NASDAQ: IMUX

Our most advanced drug candidate, vidofludimus calcium (IMU-838), is being tested in ongoing multiple sclerosis (“MS”) trials as part of its overall clinical development program in order to support potential regulatory approvals for patients with MS in major markets.

The Phase 3 ENSURE program of vidofludimus calcium in RMS, comprising twin studies evaluating efficacy, safety, and tolerability of vidofludimus calcium versus placebo, is currently ongoing. In October 2024, we announced a positive outcome of an interim analysis of the ENSURE program, with an unblinded Independent Data Monitoring Committee ("IDMC") confirming that the predetermined futility criteria have not been met and recommending that both ENSURE trials should continue without changes, including no need for a potential increase of the sample size. In June 2025, we announced completion of enrollment for both ENSURE trials. Each of the trials enrolled adult patients with active RMS at more than 100 sites in 15 countries. In total, 1,121 patients in ENSURE-1 and 1,100 patients in ENSURE-2 have been randomized in a double-blinded fashion to either 30 mg daily doses of vidofludimus calcium or placebo. The top-line data for both ENSURE trials is expected by the end of 2026. Although we currently believe that this goal is achievable, it is dependent on numerous factors, most of which are not under our direct control and can be difficult to predict. We plan to periodically review this assessment and provide updates of material changes as appropriate.

Our Phase 2 CALLIPER trial of vidofludimus calcium in PMS was designed to corroborate vidofludimus calcium’s neuroprotective potential and to evaluate the clinical efficacy, safety and tolerability of vidofludimus calcium in a broad set of

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PMS patients to determine the suitability of advancing to a confirmatory Phase 3 program. In 2025, we announced the results from the CALLIPER trial, showing substantial and medically relevant reductions in 24-week confirmed disability progression (“24wCDW”) across patient populations and subgroups without evidence of focal inflammation; substantial and statistically significant data regarding 24-week confirmed disability improvement (“24wCDI”); and reductions in the annualized rate of thalamic brain volume loss and volume of new or enlarging T2 lesions. The data also confirmed the favorable safety and tolerability profile of vidofludimus calcium already observed in previous clinical trials.

If approved, we believe that vidofludimus calcium, with combined neuroprotective, anti-inflammatory, and antiviral effects as well as a favorable safety and tolerability profile, has the potential to be a unique treatment option targeted to the complex pathophysiology of MS. Preclinical data showed that vidofludimus calcium activates the neuroprotective transcription factor Nurr1, which is associated with direct neuroprotective effects and may enhance the potential benefit for patients. Additionally, vidofludimus calcium is a selective inhibitor of the enzyme dihydroorotate dehydrogenase (“DHODH”), which is a key enzyme in the metabolism of overactive immune cells and virus-infected cells. This mechanism is associated with the anti-inflammatory and antiviral effects of vidofludimus calcium. We believe that the combined mechanisms of vidofludimus calcium are unique in the MS space and support the therapeutic performance observed in our Phase 2 EMPhASIS trial in RRMS patients and in our Phase 2 CALLIPER trial in PMS patients. Vidofludimus calcium has shown a consistent pharmacokinetic, safety and tolerability profile in clinical trials reported, to date, and has already been exposed to more than 3,400 human subjects and patients in either of the drug’s formulations.

IMU-856 is an orally available and systemically acting small molecule modulator that targets Sirtuin 6 (“SIRT6”), a protein which serves as a transcriptional regulator of intestinal barrier function and regeneration of bowel epithelium. Based on preclinical data, we believe this compound may represent a unique treatment approach, as the mechanism of action targets the restoration of the intestinal barrier function and bowel wall architecture in patients suffering from gastrointestinal diseases such as celiac disease, IBD, GvHD and other intestinal barrier function associated diseases. Based on preclinical investigations demonstrating no suppression of immune cells, IMU-856 may have the potential to maintain immune surveillance for patients during therapy, which would be an important advantage versus immunosuppressive medications and may allow the potential for combination with available treatments in multiple gastroenterological diseases.

Data from a Phase 1b clinical trial in celiac disease patients during periods of gluten-free diet and gluten challenge demonstrated positive effects for IMU-856 over placebo in four key dimensions of celiac disease pathophysiology: protection of the gut architecture, improvement of patients’ symptoms, biomarker response, and enhancement of nutrient absorption. IMU-856 was also observed to be safe and well-tolerated in this trial. In a post hoc analysis of this Phase 1b clinical trial, IMU-856 demonstrated a dose-dependent increase of endogenous glucagon-like peptide-1 (“GLP-1”) levels. IMU-856 also showed a dose-dependent reduction of body weight gain and food consumption in preclinical in vivo testing. Contingent on financing, licensing or partnering, we are currently preparing further clinical testing of IMU-856.

We have selected the IMU-381 program to leverage our Nurr1 platform for neurologic, gastrointestinal and other autoimmune diseases. The platform comprises next-generation molecules, including a series of chemical derivatives, with improved overall properties. The IMU-381 program is currently in preclinical testing.

Additional research and development activities remain ongoing through preclinical research examining the potential to treat a broad set of neuroinflammatory, autoimmune and viral diseases with new molecules leveraging our chemical and pharmacological research platform as well as generated intellectual property in these areas. We are also exploring several options to possibly support further development of certain assets and technologies, including a potential spin-off into a new company and potential licensing transactions. Through our wholly-owned subsidiary Gliomic Therapeutics Inc., we are pursuing the use of new compounds in brain cancers leveraging our expertise in DHODH inhibition.

We expect to continue to lead most of our research and development activities from our Gräfelfing, Germany location, where dedicated scientific, regulatory, clinical and medical teams conduct their activities. Due to these teams' key relationships with local and international service providers and academic partners, we anticipate that this should result in more timely and cost-effective execution of our development programs. In addition, we are using our subsidiary in Melbourne, Australia to perform research and development activities in the Australasia region. We also conduct preclinical work in our laboratory in Martinsried, Germany and in Halle/Saale, Germany and through a collaboration with the Fraunhofer Institute.

Our business, operating results, financial condition and growth prospects are subject to significant risks and uncertainties, including delays in clinical trials, the failure of our clinical trials to meet their endpoints, failure to obtain regulatory approval and failure to obtain needed additional funding on acceptable terms, if at all, to complete the development and commercialization of our three development programs.

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Strategy

We are focused on the development of new molecules that maximize the therapeutic benefits for patients by uniquely addressing biologically relevant immunological targets. We take advantage of our established research and development infrastructure and operations in Germany and Australia to more efficiently develop our product candidates in indications of high unmet need and where the product candidates have the potential to elevate the standard of care for the benefit of patients. Given the mechanisms of action and the data generated for our product candidates, to date, we continue to execute on the clinical development of our programs for established indications as well as explore additional indications where patients could potentially benefit from the unique profiles of each product candidate.

We are currently focused on maximizing the potential of our development programs through the following strategic initiatives:

•Executing the ongoing Phase 3 ENSURE clinical trials of vidofludimus calcium in RMS.

•Determining appropriate next steps for vidofludimus calcium in PMS, following the successful completion of the Phase 2 CALLIPER clinical trial and feedback from healthcare authorities.

•Executing the IMU-856 development program, including preparation of additional clinical testing.

•Continuing preclinical research to complement the existing clinical activities, explore additional indications for potential future development and generating additional molecules for potential future development.

•Facilitating readiness for potential commercial launch of our product candidates, if regulatory approvals are received, through targeted and stage-appropriate pre-commercial activities.

•Evaluating potential strategic collaborations for each product candidate in order to complement our existing research and development capabilities and to facilitate potential commercialization of these product candidates by taking advantage of the resources and capabilities of strategic collaborators in order to enhance the potential and value of each product candidate.

Liquidity and Financial Condition

We have no products approved for commercial sale and have not generated any revenue from product sales. We have never been profitable and have incurred operating losses in each year since inception in 2016. We have an accumulated deficit of approximately $608.6 million as of December 31, 2025 and $511.4 million as of December 31, 2024. Substantially all of our operating losses resulted from expenses incurred in connection with our research and development programs and from general and administrative costs associated with our operations.

We expect to incur significant expenses and increasing operating losses for the foreseeable future as we initiate and continue the development of our product candidates and add personnel necessary to advance our pipeline of product candidates as well as prepare for potential commercialization of vidofludimus calcium. We expect that our operating losses will fluctuate significantly from quarter-to-quarter and year-to-year due to timing of development programs.

From inception through December 31, 2025, we have raised net cash of approximately $496.3 million from private and public offerings of preferred stock, common stock, pre-funded warrants and tranche rights. As of December 31, 2025, we had cash and cash equivalents of approximately $15.5 million. On February 17, 2026, we announced the closing of a private placement with net cash proceeds of approximately $187.0 million. With these funds we expect to be able to fund our operations beyond twelve months from the date of the issuance of the accompanying consolidated financial statements.

Key Status Updates

February 2026 Private Placement

Securities Purchase Agreement

On February 12, 2026, we into a securities purchase agreement (the “February Securities Purchase Agreement”) with certain accredited investors (the “February Investors”), pursuant to which we agreed to issue and sell, in a private placement (the “February 2026 Offering”), pre-funded warrants (the “February 2026 Pre-Funded Warrants”, and the shares of Common Stock issuable upon exercise of the February 2026 Pre-Funded Warrants, the “February 2026 Pre-Funded Warrant Shares”) to purchase up to 0.0001 shares of Common Stock, with each February 2026 Pre-Funded Warrant accompanied by a warrant to purchase (i) a share of Common Stock or (ii) a pre-funded warrant to purchase a share of Common Stock (collectively, the “February 2026 Common Warrants” and together with the February 2026 Pre-Funded Warrants, the “February 2026 Warrants”, and the shares of Common Stock issuable upon exercise of the February 2026 Common Warrants, the “February 2026 Common Warrant Shares”, and together with the February 2026 Pre-Funded Warrant Shares, the “February 2026 Warrant Shares”).

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The purchase price for each February 2026 Pre-Funded Warrant and accompanying February 2026 Common Warrant was $0.873120. Each February 2026 Pre-Funded Warrant is immediately exercisable at a price of $0.0001 per share. Each February 2026 Common Warrant is exercisable at a price $0.873220 per share (subject to adjustment as set forth therein) following the completion of the Reverse Stock Split (as defined below) until the earlier of (i) 30 trading days following the date of our initial public announcement of topline data from its Phase 3 ENSURE trials (for the avoidance of doubt, the later date of the initial public announcement of topline data from ENSURE-1 or ENSURE-2, if announced separately) (the “Topline Data Announcement”), (ii) immediately upon the exercise of the February 2026 Pre-Funded Warrants if such exercise of February 2026 Pre-Funded Warrants is prior to the Topline Data Announcement, provided that if the February 2026 Pre-Funded Warrant is not exercised in full, the February 2026 Common Warrant expires proportionally only to the extent the Pre-Funded Warrant is exercised, and (iii) February 17, 2031.

The Offering closed on February 17, 2026 (the “February 2026 Closing Date”).

The aggregate gross proceeds to the Company from the issuance and sale of the February 2026 Warrants was approximately $200 million, before deducting fees to be paid to the placement agents and financial advisors of the Company and other estimated offering expenses payable by the Company. The aggregate exercise price of the February 2026 Warrants is approximately $200 million.

