Latest news with #IL-6
Hans India
22 minutes ago
- Health
- Hans India
Covid and flu viruses can wake up breast cancer cells spread in lungs: Study
New Delhi: Common respiratory infections, including Covid-19 and influenza, can awaken dormant breast cancer cells that have spread to the lungs, setting the stage for new metastatic tumours, according to a new study. The findings published in the journal Nature, based on mouse studies as well as meta-analysis of human patients, support research showing increases in death and metastatic lung disease among cancer survivors infected with SARS-CoV-2 -- the virus that causes Covid. "Our findings indicate that individuals with a history of cancer may benefit from taking precautions against respiratory viruses, such as vaccination when available, and discussing any concerns with their health care providers," said Julio Aguirre-Ghiso, from the Albert Einstein College of Medicine, US. Previous evidence suggests that inflammatory processes can awaken disseminated cancer cells (DCCs) -- cells that have broken away from a primary tumour and spread to distant organs, often lying dormant for extended periods. An increase in cancer death rates during the Covid pandemic bolstered the idea that severe inflammation may be waking up the dormant DCCs, Aguirre-Ghiso said. The team tested the hypothesis on mice and exposed them to SARS-CoV-2 or the influenza virus -- both triggered the awakening of dormant DCCs in the lungs, leading to a massive expansion of metastatic cells within days of infection and the appearance of metastatic lesions within two weeks. Molecular analyses revealed that the awakening of dormant DCCs is driven by interleukin-6 (IL-6), a protein that immune cells release in response to infections or injuries. This suggested that using IL-6 inhibitors or other targeted immunotherapies might prevent or lessen the resurgence of metastasis. Further, to understand the implications in humans, the team analysed two large databases and found that respiratory infections in cancer patients in remission are linked to cancer metastasis. "The effect was most pronounced in the first year after infection," said Roel Vermeulen, from Utrecht University, The Netherlands. The rapid progression to cancer mirrors the observed quick expansion of dormant cancer cells in animal models. "Our findings suggest that cancer survivors may be at increased risk of metastatic relapse after common respiratory viral infections," said Vermeulen. "It is important to note that our study focused on the period before Covid-19 vaccines were available."
Business Wire
7 days ago
- Health
- Business Wire
Coya Therapeutics Announces Publication of Scientific Research Linking Inflammation and Oxidative Stress to the Progression of Parkinson's Disease
HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (NASDAQ: COYA) ('Coya' or the 'Company'), a clinical-stage biotechnology company focused on developing biologics that enhance regulatory T cell (Treg) function in patients with neurodegenerative disorders, announces the publication of a new research study, partially funded by Coya. The study, led by Drs. Aaron Thome, a scientific advisor to Coya, and Stanley H. Appel, the chairperson of Coya's Scientific Advisory Board, explores the role of immune dysfunction in the pathogenesis of PD. It was published in the scientific journal Frontiers of Immunology, which can be accessed here. PD is one of the most prevalent neurodegenerative disorders, marked by the progressive loss of dopaminergic neurons in the substantia nigra. This degeneration leads to motor symptoms such as tremors, rigidity, and bradykinesia, as well as non-motor symptoms, including cognitive impairment, autonomic dysfunction, and psychiatric disturbances. Peripheral immune dysfunction, characterized by altered cytokine levels and dysregulated immune cell function, appears to play a significant role in PD pathogenesis. Dr Stanley Appel, Director Johnston Center for Cellular Therapeutics at Houston Methodist Hospital commented: 'The data offer strong insights into how peripheral inflammation is a key driver of the pathophysiology of PD. During the early stages of disease, myeloid cells are anti-inflammatory, but in later stages there is increased oxidative stress and proinflammatory signaling that promote peripheral and CNS dysfunction. The observed correlation of peripheral monocytes with disease burden and progression further supports the proposed dual effect of COYA 302. This therapy is designed to both enhance the anti-inflammatory function of Tregs and suppress the inflammation caused by monocytes and macrophages.' 'Results of this novel research study confirm our findings in other serious neurodegenerative diseases driven by sustained inflammation and strengthen our multitargeted immunomodulatory approach as a strategy for treating severe conditions with high unmet needs' Dr Fred Grossman, Chief Medical Officer, added. Highlights of Study Results This cross-sectional study in peripheral blood monocytes isolated from patients with PD and age- and sex-matched controls showed differential expression of inflammatory, immunoregulatory, and chemotactic receptor transcripts, as summarized below: Upregulation of the pro-inflammatory cytokine interleukin 6 (IL-6) and interleukin 1 beta (IL-1b) transcripts was observed in PD monocytes compared to control monocytes, and its expression increased with advanced stages of PD. The chemokine receptor C-C receptor type 2 (CCR2), which facilitates monocyte migration to sites of inflammation, was upregulated in PD monocytes compared to controls. Additionally, CCR2 expression was increased in early PD and continued to rise with advancing disease stages. Transcripts of the mannose receptor (MRC1/CD206), a marker of alternatively activated (M2) myeloid cells, were upregulated in early-stage PD monocytes but declined with disease progression, resulting in decreased expression in late-stage disease. CD163, a scavenger receptor associated with immunoregulation and protection from oxidative stress, was increased in monocytes from PD patients. CD163 transcripts were low in early-stage PD but increased with disease progression. