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Immunic Presents Key Vidofludimus Calcium Data at the 40th Congress of ECTRIMS, Highlighting Its Therapeutic Potential in Multiple Sclerosis

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Immunic, Inc. (Nasdaq: IMUX) presented key data on vidofludimus calcium (IMU-838) at the 40th Congress of ECTRIMS, highlighting its potential in multiple sclerosis (MS) treatment. The data included:

1. Neurofilament light chain (NfL) reduction: In the CALLIPER trial interim analysis, vidofludimus calcium reduced serum NfL levels by 22.4% compared to placebo after 24 weeks, consistent across progressive MS subtypes.

2. Potential fatigue reduction: Clinical signals suggest vidofludimus calcium may reduce fatigue in MS patients by preventing Epstein-Barr virus reactivation.

3. Neuroprotective effects: Preclinical data showed improved neuronal survival, likely driven by Nurr1 activation.

4. T cell modulation: Vidofludimus calcium reduced or prevented development of pathogenic peripheral T helper cells in preclinical experiments.

The company expects to release CALLIPER top-line data in April 2025.

Immunic, Inc. (Nasdaq: IMUX) ha presentato dati chiave su vidofludimus calcio (IMU-838) al 40° Congresso di ECTRIMS, evidenziando il suo potenziale nel trattamento della sclerosi multipla (SM). I dati includevano:

1. Riduzione della catena leggera della neurofilamenta (NfL): Nell'analisi intermedia dello studio CALLIPER, vidofludimus calcio ha ridotto i livelli sierici di NfL del 22,4% rispetto al placebo dopo 24 settimane, risultando coerente attraverso i sottotipi progressivi della SM.

2. Potenziale riduzione della fatica: Segnali clinici suggeriscono che vidofludimus calcio potrebbe ridurre la fatica nei pazienti affetti da SM prevenendo la riattivazione del virus di Epstein-Barr.

3. Effetti neuroprotettivi: Dati preclinici hanno mostrato un miglioramento della sopravvivenza neuronale, probabilmente guidato dall'attivazione di Nurr1.

4. Modulazione delle cellule T: Vidofludimus calcio ha ridotto o prevenuto lo sviluppo di cellule T helper periferiche patogene in esperimenti preclinici.

L'azienda prevede di pubblicare i dati definitivi dello studio CALLIPER nell'aprile 2025.

Immunic, Inc. (Nasdaq: IMUX) presentó datos clave sobre vidofludimus calcio (IMU-838) en el 40° Congreso de ECTRIMS, destacando su potencial en el tratamiento de la esclerosis múltiple (EM). Los datos incluyeron:

1. Reducción de la cadena ligera de neurofilamentos (NfL): En el análisis intermedio del ensayo CALLIPER, vidofludimus calcio redujo los niveles de NfL en suero en un 22.4% en comparación con el placebo después de 24 semanas, siendo consistente en los subtipos progresivos de EM.

2. Posible reducción de la fatiga: Señales clínicas sugieren que vidofludimus calcio podría reducir la fatiga en pacientes con EM al prevenir la reactivación del virus de Epstein-Barr.

3. Efectos neuroprotectores: Datos preclínicos mostraron una mejora en la supervivencia neuronal, probablemente impulsada por la activación de Nurr1.

4. Modulación de células T: Vidofludimus calcio redujo o previno el desarrollo de células T helper periféricas patogénicas en experimentos preclínicos.

La empresa espera publicar los datos finales del estudio CALLIPER en abril de 2025.

Immunic, Inc. (Nasdaq: IMUX)는 40회 ECTRIMS 학회에서 다발성 경화증(MS) 치료에 대한 가능성을 강조하며 비도플루디무스 칼슘(IMU-838)에 대한 주요 데이터를 발표했습니다. 데이터는 다음과 같습니다:

1. 신경 필라멘트 경량 사슬(NfL) 감소: CALLIPER 시험의 중간 분석에서 비도플루디무스 칼슘은 24주 후에 플라시보 대비 혈청 NfL 수치를 22.4% 감소시켰으며, 진행성 MS의 하위 유형에서 일관성을 보였습니다.

