab in several indications and other virally induced ARDS, HS and CSU, and statements regarding the timing of initiation and completion of studies or trials and related preparatory work, the period during which the results of the trials will become available, the costs of such trials and our research and development programs generally; our interactions with and the receptiveness and approval by regulators regarding the results of clinical trials and potential regulatory approval or authorization pathways, including our BLA submission for GOHIBIC (vilobelimab); the timing and outcome of any discussions or submission of filings for regulatory approval of vilobelimab, izicopan or any other product candidate, and the timing of and our ability to obtain and maintain full regulatory approval and/or market authorization of vilobelimab or izicopan for any indication; our ability to leverage our proprietary anti-C5a and anti-C5aR technologies to discover and develop therapies to treat complement-mediated immunological and inflammatory diseases; our ability to protect, maintain and enforce our intellectual property protection for vilobelimab, izicopan and any other product candidates, and the scope of such protection; whether the FDA or any comparable foreign regulatory authority will accept or agree with the number, design, size, conduct or implementation of our clinical trials, including any proposed primary or secondary endpoints for such trials; the success of our future clinical trials for vilobelimab, izicopan and any other product candidates and whether such clinical results will reflect results seen in previously conducted preclinical studies and clinical trials; our expectations regarding the size of the patient populations for, the market opportunity for, the medical need for and clinical utility of vilobelimab, izicopan or any other product candidates, if approved or authorized for commercial use; our manufacturing capabilities and strategy, including the scalability and cost of our manufacturing methods and processes and the optimization of our manufacturing methods and processes, and our ability to continue to rely on our existing third-party manufacturers and our ability to engage additional third-party manufacturers for our planned future clinical trials and for commercial supply of any development candidate in the United States and Europe; our estimates of our expenses, ongoing losses, future revenue, capital requirements and our needs for or ability to obtain additional financing; our ability to defend against liability claims resulting from the testing of our product candidates in the clinic or, if, approved or authorized, any commercial sales; if any of our product candidates obtain regulatory approval or authorization, our ability to comply with and satisfy ongoing drug regulatory obligations and continued regulatory overview; our ability to comply with enacted and future legislation in seeking marketing approval or commercialization; our future growth and ability to compete, which depends on our retaining key personnel and recruiting additional qualified personnel; our competitive position and the development of and projections relating to our competitors in the development of C5a and C5aR inhibitors and other therapeutic products being developed in similar medical conditions in which vilobelimab, izicopan or any other of our product candidates is being developed or our industry; and other risk factors discussed under the “ITEM 3. Key information––Risk factors” section of our Annual Report on Form 20-F. Because forward-looking statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified and some of which are beyond our control, you should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur and actual results could differ materially from those projected in the forward-looking statements. You should refer to the “ITEM 3. Key information––Risk factors” section of our Annual Report and risks described in our subsequent SEC filings for a discussion of important factors that may cause our actual results to differ materially from those expressed or implied by our forward-looking statements. Moreover, we operate in an evolving environment. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties. As a result of these factors, we cannot assure you that the forward-looking statements in this presentation or in our Annual Report will prove to be accurate. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise. You should, however, review the factors and risks and other information we describe in the reports we will file from time to time with the SEC after the date of this presentation.  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. While we believe these third-party sources to be reliable as of the date of this presentation, we have not independently verified, and make no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. All market data and other information from third-party sources involve a number of assumptions and limitations, and there can be no guarantee as to the accuracy or reliability of such assumptions. Further, while we believe our own internal research is reliable, such research has not been verified by any independent source.  About InflaRx  InflaRx (Nasdaq: IFRX) is a biopharmaceutical company pioneering anti-inflammatory therapeutics by applying its proprietary anti-C5a and anti-C5aR technologies to discover, develop and commercialize highly potent and specific inhibitors of the complement activation factor C5a and its receptor, C5aR. C5a is a powerful inflammatory mediator involved in the progression of a wide variety of inflammatory diseases. InflaRx‘s lead program is izicopan (INF904), an orally administered small molecule inhibitor of C5a-induced signaling via the C5a receptor, which has shown promising PK/PD characteristics as well as therapeutic potential in Phase 1 and Phase 2a clinical studies. The company is developing izicopan for the treatment of several inflammatory diseases, including hidradenitis suppurativa (HS). The Company has also developed vilobelimab, a novel, intravenously delivered, first-in-class, anti-C5a monoclonal antibody that selectively binds to free C5a and has demonstrated disease-modifying clinical activity and tolerability in multiple clinical studies.  InflaRx was founded in 2007, and the group has offices and subsidiaries in Jena and Munich, Germany, as well as Ann Arbor, MI, USA. For further information, please visit www.inflarx.de. InflaRx GmbH (Germany) and InflaRx Pharmaceuticals Inc. (USA) are wholly owned subsidiaries of InflaRx N.V. (together, InflaRx).  CONTROLLING INFLAMMATION 

