Placebo effects have puzzled and intrigued researchers for decades but, despite playing an important role in modern trial design and treatment development, they remain relatively mysterious. With the development of new treatments in psychiatry, especially psychedelic-assisted psychotherapy, placebo effects are under the spotlight. In this issue, The Lancet Psychiatry presents two Review articles by Matthew Burke and colleagues on reconceptualising placebo and nocebo effects.
[Comment] Assessing adolescents’ use of artificial intelligence in psychiatric practice
In a recent clinical encounter with one of the authors (AP), a young boy with autism insisted that his mother hated him—because ChatGPT said so. After asking whether a parent who sets limits must dislike their child, he interpreted the bot’s confident, literal response as truth. By the time the boy arrived at the clinic, this exchange had already reshaped his affect, relationships, and risk. Encounters like this are increasingly common, and many adolescents now present with beliefs—and sometimes safety concerns—influenced by generative artificial intelligence (AI).
Determinants of Digital Health Literacy Among Patients With Serious Mental Illness: Cross-Sectional Survey
Background: Individuals with serious mental illness increasingly use digital devices and the internet to access health information and services but often face challenges when navigating digital tools, which may limit the benefits they receive from online health resources and digital health care services. Objective: The objective of our study was to assess digital health literacy among individuals with serious mental illness and identify factors influencing this literacy. Methods: Participants were recruited, using convenience sampling, from 2 psychiatric clinics, 1 day-care center, and 4 halfway houses in Taipei, Taiwan, between May 2024 and February 2025. Self-reported data were collected using a survey that incorporated the eHealth Literacy Scale, the Attitudes Toward Computer/Internet Questionnaire, and the Mobile Device Proficiency Questionnaire. Generalized linear modeling was applied to identify factors associated with digital health literacy. Results: Among 255 participants included in the analysis, 83.5% (n=213) reported owning at least 1 digital device. Digital health literacy was significantly lower among individuals who reported greater perceived difficulty in using digital tools (=−1.533, 95% CI −2.350 to −0.717; <.001) and higher distrust in online information (=−0.986, 95% CI −1.916 to −0.056; =.04). By contrast, greater mobile device proficiency (=0.144, 95% CI 0.008‐0.281; =.04) and self-efficacy (=1.777, 95% CI 0.376‐3.177; =.01) were positively associated with digital health literacy. Conclusions: Despite widespread device ownership, digital health literacy was varied and generally suboptimal among patients with serious mental illness. Perceived difficulty and distrust emerged as major barriers; proficiency and self-efficacy facilitated higher literacy. These findings highlight the need for mental health professionals to integrate tailored digital skills training, confidence-building strategies, and ongoing support into digital health interventions for individuals with serious mental illnesses.
<![CDATA[Discover how art, film, and poetry return to the APA meeting—and why psychiatrists practice creativity in every patient encounter.]]>
Pregnancy Sickness Study Identifies New Genetic Links
The University of Southern California (USC) research team that identified the hormone-encoding gene GDF15 as a key driver of pregnancy sickness has identified nine additional genes linked to its most severe form, hyperemesis gravidarum (HG). Six of the identified genes had not been previously linked to the condition.
The Keck School of Medicine of USC team and international collaborators conducted a genome-wide association study (GWAS), scanning the entire genome for differences between women who developed HG during pregnancy and those who did not. They analyzed data from more than 10,000 women with the condition and more than 450,000 controls across European, Asian, African, and Latino ancestries. Their findings offer new clues about the condition and new hope for those affected.
Marlena Fejzo, PhD, a clinical assistant professor of population and public health sciences in the Center for Genetic Epidemiology at the Keck School of Medicine, led the present study and earlier research linking GDF15 to HG. Fejzo told GEN, “The study is much larger than previous studies and on a more diverse population allowing for identification of new genes associated with HG … The new genes give us new directions to explore for prediction, diagnosis, treatment, and response to therapies.”
