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Gladstone Institutes conducts biomedical research in areas such as cardiovascular disease, HIV, dementia, and diseases of the brain and eye. It runs basic and translational science programs to understand disease mechanisms and develop therapies, using techniques like CRISPR gene editing and stem cell research, often in collaboration with UCSF. Its work is organized around centers and directorates, with an emphasis on team-based investigation and training. Unlike many industry-funded firms, Gladstone is a nonprofit research institute that relies on philanthropy and partnerships to push scientific discoveries toward medical advances. The goal is to use science and technology to overcome major unsolved diseases and improve human health.
Industries
Biotechnology
Healthcare
Company Size
501-1,000
Company Stage
Grant
Total Funding
$250K
Headquarters
San Francisco, California
Founded
1979
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New toolkit turns macrophages into better cancer fighters. A team of scientists from Gladstone and UCSF developed a new method to genetically edit myeloid cells, immune cells that act as the body's first responders. For more than a decade, scientists have used CRISPR gene editing to study the DNA sequences that control human T cells and to reprogram their functions, including massive efforts to develop improved living cancer drugs known as CAR-T therapies. But T cells are only one branch of the human immune system. Myeloid cells - a group of immune cells that include monocytes, macrophages, and dendritic cells - have remained largely off-limits to this kind of engineering, even though these cells are often the first responders to infection, injury, and tumors. Now, researchers at Gladstone Institutes and UC San Francisco (UCSF), along with collaborators at several other institutions, have developed a toolkit to deploy CRISPR in myeloid cells. Their approach, described in Nature Biotechnology, uses virus-like particles - empty viral shells repurposed as delivery vehicles - to carry gene-editing machinery into the immune cells. "We had a realization that we weren't really tapping into this whole other arm of the immune system to help fight some of the most difficult diseases out there," says Julia Carnevale, MD, an affiliate investigator at Gladstone, an assistant professor of hematology and oncology at UCSF, and co-senior author of the study. "We wanted to unlock the power of these other cells." Carnevale and her colleagues identified a gene that acts as a brake on inflammation - removing this gene could help cells be better at fighting cancer cells. Using the new toolkit, the team screened thousands of genes inside living human macrophages and identified a gene that acts as a brake on inflammation. Removing that brake from re-engineered macrophages made the cells dramatically better at fighting cancer cells. "We now have a whole toolbox of CRISPR perturbations we can make in myeloid cells, which took us a decade to build up in T cells," adds Alex Marson, MD, PhD, director of the Gladstone-UCSF Institute of Genomic Immunology and co-senior author of the study. "Beyond our initial observations with these tools in macrophages, this is an important technology resource for the field." A better delivery system. Myeloid cells have been notoriously difficult to engineer. The standard method for getting CRISPR gene editing machinery into cells, called electroporation, uses a jolt of electricity to poke temporary holes in a cell's outer membrane. It works well in T cells, but in monocytes, macrophages, and dendritic cells, it renders them unresponsive - likely because the cells are so sensitive to stress as a function of their job. "The old way of editing works well to edit genes, but the surprise was that, for myeloid cells, it left the cells dysfunctional," Marson says. As they searched for genes that control inflammation in myeloid cells, the research team co-led by Marson combined different technologies to create a new system that allowed them to test thousands of genes at once. In the new work, Marson and Carnevale's labs turned to virus-like particles that can carry proteins, including gene editing machinery, into a cell through their infection mechanism. Beyond simply deleting genes, the team showed they could use the new system to make targeted single-letter DNA changes (called base editing), silence genes without deleting their sequences, and even insert large new stretches of DNA. "This system can allow us achieve high editing efficiency, and also use the same platform for base editing and epigenetic silencing," says Hyuncheol Jung, PhD, co-first author of the study and a postdoctoral scholar in the Carnevale and Marson labs. "So instead of building a new delivery method for every kind of edit we want to make, we have one flexible toolkit that can do all of them in these cells." An inflammatory brake. To search in an unbiased way for genes that control inflammation in myeloid cells, the team needed to be able to test thousands of genes at once and trace which gene had been disabled in which cell. That required a second