 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 clinical data with C5a antibodies vilobelimab and BDB-001  AAV market growth and regulatory scrutiny related to the marketed comparator, avacopan, has provided InflaRx a clear and present opportunity with its next generation C5aR inhibitor, izicopan  By improving upon the significant limitations of the marketed comparator, izicopan has potential best-in-class properties  Faster onset of action and higher target coverage leading to potentially differentiated efficacy  Cleaner safety profile with low risk of liver toxicity and drug-drug interactions  More convenient dosing with the potential for lower pill burden and once-daily dosing  Given its class-leading properties izicopan has the potential to improve upon the ~$1.3B peak sales estimate* of avacopan  Izicopan could also address significant unmet needs and large commercial markets across broader I&I, including renal indications such as aHUS, IgAN, C3 glomerulopathy, and others  Strong IP position and a team with proven track record of delivering clinical and regulatory successes  I&I [immunology & inflammation]. AAV [ANCA-associated vasculitis]. aHUS [atypical hemolytic uremic syndrome]. IgAN [immunoglobulin-A nephropathy]. * FactSet estimates, March 2026.  4 

 Indication  PreClin  Phase 1  Phase 2  Phase 3  MARKET  STATUS & Milestones  ANCA-associated vasculitis  other renal indications  HS + CSU  broader I&I  Phase 2b planning ongoing  Additional renal indications such as aHUS, IgAN, C3G, and others  Topline Phase 2a reported  Additional indications in immuno-dermatology, hematology, neurology and others  izicopan   Oral C5aR inhibitor  I&I  InflaRx Pipeline: Targeting the C5a–C5aR1 axis to control inflammation  vilobelimab  C5a inhibitor  critical COVID-19  SARS-CoV-2-induced ARDS  broader ARDS  US EUA granted*  Approved by European Commission*  Phase 2 “Just Breathe” ASPR/BARDA clinical platform study  Critical Care  DERM  vilobelimab  C5a inhibitor  pyoderma gangrenosum  Phase 3 reported**  OTHER  IFX002  C5a inhibitor   vilobelimab  life-cycle approach  For optimized use in chronic inflammatory indications  *Commercial partnering and distribution options in the US and EU being considered.  ** Phase 3 stopped early for futility at interim analysis, FDA interaction considered.  aHUS [atypical hemolytic uremic syndrome]. IgAN [immunoglobulin-A nephropathy]. C3G [anti-C3 glomerulopathy].  5 

 Izicopan prevents binding of C5a to C5aR1  Advantages of blocking C5aR with izicopan  Blocking C5 or further upstream (e.g., with eculizumab and related antibodies) does not adequately inhibit C5a/C5aR1 signaling  A small molecule oral compound should have better tissue penetration and better ability to control C5a/C5aR1 signaling at the site of inflammation  C5aR1 is selectively expressed on various immune and tissue cells, and blocking C5aR1 will not be impacted by increasing C5a generation  scissile bond  MG7 domain  C5a  C5aR1  through C5 convertases (complement mediated)   through enzymatic cleavage at scissile bond (thrombin, trypsin, elastase, etc.)  Classical  Lectin  Alternative  Complement Pathways  Antibody binding  Mannose binding  Foreign surfaces  C3 activation  C5-convertases  1  2  C5  izicopan  6 

 *InflaRx data on file: PK Results From Single Ascending Dose (SAD) Phase 1 study – note: Avacopan data (Becker et al, 2016, PLoS One) are superimposed in graph for orientation. Avacopan was not included as a comparator in INF904 Phase I study. PD Results from multiple ascending dose (MAD) Phase 1 study.   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% blocking of C5a activity   Faster achievement of therapeutic exposure - within the first week vs 13 weeks for avacopan  Dosing advantages  30mg per capsule (vs 10mg for avacopan) and potential for once-daily dosing  Improved safety profile   No signals of safety concern (>180 humans exposed, clean GLP toxicology studies)  No time dependent CYP3A4 inhibition (IC50 > 100 μM) as measured via Ki-based TDI study  Izicopan potential advantages  Faster onset of action + higher target coverage + differentiated efficacy  Cleaner safety profile with low risk of liver toxicity and drug-drug interactions  More convenient dosing, with lower pill burden and QD potential  Avacopan steady state (week 13)  Izicopan 60mg CSU  Izicopan 60mg HS  1: Preliminary PK results of pooled patients: 10 - 11 HS patients (60mg bid) and 10 -11 CSU patients (60mg bid). Steady state plasma levels of avacopan (NDA filing for ANCA-associated vasculitis, 75-100 patients) are reached by 13 weeks and the accumulation is approximately 4-fold.  7 