Leerink Partners LLC acted as lead placement agent for the Offering, Stifel, Guggenheim Securities, William Blair, LifeSci Capital, B. Riley Securities and Brookline Capital Markets, a division of Arcadia Securities, LLC also acted as placement agents for the February 2026 Offering. As compensation in connection with the February 2026 Offering, we agreed to pay the placement agents a fee equal to 6% of the aggregate gross proceeds received by us (i) upon the issuance of the February 2026 Warrants at closing and (ii) upon the cash exercise of the February 2026 Common Warrants.

The Offering

We intend to use the net proceeds from the February 2026 Offering to fund our clinical trials and operations and for working capital and other general corporate purposes.

The securities issued in the February 2026 Offering have not been registered under the Securities Act, and until so registered the securities may not be offered or sold absent registration or availability of an applicable exemption from registration. There is no established public trading market for the February 2026 Warrants, and we do not intend to list such securities on any national securities exchange or nationally recognized trading system.

In connection with the February 2026 Offering, we and each February 2026 Investor entered into a registration rights agreement simultaneously with the February 2026 Securities Purchase Agreement (the “February 2026 Registration Rights Agreement”). Pursuant to the February 2026 Registration Rights Agreement, as promptly as reasonably practicable following the February 2026 Closing Date but, in any event, not later than 45 days thereafter (the “Filing Date”) we shall file a resale registration statement on Form S-3 (or Form S-1 if Form S-3 is not available) providing for the resale by the Investors of the Registrable Securities (as defined in the February 2026 Registration Rights Agreement) and to use reasonable best efforts to cause such resale registration statement to be declared effective by the staff of the Securities and Exchange Commission (the “SEC”) at the earliest possible date but no later than the earlier of (a) the 60th calendar day following the Filing Date if the SEC notifies us that it will review the registration statement and (b) the fifth business day after we are notified by the SEC that the registration statement will not be “reviewed” or will not be subject to further review or (ii) the fifth business day following the receipt of Reverse Split Stockholder Approval (as defined below) and the consummation of the Reverse Stock Split.

The February 2026 Securities Purchase Agreement and February 2026 Registration Rights Agreement contain certain representations and warranties, covenants and indemnities customary for similar transactions. The representations, warranties and covenants contained in the February 2026 Securities Purchase Agreement and February 2026 Registration Rights Agreement were made solely for the benefit of the parties to the February 2026 Securities Purchase Agreement and February 2026 Registration Rights Agreement, respectively, and may be subject to limitations agreed upon by the contracting parties.

Special Meeting and Reverse Stock Split

The February 2026 Securities Purchase Agreement provides that no later than three days following the February 2026 Closing Date, we must file a preliminary proxy statement with the SEC for the purpose of receiving stockholder approval (“Reverse Split Stockholder Approval”) of an amendment to our certificate of incorporation to effect a reverse stock split of the Company’s issued and outstanding Common Stock, at a ratio of not less than 10:1 (the “Reverse Stock Split”). The Company filed this proxy statement on February 20, 2026.

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Royalty Purchase Agreement

As previously disclosed, on June 3, 2025, the Company issued series B common stock warrants to purchase up to an aggregate of 86,666,667 shares of Common Stock (or prefunded warrants to purchase shares of Common Stock) in an underwritten public offering (the “Series B Warrants”). On February 12, 2026, the Company entered into a purchase and sale agreement (the “Royalty Purchase Agreement”) with certain Series B Warrant holders who had purchased a predetermined number of Series B Warrants (each a “Participating Series B Holder”) and BVF Partners, L.P. (“BVF”), acting as royalty interest agent (the “Warrant Exchange”).

Pursuant to the Royalty Purchase Agreement, the Participating Series B Holders will exchange an aggregate of 51,087,000 Series B Warrants for a pro rata share of an aggregate 5% synthetic royalty on future sales of the Company’s vidofludimus calcium program in any country (the “Royalty Interests”). The pro rata share for each Participating Series B Holder is equal to the number of Series B Warrants exchanged by such Participating Series B Holder divided by the number of Series B Warrants exchanged by all Participating Series B Holders (expressed as a percentage). Royalty Interests will be due and payable quarterly by the Company to the Participating Series B Holders following the First Commercial Sale (as defined in the Royalty Purchase Agreement).

Pursuant to the Royalty Purchase Agreement, the Company has agreed to specified affirmative and negative covenants, including without limitation covenants regarding periodic reporting of information by the Company to the Participating Series B Holders, and audits of royalties paid under the Royalty Purchase Agreement. The Royalty Purchase Agreement also contains representations and warranties, other covenants, indemnification obligations, and other provisions customary for transactions of this nature.

On the Closing Date, Series B Warrants to purchase up to an aggregate of 51,087,000 shares of Common Stock were surrendered by Participating Series B Holders and cancelled, and Series B Warrants to purchase up to an aggregate of 35,579,667 shares of Common Stock remain issued and outstanding.

Changes to the Board of Directors – Appointment of Director

On February 12, 2026, our board of directors (the “Board”), following the recommendation of the Nominating and Corporate Governance Committee of the Board (the “Committee”), appointed Thor Nagel, an Analyst with BVF, to the Board until the 2026 annual meeting of stockholders as a Class III director or until his respective successors are duly elected and qualified.

Changes to the Board of Directors – Appointment of Chair

On February 12, 2026, following the recommendation of the Committee, the Board appointed Simona Skerjanec, a member of the Board since July 2024, to serve as Interim Chairperson of the Board. Dr. Duane Nash, former Chairman, remains a member of the Board.

Changes to the Board of Directors – Resignation of Director

On February 12, 2026, Maria Törnsén resigned as a member of the Board in connection with the February Offering. The resignation of Ms. Törnsén was not the result of any disagreement with the Company on any matter relating to the Company’s operations, policies, or practices. The Board and the Company are deeply grateful for Ms. Törnsén’s service, dedication, and contributions to the Company.

CEO Search

Our Co-Founder and Chief Executive Officer, Dr. Daniel Vitt, and the Board will begin a search for a new CEO with deep commercial expertise in the MS space to lead Immunic through its next stage of growth and into commercialization. Subsequently, Dr. Vitt plans to transition to a new senior executive role focused on strengthening the company's scientific strategy and driving portfolio advancement. He will continue to support the organization in this capacity and as a member of the Board of Directors.

Presented Additional Phase 2 CALLIPER Trial Data for Vidofludimus Calcium at the ACTRIMS Forum 2026

On February 4, 2026, we announced the presentation of additional data from our Phase 2 CALLIPER trial of vidofludimus calcium in patients with PMS at the Americas Committee for Treatment and Research in Multiple Sclerosis (“ACTRIMS”) Forum 2026. The findings presented in two poster presentations provide additional evidence of vidofludimus calcium’s effects on key biological drivers of disease progression, including antiviral immune responses linked to Epstein-Barr virus (“EBV”)

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and magnetic resonance imaging (“MRI”) markers of both acute-focal and chronic-compartmentalized inflammation. The findings further reinforce our belief that vidofludimus calcium has the potential to address underlying mechanisms of disease progression in MS patients.

Presented Key Vidofludimus Calcium Data at the 41st Congress of ECTRIMS, Highlighting Its Potential in MS

On September 24, 2025, we announced presentations of key vidofludimus calcium data at the 41st Congress of the European Committee for Treatment and Research in Multiple Sclerosis (“ECTRIMS”). The results from our Phase 2 CALLIPER trial in PMS, also selected for the Best of ECTRIMS 2025 slide deck, highlighted vidofludimus calcium's neuroprotective potential and its promise to slow disease progression in patients with or without focal inflammation. Importantly, the consistent 24wCDW results across patient populations and subgroups, including in patients without evidence of baseline inflammatory gadolinium-enhancing (“Gd+”) lesions during MRI, were seen both in the overall population and in the primary progressive multiple sclerosis (“PPMS”) and non-active secondary progressive multiple sclerosis (“naSPMS”) subgroups. Additionally, data regarding 24wCDI showed an over two-fold probability for vidofludimus calcium over placebo, statistically significant in the overall PMS population, with consistent trends across the subtypes. The CALLIPER findings support our hypothesis of clinically measurable neuroprotective effects of vidofludimus calcium, consistent with its Nurr1 activation mechanism. We believe that, since 24wCDW is an accepted regulatory endpoint to demonstrate clinical benefit in PMS, this evidence of clinical activity merits further investigation and de-risks a potential Phase 3 program.

Moreover, at ECTRIMS, we also presented additional long-term data from the open-label extension (“OLE”) period of our Phase 2 EMPhASIS trial in RRMS which further reinforced the robust efficacy signals and favorable safety and tolerability observed, to date. The long-term EMPhASIS OLE data demonstrated that vidofludimus calcium was well-tolerated in patients with RRMS for treatment durations of up to 5.5 years. Among 182 patients remaining on therapy as of January 14, 2025, cumulative exposure totaled approximately 952 treatment years, with an annualized discontinuation rate of only approximately 6.4%. The most common treatment-emergent adverse events were mild, with low rates of renal and liver-related events and no new safety signals observed. Serious adverse events were infrequent and none were deemed related to treatment. These results suggest a favorable long-term safety and tolerability profile for vidofludimus calcium in RRMS.

Received Notice of Allowance from the United States Patent and Trademark Office Protecting Vidofludimus Calcium's Dose Strengths in PMS

On September 9, 2025, we announced that we received a Notice of Allowance from the United States Patent and Trademark Office (“USPTO”) for patent application 18/529,946, entitled "Treatment of multiple sclerosis comprising DHODH inhibitors." Specifically, the resulting patent covers dose strengths associated with vidofludimus calcium and other salt forms as well as free acid forms, at a daily dose of about 10 mg to 45 mg, for the treatment of PMS, including the sub-groups PPMS and secondary progressive multiple sclerosis (“SPMS”). The patent is expected to provide protection into 2041, and a potential Patent Term Extension may offer additional market exclusivity in the United States. Allowance of this new key patent represents a significant advancement for vidofludimus calcium program in PMS and further strengthens its robust, multi-layered intellectual property portfolio.

New, Positive Long-Term Open-Label Extension Data from Phase 2 EMPhASIS Trial of Vidofludimus Calcium in RRMS

On June 24, 2025, we announced new long-term OLE data from our Phase 2 EMPhASIS trial in patients with RRMS. The data at week 144 showed that 92.3% of patients remained free of 12wCDW, and 92.7% free of 24wCDW. A total of 29 CDW events were confirmed at 12 weeks following the trigger event through week 144. Of these, 44.8% were associated with relapse-associated worsening (“RAW”), while only 13.8% were associated with progression independent of relapse activity (“PIRA”). Additionally, the cumulative data available from the EMPhASIS OLE period, thus far, further reinforces the favorable safety and tolerability profile of vidofludimus calcium, showing low discontinuation rates and low rates of treatment-emergent and serious adverse events. Importantly, no new safety signals have emerged during treatment durations up to 5.5 years.

The Phase 2 EMPhASIS trial in RRMS includes an optional OLE period for up to 9.5 years to evaluate long-term safety and tolerability of vidofludimus calcium. Of the 268 patients that started the double-blind main treatment period, 254 patients continued in the OLE period. At the time of data cutoff on January 14, 2025, 182 patients (71.6% of patients starting OLE) were evaluated up to week 144, which translates into approximately 952 overall treatment years.