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A or PGC-1α), an important transcriptional activator, exhibited a slight but non-significant increase in early-stage PD monocytes. However, its transcript levels progressively declined as the disease advanced. Glutathione peroxidase 4 (GPX4), an antioxidant enzyme implicated in PD, was elevated in PD monocytes compared to controls. When stratified by disease stage, GPX4 expression increased early but declined in later stages of disease. Sirtuin 1 (SIRT1) and Sirtuin 3 (SIRT3) are NAD⁺-dependent deacetylases with critical roles in oxidative stress responses, mitochondrial regulation, and inflammation. SIRT1 transcripts were upregulated in PD monocytes relative to controls; expression increased during early and intermediate disease stages but declined with disease progression. Conversely, SIRT3 transcripts were reduced in PD monocytes, with early stage decreases that became more pronounced as disease advanced. About COYA 302 COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 comprises proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS. These mechanisms may have additive or synergistic effects. COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency. About Parkinson's Disease Parkinson's disease is a type of neurologic movement disorder, affecting the brain and causing difficulty with movements, or motor symptoms. It is characterized by its most common motor symptoms - tremors (a form of rhythmic shaking), stiffness or rigidity of the muscles, and slowness of movement (called bradykinesia) - but also manifests in non-motor symptoms including sleep problems, constipation, anxiety, depression, and fatigue, among others, which can be present well before any visible motor symptoms. It is a chronic and progressive condition, meaning that the symptoms become worse over time and can affect the ability to perform common daily activities. There are an estimated 1 million people in the U.S. living with Parkinson's disease and more than 10 million people worldwide. Most people who develop the symptoms of Parkinson's disease do so after the age of 50, but Parkinson's disease can affect younger persons as well. Approximately 10% of Parkinson's diagnoses occur before age 50. 1,2 1. National Institute of Neurological Disorders and Stroke website (accessed July 2025). 2. Parkinson's Foundation website (accessed July 2025). About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells ('Tregs') to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions, including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya's investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya's therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. For more information about Coya, please visit Forward-Looking Statements This press release contains 'forward-looking' statements that are based on our management's beliefs and assumptions and on information currently available to management. Forward-looking statements include all statements other than statements of historical fact contained in this press release, including information concerning our business plans and objectives, current and future clinical and preclinical development activities, timing and success of our ongoing and planned clinical trials and related data, the timing of announcements, updates and results of our clinical trials and related data, our ability to obtain and maintain regulatory approval, the potential therapeutic benefits and economic value of our product candidates, competitive position, industry environment and potential market opportunities. The words 'believe,' 'may,' 'will,' 'estimate,' 'continue,' 'anticipate,' 'intend,' 'expect,' and similar expressions are intended to identify forward-looking statements. Forward-looking statements are subject to known and unknown risks, uncertainties, assumptions and other factors including, but not limited to, those related to risks associated the success, cost and timing of our product candidate development activities and ongoing and planned clinical trials; our plans to develop and commercialize targeted therapeutics; the progress of patient enrollment and dosing in our preclinical or clinical trials; the ability of our product candidates to achieve applicable endpoints in the clinical trials; the safety profile of our product candidates; the potential for data from our clinical trials to support a marketing application, as well as the timing of these events; our ability to obtain funding for our operations; development and commercialization of our product candidates; the timing of and our ability to obtain and maintain regulatory approvals; the rate and degree of market acceptance and clinical utility of our product candidates; the size and growth potential of the markets for our product candidates, and our ability to serve those markets; our commercialization, marketing and manufacturing capabilities and strategy; future agreements with third parties in connection with the commercialization of our product candidates; our expectations regarding our ability to obtain and maintain intellectual property protection; our dependence on third party manufacturers; the success of competing therapies or products that are or may become available; our ability to attract and retain key scientific or management personnel; our ability to identify additional product candidates with significant commercial potential consistent with our commercial objectives; and our estimates regarding expenses, future revenue, capital requirements and needs for additional financing. We have based these forward-looking statements largely on our current expectations and projections about future events and trends that we believe may affect our financial condition, results of operations, business strategy, short-term and long-term business operations and objectives, and financial needs. Moreover, we operate in a very competitive and rapidly changing environment, and new risks may emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed herein may not occur and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Although our management believes that the expectations reflected in our forward-looking statements are reasonable, we cannot guarantee that the future results, levels of activity, performance or events and circumstances described in the forward-looking statements will be achieved or occur. We undertake no obligation to publicly update any forward-looking statements, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.