 Feature  Avacopan  Izicopan  Key differentiation for izicopan  Medicinal chemistry  Used as a lead compound series for the development of izicopan  Further structure-activity optimization performed  Izicopan has improved PK/PD profiling in humans and improved safety features (e.g. metabolic stability and CYP inhibition)  Chirality  2 chiral centers  3 chiral centers  The extra stereocenter in izicopan provides additional conformational control, significantly improving physiochemical properties and druggability  Solid-state form  Crystalline  Amorphous  The amorphous form of izicopan supports faster absorption and quicker attainment of therapeutic exposure  Izicopan therapeutic exposure reached in days to one week, vs 13 weeks for avacopan  CYP inhibition  Time dependent inhibitor of CYP3A4  Ki/Kinact assay demonstrates:  No inhibition of CYP3A4 (IC50 >100 μM)  No time dependent inhibition (TDI)  Avacopan CYP3A4 inhibition raises risk of drug–drug interactions and may slow clearance of co-medications (incl. steroids), potentially contributing to liver toxicity. This is not a concern with izicopan  Metabolic stability  Lower stability and high CYP-mediated turnover in human liver microsome (HLM) and human hepatocyte (HH)  Very high stability and very low CYP-mediated turnover in HLM and HH   Izicopan demonstrates high metabolic stability, with very low intrinsic clearance and long half-lives in both HLM and HH, compared with avacopan, suggesting a substantially reduced risk of reactive metabolite formation.  GSH-trapping in vitro  (reactive metabolites)  Rapid and high-level of formation of multiple structurally diverse thiol conjugates, indicating extensive oxidative bioactivation via multiple pathways  Minimal formation of thiol conjugates, with levels remaining consistently low throughout the incubation, supporting a low oxidative bioactivation profile  Total reactive conjugate signal for avacopan exceeding 100-fold higher than izicopan at early time points (5 and 10 minutes), consistent with rapid initial bioactivation. This elevated reactive metabolite burden persisted over time, with avacopan remaining more than 10-fold higher than izicopan at 20 and 40 min  Izicopan’s improved chemistry, metabolic & safety features  8 

 Izicopan shows ~2x the inhibitory effect in vivo compared to avacopan  Inhibition of in vivo neutrophil activation by izicopan compared to avacopan*  Experiment: Challenge of rodents with C5a leads to neutrophil activation and consequent adherence (sticking) of neutrophils to the endothelial cell wall of vessels = mimicking a neutropenia (vehicle). This effect can be completely inhibited when C5aR activation is blocked.  Note: Izicopan dosing within this experiment exerts an approximately 4.5-fold higher plasma level 8 h after dosing when compared to the identical dosing with avacopan*.  Plasma concentration sampled at 8 hours:   izicopan doubled the in vivo inhibitory effect at comparable dose when tested head-to-head with avacopan.  The strongly improved PK features of izicopan (plasma exposure) may drive the ability to increase efficacy in vivo.  Izicopan = 538 ng/mL  Avacopan-like molecule = 119 ng/mL   2X  APPROXIMATELY  +  9  Izicopan  Source: InflaRx data on file.   *Avacopan synthesized based on the published structure and publicly available data.   Avacopan 

 ANCA-associated vasculitis (AAV)  CONTROLLING INFLAMMATION 

 ANCA-associated vasculitis (AAV)  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 affecting small vessels associated with anti-neutrophil cytoplasmic antibodies (ANCA) leading to complement activation  Prevalence  Orphan drug market  Roughly 60K - 120K in US (2021 estimate) – increasing likely due to advanced diagnosis  Roughly 75K patients in Europe  In China, microscopic polyangiitis (MPA; p-ANCA/MPO; 80-90%) is more common than GPA (granulomatosis with polyangiitis; c-ANCA/PR3) vs western countries with ~60% p-ANCA (less severe form)  Renal function is commonly impaired with prevalence in MPA > GPA   Current treatment & medical need  Induction of remission critical during flare phases  Induction treatment differs from maintenance therapy and consists of high dose corticosteroids plus either cyclophosphamide or rituximab  Induction of remission therapy has significant side effects   Source: Chen, Jayne and Zhao. Complement in ANCA-associated vasculitis: mechanism and implication for management.  A life-threatening autoimmune condition  Expression of complement activation products in renal samples from patients with AAV.  Immuno-histochemistry staining of Bb, C3d and C5b–9 in the glomerulus (a-f) and small vessels (g-l).  11 