2. 피로 감소 가능성: 클리닉 신호는 비도플루디무스 칼슘이 Epstein-Barr 바이러스의 재활성화를 방지함으로써 MS 환자의 피로를 감소시킬 수 있음을 시사합니다.

3. 신경 보호 효과: 전임상 데이터는 Nurr1 활성화로 인해 향상된 신경 생존률을 보여주었습니다.

4. T 세포 조절: 비도플루디무스 칼슘은 전임상 실험에서 병원성 말초 T 보조 세포의 발달을 감소시키거나 예방했습니다.

회사는 CALLIPER 최종 데이터를 2025년 4월에 발표할 것으로 예상하고 있습니다.

Immunic, Inc. (Nasdaq: IMUX) a présenté des données clés sur le vidofludimus calcium (IMU-838) lors du 40ème Congrès de l'ECTRIMS, mettant en évidence son potentiel dans le traitement de la sclérose en plaques (SEP). Les données comprenaient :

1. Réduction de la chaîne légère des neurofilaments (NfL) : Lors de l'analyse intermédiaire de l'essai CALLIPER, le vidofludimus calcium a réduit les niveaux de NfL sériques de 22,4 % par rapport au placebo après 24 semaines, avec une cohérence observée à travers les sous-types progressifs de SEP.

2. Réduction potentielle de la fatigue : Des signaux cliniques suggèrent que le vidofludimus calcium pourrait réduire la fatigue chez les patients atteints de SEP en empêchant la réactivation du virus d'Epstein-Barr.

3. Effets neuroprotecteurs : Les données précliniques ont montré une amélioration de la survie neuronale, probablement induite par l'activation de Nurr1.

4. Modulation des cellules T : Le vidofludimus calcium a réduit ou empêché le développement de cellules T auxiliaires périphériques pathogènes dans des expériences précliniques.

L'entreprise s'attend à publier les données finales de l'étude CALLIPER en avril 2025.

Immunic, Inc. (Nasdaq: IMUX) hat auf dem 40. ECTRIMS-Kongress wichtige Daten zu Vidofludimus-Calcium (IMU-838) vorgestellt, die das Potenzial in der Behandlung der Multiplen Sklerose (MS) hervorheben. Die Daten umfassten:

1. Reduktion der neurofilamentären leichten Kette (NfL): In der Zwischenanalyse der CALLIPER-Studie reduzierte Vidofludimus-Calcium die serum NfL-Werte nach 24 Wochen um 22,4% im Vergleich zur plazebokontrollierten Gruppe, was sich über die progressiven MS-Subtypen hinweg als konsistent erwies.

2. Potenzielle Ermüdungsreduktion: Klinische Hinweise deuten darauf hin, dass Vidofludimus-Calcium möglicherweise die Müdigkeit bei MS-Patienten reduzieren kann, indem es eine Reaktivierung des Epstein-Barr-Virus verhindert.

3. Neuroprotektive Effekte: Präklinische Daten zeigten eine verbesserte neuronale Überlebensfähigkeit, vermutlich durch die Aktivierung von Nurr1.

4. T-Zell-Modulation: Vidofludimus-Calcium reduzierte oder verhinderte die Entwicklung pathogener peripherer T-Helferzellen in präklinischen Experimenten.

Das Unternehmen erwartet, im April 2025 die endgültigen Daten der CALLIPER-Studie zu veröffentlichen.

Positive
  • Vidofludimus calcium reduced serum NfL levels by 22.4% compared to placebo in the CALLIPER trial interim analysis
  • Consistent treatment effects observed across progressive MS subtypes
  • Potential to reduce fatigue in MS patients by preventing Epstein-Barr virus reactivation
  • Preclinical data showed improved neuronal survival and neuroprotective effects
  • Reduced or prevented development of pathogenic peripheral T helper cells in preclinical experiments
  • CALLIPER top-line data expected in April 2025
Negative
  • None.

Insights

The interim analysis of the CALLIPER trial shows promising results for vidofludimus calcium in progressive MS. The 22.4% reduction in serum NfL levels compared to placebo is significant, as NfL is a key biomarker for neuronal damage. Importantly, this effect was consistent across different MS subtypes and patient subgroups, suggesting broad applicability.

