Radically different
Now leading Sovato as the telesurgery software startup’s CEO, former Intuitive EVP and Chief Digital Officer Brian Miller sees a big opportunity to realize the full potential of remote medical procedures. In a Medical Design & Outsourcing interview ahead of the announcement that he’s joined Sovato, Miller — who joined Sovato co-founder Yulun Wang’s Computer…
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Gilead Sciences has agreed to acquire German-based Tubulis for up to $5 billion, the companies said today, in a deal designed to expand the buyer’s antibody–drug conjugate (ADC) capabilities with a focus on fighting cancer.
Headquartered in Munich, privately held Tubulis has developed next-generation ADC candidates based on its own conjugation, linker and payload technologies intended to more selectively deliver diverse payloads to tumors deemed to be of high unmet need. The companies said Tubulis’ programs and platforms have broad potential across multiple tumor types, complementing Gilead’s development and commercialization expertise in oncology.
“We like the strategic fit and deal terms of the Tubulis (private) acquisition,” Daina M. Graybosch, PhD, senior managing director, immuno-oncology and a senior research analyst at Leerink Partners, wrote this morning in a research note. “This is more than an oncology bolt-on; we see real platform value in application of Tubulis’ ADC technologies to other therapeutic areas, namely virology.”
Tubulis’ lead pipeline candidate, TUB-040, is a sodium-dependent phosphate transport protein 2B (NaPi2b)-targeting topoisomerase-I inhibitor (TOPO1i) ADC that is now under study in the Phase Ib/II NAPISTAR1-01 trial (NCT06303505) assessing its safety, pharmacokinetics, and preliminary efficacy as a treatment for platinum-resistant ovarian cancer and non-small cell lung cancer (NSCLC).
In October at the European Society for Medical Oncology (ESMO), Graybosch noted, Tubulis presented data for TUB-040 showing a confirmed 50% overall response rate (ORR) and a 60% unconfirmed ORR across dose levels and irrespective of target antigen—results that were competitive with more mature datasets from leading TOPO1i ADCs.
“Though the dataset was early, and our primary outgoing question was how durability would mature, we suspect that Gilead saw durability maturing positively in their diligence,” Graybosch added. “If TUB-040 proves active in NSCLC, the program could complement their Trodelvy and IO [immune-oncology] lung programs. We wonder if Gilead saw early clinical NSCLC data in their diligence and if excitement around the emerging signal drove some of Tubulis’ valuation.”
Another Tubulis pipeline candidate, TUB-030, is a 5T4-targeting ADC that according to the companies has shown promising initial clinical data across various solid tumor types. TUB-030 is currently under study in the Phase I/IIa 5-STAR 1-01 trial (NCT06657222), a first-in-human study which aims to evaluate the safety, tolerability, pharmacokinetics, and efficacy of TUB-030 as a monotherapy in patients with advanced solid tumors. Tubulis has said it is developing TUB-030 for up to 13 undisclosed solid tumor indications.
The acquisition deal follows a two-year, up-to-$465 million collaboration with Tubulis launched in December 2024. Gilead gained access to Tubulis’ Tubutecan and Alco5 platforms after signing an exclusive option and license agreement to discover and develop an ADC against a solid tumor target.
At the time, Gilead agreed to pay Tubulis $20 million upfront, received an option that if exercised would have given Tubulis an additional $30 million—plus up to $415 million in payments tied to achieving development and commercialization milestones, as well as mid-single to low double-digit tiered royalties on sales of marketed products resulting from the collaboration.
“Today’s agreement follows a two-year collaboration with Tubulis, which has given us strong conviction in their programs and research capabilities,” Gilead Chairman and CEO Daniel O’Day said in a statement. “The agreement to acquire Tubulis is a significant milestone in Gilead’s progress in oncology. The company brings a clinical-stage candidate that is a potential new treatment for ovarian cancer, as well as a next-generation ADC platform and a promising early pipeline.”
“Bringing this potential into Gilead would further expand what is already the strongest and most diverse pipeline in our company’s history,” O’Day declared.
Investors appeared less enthusiastic about the acquisition, as shares of Gilead dipped 1.7% in early Tuesday trading to $137.80 as of 12:01 p.m. ET.