 C5a-driven vicious cycle in ANCA  ANCAs trigger complement activation/C5a generation, leading to neutrophil activation   ANCAs can activate primed neutrophils to undergo respiratory burst and degranulation,  as well as NETosis  Neutrophil activation can lead to endothelial cell injury, NETosis and tissue damage, enhancing complement activation and C5a production  Forming a vicious cycle: ANCA/C5a -- neutrophil activation – vascular injury and NETosis – C5a generation  Proposed model for the interaction of ANCA, neutrophils and complement activation in the pathogenesis of AAV  Chen et al. Nat Rev Nephrol 2017, 13(6):359  Neutrophil activation  (O2-, enzymes, NETs)  Booster of cytokines   Vascular damage/TMA  Tissue damage  The key role of C5a/C5aR in AAV pathophysiology  12 

 Izicopan in AAV – A proven large market opportunity  * March 2026: Guggenheim Securities, market research, Yatin Suneja – Figures and estimates by Guggenheim Securities, FactSet, Evaluate Pharma.  ** April 2026: LifeSci Capital, market research, Sam Slutsky – Survey of 21 US physicians.  What US physicians think**  C5aR inhibition is typically initiated during major flares  Treatment duration varies between 6 and 48 months  C5aR inhibition is mainly used by physicians for:  Glucocorticoid reduction  Renal function preservation  Avacopan tox signals are an issue for physicians  “Product X” with an improved tox profile, faster onset of action and once-daily dosing could capture strong share of new AAV patient starts, and promote switching from avacopan:  Survey: “Product X” share of new patient starts could be 55% vs 15% for avacopan  Survey: 45% of current avacopan patients could switch to “Product X”  C5aR inhibition is a well established and accepted MoA in AAV  Izicopan´s profile could significantly expand the market >$1.3bn  Market for C5aR inhibitor avacopan (marketed as Tavneos) estimated to be ~$1.3B*  MoA has been established and accepted to drive organ dysfunction in AAV  With avacopan under regulatory scrutiny, a safer drug with faster onset and more convenient dosing could significantly expand this opportunity  $230  $454  $681  $805  $921  $1,041  $1,165  $1,270  Note: Ex-US Tavneos sales include sales booked by Amgen ex-US marketing partners.  13 

 Izicopan in AAV – Capturing the opportunity  Steroid-reducing / rapid taper label  Avacopan label does not state steroid-sparing  Demonstrate early benefit (potentially label relevant)  Early reduction of proteinuria (w4)  Improve eGFR (w26 / w52)  Improve time to remission (BVAS-0)  Clean label (no liver tox)  Lower capsule intake or once-daily dosing  “Steroids have much more toxicity than just infection. Steroids are incredible medicines - they help control these conditions, but used long-term and high dose cumulative use of these medications are extraordinarily toxic to the body, so you want to lower their use to zero, if possible.” – interview # 2  Goal: ‘Rock the Boat’ Scenario   Development improvements to focus on izicopan advantages   Key Development Improvements   Overall Goal  Increase signal delta to placebo especially during early major flare phase while demonstrating a rapid steroid tapering / reduction  Study Design Aspects  Enrolling fast = get patients on izicopan early in the flare  No mandatory GC tapering before initiation of dosing  Enrich for / allow patients with severe renal impairment  Fix SOC remission induction treatment to rituximab  Aggressive rapid steroid taper in treatment arm(s) tested versus standard steroid tapering in placebo arm  GC [glucocorticoids]. SOC [standard of care].   14  * IFRX proprietary market research. 