Fejzo is first author of the team’s published report in Nature Genetics (“Multi-ancestry genome-wide association study of severe pregnancy nausea and vomiting”), in which the team stated, “Potential roles for candidate genes in appetite, insulin signaling, and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues.”
HG, which affects about 2% of women, causes nausea and vomiting so severe that eating can become extremely difficult. “Most pregnancies are affected by nausea and vomiting (NVP), but in 0.3–10.8% of pregnancies the symptoms can be severe enough to cause maternal weight loss and adverse maternal and fetal outcomes,” the authors wrote. HG in its most severe form can even be life threatening.
HG was long misunderstood and often dismissed as psychological, growing evidence shows that it has a strong biological and genetic basis and can lead to severe malnourishment, putting both mother and baby at risk. Current treatments for HG are frequently ineffective in improving patient symptoms, the authors further pointed out, and so increase the risk of pregnancy termination, postpartum depression, and suicidal ideation, along with other maternal and offspring comorbidities. “Therefore, understanding of HG etiology is critical to begin to address the negative impact severe NVP has on maternal and child health.”
While historical hypotheses have previously centered around human chorionic gonadotropin (hCG), recent large-scale genetic studies have implicated the GDF15 gene encoding growth differentiation factor-15—a hormone associated with nausea and vomiting, the authors further pointed out. Earlier research by Fejzo and an international team had shown that the link between HG and GDF15 lies in women’s sensitivity to the hormone. They found that women exposed to lower levels of the hormone before pregnancy because of a mutation in the gene experience more severe symptoms, while women exposed to higher levels of the hormone before pregnancy have less severe nausea and vomiting symptoms.
“GDF15 was identified as the greatest genetic risk factor for HG in both a genome-wide and an exome-wide association study, and a rare mutation in GDF15 was associated with a greater than tenfold increased risk for HG,” the scientists noted in their newly reported study. Fejzo explained to GEN, “The mutation in GDF15 is rare. People who carry the mutation have abnormally low levels of GDF15 when they are not pregnant and that increases their risk of being hypersensitive to it during pregnancy when it is produced in massive amounts by the placenta.”
Commenting on their prior work implicating a role for GDF15 and HG, Fejzo further explained to GEN, “In our first GWAS study we found the association between the GDF15 gene and HG. Next, we published a whole-exome sequencing study that identified a mutation in GDF15 associated with HG. Then we published our study in Nature which provided strong evidence that hypersensitivity to the rise of GDF15 in pregnancy (due to low pre-pregnancy GDF15 in circulation) is the main driver of the condition.”
For their newly reported study the researchers carried out a multi-ancestry genome-wide association study of 10,974 HG/excessive vomiting in pregnancy cases and 461,461 controls across European, Asian, African, and Latino ancestries from nine contributing studies.
The results identified 10 genes that were linked to HG, including four that had previously been identified, and six new genes. “Because this is the largest study of HG ever conducted, we’ve been able to tease out important new details that were previously unknown,” said Fejzo. “The fact that we’ve studied women from multiple ancestry groups suggests that these results may be generalizable across a broad population.”
The four genes previously identified were growth differentiation factor 15 (GDF15), GFRAL, which produces the receptor for the GDF15 hormone of the same name, and IGFBP7 and PGR, both of which are involved in development of the placenta. The strongest link by far was to GDF15, which rises sharply during pregnancy. “We know that GDF15 and it’s receptor GFRAL are the main drivers and are in a signaling pathway that causes aversions, nausea, and vomiting,” Fejzo told GEN. “More work needs to be done to explore the other associations, but since studies suggest manipulating progesterone and/or IGFBP7 may not be safe in pregnancy, current studies are focusing on the GDF15 pathway.”
The six newly identified genes offer further clues that might help explain the basis of HG or point to new ways of treating it. They include FSHB, TCFL72 SLITRK1, SYN3, IGSF11, and CDH9. “Now that we’ve more than doubled the genes associated with HG, we can dig deeper into the biology behind this condition, as well as new possible pathways for treating it,” Fejzo said. Speaking to GEN, the researchers noted, “Because the new associations are novel, we need to understand the roles they may play in normal pregnancy and then compare that to pregnancies affected by HG.”