Tubulis is Gilead’s third announced acquisition this year. The biotech giant announced plans in March to buy Ouro Medicines for up to $2.18 billion, and in February agreed to acquire Arcellx for up to $7.8 billion—for which it agreed last week to extend its tender offer until 5 p.m. ET on April 24.
Under the acquisition deal, Gilead agreed to acquire all of the outstanding equity of Tubulis for $3.15 billion in upfront cash payable at closing, and up to $1.85 billion in payments tied to milestones.
The transaction is expected to close in the second quarter subject to expiration or termination of specified regulatory filings and other customary conditions.
Upon closing of the deal, Tubulis will operate as a dedicated ADC research organization within Gilead, with the Munich site serving as a hub for ADC innovation, building on its integrated discovery, manufacturing, and clinical capabilities to advance next generation ADCs.
Gilead said it plans to finance the transaction with a combination of cash on hand and senior unsecured notes. Gilead finished 2025 with $10.605 billion of cash, cash equivalents and marketable debt securities, up from $9.991 billion as of December 31, 2024.
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Good morning. Here in Chicago, cherry blossoms are blooming, rat birth control is working, and it finally feels like spring may be upon us.
As part of President Trump’s 2027 budget blueprint, the FDA has proposed policies aimed at encouraging domestic development and manufacturing of drugs, such as making it easier for drugmakers to move into clinical testing in the U.S. and giving an “exclusivity” period to U.S.-based generics manufacturers.
A new study published in Nature Chemical Biology titled, “Munc13-4–STX7 inhibitors impair endosomal TLR activation and systemic inflammation,” scientists from Scripps Research have developed a new class of drug compounds, called ENDOtollins, that reduce harmful inflammation while maintaining the body’s ability to fight infections. The results offer new directions to treat autoimmune diseases, such as lupus, and rheumatoid and juvenile arthritis, which together affect more than 15 million Americans.
“A key component of our approach is to begin by understanding the biological mechanisms at play,” said Sergio Catz, PhD, professor at Scripps Research and corresponding author of the study. “By accomplishing this first, we can more easily target the pathway driving inflammation without affecting other important processes.”
Current autoimmune disease treatments, such as hydroxychloroquine, function by broadly blocking endosomes. While effective, this approach can lead to significant side effects, including gastrointestinal problems and, less commonly, vision damage, that cause patients to stop treatment.
The authors focused on two proteins, Munc13-4 and syntaxin 7, that bind together to activate Toll-like receptors (TLRs), immune sensors that activate endosomes. This mechanism plays a key role in detecting foreign DNA and RNA from viruses and bacteria. In autoimmune diseases, TLRs become overactive and trigger chronic, damaging inflammation in the absence of a threat.
The team screened roughly 32,000 compounds and identified molecules that specifically block the Munc13-4–syntaxin 7 interaction without disrupting other cellular functions. Given that Munc13-4 is found mainly in immune cells, the compounds offer a targeted approach to reduce inflammation.
“Most treatments for autoimmune diseases manage symptoms; they don’t change the underlying course of the disease,” said Hugh Rosen, MD, PhD, professor at Scripps Research and co-author of the study. “What’s exciting about this approach is its potential to be disease-modifying: targeting the specific molecular machinery that drives inflammation, rather than broadly suppressing the immune system.”
Notably, the study screened compounds in an intact cellular environment which contrasts from many drug screening approaches, which extract proteins from the cell.
“By maintaining the proteins in their natural environment, we increase the likelihood that compounds we find will actually work in living cells,” said Jennifer Johnson, PhD, first author and senior staff scientist at Scripps Research.
The most potent compound, ENDO12, reduced inflammation in animal models that were also given a TLR-activating molecule. Blood levels of inflammatory markers, including immune system activators IL-6 and IFN-γ, and the enzyme myeloperoxidase, dropped significantly in animals that were treated.
ENDO12 treated animals demonstrated normal antiviral immune response when exposed to a virus. This selectivity addresses the concern that dampening inflammation with immunosuppressive drugs may leave patients vulnerable to infections.
Looking ahead, the team will test ENDOtollins in models that more closely mimic human autoimmune diseases and evaluate the compounds’ chemistry for potential clinical use.
Beyond autoimmune conditions, the researchers suggest ENDOtollins might help treat cytokine storms, the dangerous immune overreactions seen in patients with severe COVID-19 and as a side effect of CAR T cancer therapy. Both involve excessive IL-6 and runaway inflammation.