 GC indiv.  GC indiv.  Izicopan AAV Phase 2 trial – Base case / current planning stage   BVAS [Birmingham Vasculitis Assessment Score]. CYC [cyclophosphamide]. GC [glucocorticoids]. IZI [izicopan]. RTX [rituximab]. SOC [standard of care maintenance]. NGAL [neutrophil gelatinase-associated lipocalin]. MCP-1 [monocyte chemoattractant protein-1].  TEAEs [treatment emergent adverse events]. SAEs [serious adverse events]. TRAEs [treatment-related adverse events].  Arm 3:* IZI dose 1 BID + Rapid GC Taper + RTX  Arm 1: Placebo + Standard GC Taper + RTX  w 26  IZI dose 1 BID / QD + RTX  Placebo + RTX  Remission Maintenance  Remission Induction  Screening  GC indiv  2  4  6  8  10  12  14  16  18  20  0  2  4  6  8  10  12  14  16  18  20  0  Phase 2 over 12 mos with unblinded analysis for primary endpoint at wk 26 (6 mos), GC tapering according to SOC (PEXIVAS), izicopan arm rapid GC tapering within 4-6 wks  * Possibility to add an additional dosing arm with same GC tapering regimen switching to QD earlier – will depend on regulatory discussions  w 52  Arm 2: IZI dose 1 BID + Standard GC Taper + RTX  Izi dose 1 BID + RTX  2  4  6  8  10  12  14  16  18  20  0  Endpoint analyses   Primary: Safety  TEAEs, SAEs, TRAEs, infections + descriptive BVAS-0 non-inferiority week 26   Secondary efficacy focus  Early Proteinuria reduction: UACR delta ≥30% to placebo at Wk 4 (≥ 20% at w 2)  eGFR week 26 / 52  Time to BVAS-0 (clinical remission) + # of patients with BVAS-0 per early time points  Secondary other  Pharmacokinetics (PK)  Time in clinical remission 12 mos  GC infections / toxicity  Urine NGAL / MCP-1, other biomarkers  n = approximately 30-50 per arm  15 

 GC indiv.  GC indiv.  Izicopan AAV Phase 3 trial – Base case / current planning stage  Arm 2: IZI dose X BID/QD + Rapid GC Taper + RTX  Arm 1: Placebo + Standard GC Taper + RTX  w 26  IZI dose X BD/QD + SOC  Placebo + SOC  Remission Maintenance  Remission Induction  Screening  2  4  6  8  10  12  14  16  18  20  0  2  4  6  8  10  12  14  16  18  20  0  Phase 3 over 12 mos with unblinded analysis including for primary endpoint, GC tapering according to SOC (PEXIVAS), izicopan arm rapid GC tapering within 4-6 wks  w 52  Endpoint Analyses Scenario I  Primary endpoint*  Non-inferiority BVAS-0 (w26 + w52)+   Superiority eGFR (w26 / 52) or time to BVAS-0  Secondary endpoints  Early proteinuria reduction: UACR (w4)  Safety : TEAEs, SAEs, TRAEs,  Time in clinical remission 12 mos  GC related infections / toxicity  QOL  Endpoint Analyses Scenario II  Primary endpoint*  Superiority eGFR week 26 / 52 or time to BVAS-0  Secondary endpoints:  Safety: TEAEs, SAEs, TRAEs, + BVAS non-inferiority week 26 / week 52  Early proteinuria reduction: UACR (w4)  Time in clinical remission 12 mos  GC related infections / toxicity  QOL   Choice of primary will depend on outcome of phase II and interaction with FDA  n = approximately 150 - 170 per arm, depending on final endpoint choice and powering   * Primary endpoint efficacy will depend on Phase 2 results; potential alternatives include absolute BVAS reduction, composite measures (BVAS + renal outcomes)  BVAS [Birmingham Vasculitis Assessment Score]. CYC [cyclophosphamide]. GC [glucocorticoids]. IZI [izicopan]. RTX [rituximab].  16 

 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 regulatory path could include  Use of a “seamless” trial strategy for a ”one-shot” Phase 2 - 3 registrational trial approach  Seamless trial strategy could explore 2 doses in its first phase, including once-daily dosing, transitioning to a second phase focusing on one dosing regimen in the Phase 3 part  Potential to reduce time to the commercial market by 6 to 12 months  17 

 Additional renal indications  Development opportunities  CONTROLLING INFLAMMATION 

 C5aR proof-of-concept in AAV, other renal diseases, and broader I&I  ANCA-associated vasculitis (AAV)  Atypical hemolytic uremic syndrome (aHUS)   Immunoglobulin A nephropathy (IgAN)  Anti-C3 glomerulopathy (C3G)  nephrology  avacopan  Clinical POC for C5aR inhibitor   AAV: Approved   C3G: Phase 2 (n=22)   IgAN: Phase 2a (n=7)   aHUS: Ex-vivo (n=5)  Hidradenitis suppurativa  Chronic spontaneous urticaria  immuno-dermatology  izicopan  Phase 2a completed  Option to develop with partner  Strong preclinical POC demonstrated with C5aR inhibition  respiratory  gynecology  neurology  19 