The drug's potential to reduce fatigue by preventing EBV reactivation is intriguing, given the emerging link between EBV and MS. The 50% reduction in fatigue symptoms observed in the CALVID-1 trial for PCS patients is noteworthy and warrants further investigation in MS patients.

The preclinical data on Nurr1 activation and neuroprotection provide a strong mechanistic rationale for vidofludimus calcium's potential in MS. Upregulation of key neuroprotective genes like BDNF and SOD1 could translate to improved neuronal survival and reduced disease progression.

Immunic's presentation at ECTRIMS showcases the potential of vidofludimus calcium as a competitive player in the MS market. The consistent NfL reduction across patient subgroups could position the drug as a broad-spectrum treatment for progressive MS, a segment with significant unmet needs.

The upcoming CALLIPER top-line data in April 2025 will be a critical catalyst for Immunic's stock. Positive results could significantly boost investor confidence and potentially lead to partnerships or increased funding opportunities. The drug's oral administration and promising safety profile could give it a competitive edge in the crowded MS market.

However, investors should note that while the interim data is encouraging, final trial results and regulatory approval are still pending. The company's financial runway and ability to fund ongoing trials should be closely monitored.

– Vidofludimus Calcium Consistently Reduced Neurofilament Light Chain Levels, Compared to Placebo, in the Interim Analysis of the Phase 2 CALLIPER Trial, Across Age and Disability Levels at Baseline For All Progressive Multiple Sclerosis Subtypes –

– Clinical Signal Shown for Vidofludimus Calcium on Post COVID Fatigue May Be Related to Epstein-Barr Virus Reactivation; Preventing This Reactivation May Contribute to Fatigue Reduction in Multiple Sclerosis Patients –

– Preclinical Data Showed Improved Neuronal Survival, Likely Driven by Vidofludimus Calcium's Induction of Nurr1 Activation, as Demonstrated by Primary Target Gene Regulation

In Preclinical Experiments, Vidofludimus Calcium Reduced or Prevented Development of Pathogenic Peripheral T Helper Cells, Which Could be One of the Treatment Pathways in Multiple Sclerosis –

NEW YORK, Sept. 18, 2024 /PRNewswire/ -- Immunic, Inc. (Nasdaq: IMUX), a biotechnology company developing a clinical pipeline of orally administered, small molecule therapies for chronic inflammatory and autoimmune diseases, today announced the presentation of key data at the 40th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), highlighting Immunic's lead asset, nuclear receptor related 1 (Nurr1) activator, vidofludimus calcium's (IMU-838) therapeutic potential in multiple sclerosis (MS). The data will be presented in an oral poster presentation and three ePosters at this conference, being held September 18-20, 2024, in Copenhagen, Denmark. Additionally, members of Immunic will be available throughout the event at booth #60.

"Having four poster presentations on our lead asset, vidofludimus calcium, at the prestigious ECTRIMS Congress, illustrates the strength of the data generated for our drug candidate, to date, and its potential to become a new treatment option for MS," stated Daniel Vitt, Ph.D., Chief Executive Officer of Immunic. "We are particularly excited to have the opportunity to present data on various aspects of vidofludimus calcium's profile, including the neurofilament light chain (NfL) interim data from our phase 2 CALLIPER trial, antiviral data suggesting an effect on reducing fatigue, Nurr1 target data supporting a neuroprotective profile, and pathogenic T cell data further supporting the drug's anti-inflammatory effects."

Dr. Vitt added, "As previously reported, in the interim analysis of our CALLIPER trial, we observed a clear separation from placebo in serum NfL levels among all patients with progressive multiple sclerosis (PMS) as well as its subtypes. These observations support the potential effectiveness of vidofludimus calcium in slowing disease progression in PMS and further substantiate its neuroprotective capabilities through the activation of Nurr1. Our next major data readout for this asset is the CALLIPER top-line data, which we expect to release in April of next year. We believe that, if the CALLIPER trial is successful in showing a beneficial effect of vidofludimus calcium, this data, along with that from the ENSURE program and vidofludimus calcium's already established, strong safety and tolerability profile, may allow for a meaningful clinical differentiation of vidofludimus calcium compared to other MS medications, providing potentially attractive commercial positioning."