While translating these findings into treatments for patients remains a long-term goal, Catz emphasizes that the mechanistic insights are valuable in their own right. ENDOtollins can serve as precision tools to probe other cellular processes regulated by endosomes and lysosomes, including pathways implicated in neurodegeneration and immune dysfunction.
The post Autoimmune Disease-Related Inflammation Reduced with ENDOtollins Drug appeared first on GEN – Genetic Engineering and Biotechnology News.
Nature Biotechnology, Published online: 07 April 2026; doi:10.1038/s41587-026-03110-7
Progress toward a true virtual cell will depend on uniting AI’s pattern-finding power with the causal rigor of mechanistic models.
Microplastics have become a defining environmental signature of modern life, turning up in oceans, soil, food, drinking water, and even the air. But their biological fate inside the human body remains far less understood. A new study suggests that these particles may be doing more than simply passing through. Instead, they may be accumulating in one of the body’s most overlooked fluids—bile—and leaving behind measurable cellular damage that could shape future thinking about environmentally driven biliary injury and long‑term health effects. As the authors noted in their abstract, “the long-term accumulation patterns and chronic toxic effects of microplastics within the human biliary system are largely unknown,” underscoring the need for deeper investigation into how these particles behave in the enterohepatic circulation.
Researchers from the Tenth Affiliated Hospital of Southern Medical University (Dongguan People’s Hospital), Sun Yat-sen University, Guilin Medical University, and collaborating institutions reported the findings in Environmental Science and Ecotechnology. Their study, “Microplastics accumulate in human bile and drive cholangiocyte senescence,” provides the first direct evidence that microplastics are not only present in bile but may also contribute to mitochondrial dysfunction and premature aging in cholangiocytes, the epithelial cells that line the bile ducts.
The team collected bile from 14 surgical patients (five without gallstones and nine with gallstones) and used a multimodal analytical approach—pyrolysis–gas chromatography–mass spectrometry, laser direct infrared spectroscopy, and scanning electron microscopy—to characterize the particles. According to the paper, “we show the universal presence of microplastics in human bile,” identifying six polymer types dominated by polyethylene terephthalate and polyethylene, with most particles measuring 20–50 μm. Patients with gallstones carried substantially higher microplastic burdens, raising questions about whether biliary stasis or altered bile composition may influence microplastic retention.
To probe biological effects, the researchers exposed cultured human cholangiocytes to low-dose polystyrene nanoplastics for seven days, simulating chronic exposure. The cells exhibited mitochondrial dysfunction, elevated reactive oxygen species, reduced ATP, Drp1‑mediated mitochondrial fission, and G1 cell‑cycle arrest—hallmarks of senescence. As the authors wrote, chronic exposure “induces mitochondrial dysfunction-associated senescence in cholangiocytes,” suggesting a mechanistic link between environmental microplastics and biliary aging.
One of the most intriguing findings is that melatonin, a widely used antioxidant, partially reversed the mitochondrial and inflammatory damage. While far from a therapeutic recommendation, the result hints at a potential intervention point and gives the study translational relevance.
The work reframes the biliary system as something far more active than a simple transit channel. The data indicate that bile can serve as a reservoir for microplastics and that prolonged exposure may age cholangiocytes by driving mitochondrial dysfunction. The partial rescue with melatonin adds a mechanistic foothold for future intervention, even as the authors caution that broader human studies are essential.
For biotech, the implications are broad. The work highlights bile as a clinically accessible matrix for exposure assessment, opening the door to new diagnostics for environmental toxicology. The mitochondrial stress signature aligns with pathways already being targeted by companies developing senolytics, mitoprotective agents, and anti‑inflammatory therapeutics. The authors wrote that the research provides “a mechanistic foundation for assessing the health risks of plastic pollution and developing therapeutic interventions for environmentally driven biliary disorders.”
The post Microplastics in Human Bile Drive Mitochondrial Dysfunction and Senescence appeared first on GEN – Genetic Engineering and Biotechnology News.
Rodolphe Barrangou, PhD, is the T. R. Klaenhammer Distinguished Professor at North Carolina State University, where he leads the CRISPR Lab. Rodolphe spent nine years at Danisco and DuPont, where he made seminal contributions in the functional characterization of CRISPR as a microbial immune system. He has been at NC State since 2013.