Business Insider
04-07-2025
- Health
- Business Insider
Just 1 cup of black beans curbs inflammation in your body. Here are 4 science-backed recipes to boost your health.
Beans, beans, the magical fruit. The more you eat, the more you … can cut down on dangerous, chronic low-grade inflammation. Researchers at Illinois Institute of Technology recently discovered just how much black beans can help lower inflammation in a remarkable trial. They gave roughly two dozen people with prediabetes a three-month supply of canned beans. The directions were simple: incorporate one cup of black beans into your diet, every single day for 12 weeks. (In a control group, participants ate white rice instead). Some people mixed their beans into soups, others topped their salads with black beans. Each person in the bean-eating group just had to ensure they were eating a cup per day. It's something that people living in the longevity Blue Zones around the world already do automatically, through force of habit. With this study, there's fresh evidence that their technique can help anybody who is at risk of developing chronic diseases improve their health and longevity. Black beans owe their dark, deep hue to plant chemicals that may also help fend off inflammation In this small study, eating black beans had a big impact on people's levels of a protein called interleukin-6 (IL-6) which is a key marker of inflammation. During the course of the study, black bean eaters reduced their average IL-6 levels from 2.57 picograms per milliliter to 1.88, a significant decrease. Lead researcher Indika Edirisinghe, a professor of food science and nutrition at IIT, says he suspects a big part of the reason why black beans are so great at lowering chronic, low-grade inflammation has to do with the chemicals that give them their rich, deep black coloring. "They have something called polyphenolic compounds," Edirisinghe told Business Insider. "The polyphenolic compounds are bioactive, and they have antioxidant and anti-inflammatory activity." Just in case participants were stumped on how to start incorporating more black beans into each day, they were given a lifeline: Edirisinghe and his team offered participants several mouthwatering bean recipes, including one for black bean brownies, a chicken and black bean chili, a bean "caviar" snack dip, and a colorful bean salad in a jar. "There's no rocket science," Edirisinghe said. "It's very simple, and there's a great opportunity here to become healthy." Here are 4 of the easy — and tasty — black bean recipes patients used during the study Taco salad in a jar Ingredients: 1 15-oz. can of black beans, rinsed and warmed up 1 lb. ground turkey 2 cups of frozen corn, thawed and warmed up 1 head of romaine, chopped 1 cup of shredded pepperjack cheese 1 cup of diced tomatoes 1 tbsp. taco seasoning 2 tbsp. extra virgin olive oil Salt Directions: In a large skillet, heat the olive oil over medium-high heat Add the turkey and season with taco seasoning and salt Cook the turkey, breaking it up with a spoon or spatula, until it is golden and cooked through, about eight to 10 minutes. Then set it aside for five minutes to let it cool. Using six mason jars, layer the turkey, then black beans, corn, romaine, cheese, and tomatoes Refrigerate until ready to eat. (Makes a great lunch!) Black bean brownies 1 15-oz. can of black beans, drained and rinsed 1/2 cup of oats 1/2 tsp. baking powder 2 tbsp. cacao powder 1/4 tsp. salt 1/2 cup maple syrup 1/4 cup coconut oil 2 tsp. vanilla extract 1/3 cup chocolate chips, plus extra for topping Directions: Preheat your oven to 350F Combine all the ingredients except the chocolate chips in a food processor, and blend until very smooth. (If you don't have a food processor, a blender can work, but the consistency won't be as smooth.) Stir in the chips Pour into a well greased 8x8 pan Sprinkle extra chips on top, if you like Cook brownies for 15 to 18 minutes Let cool for at least 10 minutes before