Completion of Enrollment for Both Phase 3 ENSURE Trials of Vidofludimus Calcium in RMS

On June 5, 2025, we announced completion of enrollment for both Phase 3 ENSURE trials. The ENSURE program comprises two identical multicenter, randomized, double-blind Phase 3 trials designed to evaluate the efficacy, safety and tolerability of vidofludimus calcium versus placebo in RMS patients. Each of the trials, titled ENSURE-1 and ENSURE-2,

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enrolled adult patients with active RMS at more than 100 sites in 15 countries, including the United States, India and countries in the Middle East and North Africa (“MENA”) region, Latin America, and Central and Eastern Europe. In total, 1,121 patients in ENSURE-1 and 1,100 patients in ENSURE-2 have been randomized in a double-blinded fashion to either 30 mg daily doses of vidofludimus calcium or placebo. The primary endpoint for both trials is time to first relapse up to 72 weeks. Secondary endpoints include time to confirmed disability worsening based on the expanded disability status scale ("EDSS"), volume of new T2-lesions, time to sustained clinically relevant changes in cognition, and MRI-based endpoints. The top-line data from both ENSURE trials is expected by the end of 2026, which should allow for a synchronized readout and a pooled assessment of the confirmed disability worsening secondary endpoint.

Additional Data from Phase 2 CALLIPER Trial of Vidofludimus Calcium in PMS

On June 5, 2025, we also announced additional data from our Phase 2 CALLIPER trial in PMS, further supporting the positive top-line results announced on April 30, 2025. Building on the top-line data showing reductions in the relative risk of 24wCDW events based on the EDSS at the end of the main treatment period, data for the secondary endpoint of time to 24wCDW based on the EDSS further reinforced the neuroprotective potential of vidofludimus calcium in the overall PMS patient population and in the PPMS, naSPMS and active secondary progressive multiple sclerosis (“aSPMS”) subtypes. Similarly, consistent with the top-line data, further analyses of subpopulations – both with and without inflammatory gadolinium-enhanced lesion activity at baseline, who are largely shown to not benefit from current anti-inflammatory therapies – continued to demonstrate promising results for the overall study population as well as the PPMS and naSPMS subtypes.

Vidofludimus Calcium Reduced Risk of Disability Worsening in Progressive Multiple Sclerosis Patients from Phase 2 CALLIPER Trial

On April 30, 2025, we announced the results from our Phase 2 CALLIPER trial of vidofludimus calcium in patients with PMS. In the overall PMS patient population, vidofludimus calcium reduced the relative risk of 24wCDW events based on changes in the EDSS compared to placebo. Further analyses by disease subtype demonstrated that vidofludimus calcium was associated with similar reductions in the relative risk of 24wCDW events in the PPMS and the naSPMS study populations compared to placebo. A consistent reduction of disability worsening was observed in the different subpopulations with or without inflammatory gadolinium-enhanced lesion activity at baseline and during the study. Vidofludimus calcium reduced the relative risk of 24wCDW events in patients without gadolinium-enhancing lesions at baseline compared to placebo.

While vidofludimus calcium had a modest benefit on the exploratory primary MRI endpoint, it substantially reduced the annualized rate of thalamic brain volume loss in patients with PMS compared to placebo. The total volume of new or enlarging T2 lesions showed a substantial difference between vidofludimus calcium and placebo over time, with vidofludimus calcium decreasing and placebo increasing.

The top-line CALLIPER data set supports the favorable safety and tolerability profile of vidofludimus calcium already observed in previous clinical trials. No new safety signals were identified.

IMU-856 Demonstrated Dose-Dependent Increase of GLP-1 in Celiac Disease Patients and Corresponding Effects in Preclinical Testing

On February 20, 2025, we announced that IMU-856 demonstrated a dose-dependent increase of endogenous GLP-1 levels in a post hoc analysis of patients from our Phase 1b clinical trial in celiac disease. IMU-856 also showed a dose-dependent reduction of body weight gain and food consumption in preclinical in vivo testing.

The post hoc analysis of our Phase 1b clinical trial of IMU-856 in celiac disease patients measured blood concentrations of GLP-1, between baseline and day 28, in a fasting state. A highly statistically significant (day 29: 80 mg p=0.014; 160 mg p=0.003) and dose-dependent increase of GLP-1 versus placebo control was detectable, even in the small patient population in this Phase 1b clinical trial (baseline: N placebo = 11, N 80 mg IMU-856 = 13, N 160 mg IMU-856 = 13). These clinical findings were corroborated by effects observed in a 6-month preclinical in vivo study, where IMU-856 was found to reduce body weight gain accompanied by food consumption in a dose-dependent fashion up to -40 %, compared to the control group, which was found to be linked to reduced food intake.

April 2025 Offering

On April 9, 2025, we entered into a securities purchase agreement with certain institutional and accredited investors relating to the issuance and sale of an aggregate of 5,666,667 shares of our Common Stock (the “April 2025 Shares”). The purchase price per share was $0.90 for aggregate gross proceeds of approximately $5.1 million. The offer and sale of the shares is referred to herein as the “April 2025 Offering.” The April 2025 Offering closed on April 10, 2025.

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In addition, on April 9, 2025, the Company entered into a placement agency agreement with Titan Partners Group LLC, a division of American Capital Partners, LLC (the “Placement Agent”), relating to the April 2025 Offering. Pursuant to the Placement Agency Agreement, the Company agreed to pay the Placement Agent a cash fee of 6.0% of the gross proceeds from the April 2025 Offering raised from investors and to reimburse the Placement Agent for certain costs incurred in connection therewith. Additionally, upon the closing of the April 2025 Offering, the Company agreed to issue to the Placement Agent, or its designees, warrants to purchase up to an aggregate of 283,334 shares of common stock, representing 5.0% of the shares sold in the April 2025 Offering (the “Placement Agent Warrants”). The Placement Agent Warrants are exercisable, in whole or in part, for five years from the anniversary of the Placement Agency Agreement, at an initial exercise price per share of common stock of $1.125, which is equal to 125% of the price per share to investors in the April 2025 Offering. The Placement Agent Warrants and the shares of common stock underlying the Placement Agent Warrants were offered pursuant to the exemptions from registration provided in Section 4(a)(2) under the Securities Act and Regulation D promulgated thereunder.

The net proceeds to the Company from the April 2025 Offering, after deducting commissions and the Company’s offering expenses, was approximately $4.7 million.

The April 2025 shares were registered under the Securities Act, on the Company’s Registration Statement on Form S-3 (Registration No. 333-275717), previously filed with the SEC, and declared effective on May 31, 2024.

May 2025 Equity Offering

On May 28, 2025, we entered into an underwriting agreement (the “May 2025 Underwriting Agreement”) with Leerink Partners LLC, for the issuance and sale of (i) pre-funded warrants to purchase an aggregate of 86,666,667 shares of Common stock (the “May 2025 Pre-Funded Warrants”), (ii) accompanying series A warrants to purchase an aggregate of 86,666,667 shares of Common Stock (or Pre-Funded Warrants) (the “Series A Warrants”), and (iii) accompanying series B warrants to purchase an aggregate of 86,666,667 shares of Common Stock (or Pre-Funded Warrants) (the “Series B Warrants”) (the “May 2025 Offering”). The price per May 2025 Pre-Funded Warrant and accompanying Series A Warrant and Series B Warrant was $0.7499.

Each Pre-Funded Warrant is immediately exercisable for one share of Common Stock at an exercise price of $0.0001 per share and will expire when exercised in full. The Series A Warrants are exercisable for one share of Common Stock at an exercise price of $0.75 per share. All but 10,666,667 of the Series A Warrants expired on December 31, 2025. The expiration date for the remaining 10,666,667 Series A Warrants was extended to February 28, 2026. Each Series B Warrant is exercisable on the earlier of (i) October 1, 2025, (ii) the first day following any five trading days during which the volume weighted average price for the Common Stock of the Company during such five trading day period is $1.25 or greater (the “VWAP Target”), or (iii) immediately prior to the consummation of a Fundamental Transaction (as defined in the Series B Warrants) for one share of Common Stock at an exercise price of $0.75 per share and will expire five years from the date of issuance. The holder of the Pre-Funded Warrants and Series B Warrants may also satisfy its obligation to pay the exercise price through a “cashless exercise,” in which the holder receives the net value of such warrant in shares of Common Stock determined according to the formula set forth in the applicable warrant.

The aggregate proceeds from the May 2025 Offering were approximately $65 million before deducting underwriting discounts and commissions and offering expenses payable by the Company in connection with the May 2025 Offering. On February 12, 2026, as part of the Royalty Purchase Agreement, 51,087,000 warrants were exchanged for the right to share a 5% royalty and 35,579,667 Series B warrants are still outstanding (see note 12 "Subsequent events"). The Company may receive up to an aggregate of approximately $27 million of additional gross proceeds if the remaining Series B Warrants are exercised in full for cash and up to $8.0 million gross proceeds if the remaining Series A Warrants are exercised for cash. Pursuant to the Placement Agency Agreement, the Company agreed to pay the Placement Agent a cash fee of 6.0% of the gross proceeds from the May 2025 Offering raised from investors and to reimburse the Placement Agent for certain costs incurred in connection therewith.

The May 2025 Offering was made pursuant to an effective registration statement on Form S-3 (Registration Statement No. 333-275717), as amended, previously filed with the SEC on November 22, 2023, and declared effective by the SEC on May 31, 2024, as supplemented by the preliminary prospectus supplement, dated May 28, 2025, and a final prospectus supplement filed with the SEC pursuant to Rule 424(b) under the Securities Act, on May 30, 2025. The closing of the May 2025 Offering took place on June 3, 2025.

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Transfer of Nasdaq Market Listing and Notice of Non-Compliance with Nasdaq Listing Rule 5450(a)(1)

On January 5, 2026, we were notified by the Nasdaq Listing Qualifications Department of The Nasdaq Stock Market LLC (“Nasdaq”) that our application to transfer the listing of our Common Stock from the Nasdaq Global Select Market to the Nasdaq Capital Market had been approved (the “Approval”). The common stock was transferred to the Nasdaq Capital Market at the opening of business on January 7, 2026. The common stock will continue to trade under the symbol “IMUX.” The Nasdaq Capital Market operates in substantially the same manner as the Nasdaq Global Select Market, and listed companies must meet certain financial requirements and comply with Nasdaq’s corporate governance requirements.

As previously disclosed, on June 27, 2025, we received a letter from Nasdaq indicating that we were not in compliance with Nasdaq Listing Rule 5450(a)(1) because the closing bid price per share for Common Stock had closed below $1.00 for the previous 30 consecutive business days (the “Bid Price Rule”). We were given a 180-day grace period, until December 24, 2025, to regain compliance with the rule. We had not regained compliance with the Bid Price Rule by December 24, 2025. Therefore, we transferred the listing of our Common Stock from the Nasdaq Global Select Market to the Nasdaq Capital Market. As a result of the Approval, we have been granted an additional 180-day grace period, or until June 22, 2026, to regain compliance with the Bid Price Rule. To regain compliance with the Bid Price Rule and qualify for continued listing on the Nasdaq Capital Market, the minimum bid price per share of the Common Stock must be at least $1.00 for at least 10 consecutive business days on or prior to June 22, 2026. If we fail to regain compliance during the additional compliance period, then Nasdaq will notify us of its determination to delist the Common Stock, at which point we would have an opportunity to appeal the delisting determination to a Nasdaq Listing Qualifications Panel (the “Panel”), but there can be no assurance that the Panel would grant our request for continued listing. As a condition of the Approval imposed by Nasdaq Listing Rule 5810(c)(3)(a)(i), we notified Nasdaq that it would seek to implement a reverse stock split, if necessary, to regain compliance with the Bid Price Rule. The Company filed a proxy statement to obtain shareholder approval for a reverse stock split on February 20, 2026.