Dr. Vitt continued, "Fatigue is one of the most common and most debilitating symptoms for both post-Covid Syndrome (PCS) and MS. Third-party research has recognized Epstein-Barr virus (EBV) reactivation as a potential cause for PCS fatigue. Notably, data has demonstrated not only vidofludimus calcium's antiviral effects, but also its potential ability to prevent reactivation of EBV. We aim to confirm vidofludimus calcium's potential to reduce fatigue in MS patients in our ongoing CALLIPER and phase 3 ENSURE trials and in the recently initiated investigator-sponsored phase 2 RAPID_REVIVE trial in PCS patients. Additionally, results from an animal model suggest that vidofludimus calcium reduces or prevents the development of pathogenic peripheral T helper cells. Besides its effect on pathogenic immune cells, preclinical evidence further suggests a neuroprotective role of vidofludimus calcium via activation of Nurr1. Preclinical data support Nurr1-driven direct neuroprotective effects by vidofludimus calcium enhancing neuronal survival and indirect effects by reducing neurotoxic activation of microglia cells. The combination of neuroprotective and anti-inflammatory effects of vidofludimus calcium represents a potential beneficial profile for effective treatment of MS."

Oral Poster Presentation:

  • Title: Serum Neurofilament Changes in Progressive MS: Exploring the Impact of Vidofludimus Calcium by Age and Disability in the CALLIPER Study Interim Analysis
  • Presenting Author: Robert J. Fox, M.D., Staff Neurologist, Mellen Center for Multiple Sclerosis, Vice-Chair for Research, Neurological Institute, Cleveland Clinic, Cleveland, Ohio
  • Poster Number: P753
  • Session Title: Poster Session 2
  • Date: Thursday, September 19, 2024
  • Time: 4:45 pm – 6:45 pm CEST

In the phase 2 CALLIPER trial interim analysis of 203 patients, serum NfL levels were reduced by 22.4% (p=0.01, post hoc) after 24 weeks of vidofludimus calcium treatment compared to placebo, with consistent treatment effects across each progressive MS subtype, including primary progressive MS as well as active and non-active secondary progressive MS. The vidofludimus calcium group showed a 10% decrease in NfL versus a 20% increase for placebo among those with an Expanded Disability Status Scale (EDSS) score ≤ 5.5; and a 2% decrease for vidofludimus calcium versus a 12% increase for placebo among those with an EDSS score >5.5. Similarly, among patients aged ≤ 45 years, the reduction was 11.6% for vidofludimus calcium versus a 15% increase for placebo, while for those aged > 55 years, it was a 10% decrease versus a 13% increase, respectively. The data suggest that vidofludimus calcium treatment consistently reduces NfL levels compared to placebo across different patient subgroups based on age and disability scores at baseline.

ePosters:

  • Title: Exploring the Potential of Vidofludimus Calcium to Reduce Fatigue in Multiple Sclerosis by Preventing Epstein-Barr Virus Reactivation
  • ePoster Number: P1119

Analysis of the antiviral activity of vidofludimus calcium in vitro revealed a dose-dependent reduction of lytic EBV reactivation in B cells and an anti-EBV effect in epithelial cells. Results of a post-hoc analysis of PCS symptoms in the phase 2 CALVID-1 trial indicated a potential contribution of vidofludimus calcium to the prevention of long-term fatigue. 80% of patients who received placebo reported fatigue compared to 50% who received 45 mg vidofludimus calcium. Fatigue decreased in both treatment groups in the next 9-17 weeks to 33% for placebo and 17% for vidofludimus calcium. A clinical signal for vidofludimus calcium on PCS fatigue was observed which might be related to EBV reactivation. By preventing this reactivation, vidofludimus calcium may contribute to fatigue reduction in MS patients as well. This hypothesis will be further assessed by determining effects on fatigue using patient questionnaires as well as analyses of the anti-EBV effect in the ongoing CALLIPER, ENSURE, and RAPID_REVIVE clinical trials.

