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Seres to lay off staff, pause top program in latest reboot

Seres Therapeutics, a cash-strapped developer of microbiome drugs, will cut staff and pause its lead program as part of a reboot that’ll see the company focus resources on earlier prospects for immune diseases. The Cambridge, Massachusetts-based company said T

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Seres Therapeutics, a cash-strapped developer of microbiome drugs, will cut staff and pause its lead program as part of a reboot that’ll see the company focus resources on earlier prospects for immune diseases. The Cambridge, Massachusetts-based company said Thursday it will stop investing in that top program — SER-155, a therapy meant to alleviate complications from stem cell transplants — while seeking funding to move the treatment forward. In the meantime, Seres will prioritize “high-value earlier-stage” programs in immunological conditions and reduce its workforce by about 30%. Those efforts are expected to extend Seres’ cash runway into the third quarter of 2026, the company said in a statement. “As we shift our operational focus to our promising earlier-stage pipeline, we are now in a position to streamline our organization and cost structure,” added co-CEOs Thomas DesRosier and Marella Thorell, in the statement. Seres has long been at the forefront of drug research involving the human microbiome, the trillions of microbes colonizing the human body. The company was formed by Flagship Pioneering, went public in 2015 and, since then, helped bring one of the first microbiome drugs to market — a pill called Vowst for a type of tough-to-treat bacterial infection. But Seres has also dealt with a number of setbacks along the way that have depressed its share price and left it scrambling for cash. An effort to bring an earlier, immunology-focused microbiome drug failed to produce positive results. Seres also struggled to grow Vowst sales , restructured and in 2024, offloaded the medication to its long-time partner, Nestlé Health Science. That deal helped Seres clear debt payments and advance testing of SER-155. But while it’s since accumulated early data and finalized the protocol for a potential Phase 2 study, Seres has again been on shaky footing. Previous CEO Eric Shaff stepped down last year, paving the way for co-leaders DesRosier and Thorell. At the time, the company was exploring “various deal structures” to finance mid-stage development. The company received additional breathing room via a $25 million payment from Nestle, but wasn’t able to secure the needed funding in the ensuing months to start Phase 2 testing of SER-155. As of late November, it only had enough cash to operate through the second quarter of 2026. Now, Seres is pivoting again, choosing instead to halt the SER-155 program altogether while cutting staff and pouring money into different drug programs. Among those candidates is SER-603, which targets immune conditions such as candidate in ulcerative colitis, Crohn's disease, and immune checkpoint-related enterocolitis. Seres is working with Memorial Sloan Kettering Cancer Center on an investigator-sponsored trial evaluating SER-155. Discussions regarding “potential collaborations” for its other programs are ongoing, the company said.

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01Why Muscle Cells Might Do Some Heavy Lifting

Brown was studying gene therapy in the 1990s when he designed a technology to turn mRNA expression on or off in different cells. For the new mouse study, published in Nature Biotechnology , he adapted the technology to turn off mRNA expression in dendritic cells, muscle cells, or liver cells. The researchers then vaccinated the mice with each version, delivering the vaccines both intravenously and intramuscularly. “The results were pretty stunning,” Brown said. When mRNA expression was turned off in muscle cells, T-cell response went down, suggesting muscle cells play a role in immunity. When expression was turned off in liver cells, T-cell expression tripled — indicating liver cells dampen immunity. Turning off expression in dendritic cells had no effect on T-cell activation, though it did reduce the number of killer T cells by as much as half. (Interestingly, no such reduction occurred when the antigen was SARS-CoV-2 spike. Brown is now investigating why different antigens had varying effects.) Knowing all this is crucial for designing effective mRNA vaccines and therapies. That’s because different mRNA therapies require different strategies. Cancer vaccines must boost tumor-fighting killer (CD8+) T cells. For genetic disease treatments, scientists want to avoid triggering the immune system to prevent killing the very cells the mRNA is meant to modify. “Understanding the immunology is extremely important for this class of drug,” Brown said. The finding doesn’t mean dendritic cells aren’t important for mRNA vaccines to work. “It just means that the mRNA doesn’t have to get into those cells to induce an immune response,” Brown said. Instead, the antigen can be transferred to those dendritic cells.