delivery tool: a modified virus that could both carry genetic instructions into each cell and permanently record which instruction it had received. That's where the researchers hit a new obstacle. Myeloid cells carry a built-in defense that normally blocks viruses from writing anything into their DNA. To overcome this, the team borrowed a trick from HIV; they used a protein that disables the immune defense. Paired with their virus-like-particle delivery, this combined system, called SLICeVLP, let them test the effect of removing thousands of different genes, one at a time, from living macrophages. The two first authors of the study, Hyuncheol Jung (left) and Pascal Devant (right), helped develop a toolkit that can now be used by many scientists studying myeloid cell biology in the lab. Running multiple separate screens, the researchers looked for genes that control different facets of immune activation in macrophages. The same gene rose to the top across multiple screens: TNFAIP3, which encodes a protein called A20. A20 was already known from mouse studies to act as a brake that keeps macrophages from becoming overly inflammatory, but there had been no way to target that brake directly in human macrophages. Now, for the first time, the researchers had an easy way to test whether disabling A20 could be useful therapeutically. They began with CAR-macrophages - macrophages that have been engineered with cancer-targeting receptors, similar in concept to the CAR-T cells. Then, they used their system to remove the TNFAIP3 gene encoding A20. The edited cells became more inflammatory, significantly better at killing cancer cells, and more resistant to the immune-suppressing signals that tumors produce to shut down the immune system. "Our screens helped us prioritize certain genes over others as potential targets," says Pascal Devant, PhD, co-first author of the study and a postdoctoral scholar in Marson's lab. "The question is always: what's a gene you'd actually want to target in a therapy?" Toward the future. The new myeloid gene editing system isn't yet ready to test in human therapeutics - the scientists found some small unintended genetic changes in cells edited with the base editing machinery, for instance. But they see the tool as the beginning of a new era of exploring myeloid cell biology in the lab. "We've had a lot of interest from people studying anything from neurobiology to atherosclerosis of the cardiovascular system," Marson says. "This toolset can help a lot of scientists probe these cells in whole new ways, in the context of whatever disease they're studying, from cancer to autoinflammatory and infectious diseases." The researchers are continuing to fine-tune the editing toolset, as well as scale it up to make more genetic edits and in more myeloid cell types. "We're excited to see what people do with this technology," Carnevale says. For Media Julie Langelier Associate Director, Communications 415.734.5000 Email About the Study The paper, "Virus-like particles enable targeted gene engineering and pooled CRISPR screening in primary human myeloid cells," was published in the journal Nature Biotechnology on August 17, 2026. In addition to Carnevale, Marson, Devant, and Jung, authors are Mineto Ota, Emma Dann, Ronghui Zhu, Chandrima Modak, Ana Vasquez-Ibarra, Zachary Steinhart, Jae Hyun J. Lee, Vincent Allain, Brian R. Shy, Justin Eyquem, and Jennifer A. Doudna of Gladstone; Carter Ching, Luis Sandoval, Jae Hyung Jung, Esha Urs, Peixin Amy Chen, and Luke A. Gilbert of UC San Francisco; Jonathan K. Pritchard of Stanford University; Jennifer R. Hamilton (now at Azalea Therapeutics), Wayne Ngo, Da Xu, and James K. Nuñez of UC Berkeley; Meirui An and David R. Liu of the Broad Institute of MIT and Harvard; and Takuya Tada and Nathaniel R. Landau of NYU Grossman School of Medicine. The work was supported by the National Institutes of Health (grants DA046100, AI122390, R35GM155044, K08CA252605, DP2CA311215, U54AI170792, P01AI55393, R01DK129364, and R01CA276368), the Laboratory for Genomics Research, the Bakar Fellows Program, the Weill Neurohub Fellows Program, the Astellas Foundation for Research on Metabolic Disorder, the Chugai Foundation for Innovative Drug Discovery Science, the Parker Institute for Cancer Immunotherapy, the Burroughs Wellcome Fund, the Damon Runyon Cancer Research Foundation, the CRISPR Cures for Cancer Initiative; the Lydia Preisler Shorenstein Donor Advised Fund, the Pascarella Scholars Fund, the Simons Foundation, K. Jordan, the Jane Coffin Childs Fund for Medical Research, the National Research Foundation of Korea Postdoctoral Overseas Training Program (RS-2023-00242661), the Chan Zuckerberg Initiative Foundation (CZIF2025-011112), the Silicon Valley Community Foundation, and the Weill Cancer Hub West. About Gladstone Institutes Gladstone Institutes is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. Established in 1979, it is located in the epicenter of biomedical and technological innovation, in the Mission Bay neighborhood of San Francisco. Gladstone has created a research model that disrupts how science is done, funds big ideas, and attracts the brightest minds.