Product Acquisition History

Our wholly-owned German subsidiary Immunic AG acquired vidofludimus calcium in September 2016 through an asset acquisition from 4SC AG (hereinafter, “4SC”), a publicly traded company based in Planegg-Martinsried, Germany. On March 31, 2021, Immunic AG and 4SC entered into a Settlement Agreement, pursuant to which Immunic AG settled its remaining obligation of a 4.4% royalty on net sales for $17.25 million. The payment was made 50% in cash and 50% in shares of Immunic’s common stock.

Our rights to IMU-856 are secured pursuant to an option and license agreement (the “Daiichi Sankyo Option”) with Daiichi Sankyo Co., Ltd. (hereinafter, "Daiichi Sankyo") in Tokyo, Japan. On January 5, 2020, Immunic AG exercised its option under the Daiichi Sankyo Option to acquire the exclusive global rights to commercialize IMU-856. The license also grants Immunic AG the rights to Daiichi Sankyo’s patent application related to IMU-856. Concurrent with the option exercise, Immunic AG paid to Daiichi Sankyo a one-time upfront licensing fee. Going forward, Daiichi Sankyo is eligible to receive future development, regulatory and sales milestone payments, as well as royalties related to IMU-856.

Leadership

We are led by a team of dedicated and committed experienced professionals with an entrepreneurial spirit and track record of successful licensing transactions in the healthcare industry, worldwide. The team brings together several decades of leadership experience in the pharmaceutical industry with a strong scientific background and sound knowledge in drug discovery, product development, chemistry, manufacturing and controls processes, intellectual property, clinical trial design, health economics and market access, commercial launch, merger and acquisitions, capital markets, corporate finance, business development, regulatory affairs and project valuation. Our team members are inventors on project-related patents and have successfully published project-related scientific publications.

Product Candidates

Vidofludimus Calcium (IMU-838)

Vidofludimus calcium is a small molecule investigational drug in development as an oral next-generation treatment option for patients with MS and other chronic inflammatory and autoimmune diseases. If approved, we believe that vidofludimus calcium, with combined neuroprotective, anti-inflammatory, and antiviral effects as well as a favorable safety and tolerability profile, has the potential to be a unique treatment option targeted to the complex pathophysiology of MS.

Preclinical data showed that vidofludimus calcium activates the neuroprotective transcription factor Nurr1, which is associated with direct neuroprotective properties and may enhance the potential benefit for patients. Nurr1 activation mediates its neuroprotective function by acting in microglia, astrocytes and neurons. In microglia and astrocytes, Nurr1 activation leads

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to a reduction of pro-inflammatory cytokines and blocks the production of direct neurotoxic agents like reactive oxygen species (“ROS”) and nitric oxide (“NO”). Enhanced Nurr1 activity in neurons mediates neuronal survival and differentiation, as well as improved neurotransmission. Therefore, activation of Nurr1 by vidofludimus calcium may halt neurodegeneration and disability progression in patients suffering from MS and other degenerative diseases.

Additionally, vidofludimus calcium is a selective inhibitor of the enzyme DHODH, which is a key enzyme in the metabolism of overactive immune cells and virus-infected cells. This mechanism is associated with the anti-inflammatory and antiviral effects of vidofludimus calcium. By inhibiting DHODH, a key enzyme of pyrimidine de novo biosynthesis, highly metabolically active T and B immune cells experience metabolic stress, which leads to a modulation of their activity and function. By addressing only highly metabolically active immune cells, vidofludimus calcium may reduce focal inflammation in the brain, without impacting normal acting immune cells.

Based on the selectivity toward metabolically activated cells, with a high need for ribonucleic acid and deoxyribonucleic acid production, DHODH inhibition also leads to a direct antiviral effect, which has been observed in various virus infected cells, such as EBV infections, hepatitis C virus infections, severe acute respiratory syndrome coronavirus 2 (“SARS-CoV-2”) infections, cytomegalovirus infections and even hemorrhagic fever-causing viruses, such as Arena virus infections. Treatment with vidofludimus calcium may avoid virus infections and reactivations, one of the major drawbacks of the long-term use of traditional immunomodulators. In addition, the blockage of reactivation of EBV could be of highest importance for MS patients, as infection with and reactivation of EBV was brought into connection with disease onset and progression (Bjornevik et al., 2022/Lanz et al., 2022/Schneider-Hohendorf et al., 2022).

Efficacy of vidofludimus has been observed in several animal disease models for MS, IBD, as well as systemic lupus erythematosus and transplant rejection. Previous filings by us with the SEC have summarized the development history of vidofludimus and the previous amorphous formulation of the free acid form of vidofludimus. After the asset acquisition from 4SC, we developed and filed several new patent applications for a new specific polymorph of the calcium salt formulation of vidofludimus, vidofludimus calcium, which we believe exhibits improved physicochemical and pharmacokinetic (“PK”) properties.

In 2017, we completed two Phase 1 studies of single or repeated once-daily doses of vidofludimus calcium in healthy human subjects, where we observed results supporting tolerability of repeated daily dosing of up to 50 mg of vidofludimus calcium.

We also completed a Phase 1 trial in a total of 24 patients with either no liver function impairment or liver disease of Child-Pugh A Child-Pugh B grade which was designed to explore dose optimization of vidofludimus calcium. The study showed little influence on the PK of vidofludimus calcium in patients with Child-Pugh A Child-Pugh B liver impairment.

Currently, several clinical pharmacology studies and related analyses are ongoing that are intended to support regulatory filings of vidofludimus calcium.

Indication: Multiple Sclerosis

Diagnosis and Prevalence

MS is an autoimmune disease that affects the brain, spinal cord and optic nerve. In MS, myelin, the coating that protects the nerves, is attacked and damaged by the immune system. Thus, MS is considered an immune-mediated demyelinating disease of the central nervous system ("CNS"). MS is a progressive disease which, without effective treatment, leads to severe disability. We are developing vidofludimus calcium for the treatment of RMS and PMS.

RMS is the most common form of MS. Approximately 85% of patients with MS are expected to develop RMS, with some patients developing more progressive forms of the disease. RMS is characterized by clearly defined attacks of new or increasing neurologic symptoms. These relapses are followed by periods of remissions, or partial or complete recovery. During remissions, all symptoms may disappear, or some symptoms may continue and become permanent.

PMS includes primary progressive MS (“PPMS”) and secondary progressive MS (“SPMS”). PPMS is characterized by steadily worsening neurologic function from the onset of symptoms without initial relapse or remissions. SPMS is identified following an initial relapsing-remitting course, after which the disease becomes more steadily progressive, with or without other disease activity present. Active SPMS, the progressive disease form where relapses and MRI lesions are still present, is generally counted to the RMS spectrum. The forms of SPMS that are considered part of the PMS spectrum are non-active SPMS (where disability worsening occurs despite no relapses observed in the last 24 months and no MRI lesions present in the last 12 months) or non-relapsing SPMS (where no relapses occurred in the last 24 months, but MRI lesions may be present at any time).

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MS is a disease with unpredictable symptoms that can vary widely. Common early signs of MS include vision problems, tingling and numbness or other unspecific neurological symptoms. Diagnosis of MS can be confirmed via blood tests and a spinal tap, in which a small sample of fluid is removed from the spinal cord. However, most important for diagnosis are characteristic CNS lesions detected by MRI.

According to the National Multiple Sclerosis Society (2019), there are nearly one million patients in the United States living with MS. The MS International Federation (2021) indicates there are more than one million patients with MS in Europe as well. The disease has a large economic impact as it affects mainly young adults in the prime working age, peaking around 30 years old, although MS can occur in children and in adults. MS is up to three times more common in women than in men (Green J, Dunn WH 2012). MS affects twice as many women and men in certain age cohorts and is more common in areas inhabited by people of northern European ancestry, such as Europe, the United States, Canada, New Zealand and parts of Australia.

Evolution in Understanding of Disease Drivers of MS

The presence of a “smoldering disease” in the background of MS that leads to PIRA was suggested by a large meta-analysis of clinical data in more than 35,000 MS patients (Lublin et al., 2022). PIRA was traditionally believed to be the dominant driver of disease worsening in PMS and this was confirmed by this study as well. However, the study also found that approximately half of the disability accumulating in RMS patients were not related to relapse activity. This suggests that other mechanisms including PIRA already contribute half of the disability to disease progression in RMS – already from early stages of the disease. In addition, this investigation found that currently available drugs were able to delay or avoid disability associated with relapse activity but were unable to diminish the impact of PIRA. This confirms that PIRA presumably is caused by a process that is not addressed by currently used anti-inflammatory medications which predominantly address focal inflammation in MS. Therefore, the medical need to find treatments with a neuroprotective potential to substantially influence PIRA remains high.

Bjornevik et al. (2022) shed additional light on the role of EBV infection previously postulated to trigger MS. They analyzed EBV antibodies in serum from 801 individuals who developed MS among a cohort of more than 10 million people active in the US military over a 20-year period (1993 to 2013). Risk of MS increased 32-fold after infection with EBV but was not increased after infection with other viruses, including the similarly transmitted cytomegalovirus. Serum levels of neurofilament light chain (“NfL”), a biomarker of axonal damage, increased only after EBV seroconversion. These findings cannot be explained by any known risk factor for MS and suggest EBV as the leading cause of MS. In addition, antibody producing cells directed against the latent EBV protein EBNA1 were found in the cerebrospinal fluid of MS patients. Cross reactivity of anti-EBNA1 antibodies against GlialCAM, a protein that is predominantly expressed in glial cells in the CNS and potentially important in the myelination process of axons, further corroborates the connection between EBV infections and pathologic processes in MS (Lanz et al., 2022). Schneider-Hohendorf et al. (2022) investigated the T cell repertoire in MS patients and control populations, basically highlighting the top antigens that are seen by T cells on an ongoing basis. The study found that EBV-related antigens were on top of the list of antigens seen by T cells in MS patients but not in other EBV-infected populations. These results suggest that ongoing EBV reactivation seems to be an ongoing trigger for the immune system in MS patients and may be the trigger for disease progression and ongoing neurodegenerative processes.

Current Treatment Options

There are currently two main approaches to treating RMS. Some therapies, such as short-term corticosteroid medications, are used for treating relapses of MS symptoms. Other approaches are used as long-term treatments to reduce the number of relapses and prevent or slow down disability progression. The latter are referred to as disease-modifying therapies. We intend to develop vidofludimus calcium as a disease-modifying therapy for MS.

Historically, the initial treatment options for RMS patients are often beta interferons (either as interferon beta-1a or interferon beta-1b) or glatiramer acetate, all of which are given by injection. In addition, there are several oral medications, such as dimethyl fumarate, fingolimod, siponimod, ponesimod, teriflunomide, ozanimod or cladribine, and biologics, such as natalizumab, ocrelizumab, ublituximab, ofatumumab or alemtuzumab, approved for commercial use in MS in various countries. All of these medications are commonly used across the spectrum of patients with RMS. Some of these drugs have generic versions available in some countries and other drugs will become generic in the next years.

With regard to PMS, there is currently only one drug approved: Ocrevus® (ocrelizumab) specifically for the treatment of PPMS. There are no relevant treatments available in the United States for non-active SPMS. Other available medications in MS have previously been tested in different forms of PMS, such as siponimod in the Phase 3 EXPAND trial in SPMS patients. Although the study found a statistically significant effect in active SPMS patients, the treatment for non-active SPMS patients

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remained elusive. It also highlighted the fact that currently available anti-inflammatory treatments in RMS may in general have no utility in non-active SPMS as the disease progress may be predominantly driven by “smoldering disease” rather than focal inflammation. Therefore, the unmet medical need in PMS remains high, in particular for the non-active SPMS patient population, where the highest medical need for new therapies exists.