Of the newly identified genes, TCF7L2 stands out because it is one of the strongest genetic risk factors for type 2 diabetes and is also associated with gestational diabetes. “This is a brand-new target, and it’s not yet clear what it’s doing in pregnancy,” Fejzo said. In further commentary to GEN, Fejzo added, “The TCF7L2 gene is a type 2 diabetes-associated gene and a transcription factor that may control glucagon-like peptide-1 (GLP-1) expression and has been associated with liraglutide effects resulting in greater weight loss in obesity. So understanding its role in that rapidly evolving therapeutic arena has potential.”
Several of the other genes identified are involved in appetite and nausea, as well as brain plasticity, or how the brain learns and adapts to new information. Fejzo suggests the brain may learn to associate certain foods with feeling sick, leading to strong, lasting aversions during pregnancy. More research is needed to explore this possibility. “Other genes are associated with learning flexibility so we hypothesize that they may play a role in conditioned taste aversion and may provide new targets to alter or dampen learned aversions,” Fejzo told GEN. Historically, people believed the pregnancy hormone hCG was the cause, but we found no evidence to support that and instead, fascinatingly, we found a link to the follicle stimulating hormone receptor.”
Of the ten candidate genes six—GDF15, GFRAL, IGFBP7, PGR, TCF7L2 and SYN3—have been linked with cachexia—a wasting condition with similar symptoms to HG, including loss of appetite, weight loss and muscle wasting, the scientists noted. “Manipulation of GDF15, GFRAL, IGFBP7, PGR and TCF7L2 in animal models has shown effectiveness in reducing symptoms of cachexia. Thus, assuming analogous functions for these factors in HG, there is both genetic and biological support for causal and potentially reversible contributions for these genes in NVP.”
The researchers also found that some genes linked to HG were associated with other pregnancy outcomes. “This study also identified individual associations between risk genes and adverse outcomes including shorter pregnancy duration, pre-eclampsia, and birth weight,” they noted.
Several medications are available for treating HG, but even the most effective, Zofran, only partly relieves symptoms for about half of patients. The new findings reveal new potential treatment targets and could possibly also help match existing medications to patients based on their genetic profiles. “The ten genetic associations provide intriguing avenues to advance our understanding and pursue therapeutic pathways for a common pregnancy condition that in its most severe form is associated with substantial morbidity and even mortality for mothers and exposed offspring,” the scientists concluded.
Fejzo and her team just received approval to launch a clinical trial of metformin, a widely used diabetes medicine that increases GDF15 levels. The study will test whether taking metformin before pregnancy can desensitize women to the hormone, potentially reducing nausea and vomiting or preventing HG in women who have had it before. GEN was told, “We will be initiating a clinical trial to increase GDF15 prior to pregnancy in patients with a history of HG and planning to conceive to desensitize them to the hormone’s rapid rise in early pregnancy. We and others have shown preliminary evidence that this approach may work as in our retrospective study pre-pregnancy metformin use was associated with a significant reduction in HG risk.”
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Cancer Cell Apoptosis Avoided by Membrane Oligomerization
Apoptosis in cancer cells may be easier to unleash than previously thought, according to new research led by scientists at Umeå University and collaborators. That finding could open up more cancers to treatment with anti-apoptotic drugs. The team used neutron reflectometry (NR) and ATR-FTIR to detail communication between proteins in and around the mitochondrial outer membrane (MOM).
“We use neutrons as a kind of ‘x-ray’ magnifying glass to study how various proteins talk to each other inside the cell,” Gerhard Gröbner, PhD, told Inside Precision Medicine. He is a professor at Umeå University and senior author of a new study that looks at the role of the Bax protein in apoptosis. The findings appear in ACS Chemical Biology.
Apoptosis is a form of programmed cell death that removes old or damaged cells, enabling the immune system to function properly. When apoptosis does not work as it should, as in many cancers, cells can divide uncontrollably and form tumors.