  • Title: Vidofludimus Calcium Activity on Nurr1 in Preclinical Models: A Potential Neuroprotective Function in Multiple Sclerosis
  • ePoster Number: P1410

Vidofludimus calcium enhanced the expression of Nurr1 target genes important for neuronal survival, such as brain derived neurotrophic factor (BDNF) and superoxide dismutase 1 (SOD1), in a rat neuronal cell line. Additionally, it upregulated key Nurr1 target genes, such as tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT2), in human microglial and murine neuronal cell lines, which could contribute to neuronal protection. Vidofludimus calcium protected neurons under pro-apoptotic conditions, reduced gene expression of IL-6, TNFa and IFNg in human microglia stimulated with lipopolysaccharide (LPS), and increased BDNF levels in human peripheral blood mononuclear cells (PBMCs) stimulated with LPS. Vidofludimus calcium effectively attenuated disease severity in an experimental autoimmune encephalomyelitis (EAE) model. Treatment with vidofludimus calcium led to reduced immune cell infiltration, including decreased numbers of pathogenic T cells producing IL-17A, GM-CSF, and IFNγ. Preliminary data showed that mice receiving vidofludimus calcium exhibit elevated levels of BDNF in the blood and enhanced expression of Nurr1 and its target gene TH in the central nervous system.

  • Title: Vidofludimus Calcium Shows T Helper Cell Modulatory Effects in Murine Experimental Autoimmune Encephalomyelitis: One of the Potential Mode of Action Pathways for MS Treatment
  • ePoster Number: P1390

Vidofludimus calcium given prophylactically reduced disease severity and prevented disease development (63% and 15% symptom free in vidofludimus calcium and vehicle, respectively). This was reflected in the strong reduction of infiltrating T helper (Th) cells in the spinal cord as well as reduced numbers of proinflammatory Th cells in the periphery (draining lymph nodes, dLN). Vidofludimus calcium treatment, given after symptom onset, reduced disease progression compared to vehicle. This was supported by lower numbers of infiltrating proinflammatory Th cells into the spinal cord, while no significant difference was seen in the periphery compared to vehicle. The effect of vidofludimus calcium was assessed on myelin oligodendrocyte glycoprotein (MOG) antigen-specific Th cells (2D2) on day 7 after disease induction. Although vidofludimus calcium seems to increase MOG-specific follicular T helper (Tfh) cells in the periphery (dLN), the progression to develop into pathogenic Th cells was inhibited and the development of regulatory T cells was increased. Overall, vidofludimus calcium reduces or prevents development of pathogenic peripheral Th cells.

All poster presentations will be accessible on the "Events and Presentations" section of Immunic's website at: https://ir.imux.com/events-and-presentations.

About Vidofludimus Calcium (IMU-838)
Vidofludimus calcium is a small molecule investigational drug in development as an oral next-generation treatment option for patients with multiple sclerosis and other chronic inflammatory and autoimmune diseases. The selective immune modulator activates the neuroprotective transcription factor nuclear receptor related 1 (Nurr1), which is associated with direct neuroprotective properties. Additionally, vidofludimus calcium is a known 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 anti-viral effects of vidofludimus calcium. Vidofludimus calcium has been observed to selectively act on hyperactive T and B cells while leaving other immune cells largely unaffected and enabling normal immune system function, e.g., in fighting infections. To date, vidofludimus calcium has been tested in more than 1,800 individuals and has shown an attractive pharmacokinetic, safety and tolerability profile. Vidofludimus calcium is not yet licensed or approved in any country.

About Immunic, Inc.
Immunic, Inc. (Nasdaq: IMUX) is a biotechnology company developing a clinical pipeline of orally administered, small molecule therapies for chronic inflammatory and autoimmune diseases. The company's lead development program, vidofludimus calcium (IMU-838), is currently in phase 3 and phase 2 clinical trials for the treatment of relapsing and progressive multiple sclerosis, respectively, and has shown therapeutic activity in phase 2 clinical trials in patients suffering from relapsing-remitting multiple sclerosis, progressive multiple sclerosis and moderate-to-severe ulcerative colitis. Vidofludimus calcium combines neuroprotective effects, through its mechanism as a first-in-class nuclear receptor related 1 (Nurr1) activator, with additional anti-inflammatory and anti-viral effects, by selectively inhibiting the enzyme dihydroorotate dehydrogenase (DHODH). IMU-856, which targets the protein Sirtuin 6 (SIRT6), is intended to restore intestinal barrier function and regenerate bowel epithelium, which could potentially be applicable in numerous gastrointestinal diseases, such as celiac disease, for which it is currently in preparations for a phase 2 clinical trial. IMU-381, which currently is in preclinical testing, is a next generation molecule being developed to specifically address the needs of gastrointestinal diseases. For further information, please visit: www.imux.com.