Bruton's tyrosine kinase inhibitors (“BTKi”) have been developed and assessed for both relapsing forms of MS and progressive forms such as PPMS and SPMS. Evobrutinib’s development was ultimately stopped after Phase 3 trials failed to meet their primary endpoints, leading to discontinuation for lack of efficacy. Tolebrutinib’s development faced regulatory challenges due to reports of liver toxicity, resulting in a partial clinical hold by the U.S. Food and Drug Administration (“FDA”). Most recently, Phase 3 trials for this product failed to meet their primary endpoint in the RMS indication, and in December 2025, the FDA issued a complete response letter clarifying they could not establish a favorable benefit-risk profile for tolebrutinib for indication non-relapsing SPMS. Fenebrutinib remains in Phase 3 studies, with one of two studies in RMS reported to have met the primary endpoint, and an additional Phase 3 study in PPMS reported to have met the primary endpoint as well. Remibrutinib also continues its clinical development.

It is generally accepted that current disease-modifying therapies (“DMTs”) are effective in controlling acute focal neuroinflammation resulting in symptoms related to a relapse, however, so far, available DMTs seem to lack significant efficacy effects against progression of the disease independent of MS activity and relapses resulting from smoldering processes such as compartmentalized neuroinflammation and neurodegeneration. These, together with improved safety and tolerability profiles, are considered key unmet needs for the treatment of MS.

There is no specific guidance on which therapies or medications are used in which sequence of the MS disease course. Typically, treatments are escalated over time, considering:

•Level and progression of MS disease activity (relapse(s), disability worsening, MRI lesions),

•Risks of long-term immunosuppression,

•Patient preferences or risks perceptions, and

•Safety/tolerability aspects.

Many drugs approved for patients with RMS work through anti-inflammatory mechanisms by suppressing the immune system, either broadly or by targeting classes of immune cells, altering how the immune system functions and fights certain infections. As a result, people who take these therapies are at higher risk for John Cunningham virus infection or re-activation, which is believed to be the cause of a rare and often lethal viral disease of the brain called progressive multifocal leukoencephalopathy ("PML"). To date, occurrences of PML have been reported in individuals with RMS treated with natalizumab, ocrelizumab, dimethyl fumarate and fingolimod. No case of PML has yet been reported for the DHODH inhibitor teriflunomide, which has been one of the key differentiators of teriflunomide from other disease-modifying therapies in RMS. The active moiety of vidofludimus calcium has also shown direct antiviral effects in multiple models of virus-infected cells, which we believe is caused by DHODH inhibition. Of specific interest, vidofludimus calcium reduces the reactivation of EBV in a dose dependent fashion which was demonstrated in latently EBV-infected cell models. Subject to further clinical trials, we believe that could be an important potential differentiator against other drug classes in RMS.

Current Development Plan and Clinical Studies

Depending on the results of our ongoing clinical trials, we believe that vidofludimus calcium has the potential to demonstrate medically important advantages versus other treatments, due to its safety and tolerability profile as well as its neuroprotective, anti-inflammatory, and anti-viral effects observed, to date. Vidofludimus calcium could provide MS patients with a distinctive therapy that is uniquely matched to the biological drivers of MS. In clinical trials, to date, it has shown data indicating:

•Lower rates of confirmed disability worsening and increased rates of confirmed disability improvement.

•Robust MRI lesion suppression, comparing favorably to other medications commercially available for RMS.

•A robust decrease in serum NfL, a biomarker for axonal damage, observed in patients with both RMS and PMS.

•Potent Nurr1 activation, which is involved in protection of relevant neurons from cell death.

•A targeted effect on hyperactive immune cells without suppression of normal immune function.

•Favorable safety and tolerability profile, with low rates of treatment-emergent adverse events, serious adverse events and adverse events leading to treatment discontinuations, distinguishing vidofludimus calcium from other oral RMS treatments.

•A very low discontinuation rate for MS patients, which indicates an encouraging combination of tolerability and efficacy as well as maintenance of normal quality-of-life.

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•A broad spectrum antiviral effect, which may support lowering the rate of viral infections and reactivations, including EBV reactivation, potentially resulting in slowing potential EBV-related neurodegenerative processes.

Phase 2 Clinical Trial of Vidofludimus Calcium in RRMS (EMPhASIS Trial)

Our Phase 2 EMPhASIS trial of vidofludimus calcium in RRMS consisted of two cohorts: The full data set of Cohort 1, which evaluated efficacy and safety of 30 mg or 45 mg once daily vidofludimus calcium compared to placebo, was published in August and September 2020, respectively. The Cohort 1 results were subsequently published in the peer reviewed journal, Annals of Clinical and Translational Neurology (Fox et al., 2022). The results of Cohort 2, which evaluated efficacy and safety of 10 mg once daily vidofludimus calcium compared to placebo, were published in February 2022. The combined Cohort 1 and 2 results were published in the peer reviewed journal, Neurology® Neuroimmunology & Neuroinflammation, an official journal of the American Academy of Neurology (Fox et al., 2024).

On August 2, 2020, we announced positive top-line data from our Phase 2 EMPhASIS trial of vidofludimus calcium in patients with RRMS. The trial achieved statistical significance on all primary and key secondary endpoints, indicating activity in RRMS patients. In particular, the trial met its primary endpoint, demonstrating a statistically significant reduction in the cumulative number of combined unique active (“CUA”) MRI lesions up to week 24 in patients receiving 45 mg of vidofludimus calcium once daily, by 62% (p=0.0002), as compared to placebo. The trial also met its key secondary endpoint, showing a statistically significant reduction in the cumulative number of CUA MRI lesions for the 30 mg once daily dose by 70% (p<0.0001), as compared to placebo. On September 11, 2020, we published the full unblinded clinical data set from our Phase 2 EMPhASIS trial of vidofludimus calcium in patients with RRMS. The data confirmed and expanded on the previously announced top-line results.

On April 15, 2021, we announced interim data from Cohort 2 after 59 randomized patients completed week 12 MRI assessments. We concluded from this data, along with previously published data from Cohort 1, that 30 mg once daily vidofludimus calcium is the most appropriate anti-inflammatory dose for Phase 3 clinical trials in patients with RMS.

On February 24, 2022, we published final data from Cohort 2 showing that the anti-inflammatory effects of vidofludimus calcium at the 10 mg dose were observed to be lower (13% reduction of gadolinium-enhancing MRI lesions up to 24 weeks, as compared to placebo) than those found with the 30 mg vidofludimus calcium dose in the pooled Cohort 1 and 2 data (78% reduction), providing further support for the selection of 30 mg dosing in the ongoing ENSURE trials in RMS. Final Cohort 2 data also provided evidence of dose-proportional neuroprotective activity. For instance, the highest decrease of the biomarker serum NfL was observed with the 45 mg dose of vidofludimus calcium versus placebo (-26.0% median of differences between percentage change of serum neurofilament, Hodges-Lehmann estimation), a substantial decrease was seen with the 30 mg dose (-18.0%), while the smallest decrease was observed with the 10 mg dose of Cohort 2 (-9.0%). The 10 mg group in Cohort 2 also showed a signal with respect to improvement in EDSS, consistent with those signals seen with the higher doses in Cohort 1, although all of these early signals need to be confirmed in a larger patient population with longer follow-up periods. Taken together, these last two observations suggest that higher doses, such as 45 mg vidofludimus calcium, may be preferred doses for clinical trials in which neuroprotective effects are the main mechanism for improvement, such as in PMS.

The Phase 2 EMPhASIS trial in RRMS includes an optional long-term open-label extension (“OLE”) period for up to 9.5 years to evaluate long-term safety and tolerability of vidofludimus calcium. Of the 268 patients that started the double-blind main treatment period, 254 patients continued in the OLE period.

On November 17, 2022, we reported an interim analysis of the long-term OLE period with data extraction in October 2022, when 209 patients remained on treatment in the OLE phase, some of whom have already received more than 180 continuous weeks (approximately four years) of active treatment with vidofludimus calcium. Long-term open-label treatment with vidofludimus calcium was associated with a low rate of confirmed disability worsening over time, comparing favorably to historical trial data for currently available MS medications. During the 24-week double-blind main treatment period, 12wCDW and 24wCDW events occurred in 1.6% of subjects in the combined vidofludimus calcium treatment arms as compared to 3.7% in the placebo group. In the OLE phase, the proportion of patients free from 12wCDW was 97.6% after 48 weeks and 94.5% after 96 weeks of vidofludimus calcium treatment as compared to the start of the OLE phase. Similar results were observed for 24wCDW and sustained CDW. The OLE phase also showed low relapse activity.

On June 24, 2025, we announced additional long-term OLE data from the EMPhASIS trial. The data at week 144 showed that 92.3% of patients remained free of 12wCDW, and 92.7% free of 24wCDW. A total of 29 CDW events were confirmed at 12 weeks following the trigger event through week 144. Of these, 44.8% were associated with RAW, while only 13.8% were associated with PIRA. Additionally, the cumulative data available from the EMPhASIS OLE period, thus far, further reinforced the favorable safety and tolerability profile of vidofludimus calcium, showing low discontinuation rates and low rates of

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treatment-emergent and serious adverse events. Importantly, no new safety signals have emerged during treatment durations up to 5.5 years. The most common treatment-emergent adverse events were mild, with low rates of renal and liver-related events. Serious adverse events were infrequent and none were deemed related to treatment. At the time of data cutoff on January 14, 2025, 182 patients were evaluated up to week 144, which translates into approximately 952 overall treatment years, with a low annualized discontinuation rate of approximately 6.4%.

As of January 2026, more than 170 patients continue to be treated in the OLE phase of the EMPhASIS trial, with more than five total treatment years.

Further information regarding our EMPhASIS trial in RRMS can be found on ClinicalTrials.gov under the identifier NCT03846219.

Phase 3 Program of Vidofludimus Calcium in RMS (ENSURE-1 and ENSURE-2 Trials)

On July 1, 2021, we announced FDA clearance of our Investigational New Drug (“IND”) application for the Phase 3 ENSURE program of vidofludimus calcium in patients with RMS. The ENSURE program comprises two identical multicenter, randomized, double-blind Phase 3 clinical trials designed to evaluate the efficacy, safety, and tolerability of vidofludimus calcium versus placebo in RMS patients. The primary endpoint for both clinical trials is time to first relapse up to 72 weeks. Secondary endpoints include total number of new and /or enlarging T2 MRI lesions, time to confirmed disability worsening based on EDSS, number of gadolinium enhancing T1 MRI lesions, and other clinical and MRI-based endpoints. With regard to the endpoints assessing disability, the ENSURE program will apply a synchronized readout and a pooled assessment across both clinical trials.

The ENSURE trials are being run concurrently. The first patient in ENSURE-1 was enrolled in November 2021. The first patient in ENSURE-2 was enrolled in January 2022. On June 5, 2025, we announced completion of enrollment for both ENSURE trials. Each of the trials enrolled adult patients with active RMS at more than 100 sites in 15 countries, including the United States, India and countries in the MENA region, Latin America, and Central and Eastern Europe. In total, 1,121 patients in ENSURE-1 and 1,100 patients in ENSURE-2 have been randomized in a double-blinded fashion to either 30 mg daily doses of vidofludimus calcium or placebo. The top-line data for both ENSURE trials is expected by the end of 2026.