Many cancer therapies (e.g. drugs and radiation) are designed to trigger apoptosis in tumors. But there are also many aggressive and often incurable cancers that current anti-apoptotic therapies do not work on due to these tumors’ intensive use of survival proteins, such as Bcl-2 and its relatives, which can stop apoptotic death.
“Finding new drugs to inhibit Bcl-2 and its relatives in a wider sense would thus help treat more cancers. Currently only one Bcl-2 drug is available, and it is used for very specific leukemia,” said Gröbner.
“Going forward we will test a range of potential drug candidates to block Bcl-2 to release cell-killing proteins like Bax again to improve therapies,” he added.
The cell‑killing protein Bax protein is one of the most important proteins controlling apoptosis. Once activated, Bax can initiate apoptosis by forming pores in the membranes of mitochondria. Another key protein from the same family, the cell‑protective protein Bcl‑2, instead prevents Bax from killing tumor cells. In nearly half of all human cancers, one of the underlying problems is an increased production of Bcl‑2, which promotes tumor growth and often leads to poor response to therapy.
“In our research, we have used advanced neutron experiments to show how Bcl‑2 protects cancer cells by blocking the death‑inducing proteins that are most often activated by therapy,” said Gröbner.
The team used NR and ATR-FTIR to elucidate the molecular communication between those proteins in and around the mitochondrial outer membrane (MOM). The spatial and temporal changes across model MOM surfaces were resolved during the interaction of Bax with Bcl-2. The NR-derived membrane surface Bax distributions suggested that Bcl-2 mediated Bax sequestration through both Bcl-2/Bax heterodimerization and Bax/Bax oligomerization. Kinetic analysis revealed a two-step process: rapid formation of Bcl-2/Bax heterodimers, followed by slower Bax oligomerization on these complexes
The experiments show that Bcl‑2 can capture and bind several Bax proteins at the same time. This makes the inhibition of cell death more efficient than previously thought. Cancer cells do not need to produce extremely large amounts of Bcl‑2 to protect themselves—even a moderate increase can be sufficient.
The researchers also investigated how the composition of the mitochondrial membrane affects the interaction between the proteins. They found one particular lipid, cardiolipin, can promote apoptosis and help Bax form pores in the membrane. However, even in membranes containing cardiolipin, a sufficiently high level of Bcl‑2 can still prevent cell death.
“In the longer term, this type of knowledge could open up new opportunities for cancer treatment, for example by targeting Bcl‑2 and its protective function,” says Gröbner.
The study was carried out in collaboration between researchers from Umeå University, Lund University, the European Spallation Source (ESS) in Lund, the ISIS Neutron and Muon Source and Diamond Light Source in the United Kingdom, and the Institut Laue‑Langevin (ILL) in France.
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Pivotal Phase III Pancreatic Cancer Trial Advances RAS-Targeting Daraxonrasib
This week, Revolution Medicines (RevMed) announced positive topline results from its global Phase III trial of RAS-targeting daraxonrasib in metastatic pancreatic ductal adenocarcinoma (PDAC) patients. In RASolute 302, patients on daraxonrasib showed improvements in progression-free survival (PFS) and overall survival (OS) compared with standard of care cytotoxic chemotherapy.
“With these unprecedented results, daraxonrasib has the potential to achieve our goal of bending the mortality curve in pancreatic cancer. Unlike chemotherapy, daraxonrasib is a RAS-targeted medicine that targets RAS in its active ‘ON’ state, shutting down a key signaling pathway that drives aggressive tumor growth. This is especially important in pancreatic cancer, which is among the most RAS-driven cancers, with more than 90% of tumors harboring a RAS mutation that is the driver of the cancer,” Mark A. Goldsmith, MD, PhD, told Inside Precision Medicine. He is chief executive officer and chairman of Revolution Medicines.
Daraxonrasib patients achieved a median OS of 13.2 months versus 6.7 months for chemotherapy. The drug was generally well tolerated, with a manageable safety profile and with no new safety signals.