 Potential izicopan renal disease PoC basket studies  aHUS  Compelling biology with strong evidence for C5a/neutrophil–driven endothelial injury  Fast POC with clear, regulator-accepted TMA response (biomarker) endpoint with rapid efficacy readout  Izicopan: differentiated safety with no vaccination, low infection risk, oral therapy  Monotherapy potential or as add-on / rescue to anti-C5  IgAN  Accelerated approval via biomarker surrogate (proteinuria), with eGFR stabilization as confirmatory endpoint  Autoimmune disease with immune complex–driven pathology, where C5a/C5aR1 is a clearly defined key disease mechanism.  Aligned with growing adoption of complement therapies in this kidney disease  Izicopan: no vaccination required, and low infection risk compared with other complement inhibitor such as iptacopan.  C3G  Accelerated approval pathway based on biomarker surrogate (proteinuria), with eGFR stabilization as supportive endpoint.  Strong proof-of-concept data from avacopan support C5a/C5aR1 as a validated therapeutic target pathway.  Aligned with growing adoption of complement therapies in this kidney disease  Izicopan could have oral convenience, no vaccination requirement and low infection risk compared with pegcetacoplan.  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 complement-mediated kidney disease trials  Strong potential for rapid recruitment and efficient proof-of-concept generation  aHUS [atypical hemolytic uremic syndrome]. IgAN [immunoglobulin-A nephropathy]. C3G [anti-C3 glomerulopathy].  20 

 Renal indications  aHUS (atypical hemolytic uremic syndrome)  CONTROLLING INFLAMMATION 

 aHUS is a potentially life-threatening condition that causes small blood clots and organ damage  Caused by genetic abnormalities that result in chronic uncontrolled complement activation, leading to complement-mediated TMA (thrombotic microangiopathy) in small blood vessels throughout the body.  Prevalence: aHUS alliance Global Action estimates a prevalence rate of 6.5 per million in US, over 2,000 patients in US; rising due to more sensitive diagnostic tests. (FutureMarketInsights)  Treatment: Anti C5 Abs Soliris and Ultomiris  Primary endpoint: complete TMA response*. Soliris registration trial (N=20 and N=17); Ultomiris single-arm trial (N=56). TMA improvements can be detected within days to weeks.  Figure source: Grepmed  aHUS is a systemic TMA that affects multiple organs  * Criteria for complete TMA response  Platelet count normalization (≥150 × 109/l), LDH normalization (≤246 U/l), and 25% or better improvement in serum creatinine from baseline.   A new paradigm for aHUS: C5a likely a key driver for TMA  Avacopan PoC ex vivo data suggest that the C5a/C5aR1 pathway is essential for TMA formation in aHUS patients,   consistent with in-house InflaRx data  22 

 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 deposition was not impacted, suggesting C5a/C5aR1 axis but not C5b-9 playing a critical role in platelet aggregation in aHUS  InflaRx study using the same in-vitro model demonstrate that both izicopan and vilobelimab could effectively reduce thrombus formation induced by aHUS serum.  Suggesting a new pathogenesis for aHUS  C5a  direct EC injury  thrombogenicity  C5a/C5aR1 - neutrophil  enhancing EC injury   Versus the classic paradigm of MAC (C5b-9) playing the dominant role in EC injury in aHUS  Aiello et al. blood advances 2022 (6)  aHUS: Ex vivo PoC with avacopan  23 

 Renal indications  IgA nephropathy (IgAN)  CONTROLLING INFLAMMATION 

 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 may also occur in association with other conditions, including lupus nephritis and thrombotic microangiopathy.  Disease course and symptoms  Typically, slow-progressing; may ultimately lead to acute kidney injury and chronic kidney disease, including end-stage renal disease (ESRD)  Approximately 25% of patients develop ESRD over the disease course1,2  Complement activation is a key driver of kidney inflammation and injury in IgAN, highlighting an unmet need for a safe and effective complement inhibitor to control complement-driven damage4  Iptacopan, an oral factor B inhibitor, has achieved regulatory approval  Ultomiris (ravulizumab), an anti-C5 antibody, has recently demonstrated statistically significant reductions in proteinuria, meeting the primary endpoint in Phase 3 clinical studies  Source: NIDDK  Sources: 1: Mayo Clinic. 2: NIDDK. 3: UpToDate. 4: Duval et al. Nephrol dial transplant, 2023 (38). 5: CDA, Clarivate, Opti-Brand PMR, Adelphi, ZS conjoint 2024, Spherix, data for year 2025.   IgAN: An autoimmune condition with complement activation  25 

 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 kidney  Avacopan – Blockade of C5aR1 “PoC” in Patients with IgAN  26 