On October 22, 2024, we announced a positive outcome of an interim analysis of our Phase 3 ENSURE program. An unblinded IDMC confirmed that the predetermined futility criteria have not been met and recommended that both ENSURE trials should continue without changes. The IDMC considered if a sample size adjustment would be appropriate for either of the two trials based on factors that include statistical analysis and ultimately recommended that the sample sizes for both trials should remain unchanged.

Based on vidofludimus calcium’s highly significant activity in preventing lesion formation in our Phase 2 EMPhASIS trial in RRMS, the strong and consistent correlation observed between lesion formation and clinical relapse in third-party clinical trials, and the drug’s robust safety profile, to date, we believe that this Phase 3 program should provide a straightforward path towards potential regulatory approval of vidofludimus calcium in RMS.

Further information regarding our ENSURE program in RMS can be found on ClinicalTrials.gov under the identifiers NCT05134441 (ENSURE-1) and NCT05201638 (ENSURE-2), respectively.

Phase 2 Clinical Trial of Vidofludimus Calcium in PMS (CALLIPER Trial)

On July 1, 2021, we announced that the FDA also cleared our separate IND application for the Phase 2 CALLIPER trial of vidofludimus calcium in patients with PMS. The multicenter, randomized, double-blind, placebo-controlled trial was designed to corroborate vidofludimus calcium’s neuroprotective potential and to evaluate the clinical efficacy, safety and tolerability of vidofludimus calcium in a broad set of PMS patients to determine the suitability of advancing to a confirmatory Phase 3 program. The first patient was enrolled in September 2021. Completion of enrollment was announced in August 2023, with 467 patients with primary PMS, or active or non-active secondary PMS enrolled at more than 70 sites in North America, Western, Central and Eastern Europe. Patients were randomized to either 45 mg daily doses of vidofludimus calcium or placebo in a double-blinded fashion.

On October 9, 2023, we announced positive interim data from the CALLIPER trial, showing biomarker evidence that vidofludimus calcium’s activity extends beyond the previously observed anti-inflammatory effects, thereby further reinforcing its neuroprotective potential.

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On April 30, 2025, we announced the results from our Phase 2 CALLIPER trial. In the overall PMS patient population, vidofludimus calcium reduced the relative risk of 24wCDW events based on changes in the EDSS compared to placebo. Consistent reductions in disability worsening were observed in the PPMS and naSPMS subtypes as well as in different subpopulations with or without inflammatory gadolinium-enhanced lesion activity at baseline and during the study. While vidofludimus calcium had a modest benefit on the exploratory primary MRI endpoint, it substantially reduced the annualized rate of thalamic brain volume loss in patients with PMS compared to placebo. The total volume of new or enlarging T2 lesions showed a substantial difference between vidofludimus calcium and placebo over time, with vidofludimus calcium decreasing and placebo increasing. The top-line CALLIPER data set supports the favorable safety and tolerability profile of vidofludimus calcium already observed in previous clinical trials. No new safety signals were identified.

On June 5, 2025, we announced additional data from our Phase 2 CALLIPER trial. Building on the top-line data showing reductions in the relative risk of 24wCDW events based on the EDSS at the end of the main treatment period, data for the secondary endpoint of time to 24wCDW based on the EDSS further reinforced the neuroprotective potential of vidofludimus calcium in the overall PMS patient population and in the PPMS, naSPMS and active secondary progressive multiple sclerosis (“aSPMS”) subtypes. Similarly, consistent with the top-line data, further analyses of subpopulations – both with and without inflammatory gadolinium-enhanced lesion activity at baseline, who are largely shown to not benefit from current anti-inflammatory therapies – continued to demonstrate promising results for the overall study population as well as the PPMS and naSPMS subtypes.

On September 24, 2025, we announced presentations of key vidofludimus calcium data at the 41st Congress of ECTRIMS. The results from our Phase 2 CALLIPER trial, also selected for the Best of ECTRIMS 2025 slide deck, highlight vidofludimus calcium's neuroprotective potential and its promise to slow disease progression in patients with or without focal inflammation. Importantly, the consistent 24wCDW results across patient populations and subgroups, including in patients without evidence of baseline inflammatory Gd+ lesions during MRI, were seen both in the overall population and in the PPMS and naSPMS subgroups. Additionally, data regarding 24wCDI showed an over two-fold probability for vidofludimus calcium over placebo, statistically significant in the overall PMS population, with consistent trends across the subtypes. The CALLIPER findings support the hypothesis of neuroprotective effects of vidofludimus calcium, consistent with its Nurr1 activation mechanism. We believe that, since 24wCDW is an accepted regulatory endpoint to demonstrate clinical benefit in PMS, this evidence of clinical activity merits further investigation and de-risks a potential Phase 3 program.

We have conducted regulatory interactions with health authorities, including the FDA and the European Medicines Agency (“EMA”), following the data from the CALLIPER trial. These interactions were intended to obtain regulatory feedback on the clinical data package and to discuss potential next steps for the further development of vidofludimus calcium in PMS. The feedback received from the FDA included considerations related to the overall benefit-risk profile of vidofludimus calcium in the PMS population, the need for additional clinical data to support potential registration, and the context of available approved therapies. We believe that this feedback provides a clear path forward for starting a confirmatory program for vidofludimus calcium in PMS populations.

As of January 2026, more than 350 patients continue to be treated in the OLE phase of the CALLIPER trial.

Further information regarding our CALLIPER trial in PMS can be found on ClinicalTrials.gov under the identifier NCT05054140.

Vidofludimus Calcium Registration Plan

All of our drug development candidates require approval from the FDA (for the United States), EMA (for the European Union) and other national competent authorities (for any other territory) before they can be marketed for sale in the applicable jurisdiction. The activities required before drugs or biologics may be marketed in the United States include:

•In vitro and in vivo preclinical safety and mechanistic studies and formulation and stability studies;

•the submission to the FDA of an investigational new drug application for human clinical testing, which is known as an IND;

•adequate and well-controlled human clinical trials to demonstrate the safety and effectiveness of the drug;

•satisfactory completion of an FDA inspection of the manufacturing facility or facilities at which the drug is produced to assess compliance with current good manufacturing practice (“cGMP”), requirements to assure that the facilities, methods and controls are adequate to preserve the drug’s identity, strength, quality and purity;

•the submission to the FDA of a new drug application, which is known as an NDA, for a drug; and

•the approval by the FDA of an NDA.

The FDA reviews all available data relating to safety, efficacy and quality and assesses the risk/benefit profile of a product candidate before granting approval. The data assessed by the FDA in reviewing an NDA includes preclinical testing data,

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including animal data, chemistry, manufacturing and controls (“CMC”) data, PK, pharmacodynamic (“PD”) and drug-drug interaction data, as well as human clinical safety and efficacy data. Moreover, an agreement for a pediatric development plan (“PSP”) is required to be achieved with the FDA prior to NDA submission. Such PSP agreements have been reached with the FDA, who waived Immunic’s requirement to conduct clinical studies in pediatric patients for both RMS and PMS.

Future human clinical testing and marketing outside the United States will be subject to foreign regulatory requirements. These requirements vary by jurisdiction, may differ from those in the United States and may require us to perform additional preclinical or clinical testing regardless of whether FDA approval has been obtained. The amount of time required to obtain necessary approvals from foreign regulatory agencies may be longer or shorter than that required for FDA approval. In many countries outside of the United States, coverage, pricing and reimbursement approvals are also required.

Vidofludimus Calcium Manufacturing and Formulation

Vidofludimus calcium is formulated as a white, uncoated immediate release tablet. Dose strengths for clinical trials are 5 mg, 15 mg, 22.5 mg, 30 mg and 45 mg, and a matching placebo. The tablets are packaged in high-density polyethylene (“HDPE”) bottles, protected from moisture with desiccant in the cap. Vidofludimus calcium has been synthesized in several batches of up to 80 kg each of active pharmaceutical ingredient (“API”) and a drug product batch size of up to 500,000 tablets has been produced by manufacturers under contract with us. Our existing API manufacturer has the capacity for manufacturing of up to metric tons.

The execution of Phase 3 clinical trials usually requires the use of a commercial formulation of the investigational drug manufactured at commercially usable quantities. Manufactures under contract with us have developed and produced a formulation of vidofludimus calcium which would allow commercially usable production batches. A Phase 1 bioequivalence study between the early development stage formulation and the final formulation of vidofludimus calcium, manufactured with different manufacturing processes, was completed and showed bioequivalence regarding drug exposure curve in blood plasma (area under the curve). A confirmatory relative bioavailability and food effect study demonstrated a high bioavailability of tablets as compared to a drinking solution and confirmed the in vitro finding of a complete and fast dissolution profile in human subjects. No food effect on the uptake or elimination of vidofludimus calcium after administration of the tablets was observed.

Additional investigations regarding metabolite characterization, metabolic modeling and potential drug-drug interactions, as well as other activities relating to clinical pharmacology are either completed, ongoing or planned in anticipation for presentation to regulatory authorities.

Vidofludimus Calcium Intellectual Property, Licenses and Royalties

We follow a multi-layered intellectual property (“IP”) approach for vidofludimus calcium. Currently, 10 independent patent families are expected to provide exclusivity up to 2044 in the United States, or even beyond. Currently, 4 to 5 granted patents are ready for prospective listing in the Orange Book, the FDA's publication of Approved Drug Products with Therapeutic Equivalence Evaluations.

Vidofludimus calcium is protected by several layers of granted patents in the United States, Europe and other jurisdictions around the world. These patents are directed towards composition-of-matter for forms of vidofludimus calcium; the treatment of RRMS with a specific dose strength used in the clinical trials; the treatment of PMS with specific dose strengths used in the clinical trials; the dosing regimens, including those used in clinical trials for the treatment of MS, as well as composition-of-matter of a specific polymorph of vidofludimus calcium and a related method of production of the material. In the United States, these patents provide protection into 2041, unless extended further. In addition, pending applications are directed towards the use of vidofludimus calcium and other salt forms as well as free acid forms for treating neurodegenerative diseases, which, if granted, could provide protection up to 2044, unless extended further, and the pharmaceutical product (formulation, production process and impurity profile), which, if granted, could provide protection up to 2045, unless extended further. An additional patent, covering the treatment of long COVID, has been granted in the US and in Europe, also providing protection until 2041. Further undisclosed patent applications dedicated to strengthening the exclusivity period are currently in process. In addition to the patent exclusivity, vidofludimus calcium, as a new chemical entity, also is expected to benefit from regulatory data protection.

Vidofludimus calcium was acquired in a transaction with 4SC in September 2016. We have subsequently submitted additional patent applications for independently developed intellectual property. On March 31, 2021, our German subsidiary, Immunic AG, and 4SC entered into a Settlement Agreement, pursuant to which Immunic AG settled its remaining obligation of a 4.4% royalty on net sales for $17.25 million. The payment was made 50% in cash and 50% in shares of our common stock.

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IMU-856

IMU-856 is an orally available and systemically acting small molecule modulator that targets SIRT6, a protein which serves as a transcriptional regulator of intestinal barrier function and regeneration of bowel epithelium. Based on preclinical data, we believe this compound may represent a unique treatment approach, as the mechanism of action targets the restoration of the intestinal barrier function and bowel wall architecture in patients suffering from gastrointestinal diseases such as celiac disease, IBD, GvHD and other intestinal barrier function associated diseases.

We believe that, because IMU-856 has been shown in preclinical investigations to avoid suppression of immune cells, it may therefore have the potential to maintain immune surveillance for patients during therapy, which would be an important advantage versus immunosuppressive medications and may allow the potential for combination with available treatments in multiple gastroenterological diseases.