RAS is the key oncogenic driver of pancreatic cancer. Nearly all RAS mutations occur at KRAS position G12, but RAS mutations in other isoforms and at KRAS positions G13 and Q61 are also observed.
RevMed now intends to submit the drug for approval by regulatory authorities, including the U.S. Food and Drug Administration as part of a future New Drug Application, and for presentation at the 2026 American Society of Clinical Oncology Annual Meeting. Information about current trials of the drug are available at https://revmedclinicaltrials.com/.
“For patients with metastatic pancreatic cancer, new treatment options are urgently needed to increase survival time and improve quality of life,” said Brian M. Wolpin, MD, MPH, professor of medicine at Harvard Medical School, director of the Hale Family Center for Pancreatic Cancer Research at Dana-Farber Cancer Institute, and principal investigator for the RASolute 302 trial. “The widely anticipated results of this study indicate that daraxonrasib provides a clear and highly meaningful step forward for patients with pancreatic cancer who have experienced progression on prior treatment, typically chemotherapy. I believe that this new approach is a very important advance for the field that I expect will be practice-changing for physicians and improve the care for patients with previously treated metastatic pancreatic cancer.”
Pancreatic cancer is the most RAS-addicted of all major cancers, with more than 90% of patients harboring tumors driven by mutations in RAS proteins. These mutations span a range of RAS variants that fuel aggressive tumor behavior. Daraxonrasib, a multi-selective inhibitor of RAS(ON) proteins, is the first investigational agent in a novel class of RAS inhibitors designed to address a diverse and broad spectrum of oncogenic RAS drivers.
The RASolute 302 trial enrolled patients with pancreatic tumors harboring a wide range of RAS variants, including those with RAS G12 mutations (such as G12D, G12V, and G12R), as well as those without an identified RAS mutation. The primary endpoints of the trial were PFS and OS in patients with tumors harboring RAS G12 mutations. Secondary endpoints assessed PFS and OS in all enrolled patients (the intent-to-treat population), including those with tumors with and without (wild type) an identified RAS mutation.
Daraxonrasib is an oral RAS(ON) multi-selective, non-covalent inhibitor. Cancers driven by a broad range of common RAS mutations include PDAC, non-small cell lung cancer (NSCLC), and colorectal cancer. The drug is currently being evaluated in four global Phase III registrational trials, including three in PDAC and one in NSCLC.
Daraxonrasib works by suppressing RAS signaling through inhibition of the interaction between both wild-type and mutant RAS(ON) proteins and their downstream effectors.
Pancreatic cancer is one of the deadliest malignancies, because of its typically late-stage diagnosis, resistance to standard chemotherapy, and high mortality rate. In the U.S., recent estimates indicate that each year approximately 60,000 people will be diagnosed with pancreatic cancer, and about 50,000 people will die from it.
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Fujifilm Biotechnologies Opens New QC Lab in Denmark
Fujifilm Biotechnologies, a CDMO, celebrated the opening of its new, 2,000‑square‑meter quality control (QC) laboratory at its Hillerød, Denmark, commercial‑scale manufacturing site. The expanded QC footprint will enable bioassay and virology operations and support the site’s planned expansion, according to the company.
The laboratory features ventilation systems, personnel, and material airlocks, and an open‑plan layout. The space supports approximately 100 quality team members to conduct viral safety testing for drug substance/product release, scale capacity for complex cell‑based potency and ELISA methods, and perform raw material and critical total organic carbon cleanability studies to accelerate future partner campaigns.
The QC laboratory also incorporates robotics and an ongoing LIMS implementation across the company’s global network of sites to enable digital harmonization and data integrity.
The company doubled its Hillerød capacity in 2024 from six to 12 x 20,000 L mammalian cell culture bioreactors, increasing the complexity and volume for QC testing. The expanded production scale required expanded QC capabilities and advanced analytical equipment to support current operations and anticipated future demand. The QC lab is housed within a new 7,600-square-meter building that also features employee amenities, office and collaboration space, utility services, and an emergency generator to ensure uninterrupted operations and timely delivery of critical test results.