Gladstone Institutes receives National Recognition for Excellence in postdoc programs. Postdoctoral researchers are central to Gladstone's scientific mission, helping drive discoveries that advance the understanding and treatment of disease. Gladstone Institutes has been selected as one of 12 institutions nationwide to receive an Institutional Policy Award from the National Postdoctoral Association's new Excellence Recognition Program. The honor highlights Gladstone's strong alignment with the association's rigorous recommended policies and practices for supporting postdoctoral scholars through mentorship, professional development, workplace policies, and career advancement. "At Gladstone, we recognize that our postdoctoral scholars are primary engines of scientific advancement," says Deepak Srivastava, MD, president of Gladstone Institutes. "They are pushing the boundaries of what's possible and turning ambitious hypotheses into life-saving discoveries. Their success is, quite literally, Gladstone's success." Indeed, postdoctoral researchers are central to Gladstone's scientific mission, helping drive discoveries that advance the understanding and treatment of disease. Gladstone trains well over 100 postdoctoral scholars annually, with support spanning every stage of the training experience. Through its Postdoctoral and Graduate Student Education and Research Development Affairs office, Gladstone provides extensive professional development training, individualized career counseling, leadership development, grant and manuscript writing support, and career exploration resources. Postdoctoral scholars also benefit from structured mentoring practices, including annual individual development plans, mentor and mentee standards, and opportunities to build strong professional networks across the organization. Gladstone supports more than 100 postdoctoral scholars each year with mentorship, professional development, and career resources that help prepare the next generation of scientific leaders. "Our commitment to postdocs goes far beyond simply providing research training," says Sudha Krishnamurthy, PhD, director of Postdoctoral and Graduate Student Education and Research Development Affairs at Gladstone. "We aim to develop the whole scientist - ensuring they have the technical rigor, leadership skills, and mentorship network necessary to become the next generation of global leaders in biomedicine." Gladstone's postdocs go on to become research investigators, educators, life science industry professionals, government workers, and more, Krishnamurthy adds. The policies and programs at Gladstone recognized by the National Postdoctoral Association include transparent compensation practices, comprehensive employee benefits, dedicated services for international scholars, and resources that support mental health and well-being. "Improving the postdoctoral experience is a community effort," says Erin Heckler, PhD, vice chair of the National Postdoctoral Association's board of directors. "The NPA, recognizing the work of these institutions as examples of policies and practices, shares what progress is possible for everyone." The Institutional Policy Award acknowledges Gladstone's efforts to create a training environment where early-career scientists can develop the skills, experience, and professional networks needed to make impactful discoveries and become future leaders in biomedical research. For Media Julie Langelier Associate Director, Communications 415.734.5000 Email About Gladstone Institutes Gladstone Institutes is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. Established in 1979, it is located in the epicenter of biomedical and technological innovation, in the Mission Bay neighborhood of San Francisco. Gladstone has created a research model that disrupts how science is done, funds big ideas, and attracts the brightest minds.