For his CRISPR work, Rodolphe has received several international awards, notably the Canada Gairdner International Award, and has been elected to the National Academy of Sciences, the National Academy of Engineering, and the National Academy of Inventors. Rodolphe is a scientific co-founder of Intellia Therapeutics, Locus Biosciences, TreeCo, Ancilia Biosciences, and CRISPR Biotechnologies, and an advisor to Inari and the IGI. He is also the founding Editor in Chief of The CRISPR Journal (published by Mary Ann Liebert, Inc., a Sage partner), which launched in 2018.
Rodolphe holds a degree from Paris Descartes University and a PhD in functional genomics from NC State.
It has been almost 25 years since the acronym “CRISPR” was first coined. Since then, CRISPR has become a household word, a star of books and films, and a Nobel Prize–winning discovery. This powerful and disruptive genome editing technology has transformed countless fields, including gene therapy, xenotransplantation, de-extinction and agbiotech. Researchers continue to build on the CRISPR chassis, devising new platforms for bespoke genome editing. But major questions remain around clinical safety, commercial development, ethical deployment, and regulatory oversight.
In the first of a new series of GEN Keynote Webinars, Professor Rodolphe Barrangou, PhD (North Carolina State; EIC, The CRISPR Journal) offers a front-row perspective of the CRISPR revolution, the seminal advances, clinical highlights, and rising applications. Almost two decades ago, Barrangou provided the first experimental demonstration of the functional role of CRISPR. With numerous advisory and entrepreneurial activities in the gene editing space, Barrangou is the ideal guide to discuss CRISPR’s progress in the clinic; the state of the CRISPR toolbox; and the regulatory roadblocks and ethical challenges that will shape the application of CRISPR in agbiotech, germline editing, and other arenas.
Registration for this GEN Keynote Webinar is free. Following this live presentation, Dr. Barrangou will answer audience questions.
Produced with support from:
The post CRISPR at 25: The Past, Present, and Future of Genome Editing appeared first on GEN – Genetic Engineering and Biotechnology News.
In a new study published in Science titled, “Mitochondrial metabolism and signaling direct dendritic cell function in antitumor immunity,” researchers from St. Jude Children’s Research Hospital have uncovered a new metabolic mechanism for how tumors disable immune “gatekeeper” cells that initiate response in the presence of cancer. The results offer a new path to improve immunotherapy.
Dendritic cells alert and activate tumor-killing immune cells as a critical part of anticancer immune response. The authors found that tumors reduce dendritic cell function by minimizing mitochondrial fitness to prevent anticancer immune response. Correspondingly, boosting mitochondrial function in dendritic cells enhances antitumor immune activity and strengthens the efficacy of existing immunotherapies.
Within the nutrient-sparse tumor microenvironment, dendritic cells progressively lose mitochondrial activity, which drives cell dysfunction and weakens immune defenses against cancer. When dendritic cells with high mitochondrial activity were introduced into tumors in preclinical mouse models, results showed that immunogenic activity was restored while improving tumor control.
“We found that tumors reprogram mitochondrial metabolism in dendritic cells, reducing their ability to activate the immune system against cancer,” said Hongbo Chi, PhD, St. Jude Department of Immunology chair and corresponding author of the study. “By enhancing mitochondrial function, we could restore dendritic cell activity and rescue antitumor immunity.”
Immunotherapies for cancer, such as immune checkpoint blockade, have greatly improved care for many malignancies, but have not been successful in all cancers. To determine whether these findings could improve immunotherapy effectiveness in tumor-bearing mice, the authors evaluated the administered dendritic cells with high mitochondrial activity in combination with immune checkpoint blockade.
“We saw the most pronounced therapeutic effect in mice treated with the combination of dendritic cells that had high mitochondrial activity and immune checkpoint blockade,” said co-first author Zhiyuan You, PhD, researcher at St. Jude Department of Immunology. “Those combinations synergistically slowed or stopped tumor growth and extended survival far more than either treatment alone.”
To test long-term effects, the researchers exposed combination therapy treated mice to a new tumor after a few months. New tumor growth stopped for these mice, indicating durable, long-term immune memory.