cutting If they still look somewhat undercooked, put them in the fridge for an hour to firm up Chicken, quinoa, and black bean chili verde Ingredients: 1 15-oz. can of black beans, rinsed 1 rotisserie chicken, shredded 6 cups of chicken broth 1 cup of quinoa 1 16-oz. jar of salsa verde 3 cloves of garlic, minced 1 large onion, diced 1 tbsp. of canola oil 1 tbsp. of ground cumin Salt Sour cream and cilantro, for serving Directions: In a large pot over medium heat, heat up the oil Cook the onion and garlic until tender, about six minutes Add the cumin, and season with salt Add the beans, chicken, and salsa verde and stir until combined Add 5 cups of the chicken broth and quinoa and bring to a boil Reduce the heat and let it simmer until the quinoa is tender, about 20 minutes If the quinoa absorbs most of the liquid, add the extra cup of chicken broth Serve with sour cream and cilantro Cowboy caviar Ingredients: 1 cup of black beans 1 cup of corn 1 cup of cherry tomatoes, quartered 1 small red onion, finely chopped 2 orange bell peppers, chopped 1 avocado, chopped 1 tsp. salt 1/2 tsp. cumin 1/3 cup of lime juice 1/3 cups of extra virgin olive oil 3 tbsp. of chopped fresh cilantro 1 tbsp. of hot sauce Tortilla chips for serving Directions: In a small bowl, combine the olive oil, lime juice, cilantro, hot sauce, cumin, and salt In a large bowl, combing the remaining ingredients, except the chips Pour the dressing from the small bowl into the large bowl and toss until well combined Serve it up with the chips
Hindustan Times
20-06-2025
- Health
- Hindustan Times
Do you floss your teeth properly? Doctor explains how it can lower heart disease risk
Flossing your teeth can help reduce the risk of heart disease. Dr Kunal Sood, an anesthesiology and interventional pain medicine physician, shared an Instagram post on June 19 in which he shared that research suggests that regular flossing can lower the risk of stroke and heart disease by reducing inflammation and preventing bacterial buildup in the mouth. Also read | Should you floss before or after brushing? Dentist shares what your ideal oral care routine should be In his caption, Dr Sood wrote, 'Can flossing reduce risk of heart disease? Share to help someone cut both gum and heart risk.' Saying how 'gums set off body-wide alarms', he said: 'Plaque trapped between teeth sparks gingivitis, letting Porphyromonas gingivalis and other microbes slip into the bloodstream. Those invaders crank up C-reactive protein (CRP) and IL-6 —the same inflammatory messengers that thicken arterial plaque and boost clotting risk.' Dr Sood added that 'flossing disrupts the oral-heart highway'. 'Adding floss to twice-daily brushing removes up to 80 percent of interdental plaque — far more than brushing alone. In a seven-year study of 40,000+ adults, flossing at least once a week was linked to: 22 percent lower ischemic-stroke risk, 44 percent lower cardio-embolic-stroke risk, and 12 percent lower atrial-fibrillation risk.' A post shared by Kunal Sood, MD (@doctorsoood) Explaining why frequency — and timing — matter, Dr Sood said, 'Every floss session breaks up biofilm before it inflames gum vessels. Even weekly flossing trims systemic inflammation, but daily use keeps the bacterial 'drip' shut off almost completely.' He also shared: 1. Floss daily (string, picks, or water-flosser); if that's tough, aim for several times per week — consistency beats perfection. 2. Brush twice daily and book professional cleanings every six months; scaling alone can drop CRP within weeks. 3. Spot warning signs — bleeding gums, chronic bad breath, looseness — then schedule a periodontal check-up. 4. Reinforce the win with cardio basics: quit smoking, manage blood sugar, move daily. The same habits that protect gums fortify arteries. Note to readers: This article is for informational purposes only and not a substitute for professional medical advice. Always seek the advice of your doctor with any questions about a medical condition.