Can AI help us age better? Bay Area scientists are trying to find out. By Panashe Matemba-Mutasa, The Mercury News The Tribune Content Agency June 17, 2026 12:57 PM Gift Article A growing number of researchers are turning to artificial intelligence to understand why some people remain healthy into their 90s while others develop chronic diseases decades earlier. At labs throughout the Bay Area, the technology is fueling a wave of longevity research aimed at measuring how long people live - and how well they age. Researchers say AI can uncover early signs of age-related diseases, predict an individual's biological age and identify factors contributing to healthier lives - all by sifting through vast amounts of data to find patterns nearly impossible for humans to detect. The tools are still being refined. But scientists believe they could accelerate discoveries to improve health and independence into older adulthood. The most ambitious applications of AI in aging research, including speeding drug development and testing, remain years away, experts said. Researchers must also navigate bias within systems trained on data that may not reflect the full diversity of the population. Still, patients are already seeing some benefits, such as AI-assisted scan readings that can reduce the odds of false positives. "We're already seeing the benefits," said Nathan Price, chief scientist at the Buck Institute for Research on Aging in Novato. Any discovery won't be an anti-aging silver bullet. Social, behavioral and structural factors - including whether patients can access or choose to use those treatments - will play an equally important role, said Angie Perone, the director of the Center for the Advanced Study of Aging Services at UC Berkeley. "This is only one piece of an important puzzle," Perone said. Predicting how cells age. Scientists at Gladstone Institutes, based in San Francisco, recently launched an AI model to predict how human cells evolve with age. Trained on millions of cells, the model attempts to map the trajectory of aging, allowing researchers to forecast how cells might change and identify potential drivers of age-related decline. That marks a shift from earlier approaches, which largely compared snapshots of "young" and "old" cells. Instead, the model, developed by scientists led by physician-scientist Christina Theodoris, treats aging as a continuous process that can be learned and predicted. The team also tested some of the model's predictions in biological systems, identifying genes expected to accelerate aging and validating those effects in human heart cells and in mice. That kind of experimental follow-up is essential, experts say, though the research remains in early stages. "The real test will be whether these predictions hold up across many tissues and disease contexts," said Hani Goodarzi, a core investigator at Palo Alto-based Arc Institute, noting current tools, including animal models, are imperfect benchmarks. Significant hurdles remain. The model will require large-scale datasets that track how cells respond to drugs and genetic changes, along with validation across a wider range of tissues and diseases. And even the most accurate predictions must ultimately be translated into real-world therapies. Searching for hidden patterns. At the Buck Institute for Research on Aging, scientists are using artificial intelligence to figure out how to help people stay healthier for longer. One of the institute's AI projects integrates individual genetic information, clinical lab results, microbiome data and other health measurements. Drawing on a database containing thousands of biological measurements from research participants, the system identifies patterns and generates personalized insights about health risks and interventions. "The microbiome is highly predictive of who will lose weight," Price said, noting that AI can uncover connections hidden within vast datasets. Users can interact with the platform through a chatbot-like interface that generates graphs, health scores and detailed analyses of their data. They expect the tool to be released to the public by the end of the year. It is part of Healthspan Horizons, a large-scale research initiative supported by a $52 million grant that aims to enroll thousands of participants and better understand the biology of aging on an individual level. Detecting disease earlier. Artificial intelligence is also reshaping the way researchers study Alzheimer's disease by shifting the focus from symptoms to the biological changes occurring inside the brain. Rather than relying primarily on memory loss and other cognitive symptoms, AI is helping scientists analyze complex brain scans and other data to identify those changes earlier and more objectively. "The way we see Alzheimer's has shifted from seeing it as a clinical cognitive syndrome to a more biological disease," said Duygu Tosun-Turgut, a professor of radiology and biomedical imaging at UC San Francisco and founding director of Medical Imaging Informatics and Artificial Intelligence at the San Francisco Veterans Affairs Medical Center. That capability is particularly valuable for clinical trials. Before, researchers sometimes enrolled patients whose symptoms resembled Alzheimer's but were caused by other conditions, making it harder to determine whether experimental treatments were effective. AI can help identify people with the disease's true biological signatures, improving both patient selection and trial outcomes. Beyond research, Turgut believes AI could improve access to dementia screening and diagnosis, particularly in underserved communities. Specialized memory clinics remain scarce in many parts of the country, and studies have shown that dementia is often underdiagnosed among people with lower socioeconomic status. "Hopefully, we can develop tools that are cheap and scalable enough to be distributed to every geographic spot in the world," she said. Still, she and other researchers cautioned that AI systems are only as good as the data used to train them. Many research cohorts are disproportionately composed of highly educated participants and may not reflect the demographic diversity of the broader population. And so the promise of AI hinges on a hurdle researchers have yet to fully overcome: bias. Until these systems can consistently produce accurate, equitable results across diverse populations, human oversight remains essential. Still, scientists and startups are betting that AI will play an increasingly central role in unraveling the biology of aging, and, perhaps one day, extending healthy years of life.
