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– 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: . 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: . 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 Ukraine – Russia 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 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 [email protected] US IR Contact Rx Communications Group Paula Schwartz +1 917 633 7790 [email protected] US Media Contact KCSA Strategic Communications Caitlin Kasunich +1 212 896 1241 [email protected] SOURCE Immunic, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Data shows L1-79 offers a statistically significant improvement compared to placebo in socialization, as well as the investigator- and parent-rated global impression scales The change over placebo may be one of the largest statistically significant effects observed with the Vineland-3 Socialization standard score for a medication in autism NEW YORK, July 30, 2024 (GLOBE NEWSWIRE) -- Yamo Pharmaceuticals, a clinical stage pharmaceutical company, announced today positive topline results of its Phase 2 clinical trial evaluating the effects of L1-79 in adolescents and young adults with autism spectrum disorder (ASD). The data demonstrated a statistically significant improvement with L1-79 compared to placebo on the Vineland Adaptive Behavior Scale (Vineland-3) Socialization standard score (difference compared to placebo: 7.09, p-value = 0.02) during the first 12-weeks of the study. The Vineland-3 Socialization Domain is a well-established standardized assessment tool that looks at a person’s coping skills, ability to engage in play, and leisure and interact with others. In addition, other endpoints, such as the Clinical Global Impression of Severity of Illness (CGI-S) and the Caregiver Global Impression of Change of 3 Most Bothersome Symptoms of ASD (CGI-3P), demonstrated statistically significant improvements with L1-79 compared to placebo, corroborating the Vineland-3 findings. L1-79 was generally safe and well tolerated. There were no serious adverse events or adverse events leading to withdrawal from the trial with L1-79. “It is very encouraging to see a more than seven-point improvement in the Socialization Domain of the Vineland-3,” said J. Thomas Megerian, MD, PhD, Yamo’s Chief Medical Officer. “We believe that this is one of the largest statistically significant effects observed to-date with a medication in ASD on the Vineland-3 Socialization standard score, representing a clinically meaningful improvement in one of the core domains of function affected by ASD. The Company is eager to meet with the FDA to discuss Phase 3 plans, as well as to file for Breakthrough Therapy designation.” “We are excited to receive these results in the hope to offer patients and their families a treatment option that can impact the core symptoms of ASD,” said Chuck Bramlage, Yamo’s Chief Executive Officer. About L1-79Evidence suggests that dysfunction in the catecholaminergic system may play a role in the core symptoms of ASD. L1-79 is a tyrosine hydroxylase inhibitor expected to modulate the catecholaminergic pathways, and thereby improve the core ASD symptoms. L1-79 was granted Fast Track designation by the FDA in May of 2018. About the StudyThis Phase 2, multi-center, randomized, chronic-dosing (12-week) clinical trial was a two-period placebo-controlled crossover trial that enrolled 58 adolescent and young adults with ASD. Patients were randomized 1:1 to one of two active treatment groups: L1-79 200 mg or 300 mg. On day one of Period 1, participants in each dosing group were randomized to receive either L1-79 or placebo BID for 12-weeks. Following the conclusion of Period 1, participants underwent a six-week washout period and then crossed over into Period 2, in which each participant that received placebo in Period 1 received L1-79 and vice versa BID for another 12-weeks. Please refer to study identifier NCT05067582 at www.clinicaltrials.gov for additional clinical trial details. About Autism Spectrum DisorderAutism spectrum disorder or autism refers to a group of complex neurodevelopment disorders that is defined in the Diagnostic and Statistics Manual of Mental Disorders V (DSM-5) by “difficulties in social communication and social interaction, and restricted and repetitive behavior, interests or activities.” In the U.S., it is estimated that 1 in 36 children have ASD, with boys being 3.8 times more likely to be diagnosed than girlsi. Symptoms of repetitive and characteristic patterns of behavior and difficulties with social-communication and interaction start early in childhood and continue throughout a person’s life. While the causes of ASD are not known, research suggests that both genes and environment play important roles. Since the severity, specific types of symptoms, and causes of ASD vary between individuals, it is referred to as a “spectrum’ disorder.” Currently there are no approved pharmacological therapies which address the core symptoms of ASD. About Yamo PharmaceuticalsYamo Pharmaceuticals is a clinical stage pharmaceutical company founded in 2015 to develop L1-79, a novel therapy with the potential to improve the core symptoms of ASD. Yamo Pharmaceuticals is a privately held company. More information may be found at www.yamopharma.com. Safe Harbor StatementThis press release contains “forward-looking statements” concerning the development and commercialization of Yamo Pharmaceuticals’ products, the potential benefits and attributes of such products, and Yamo Pharmaceuticals expectations regarding its prospects. Forward-looking statements are subject to risks, assumptions and uncertainties that could cause actual future events or results to differ materially from such statements. These statements are made as of the date of this press release. Actual results may vary. Yamo Pharmaceuticals undertakes no obligation to update any forward-looking statements for any reason. Contact DataInvestor and Media ContactsChuck Bramlage, CEOcbramlage@yamopharma.com Eugene Prahin, CFOeprahin@yamopharma.com(212) 610-1570 i Maenner MJ, Warren Z, Williams AR, et al. Prevalence and Characteristics of Autism Spectrum Disorder Among Children Aged 8 Years — Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2020. MMWR Surveill Summ 2023;72(No. SS-2):1–14.