Impaired intestinal barrier function is suspected to be involved in the initiation of many chronic inflammatory or autoimmune conditions, and microbial translocation through the damaged gut mucosa has been associated with many diseases, not only of the bowel but of the whole body. To date, there are no adequate treatment strategies to ameliorate impaired barrier function.

Indication: Celiac Disease

Diagnosis and Prevalence

Celiac disease is a multifactorial, complex autoimmune disease caused by an inappropriate immune reaction against a degradation product of gluten in genetically susceptible individuals. It is characterized by impaired intestinal barrier function with villous atrophy and consecutive nutrient malabsorption. Celiac disease is estimated to affect 1 in 100 people worldwide (Celiac Disease Foundation, 2022). In the United States, alone, it is estimated that there are approximately two million people diagnosed with celiac disease (Singh et al., 2018) and an additional approximately one million people are undiagnosed, yet still at risk for long-term health complications (Choung et al., 2016).

Ongoing inflammation in patients with celiac disease can cause debilitating symptoms and serious medical complications. Many patients suffer from gastrointestinal symptoms such as diarrhea and have abnormal bowel epithelial lining (villous atrophy and crypt enlargement). Small bowel damage often leads to nutrient malabsorption that can result in a range of further clinical manifestations such as fatigue, anemia, osteopenia, weight loss, or failure to thrive in children. In addition, extra-intestinal symptoms and systemic manifestations are often present, such as dermatitis herpetiformis, infertility, or neurological and skeletal disorders. Patients with persistent villous atrophy show an increased risk of lymphoproliferative malignancy. The intestinal epithelial barrier, physiologically impermeable to macromolecules such as gliadin, is recognized to play an important role in the pathogenesis of celiac disease. In children, nutrient malabsorption can affect growth and development, in addition to causing the symptoms seen in adults.

Current Treatment Options

There is currently no known cure or medical treatment for celiac disease and patients must adhere to a strict, life-long gluten-free diet which can help manage symptoms and avoid disease flareups. However, a significant number of patients continue to experience disease activity and persistent symptoms despite a gluten-free diet as gluten is present in numerous food products, medications, household products and cosmetics as impurity. Thus, there is an increasing number of different treatment options in clinical development to reduce the burden of living with celiac disease and improve long-term health outcomes (Buriánek, Gege, Marinković, 2024). Treatment goals include resolution of bowel inflammation and relief of associated clinical signs and symptoms. This is underlined by the recently published FDA Draft Guidance (April 2022) for the development of drugs for the adjunctive treatment of gluten-free diet.

Current Development Plan and Clinical Studies

Current treatments of many conditions of the bowel are designed to inhibit inflammation, but they do not target the impaired bowel wall barrier function. IMU-856 is designed to target pathways impacting the bowel wall barrier function and aims to normalize such function. We believe that normalized bowel wall barrier function may avoid antigen triggers, which may lead to the achievement and maintenance of remission without significantly influencing the immune competency of the patient.

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We completed a double-blind, randomized, placebo-controlled Phase 1/1b clinical trial of IMU-856, which was comprised of three parts:

Part A: Single Ascending Dose Part

The first part of the Phase 1 clinical trial was a single ascending dose, double-blind, placebo-controlled study in healthy human subjects designed to assess safety, PD and PK properties of IMU-856. Healthy human subjects were randomized in a double-blinded manner to either placebo or active treatment with single ascending doses of IMU-856 at 10 mg, 20 mg, 40 mg, 80 mg, 120 mg and 160 mg.

On September 20, 2022, we announced unblinded safety, tolerability and PK results from the single ascending dose part of the Phase 1 clinical trial of IMU-856 in healthy human subjects. Single ascending doses of IMU-856 were found to be safe and well-tolerated and no maximum tolerated dose was reached. No serious adverse events occurred. Moreover, a dose-linear PK profile was observed across the investigated dose range.

Part B: Multiple Ascending Dose Part

The second portion of the Phase 1 clinical trial was a multiple ascending dose, double-blind, placebo-controlled study of IMU-856 in healthy human subjects. Healthy human subjects were dosed for 14 consecutive days with 40 mg, 80 mg or 160 mg once-daily of IMU-856 or placebo in a double-blinded manner. This part was designed to assess safety, PD and PK properties of IMU-856.

On September 20, 2022, we also announced unblinded results from the multiple ascending dose part of the ongoing Phase 1 clinical trial. Multiple ascending doses of IMU-856 were found to be safe and well-tolerated and no maximum tolerated dose was reached. Treatment-emergent adverse events were mostly mild in severity. No investigational medicinal product (“IMP”)-related serious adverse events were reported. No dose-dependent changes in laboratory parameters (including no effects on liver enzymes or in hematological parameters), vital signs, physical examination or electrocardiographic evaluations were found. PK analysis showed a quick achievement of stable steady-state plasma concentrations within the first week and stable steady-state trough levels over the 14-day treatment period with a low accumulation factor for IMU-856, allowing predictable trough levels during daily dosing. PK parameters in steady-state revealed a Tmax (time to reach maximum plasma concentration) of 2 to 3 hours post-dose, a plasma half-life of 17.4 to 21.5 hours and dose proportional increases in Cmax (maximum plasma drug concentration) and AUC (area under the concentration-time curve).

Part C: Celiac Disease Patients

The third portion of the Phase 1 clinical trial of IMU-856 was structured as a double-blind, randomized, placebo-controlled Phase 1b trial, designed to assess the safety and tolerability of IMU-856 in patients with celiac disease during periods of gluten-free diet and a 15-day gluten challenge with 6 g gluten given daily. The trial was conducted at sites in Australia and New Zealand. A total of 43 patients were enrolled in two consecutive cohorts with 80 mg or 160 mg of IMU-856 or placebo given once-daily over 28 days. Further objectives included pharmacokinetics, changes in malabsorption parameters and biomarkers for intestinal integrity, such as citrulline, as well as histological changes.

On May 4, 2023, we announced positive results from our Phase 1b clinical trial of IMU-856 in patients with celiac disease. The data demonstrated positive effects for IMU-856 over placebo in four key dimensions of celiac disease pathophysiology: protection of the gut architecture, improvement of patients’ symptoms, biomarker response, and enhancement of nutrient absorption. IMU-856 was also observed to be safe and well-tolerated in this trial. There were no IMP-related serious or severe treatment-emergent adverse events or any dose-dependency in adverse events. Moreover, the rates of treatment-emergent adverse events in non-disease-related parameters were comparable between the active treatment groups and placebo.

We believe that this data set provided initial clinical proof-of-concept for an entirely new therapeutic approach to gastrointestinal disorders by promoting regeneration of bowel architecture. The data provided first clinical evidence that IMU-856’s ability, observed in preclinical studies, to induce physiological gut cell renewal translates into clinical benefits for patients with celiac disease. Most importantly, the observed protection of intestinal villi from gluten-induced destruction, independent of targeting immune mechanisms involved specifically in celiac disease, appears to be unique among proposed therapeutic approaches and may be applicable to other gastrointestinal diseases such as IBD, short bowel syndrome and irritable bowel syndrome with diarrhea.

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Dose-Dependent Increase of GLP-1 in Celiac Disease Patients and Corresponding Effects in Preclinical Testing

On February 20, 2025, we announced that IMU-856 demonstrated a dose-dependent increase of endogenous GLP-1 levels in a post hoc analysis of patients from our Phase 1b clinical trial in celiac disease. IMU-856 also showed a dose-dependent reduction of body weight gain and food consumption in preclinical in vivo testing.

The post hoc analysis of our Phase 1b clinical trial of IMU-856 in celiac disease patients measured blood concentrations of GLP-1, between baseline and day 28, in a fasting state. A highly statistically significant (day 29: 80 mg p=0.014; 160 mg p=0.003) and dose-dependent increase of GLP-1 versus placebo control was detectable, even in the small patient population in this Phase 1b clinical trial (baseline: N placebo = 11, N 80 mg IMU-856 = 13, N 160 mg IMU-856 = 13). These clinical findings were corroborated by effects observed in a 6-month preclinical in vivo study, where IMU-856 was found to reduce body weight gain accompanied by food consumption in a dose-dependent fashion up to -40 %, compared to the control group, which was found to be linked to reduced food intake.

Effects on enteric hormones such as GLP-1 have been shown to provide additional favorable outcomes in multiple gastrointestinal diseases. The observed GLP-1 effects of IMU-856 may therefore provide an additional mechanism to strengthen its clinical value. We believe that this should be further evaluated in future clinical development.

Contingent on financing, licensing or partnering, we are currently preparing further clinical testing of IMU-856.

IMU-856 Manufacturing and Formulation

The API of the IMU-856 drug product is a small molecule compound, formulated as a tablet. For the Phase 1/1b clinical trial, IMU-856 was synthesized at up to 8 kg scale. Developed dose strengths were 10 mg, 40 mg, 80 mg and 160 mg, and a matching placebo. The tablets were packaged in HDPE bottles. The tablets were produced by a manufacturer under contract with us and finally released for the clinical trial by a vendor in Australia. For Phase 2 clinical testing, we have developed a new, improved formulation of IMU-856 for 60 mg, 150 mg and 240 mg dose strengths, which is stable and its manufacturing process robust.

IMU-856 Intellectual Property, Licenses and Royalties

Our rights to IMU-856 are secured pursuant to an option and license agreement (the “Daiichi Sankyo Option”) with Daiichi Sankyo Co., Ltd. (hereinafter, "Daiichi Sankyo") in Tokyo, Japan. On January 5, 2020, Immunic AG exercised its option under the Daiichi Sankyo Option to acquire the exclusive global rights to commercialize IMU-856. The license also grants Immunic AG the rights to Daiichi Sankyo’s patent application related to IMU-856. Concurrent with the option exercise, Immunic AG paid to Daiichi Sankyo a one-time upfront licensing fee. Going forward, Daiichi Sankyo is eligible to receive future development, regulatory and sales milestone payments, as well as royalties related to IMU-856.

A patent application covering composition-of-matter of IMU-856 and related pharmaceutical compositions has been granted in the US and other jurisdictions and is expected to provide protection into at least 2038, without accounting for potential patent term extension. In addition, pending applications for IMU-856 are directed towards the treatment of inflammatory/gastrointestinal diseases (e.g., celiac disease), reducing body weight and/or induction of satiety, and treatment of GvHD. A further undisclosed patent application dedicated to other diseases has been filed.

IMU-381

We have selected the IMU-381 program to leverage our Nurr1 platform for neurologic, gastrointestinal and other autoimmune diseases. The platform comprises next-generation molecules, including a series of chemical derivatives, with improved overall properties. The IMU-381 program is currently in preclinical testing.

Gliomic Therapeutics: Synthetic Lethality for Genetically-Defined Brain Tumors

Through our wholly-owned subsidiary Gliomic Therapeutics Inc., we are pursuing the use of new compounds in brain cancers leveraging our expertise in DHODH inhibition.

A group of prominent scientists from Harvard Medical School and the University of Texas Southwestern discovered that certain genetically defined groups of brain cancer appear to be exceptionally sensitive to DHODH inhibition. We worked with this group to develop a series of drug candidates specifically for neuro-oncology with unusually high potency, brain penetrance, and target selectivity. These candidates have been subsequently tested in vitro and in vivo, showing not only highly selective

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killing of tumor cells, but also increased survival in animals implanted intracranially with patient-derived tumor cells, as well as early evidence of very favorable tolerability in mice. In order to retain Immunic’s focus on our Phase 3 program in MS, as well as our broader clinical focus on immunologic diseases, Gliomic was spun out to pursue the use of these new compounds in brain cancers. Importantly, for critical scientific reasons, these new compounds would not be appropriate in MS, do not target Nurr1 activation and therefore are not competitive with vidofludimus calcium.