 Renal indications  C3 glomerulopathy (C3G)  CONTROLLING INFLAMMATION 

 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 cure disease; relapse is common  Prevalence1: US ~10,000 cases; China ~32,000  FDA approval of pegcetacoplan (2025) in C3G/IC-MPGN set a disease-specific precedent  Proteinuria can be a primary endpoint supported by eGFR stability and mechanistic complement biomarkers.  Alternative vs classical complement pathway activation in C3G  A predominant activation of the alternative complement pathway in C3 glomerulopathy as evidenced by C3bBb staining  Zipfel et al. Cell and Tissue Research (2021) 385  Complement activation in C3G  28  1: DRG Epidemiology Report, August 2019 

 Chemocentryx Corp Presentation 2020-Dec (Accolade Trial)  Safety   Adverse event incidence similar between the two groups  Efficacy  Rapid and sustained reduction of proteinuria  Improved kidney function (eGFR) at Week 26 after treatment (P<0.05)  Improved histological index score for disease chronicity (P<0.05)  Improvement from Baseline in UPCR  Avacopan Phase 2 data in C3G  Promising results from the avacopan Accolade Phase 2 trial  N = 22 for each group  29 

 Fast PoC execution  Streamlined regulatory pathways for rare diseases, unmet needs, and strong KOL engagement support rapid enrollment  Cost efficiency  Lower clinical trial costs can improve capital efficiency and enable larger, faster PoC studies within the same budgets  Established clinical expertise and network  Strong investigator networks including key opinion leaders and city centers such as Beijing University Hospital, and population centers, support efficient recruitment and high-quality trial execution  Clear endpoint readouts  Primary readouts based on endpoint such as proteinuria reduction (UPCR), eGFR stabilization and optional biomarker profiling to confirm mechanism  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 adoption, patient acceptance, and treatment persistence  Fast, focused, Phase 2 PoC studies: Smaller sizes, optimized for early go/no-go decision in these rare renal indications   30 

 Hidradenitis suppurativa (HS)  CONTROLLING INFLAMMATION 

 FDA has acknowledged the importance of draining tunnels (dT) as a major contributor to HS disease burden  FDA supportive of development of a new endpoint in HS, the modified Hidradenitis clinical response score (mHiSCR) which, depending on validation work in a Phase 2b trial, could be used as primary endpoint in pivotal trials.   mHiSCR incorporates reduction of dT by requiring on overall 50% abscess, nodule and dT (ANdT) count reduction from baseline and separately, a 50% dT reduction from baseline as key criteria (next to no increase in abscesses and no new dT development from baseline)  InflaRx believes mHiSCR may be suitable to meaningfully control placebo response rates in HS while catering to izicopan´s MoA  Phase 2b study could provide additional insight into the clinical utility of izicopan in HS, help validate mHiSCR and dT reduction as a label relevant endpoints and establish a dose for Phase 3  HS remains a large market opportunity for izicopan: Currently further development is only envisioned in collaboration with a partner  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 pain (NRS30)  Izicopan shows promise to be a safe oral agent with biologic-like activity and a differentiated new mechanism of action  and a market potential that could exceed $1.5B per year1  1: IFRX proprietary market research, Clarivate. dT [draining tunnel].  Outcome of FDA interactions  32 

 Appendix  CONTROLLING INFLAMMATION 

 Anaphylatoxin C5a is upstream of the cytokine network   Induces histamine release – can lead to anaphylactic reactions  Boosting effect on various pro-inflammatory cytokines from various immune cells (IL-17, IL-6, IL-8, IL-1 and others)  Drives TH1 and TH17 T-cell differentiation  Strong activator of neutrophils and macrophages  Chemotaxis of neutrophils / macrophages / monocytes into tissue  O2 radical generation + granular enzyme release from neutrophils  NETosis induction (neutrophil extracellular traps)  Essential role in many inflammatory conditions  Acute and chronic inflammation and other conditions  Over 6,000 publications on role in numerous diseases  C5a  strong amplifierof inflammation  C5aR  expressed on many immune cells  and upregulated in many tissues under disease conditions  Targeting strong pro-inflammatory mechanisms  vilobelimab intravenous mAb  izicopan  oral small molecule  C5  Cleavage of C5a  through complement pathway or enzymatic  C5a/C5aR are validated targets promoting inflammation  34 

 Strong IP positions in INF904   avacopan  Among ~100 compounds synthesized with modifications to avacopan core structure in positions C3, R8 and/or R9, izicopan was selected and showed desired blocking activities and PK profile in animals.  Property  Avacopan   Izicopan  MW  581.67  653.23  cLogP  8.19  8.15  Markush Structure  Li et al. US patent No. 11,149,009 (2021.10)  izicopan  Izicopan design: Optimized avacopan backbone structure  35 