During pregnancy, the effects of therapeutical doses of amphetamine have been investigated on birth outcomes in humans. However, a thorough investigation of the mechanisms underlying the long-term effects of embryonal exposure to addictive doses of amphetamine remains largely unexplored. Using a tiny worm, researchers have revealed the underlying mechanisms of embryonal exposure to methamphetamine (Meth) and amphetamines, a psychostimulant used to treat a variety of brain dysfunctions. Amphetamine is a psychostimulant that has been used to treat a variety of brain dysfunctions. However, it is a highly abused drug. In fact, amphetamine and amphetamine-derived compounds such as methamphetamine (Meth) are among the most abused psychostimulants in the world. The neurological effects caused by acute or chronic use of amphetamine have been broadly investigated and several studies have shown that proteins involved in the synthesis, storage, release and reuptake of dopamine (DA), a neurotransmitter that plays a role as in the "reward" center, are either direct targets of or are indirectly affected by these drugs. During pregnancy, the effects of therapeutical doses of amphetamine have been investigated on birth outcomes in humans. However, a thorough investigation of the mechanisms underlying the long-term effects of embryonal exposure to addictive doses of amphetamine remains largely unexplored. Using a tiny worm, C. elegans, Florida Atlantic University researchers are the first who investigate the underlying mechanisms within the embryo after exposure to high concentrations of amphetamines, uncovering their long-lasting effects. For the study, researchers examined whether exposure to high doses of amphetamine throughout embryogenesis causes changes in the expression and function of two major dopaminergic proteins, tyrosine hydroxylase (TH) and vesicular monoamine transporter (VMAT). TH and VMAT both play important roles in the synthesis, storage and release of dopamine -- critical for various brain functions and behaviors. Results of the study, published in the International Journal of Molecular Sciences, show that following exposure to high doses of amphetamine during embryogenesis, the expression of specific genes in the dopaminergic system (dopamine transporter, TH and VMAT) is altered in adult C. elegans via epigenetic mechanisms. These modifications in gene and, consequently, proteins expression cause behavioral changes in adult animals such that animals that received amphetamine during embryogenesis were more susceptible to amphetamine-induced behaviors. "The dopaminergic response to amphetamines and the mechanisms underlying histone methylation are highly conserved across diverse species, which is why we used C. elegans to examine the long-term effects caused by embryonal exposure to amphetamines," said Lucia Carvelli, Ph.D., senior author and an associate professor of neuroscience, FAU Harriet L. Wilkes Honors College and a member of the FAU Stiles-Nicholson Brain Institute. "Importantly, although we used C. elegans as a model system, our goal is to understand how amphetamine works in humans." One advantage of the model the researchers used is that C. elegans embryos can develop outside the uterus and in the absence of maternal care. "Our results were not influenced by possible amphetamine-induced epigenetic or behavioral modifications passed through maternal care, but they are a direct consequence of biological alterations at the embryo," said Carvelli. Behavioral data from the research show that, following embryonic exposure to amphetamine, adult animals exhibit an increased response to amphetamines. This suggests that the altered expression of TH and VMAT caused by continuous exposure to amphetamines during embryogenesis generates animals that are hypersensitive to amphetamines. "Since our results are in agreement with data showing that mice overexpressing TH exhibit enhanced amphetamine-induced behaviors, and that rats chronically treated with amphetamine exhibit a long-lasting increase in striatal reuptake of dopamine, our findings establish C. elegans as an efficient and inexpensive model to study the long-lasting physiological modifications caused by prenatal exposure to amphetamine," said Carvelli. Study co-authors are Tao Ke, Ph.D., a post-doctoral researcher in the Carvelli lab; Kate E. Poquette, an undergraduate FAU student; and Sophia L. Amro Gazze, a student at FAU High School. This research was funded by the National Institute on Drug Abuse, National Institutes of Health (grant No. DA042156), awarded to Carvelli.