At the moment, Gliomic is a very lean organization, owned entirely by Immunic, with a single employee under the direction of Immunic itself, who is focused on obtaining external funding for Gliomic. As a wholly owned entity, Gliomic coordinates all of its activities with Immunic, and Immunic retains the final authority and priority in all matters. Any moneys being spent by Gliomic now are modest, and entirely at the discretion of Immunic itself.

We plan to provide additional updates in the foreseeable future.

Government Regulation - All Products

In the United States, the FDA regulates drugs under the federal Food, Drug, and Cosmetic Act (“FDCA”), and its implementing regulations. All of Immunic’s drug development candidates require approval from the FDA (for the United States), EMA (for the European Union) and/or other national competent authorities (for any other territory) before they can be marketed for sale in the applicable jurisdiction. The activities required before drugs or biologics may be marketed in the United States include:

•In vitro and in vivo preclinical safety and mechanistic studies and formulation and stability studies;

•the submission to the FDA of an application for human clinical testing, which is known as an IND application;

•adequate and well-controlled human clinical trials to demonstrate the safety and effectiveness of the drug;

•satisfactory completion of an FDA inspection of the manufacturing facility or facilities at which the drug is produced to assess compliance with current good manufacturing practice (“cGMP”), requirements to assure that the facilities, methods and controls are adequate to preserve the drug’s identity, strength, quality and purity;

•the submission to the FDA of an NDA for a drug; and

•the approval by the FDA of an NDA.

The FDA reviews all available data relating to safety, efficacy and quality and assesses the risk/benefit profile of a product candidate before granting approval. The data assessed by the FDA in reviewing an NDA includes preclinical testing data, including animal data, CMC data, PK, PD and drug-drug interaction data, as well as human clinical safety and efficacy data. Moreover, an agreement for a PSP is required to be achieved with the FDA prior to NDA submission.

Preclinical tests include laboratory evaluations of product chemistry, toxicity and formulation, as well as animal studies. Preclinical trials must also be conducted in accordance with FDA, EMA, International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use (“ICH”) and other foreign authorities’ legal requirements, regulations or guidelines, including Good Laboratory Practice (“GLP”), an international standard meant to harmonize the conduct and quality of non-clinical studies and the archiving and reporting of findings. Before human clinical testing can begin in the US, a sponsor must submit the results of the preclinical tests and, where applicable, human clinical data obtained in trials outside of the US, together with manufacturing information and analytical data, to the FDA as part of the IND, which is a request for authorization from the FDA to administer an IND product candidate to humans in clinical trials. An IND automatically becomes effective 30 days after receipt by the FDA, unless the FDA, within the 30-day time period, places the clinical trial on a clinical hold. In such a case, the IND sponsor and the FDA must resolve any outstanding safety concerns before the clinical trial can begin. The FDA may impose a clinical hold at any time before or during clinical trials due to safety concerns about proposed or ongoing clinical trials or non-compliance with FDA requirements, and the trials may not commence or continue until the FDA notifies the sponsor that the hold has been lifted.

All clinical trials must be conducted under the supervision of one or more qualified investigators pursuant to protocols detailing, among other things, the objectives of the trial, dosing procedures, subject selection, inclusion/exclusion criteria and the safety and effectiveness criteria to be evaluated. The trial sponsor submits the protocol, as well as any subsequent protocol amendments, to the FDA as part of the IND. Sponsors must also provide all participating investigators and the FDA safety reports of any serious and unexpected adverse events and any findings from laboratory tests in animals that suggest a significant risk for human subjects. For each institution where a clinical trial will be conducted, an Institutional Review Board (“IRB”) must review and approve the clinical trial protocol and informed consent form required to be provided to each trial subject or his or her legal representative prior to a clinical trial commencing, and conduct ongoing monitoring of the study until completed or termination to assure that appropriate steps are taken to protect the human subjects participating in the research.

Human clinical trials are typically conducted in three sequential phases that may overlap or be combined:

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Phase 1: In Phase 1 clinical trials, the product candidate is initially introduced into healthy human subjects and tested for safety, dosage and tolerability, absorption, distribution, metabolism, excretion, and effect on the body.

Phase 2: Phase 2 clinical trials are conducted in a limited patient population. These studies continue to evaluate safety while gathering preliminary data on effectiveness in patients with the targeted disease or condition, especially studying the potentially therapeutically effective dose.

Phase 3: Phase 3 clinical trials further evaluate efficacy and safety in an expanded patient population, generally at geographically dispersed clinical study sites. These clinical trials are intended to establish the overall risk-benefit ratio of the product candidate and provide, if appropriate, an adequate basis for product labeling.

Post-approval studies, sometimes referred to as Phase 4 studies, may be conducted after initial marketing approval from the FDA. These studies are used to gather additional information about a product’s safety and/or efficacy in patients affected by the therapeutic indication. The FDA may require Phase 4 studies as a condition of approval of an NDA.

Clinical trials must also be conducted in accordance with legal requirements, regulations or guidelines of the FDA and comparable foreign authorities, including human subject protection requirements and current good clinical practice (“cGCP” or “GCP”). In addition, clinical trials must be conducted using product candidates produced under cGMP requirements. The FDA or the sponsor may suspend a clinical trial at any time for various reasons, including a finding that the research subjects or patients are being exposed to an unacceptable health risk. Similarly, an IRB may suspend or terminate approval of a clinical trial at an institution if the clinical trial is not being conducted in accordance with the IRB’s requirements or if the drug has been associated with unexpected serious harm to patients. In addition, some clinical trials are overseen by an independent group of qualified experts, known as a data safety monitoring board or committee, which monitors data from the trial to ensure patient safety and data integrity and may also make recommendations to alter or terminate a trial based on concerns for patient safety.

Before obtaining marketing approval for the commercial sale of any drug product, a sponsor must demonstrate in preclinical studies and well-controlled clinical trials that the product is safe and effective for its intended use and that the manufacturing facilities, processes and controls are adequate to preserve the drug’s identity, strength, quality and purity. The results of these preclinical studies and clinical trials, along with descriptions of the manufacturing process, analytical tests conducted on the chemistry of the drug, proposed labeling and other relevant information such as an agreed PSP are submitted to the FDA as part of an NDA requesting approval to market the product. The submission of an NDA is subject to the payment of substantial user fees; under certain limited circumstances, a waiver of such fees may be obtained. After the submission of an NDA, but before approval of the NDA, the manufacturing facilities used to manufacture a product candidate must be inspected by the FDA to ensure compliance with the applicable cGMP requirements. The FDA may also inspect clinical trial sites and audit clinical study data to ensure that the sponsor’s studies were properly conducted in accordance with the IND regulations, human subject protection regulations, and cGCP.

Under the current Prescription Drug User Fee Act (“PDUFA”) guidelines, the FDA goal for acting on the submission of an NDA for a new molecular entity is ten months from the date of “filing.” The FDA conducts a preliminary review of an NDA within 60 days after submission to determine whether it is sufficiently complete to permit substantive review, before accepting the NDA for filing. This two month preliminary review effectively extends the typical NDA review period to twelve months. The FDA may request additional information rather than accept an NDA for filing. In this event, the NDA must be resubmitted with the additional information. The resubmitted application also is subject to review before the FDA accepts it for filing.

Following the FDA’s evaluation of an NDA, it will issue an approval letter or a complete response letter (“CRL”). An approval letter authorizes the sponsor to begin commercial marketing of the drug for specific indications. A CRL indicates that the review cycle of the application is complete and the application will not be approved in its present form. A CRL describes the specific deficiencies in the NDA identified by the FDA. When possible, a CRL will recommend actions that the applicant might take, including providing additional clinical data, such as an additional Phase 3 clinical trial or other significant and time consuming requirements related to clinical trials, nonclinical studies or manufacturing, to place the application in condition for approval. If a CRL is issued, the sponsor must resubmit the NDA addressing all of the deficiencies identified in the letter, or withdraw the application. Even if the sponsor submits the recommended data and information, the FDA may decide that the resubmitted NDA does not satisfy the criteria for approval.

As a condition to a product’s regulatory approval, the FDA may require a sponsor to conduct Phase 4 studies designed to further assess the drug’s safety and effectiveness after NDA approval, or may require other testing and surveillance programs to monitor the safety of the approved product. The FDA may also place other conditions on approval including the requirement for a risk evaluation and mitigation strategy (“REMS”) to assure the safe use of the drug. A REMS could include medication

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guides, communication plans to healthcare professionals or other activities to assure safe use, such as provider certification or training, restricted distribution methods, and patient registries.

Research and Development

We recognized $82.0 million and $80.0 million in research and development expenses in the years ended December 31, 2025 and 2024, respectively.

Geographic Information

Substantially all of our long-lived assets were located within both the United States and Germany in 2025 and 2024.

Human Capital

As of February 1, 2026, we had 92 employees, nine of whom held M.D. degrees and 30 of whom held Ph.D. degrees. Of the employees, 68 were engaged in research and development and 24 in administration. We consider our employee relations to be good.

We emphasize several measures and objectives in managing our human capital assets, including, among others, (i) employee safety and wellness, (ii) talent acquisition and retention, (iii) employee engagement, development and training, (iv) diversity and inclusion and (v) compensation. These targeted ideals may include annual bonuses, stock-based compensation awards, a 401(k) plan, healthcare and insurance benefits, paid time-off, family leave, child-care, and employee assistance programs. We also provide our employees with access to various innovative, flexible, and convenient health and wellness programs. We designed these programs to support employees’ physical and mental health by providing tools and resources to improve or maintain their health status and encourage engagement in healthy behaviors.

Corporate Information and Website

Prior to April 12, 2019, we were a clinical-stage biotherapeutic company known as Vital Therapies, Inc. that had historically been focused on the development of a cell-based therapy targeting the treatment of acute forms of liver failure. Vital Therapies, Inc. was originally incorporated in the State of California in May of 2003 as Vitagen Acquisition Corp., subsequently changed its name to Vital Therapies, Inc. in June 2003, and reincorporated in Delaware in January 2004. In April 2019, we completed an exchange transaction with Immunic AG pursuant to which holders of ordinary shares of Immunic AG exchanged all of their shares for shares of our common stock, resulting in Immunic AG becoming our wholly owned subsidiary. Following the exchange, we changed our name to Immunic, Inc. and we became a clinical-stage biopharmaceutical company focused on the development of selective oral therapies in immunology.

Our corporate headquarters are located at 1200 Avenue of the Americas, Suite 200, New York, New York 10036. We also have an office at Lochhamer Schlag 21, 82166 Gräfelfing, Germany and a research laboratory at Fraunhoferstraße 1, 82152 Planegg, Germany. Our telephone number is (332) 255-9818.

We maintain a website at www.imux.com. The information contained on, or that can be accessed through, the website is not a part of this Annual Report on Form 10-K.

Our Annual Reports on Form 10-K, Quarterly Reports on Form 10-Q, Current Reports on Form 8-K and all amendments to those reports filed or furnished pursuant to Section 13(a) or 15(d) of the Exchange Act are available free of charge through the investor relations page of our internet website as soon as reasonably practicable after we electronically file such material with, or furnish it to, the SEC.