Source: www.medscape.com ↗
02What Comes Next

With data expected in the fourth quarter of 2026, we are prioritizing histology alongside patient-reported outcomes using the Celiac Disease Symptom Diary, one of only two instruments developed in line with U.S. Food and Drug Administration (FDA) guidance, to capture changes in symptoms such as abdominal pain and nausea. Ultimately, the broader aim is to give gastroenterologists and patients a therapeutic option for a disease that has long been managed without one. The future of drug development will not be defined by statistical significance alone, but by whether new therapies also improve the daily burden of living with celiac disease. “The first therapy to cross the line could change the field,” Geller concluded. “It would help establish celiac as a serious medical condition with options beyond a restrictive diet and open the door for what comes next.” Dr. Paul Lizzul is chief medical officer at First Tracks Biotherapeutics, a clinical ‑ stage biotechnology company advancing antibody therapeutics that modulate immune pathways implicated in autoimmune and inflammatory diseases. Marilyn Geller serves as an advisor to First Tracks Bio. Footnotes Abadie V, Jabri B. IL-15: a central regulator of celiac disease immunopathology. Immunol Rev . 2014;260(1):221-234. https://doi.org/10.1111/imr.12191. Yokoyama S, Watanabe N, Sato N, et al. Antibody-mediated blockade of IL-15 reverses the autoimmune intestinal damage in transgenic mice that overexpress IL-15 in enterocytes. Proc Natl Acad Sci U S A . 2009;106(37):15849-15854. https://doi/full/10.1073/pnas.0908834106. Anthony S, Schluns KS. Emerging roles for IL-15 in the activation and function of T-cells during immune stimulation. Research and Reports in Biology . 2015;6:25-37. https://doi.org/10.2147/RRB.S57685.

Source: www.biopharmadive.com ↗
03What the Artificial Neuron Cannot Do

Hersam’s next goal is a small circuit — perhaps 10 artificial neurons — where each one fires differently, and together they accomplish what would require thousands of conventional transistors. “ Silicon achieves complexity by having billions of identical devices,” Hersam said. “The brain is the opposite. It’s heterogeneous. The complexity is at the device level.” But Gaudet sees a gap no circuit design can yet fill: Biological neurons grow new connections and prune old ones, strengthening pathways that are used and weakening those that aren’t. Hersam’s lab’s printed neurons — or any other neuromorphic technology that mimics neuronal dynamics — can’t achieve that level of complexity yet. Brown is careful about the distance remaining between these printed neurons and the real thing. “Neurons are just so flexible,” he said. “They can totally change what they’re doing based on whether they’ve learned something and based on your emotional state. There’s a lot of hidden mysteries.” Sangwan suspects the device has more to reveal. “It’s a nonlinear dynamical system,” he said. “We don’t fully know how many different variables you need to explain it. It’s just the beginning.” Hersam, Sangwan, Brown, Holla, and Gaudet reported having no relevant financial disclosures. Disclosure information for study authors is available in the original study publication.

Source: www.medscape.com ↗
04Lifestyle Matters: How do environmental and lifestyle factors influence Alzheimer’s disease?

Dr. Harrison and Finnish neuroscientist Dr. Miia Kivipelto explore the complex interplay between genetics and lifestyle in Alzheimer's development. Learn how the groundbreaking FINGER study demonstrates potential prevention strategies, and discover the latest evidence on how environmental factors, diet, and chronic conditions influence Alzheimer's risk.

Source: www.biopharmadive.com ↗
05China: Threat or opportunity?

One of the biggest biotech news stories of recent years is China’s continued rise as a biotech and life sciences powerhouse. China conducts a quarter of all clinical trials and drug development and has almost 1,500 new drugs in development.¹ Many China-based biotechs have benefitted from government funds, out-licencing deals with large pharmas and venture capital funding. However, policymakers in the US and EU have concerns about the possible threat to their region’s biosecurity and competitiveness as centres for health and life science research. Given China’s increased importance, ICON Biotech conducted the same biotech sector survey with 100 China-based biotech leaders. The results show that Chinese biotechs face many of the same challenges as biotechs located elsewhere. They share the same funding challenges and burdens associated with increasingly complex clinical trials and regulations.

Source: www.biopharmadive.com ↗
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Peptide Therapy Guide Editorial Team

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