Gladstone Institutes receives USD 2m NIAID award for AI-guided phage therapy development. May 20, 2026 Gladstone Institutes has received a USD 2 million NIAID P01 award to establish the PhAIge Therapy Center, a multi-project preclinical program applying AI-guided engineering and molecular typing to accelerate phage therapy development against multidrug-resistant ESKAPE pathogens, with an initial focus on Klebsiella pneumoniae. The five-year grant, running through April 2031, funds two research projects and three supporting cores under principal investigator Seth Lawler Shipman. The first project develops high-throughput, sequencing-based assays to quantify rate constants across each stage of the phage infection cycle - recognition, entry, replication, packaging, and lysis - generating the granular kinetic data needed to rationally select and engineer phages with superior bactericidal activity. The second project uses multiplexed assays to rapidly characterize K. pneumoniae strains by capsule type and susceptibility profile, enabling construction of optimized, off-the-shelf phage cocktails matched to individual clinical isolates. Two specialized cores anchor the translational infrastructure. An Advanced Computational Core integrates bioinformatics pipelines, machine learning, and AI-driven modeling to predict phage-host interactions and guide candidate selection. An Organoid and Human Cell Culture Core incorporates 3D human tissue models and primary cell cultures into early screening, capturing host-pathogen dynamics that standard in vitro assays do not reflect. The program also includes an Administrative Core that manages a development and research pilot program and coordinates with clinical and industry advisors. The P01 mechanism, typically reserved for multi-investigator center-scale efforts, reflects the scope of infrastructure the Gladstone team is assembling. The combination of quantitative infection-cycle assays, AI-guided phage selection, and human-relevant tissue models represents an attempt to address a persistent bottleneck in phage therapy development: the absence of standardized, predictive preclinical tools that can reliably translate to clinical outcomes. ESKAPE pathogens - Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species - account for a substantial proportion of hospital-acquired infections globally and are associated with high rates of multidrug resistance. K. pneumoniae in particular has drawn research attention due to the diversity of its capsule types, which directly determine phage susceptibility and complicate the design of broadly effective phage preparations. NIAID's decision to fund a center structured around capsule typing and AI-guided tailspike engineering reflects the recognized complexity of matching phages to clinical bacterial isolates at scale. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/
Exclusive: biotech group leases 105,000 square feet in S.F. as it plans to hire 300 scientists. By Roland Li, Staff Writer March 25, 2026 Biomedical research nonprofit Gladstone Institutes has leased 105,000 square feet in the last major new building of San Francisco's Mission Bay, part of the company's expansion plans that include hiring 300 new scientists. The deal at 1450 Owens St. includes space for 30 new labs and is one of the city's biggest leases of 2026, so far. It includes the option for Gladstone to purchase the building in the future and is a block from its headquarters at 1650 Owens St. Get Digital Access and Stay Informed With Trusted Local News. Gladstone's work is increasingly focused on using artificial intelligence - a booming sector in Mission Bay - to speed up research around drug discovery. The new building will house the Gladstone Institute of Data Science and Biotechnology and the Gladstone-UCSF Institute of Genomic Immunology. Article continues below this ad "We embed the AI and technology with the biological questions," said Dr. Deepak Srivastava, president of Gladstone. "We are both inventors and rapid adopters of technology." Gladstone's hiring plans would increase its current staff of around 600 scientists by 50%. Research areas include heart disease, infectious diseases, cancer, and neurological diseases including Alzheimer's and Parkinson's. See more S.F. Chronicle on google. Make us