 Parameter  Unit  Dose  INF904  Avacopan*  AUCinf  h.ng/ml  3 mg  285  25  10 mg  1264  130  30 mg  5956  628  AUClast  h.ng/ml  3 mg  254  23  10 mg  1117  122  30 mg  5197  557  Cmax  ng/ml  3 mg  21.5  9  10 mg  74.8  25  30 mg  289  79  tmax  hr  3 mg  3.5  1.2  10 mg  4  1.7  30 mg  5.01  1.7  In comparison to published data for avacopan, izicopan is approximately 3-fold higher in Cmax and 10-fold higher in systemic exposure (AUClast) for comparable doses (3, 10, 30 mg)  PK results from single ascending dose (SAD) Phase 1  36  Source: Bekker et al. 2016, PLoS One; 11(10): e0164646   *Please note: Avacopan data taken from Bekker et al. 2016, PLoS One; 11(10): e0164646 are superimposed in graph for orientation. Avacopan was not included as a comparator in INF904 Phase I study.  

 PD MAD results confirm strong 90%+ C5a inhibition at C5a levels found in human diseases  This is differentiated from reported avacopan results which have shown approximately 50% inhibition at a lower challenge of 10nM C5a (7-day dosing – trough)**   Upon stimulation with 12.6 nM rhC5a (levels observed in disease state)  24 h  144 h (Day 6)  168 h (Day 7)  312 h (Day 13)  336 h (Day 14)  C5a (nM)  30QD  30BID  90BID  30QD  30BID  90BID  30QD  30BID  90BID  30QD  30BID  90BID  30QD  30BID  90BID  Blockade (%)   80  94  90  93  95  94  95  97  97  96  92  97  90  95  97  EC50 (nM)  35.6  106.2  145.6  52.4  134.7  160  74.2  149.0  268.2  92.4  126.3  465.7  94.6  110.9  238  izicopan 30 mg QD   izicopan 30 mg BID   izicopan 90 mg BID   C5a-mediated CD11b upregulation on neutrophils ex vivo  37  *EC50 (nM) is the half maximal effective C5a concentration ** Bekker et al. 2016, PLoSOne; 11(10): e0164646 

 InflaRx N.V.  CONTROLLING INFLAMMATION  Email: IR@inflarx.com  Tel: +49-3641-508180  Fax: +49-3641-508181  www.inflarx.com  Winzerlaer Str. 207745 Jena, Germany 

FAQ

What is InflaRx (IFRX) announcing about izicopan in ANCA-associated vasculitis?

InflaRx plans to develop izicopan, its oral C5a receptor inhibitor, in ANCA-associated vasculitis (AAV), a life‑threatening kidney disease. The company is conducting Phase 2 planning and assessing multiple development approaches, including a potential expedited Phase 2/3 path, to align with evolving regulatory expectations.

Which additional kidney diseases is InflaRx targeting with izicopan?

InflaRx aims to establish proof of concept for izicopan in several complement‑mediated renal diseases: aHUS, IgA nephropathy (IgAN) and C3 glomerulopathy (C3G). Open‑label studies in these indications are expected to start generating clinical data next year, alongside a pharmacokinetic bridging study in China.

How long does InflaRx expect its current cash to fund operations and development?

InflaRx estimates it has sufficient funds to support planned izicopan programs and ongoing operations through 2029. This includes proof‑of‑concept data readouts in aHUS, IgAN and C3G, the planned Phase 2 data readout in AAV, and general corporate activities over that period.

What is the commercial potential InflaRx sees for izicopan in hidradenitis suppurativa?

InflaRx believes hidradenitis suppurativa remains a significant opportunity for izicopan, with market potential that could exceed $1.5 billion per year. The company currently envisions further development in this indication only in collaboration with a partner, following supportive Phase 2a clinical data.

How does InflaRx compare izicopan to the approved C5aR inhibitor avacopan?

InflaRx describes izicopan as a potential best‑in‑class C5aR inhibitor, citing higher systemic exposure, stronger C5a blockade, a cleaner cytochrome P450 3A4 profile and more convenient dosing than avacopan. It also notes a ~$1.3 billion peak‑sales estimate for avacopan as a benchmark market opportunity.

What clinical data support izicopan’s safety and efficacy so far?

First‑in‑human and Phase 2a studies showed izicopan was well tolerated, with no reported safety signals of concern across single and multiple dosing. The drug achieved ≥90% blockade of C5a‑induced neutrophil activation and produced clinically meaningful responses in hidradenitis suppurativa and chronic spontaneous urticaria.

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