To better understand the relationship between mitochondrial function and dendritic cells, the researchers examined metabolic pathways affected by the tumor microenvironment. They identified a signaling axis composed of two proteins, OPA1 and NRF1, that regulate communication between mitochondria and the nucleus. Expression was greatly downregulated in dendritic cells during tumor progression and acted as a metabolic switch to shut down dendritic cell immunogenic activity.
“We’re seeing a direct regulation of dendritic cells by the tumor microenvironment,” said co-first author Jiyeon Kim, PhD, researcher at St. Jude Department of Immunology. “We have characterized how that results in mitochondrial reprogramming of dendritic cells to benefit cancer, giving us new opportunities to reverse the process.”
The study’s mechanistic insights enable new directions to rewire dendritic cell function and enhance cancer treatments.
“These findings reinforce the central role of dendritic cells in cancer immunity,” Chi said. “By exploring their mitochondrial function in the tumor microenvironment, we have provided a proof-of-principle of how we may be able to improve the next generation of immunotherapies.”
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OneCyte, which focuses on high-throughput single-cell analysis and cell line development technologies, and Kemp Proteins, which specializes in protein engineering and expression solutions, signed a strategic partnership agreement to deliver cell line development services for biopharmaceutical companies.
The collaboration brings together OneCyte’s proprietary single-cell platform for high-throughput and high-speed clone selection with Kemp Proteins’ molecular engineering capabilities, including its machine learning–driven platform, PROTiQ
.
Biopharma companies continue to face significant challenges in cell line development, including long development cycles, suboptimal yields, and high failure rates, particularly for novel and complex molecules, according to Konstantinos Tsioris, PhD, co-founder and president of OneCyte. These challenges can delay regulatory timelines and slow the progression of therapies into the clinic.
The OneCyte-Kemp partnership addresses these pain points by integrating predictive in silico design with rapid and high throughput experimental validation, say officials at both companies. As part of the workflow, amino acid sequences are evaluated using Kemp’s PROTiQ platform to assess developability risks, identify sequence liabilities, and generate structural insights.
The optimized candidates are then paired with OneCyte’s high-performance cell line development platform, which reportedly enables identification of elite clones with higher productivity.
Unlike traditional, rigid development workflows, this integrated approach is designed to adapt quickly to the evolving needs of new therapeutic modalities, notes Tsioris.
“By combining our single-cell technology with Kemp’s deep expertise in protein expression, we are confident that we can address the hardest challenges associated with new modalities, delivering faster timelines and industry-leading titers,” he continues.
“OneCyte’s class-leading single-cell technology, stacked on top of our molecular design and expression capabilities, will provide a powerful and differentiated solution for our global biopharma customers,” says Michael Keefe, CEO of Kemp Proteins.
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Good morning, everyone, and welcome to another working week. We hope the weekend respite was relaxing and invigorating because that oh-too-familiar routine of meetings, deadlines, and the like has returned with a vengeance. You knew this would happen, yes? To cope, we are relying, as always, on cups of stimulation. Our choice today is laced with traces of cocoa. Feel free to join us. Remember, no prescription is required. Meanwhile, here are some tidbits to help you along. Best of luck accomplishing your goals today and, of course, do keep in touch. …
In February, a small biotech company called Kezar Life Sciences reached a breakthrough with the U.S. Food and Drug Administration, agreeing to a plan for a clinical trial it hoped could lead to the approval of its treatment for a rare, debilitating liver disease called autoimmune hepatitis. The problem: The agreement came four months too late, STAT explains. The meeting to discuss trial design, a critical step in the drug development process, had been scheduled for last October. But the FDA abruptly canceled it without explanation. The company could no longer proceed as planned and, without clarity from regulators, its path forward was unclear. Kezar’s investors wanted out, and the biotech was forced to start the process of winding down.
Americans starting weight loss medicines for the first time want lower cost and greater convenience as they consider pills from Novo Nordisk and Eli Lilly, Reuters says, citing seven doctors who specialize in obesity. Novo’s Wegovy pill has been on the market since January, while Lilly’s newly approved Foundayo joins the fray this week. Interviews with the specialists show a promising landscape for oral weight loss drugs as the companies compete for share in the fast-changing obesity treatment market that is seen topping $100 billion a year in the next decade. All seven doctors said they had begun prescribing oral Wegovy, and three said they have prescribed the pill to about 10% of their patients. Of those patients, most are taking a GLP-1 for the first time, rather than switching from injectables, and have not yet reached the highest dose.