Cautionary Statement Regarding Forward-Looking Statements
This press release contains "forward-looking statements" that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this press release regarding strategy, future operations, future financial position, future revenue, projected expenses, sufficiency of cash and cash runway, expected timing, development and results of clinical trials, prospects, plans and objectives of management are forward-looking statements. Examples of such statements include, but are not limited to, statements relating to Immunic's development programs and the targeted diseases; the potential for vidofludimus calcium to safely and effectively target diseases; preclinical and clinical data for vidofludimus calcium; the timing of current and future clinical trials and anticipated clinical milestones; the nature, strategy and focus of the company and further updates with respect thereto; and the development and commercial potential of any product candidates of the company. Immunic may not actually achieve the plans, carry out the intentions or meet the expectations or projections disclosed in the forward-looking statements and you should not place undue reliance on these forward-looking statements. Such statements are based on management's current expectations and involve substantial risks and uncertainties. Actual results and performance could differ materially from those projected in the forward-looking statements as a result of many factors, including, without limitation, the COVID-19 pandemic, increasing inflation, impacts of the UkraineRussia conflict and the conflict in the Middle East on planned and ongoing clinical trials, risks and uncertainties associated with the ability to project future cash utilization and reserves needed for contingent future liabilities and business operations, the availability of sufficient financial and other resources to meet business objectives and operational requirements, the fact that the results of earlier preclinical studies and clinical trials may not be predictive of future clinical trial results, the protection and market exclusivity provided by Immunic's intellectual property, risks related to the drug development and the regulatory approval process and the impact of competitive products and technological changes. A further list and descriptions of these risks, uncertainties and other factors can be found in the section captioned "Risk Factors," in the company's Annual Report on Form 10-K for the fiscal year ended December 31, 2023, filed with the SEC on February 22, 2024, and in the company's subsequent filings with the Securities and Exchange Commission. Copies of these filings are available online at www.sec.gov or ir.imux.com/sec-filings. Any forward-looking statement made in this release speaks only as of the date of this release. Immunic disclaims any intent or obligation to update these forward-looking statements to reflect events or circumstances that exist after the date on which they were made. Immunic expressly disclaims all liability in respect to actions taken or not taken based on any or all the contents of this press release.

Contact Information

Immunic, Inc.
Jessica Breu
Vice President Investor Relations and Communications
+49 89 2080 477 09
jessica.breu@imux.com

US IR Contact 
Rx Communications Group
Paula Schwartz
+1 917 633 7790
immunic@rxir.com

US Media Contact
KCSA Strategic Communications
Caitlin Kasunich
+1 212 896 1241
ckasunich@ksca.com

Immunic, Inc. Logo (PRNewsfoto/Immunic, Inc.)

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SOURCE Immunic, Inc.

FAQ

What were the main findings of Immunic's vidofludimus calcium (IMUX) presentation at ECTRIMS 2024?

The main findings included a 22.4% reduction in serum NfL levels compared to placebo in the CALLIPER trial interim analysis, potential fatigue reduction by preventing Epstein-Barr virus reactivation, improved neuronal survival in preclinical studies, and reduction of pathogenic T helper cells in experimental models.

When is Immunic (IMUX) expecting to release the CALLIPER top-line data for vidofludimus calcium?

Immunic expects to release the CALLIPER top-line data for vidofludimus calcium in April 2025.

How did vidofludimus calcium (IMUX) affect neurofilament light chain levels in the CALLIPER trial?

In the CALLIPER trial interim analysis, vidofludimus calcium reduced serum neurofilament light chain (NfL) levels by 22.4% compared to placebo after 24 weeks of treatment, with consistent effects across progressive MS subtypes.

What potential effect did vidofludimus calcium (IMUX) show on fatigue in multiple sclerosis patients?

Clinical signals suggest that vidofludimus calcium may reduce fatigue in MS patients by preventing Epstein-Barr virus reactivation. This hypothesis will be further assessed in ongoing clinical trials.

Immunic, Inc.

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