a Preferred Source to get more of our news when you search. Gladstone is currently recruiting lab leaders from around the world. That's despite two major challenges in the past year: the Trump administration's hostility to foreign immigration and widespread federal research cuts. Article continues below this ad Around $80 million of Gladstone's $125 million annual budget comes from grants from the National Institutes of Health, and funding dropped by 10% last year, Srivastava said. "In the U.S. we've really benefited from the most brilliant minds coming here. That's certainly under threat," he said. Despite the obstacles, Gladstone is continuing its expansion plans, in part by seeking more philanthropic support. Starting in 2024, Gladstone sought to raise $350 million by 2029. Around $200 million has been raised to date. Major donors include real estate developer and former Giants owners Bob Lurie and wife Connie; real estate developer John Sobrato and wife Susan; former venture capitalist Bill Younger, who is chair of Gladstone's board, and wife Brenda; hedge fund manager William Fisher, who is the son of Gap's co-founders, and wife Sakurako; Divesh Makan, co-founder of Iconiq Capital, and Diksha Makan; and the Dolby family. "The work we're doing is too important to slow at this moment when we have greater opportunity (through technology). I just wasn't willing to slow down," Srivastava said. "Every day we go slower is more people dying." Gladstone was established in 1979 and is named for Jack David Gladstone, a real estate developer who left most of his fortune to biomedical research. The nonprofit was one of the first tenants in Mission Bay in 2004, alongside UCSF. "When I moved here, it was all abandoned warehouses. There was just two buildings. This growth is phenomenal," Srivastava said. Alexandria Real Estate Equities, a major biotech landlord, has also built numerous Mission Bay buildings including 1450 Owens St., which is the last major parcel in the area. DGA Architects and IwamotoScott Architecture designed the building. Alexandria doesn't typically start construction on new buildings until it secures an anchor tenant, but did so at 1450 Owens after requests from the city, said Joel Marcus, Alexandria's executive chairman. Construction started in 2022 and was completed in 2024. (Gladstone will build its own tenant improvements and plans to move in by early 2027.) Marcus called the building "a great place for innovative research," with state-of-the-art lab space. Around half of the building remains vacant, and Marcus said both biotech and AI tenants have shown interest in the remaining space. He called Mission Bay a "thriving metropolis" that now has biotech, AI, housing, and a major sports and entertainment complex in Chase Center. Still, the biotech industry remains in a downturn, with widespread layoffs and funding cuts. Though Gladstone is a nonprofit, it partners with for-profit companies to take drugs through clinical trials and eventual Food and Drug Administration approval. Srivastava is "starting to see the green shoots of a resurgence," with more drug approval activity and investments. "It's been a rough period," he said. "People are starting to see the convergence of AI and biotech is so powerful right now." Get inside access to the deals and developments transforming San Francisco and the Bay Area. March 25, 2026 Business Reporter Roland Li covers commercial real estate for the business desk, focusing on the Bay Area office and retail sectors. He was previously a reporter at San Francisco Business Times, where he won one award from the California News Publishers Association and three from the National Association of Real Estate Editors. He is the author of "Good Luck Have Fun: The Rise of eSports," a 2016 book on the history of the competitive video game industry. Before moving to the Bay Area in 2015, he studied and worked in New York. He freelanced for the Wall Street Journal, the New York Times and other local publications. His hobbies include swimming and urban photography.
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Industries
Biotechnology
Healthcare
Company Size
501-1,000
Company Stage
Grant
Total Funding
$250K
Headquarters
San Francisco, California
Founded
1979
Find jobs on Simplify and start your career today