Yahoo
10-06-2025
- Business
- Yahoo
Monte Rosa Therapeutics Announces FDA Clearance of IND Application for MRT-8102, a NEK7-Directed Molecular Glue Degrader for the Treatment of Multiple Inflammatory Diseases
MRT-8102, a highly selective NEK7-directed molecular glue degrader (MGD) developed to treat inflammatory conditions linked to NLRP3, IL-1β, and IL-6 dysregulation, expands Monte Rosa's clinical I&I portfolio Potency, selectivity, and long-lasting pharmacodynamics of MRT-8102 observed in preclinical studies create potential for clinical differentiation from competitive approaches for inflammatory diseases MRT-8102 Phase 1 clinical results, including data on safety, pharmacokinetics, NEK7 protein degradation, and key downstream pharmacodynamic markers, expected in H1 2026 BOSTON, June 10, 2025 (GLOBE NEWSWIRE) -- Monte Rosa Therapeutics, Inc. (Nasdaq: GLUE), a clinical-stage biotechnology company developing novel molecular glue degrader (MGD)-based medicines, today announced U.S. Food and Drug Administration (FDA) clearance of an Investigational New Drug (IND) application for MRT-8102, a NEK7-directed MGD being developed for the treatment of inflammatory diseases driven by the NLRP3 inflammasome and IL-1β. The Company plans to initiate a Phase 1 study of MRT-8102 in the coming weeks and anticipates sharing initial results in H1 2026. 'The IND clearance of MRT-8102 is another important milestone in our quest to broadly establish MGDs as a modality in immunology and inflammatory (I&I) indications. MRT-8102, following on the heels of our VAV1-directed MGD MRT-6160, is our second IND specifically for I&I indications, and represents the only clinical-stage MGD that selectively targets NEK7, with potential to address multiple inflammatory diseases, including cardio-immunology, rheumatology, and respiratory indications,' said Markus Warmuth, M.D., Chief Executive Officer of Monte Rosa Therapeutics. 'We believe MRT-8102 could provide a highly differentiated clinical profile compared to IL-1 antibodies and NLRP3 inhibitors in development based on its potency, selectivity, and long-lasting pharmacodynamics. We look forward to initiating a Phase 1 healthy volunteer study in the coming weeks, with clinical results expected in H1 2026, including data on safety, pharmacokinetics, NEK7 protein degradation, and downstream pharmacodynamic markers. As part of the Phase 1 study, we plan to establish initial proof-of-concept (POC) for cardio-immunology indications by evaluating changes in C-reactive protein (CRP) and other key inflammatory markers in a cohort of subjects with high CRP levels.' Monte Rosa believes its preclinical studies support MRT-8102's potential to address multiple inflammatory diseases driven by the NLRP3 inflammasome, IL-1β and IL-6. MRT-8102 has demonstrated nanomolar-level degradation of NEK7 in vitro with no off-target activity observed, including related NEK family proteins. In non-human primates (NHPs), oral administration of MRT-8102 resulted in near-complete inhibition of downstream inflammatory markers in ex vivo stimulation assays, as well as improvements in pathological measures in inflammatory disease models. Furthermore, in a rabbit gout model, daily oral dosing of MRT-8102 was observed to reduce pathogenic effects, including a reduction in joint swelling and histopathology scores. Preclinical GLP toxicology studies suggest a considerable safety margin for MRT-8102, with a greater than 200-fold exposure margin over the projected human efficacious dose in both rats and NHPs. In addition to MRT-8102, Monte Rosa is also working to advance a second-generation NEK7 program with enhanced CNS penetration with an IND submission expected in 2026. Monte Rosa retains full worldwide rights to MRT-8102 and its second-generation CNS-optimized NEK7 MGDs. About MRT-8102MRT-8102 is a potent, highly selective, and orally bioavailable investigational molecular glue degrader (MGD) that targets NEK7 for the treatment of inflammatory diseases linked to NLRP3, IL-1β, and IL-6 dysregulation. NEK7 has been shown to be required for NLRP3 inflammasome assembly, activation and IL-1β release both in vitro and in vivo. Aberrant NLRP3 inflammasome activation and the subsequent release of active IL-1β and interleukin-18 (IL-18) has been implicated in multiple inflammatory disorders, including cardiovascular disease, gout, osteoarthritis, neurologic disorders including Parkinson's disease and Alzheimer's disease, and metabolic disorders. In a non-human primate model, MRT-8102 was shown to potently, selectively, and durably degrade NEK7, and resulted in near-complete reductions of IL-1β and caspase-1 following ex vivo stimulation of whole blood. MRT-8102 has demonstrated a considerable safety margin (>200-fold exposure margin over projected human efficacious dose) in GLP toxicology studies. About Monte RosaMonte Rosa Therapeutics is a clinical-stage biotechnology company developing highly selective molecular glue degrader (MGD) medicines for patients living with serious diseases in the areas of oncology, autoimmune and inflammatory diseases, and more. MGDs are small molecule protein degraders that have the potential to treat many diseases that other modalities, including other degraders, cannot. Monte Rosa's QuEEN™ (Quantitative and Engineered Elimination of Neosubstrates) discovery engine combines AI-guided chemistry, diverse chemical libraries, structural biology, and proteomics to rationally design MGDs with unprecedented selectivity. Monte Rosa has developed the industry's leading pipeline of MGDs, which spans autoimmune and inflammatory diseases, oncology, and beyond. Monte Rosa has a global license agreement with Novartis to advance VAV1-directed molecular glue degraders and a strategic collaboration with Roche to discover and develop MGDs against targets in cancer and neurological diseases previously considered impossible to drug. For more information, visit Forward-Looking Statements This communication includes express and implied 'forward-looking statements,' including forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements include all statements that are not historical facts and in some cases, can be identified by terms such as 'may,' 'might,' 'will,' 'could,' 'would,' 'should,' 'expect,' 'intend,' 'plan,' 'objective,' 'anticipate,' 'believe,' 'estimate,' 'predict,' 'potential,' 'continue,' 'ongoing,' or the negative of these terms, or other comparable terminology intended to identify statements about the future. Forward-looking statements contained herein include, but are not limited to, statements about our ability to grow our product pipeline, our ability to successfully complete research and further development and commercialization of our drug candidates in current or future indications, including the timing and results of our clinical trials and our ability to conduct and complete clinical trials, statements regarding our progress and speed of development of only-in-class and first-in-class molecular glue degrader therapeutics, statements around the Company's QuEEN™ discovery engine and the Company's view of its potential to rationally design MGDs with unprecedented selectivity, statements about the advancement and timeline of our preclinical and clinical programs, pipeline and the various products therein, including the ongoing development and progress of our NEK7-directed MGD, referred to as MRT-8102, our plans to initiate a Phase 1 study of MRT-8102 in the coming weeks and our expectations for the design and advancement of such Phase 1 study, including updates related to status, safety data, pharmacokinetics, NEK7 protein degradation, and key downstream pharmacodynamic markers and timing of data read-outs, including the planned readout in the first half of 2026, the Company's statements around the potential of MRT-8102 to address multiple inflammatory diseases driven by the NLRP3 inflammasome, IL-1β and IL-6, including cardio-immunology, rheumatology, and respiratory indications and the Company's belief that MRT-8102 could provide a highly differentiated clinical profile compared to IL-1 antibodies and NLRP3 inhibitors in development based on its potency, selectivity, and long-lasting pharmacodynamics, statements relating to MRT-8102's safety margin, as well as statements around the advancement and timeline of a second-generation NEK7 program and expectations to submit an IND to the FDA in 2026, the expected potential clinical benefit of any of our candidates, advancement and application of our platform, statements around our ability to capitalize on and potential benefits resulting from our research and translational insights, including announcements related to preclinical programs, statements regarding regulatory filings for our development programs, including the planned timing of such regulatory filings, such as IND applications, and potential review by regulatory authorities, as well as our expectations of success for our programs, among others. By their nature, these statements are subject to numerous risks and uncertainties, including those risks and uncertainties set forth in our most recent Annual Report on Form 10-K for the year ended December 31, 2024, filed with the U.S. Securities and Exchange Commission on March 20, 2025, and any subsequent filings, that could cause actual results, performance or achievement to differ materially and adversely from those anticipated or implied in the statements. You should not rely upon forward-looking statements as predictions of future events. Although our management believes that the expectations reflected in our statements are reasonable, we cannot guarantee that the future results, performance, or events and circumstances described in the forward-looking statements will be achieved or occur. Recipients are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date such statements are made and should not be construed as statements of fact. We undertake no obligation to publicly update any forward-looking statements, whether as a result of new information, any future presentations, or otherwise, except as required by applicable law. Certain information contained in these materials and any statements made orally during any presentation of these materials that relate to the materials or are based on studies, publications, surveys and other data obtained from third-party sources and our own internal estimates and research. While we believe these third-party studies, publications, surveys and other data to be reliable as of the date of these materials, we have not independently verified, and make no representations as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent source has evaluated the reasonableness or accuracy of our internal estimates or research and no reliance should be made on any information or statements made in these materials relating to or based on such internal estimates and research. InvestorsAndrew Funderburkir@ MediaCory Tromblee, Scient PRmedia@