Construction of the lab was completed in last month and subsequently received approval from the Danish Medicines Agency (DKMA) following an on‑site inspection. Laboratory operations will begin in May 2026.
The new QC laboratory is part of Fujifilm Biotechnologies’ kojoX modular, connected network of manufacturing facilities, where harmonized equipment, layouts, methods, and digital systems are used to enable cross‑site workflows and consistent application of quality standards across regions, explains Christian Houborg, senior vice president and Hillerød site lead.
“Today, we are opening a world-class GMP-approved QC laboratory to elevate our quality control and be ready for the upcoming expansion, thereby continuing to manufacture advanced biological treatments for patients with severe diseases, such as cancer and rare autoimmune diseases. Together, we’re making a measurable impact for patients and partners around the world,” he said.
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It’s HAMMR Time: Duracyte Launches with “Living Pharmacy” Platform
For many patients, especially those with chronic or life-threatening diseases, treatment is not a single intervention but a relentless routine.
Cancer patients can spend years tethered to infusion schedules, returning weekly for IV therapies that dictate where they can live, travel, and work. Children with rare metabolic disorders may rely on frequent enzyme infusions, with entire rooms of supplies needed to sustain their care. And for patients in low-resource settings, life-saving biologic drugs often remain out of reach altogether due to cost and infrastructure.
These realities highlight a critical challenge in modern medicine: some of the most potent therapies are the most difficult to deliver, necessitating repeated dosing at centralized locations.
Duracyte, a newly launched biotechnology company, is pioneering a potentially transformative approach to medicine by developing a “living pharmacy” inside the human body. Its core technology, the Hybrid Advanced Molecular Manufacturing Regulator (HAMMR), is an implantable bioreactor designed to produce biologic drugs directly within patients. This innovation could fundamentally change how medicines are manufactured, delivered, and even conceived.
The founding team combines expertise across bioengineering, medicine, and biotech. Omid Veiseh, PhD, is a Rice University professor and RBL LLC managing partner focused on implantable cell therapies, while Paul Wotton, PhD, is a veteran biotech CEO with deep commercialization experience. Jonathan Rivnay, PhD, of Northwestern specializes in bioelectronics; Robert Langer, ScD, and Daniel Anderson, PhD, are MIT leaders in drug delivery and gene therapy; and Siddharth Krishnan, PhD, of Stanford, contributes expertise in wireless power and implantable devices.
Duracyte is the third venture created by RBL LLC, a Houston-based biotech studio founded by Rice University in 2024. Operating from Helix Park, RBL focuses on rapidly translating breakthrough research into real-world therapies, particularly in areas like oncology and autoimmune disease. Duracyte’s progress is further supported by ARPA-H’s THOR project, a nationwide collaboration aimed at advancing implantable biohybrid therapies from research to clinical application.
Honey, I shrunk the bioreactor
Biologic drugs, including antibodies, hormones, and enzymes, have become a cornerstone of modern medicine. They now represent a substantial share of the pharmaceutical market, treating conditions ranging from cancer to autoimmune diseases. But their production and delivery remain cumbersome.
Traditionally, biologics are manufactured in large-scale industrial bioreactors, purified, stabilized, and shipped to clinics, where they are administered via injection or intravenous infusion. This process is expensive, logistically demanding, and often burdensome for patients, who may require frequent hospital visits over months or years.
Veiseh, a professor of bioengineering at Rice University, has spent much of his career questioning whether this paradigm could be fundamentally reimagined. “What if we could bring this biomanufacturing to the patients and develop implantable bioreactors or injectable bioreactors whereby the biologic could be produced in the body?” Veiseh told Inside Precision Medicine. That question now underpins HAMMR.
At its core, HAMMR is a miniaturized, implantable bioreactor. Roughly the size of a small medical implant, the device houses genetically engineered human cells capable of producing therapeutic proteins. Unlike traditional drug delivery systems, which release pre-manufactured compounds, HAMMR generates biologics inside the patient’s body.
To accomplish this, the device replicates key functions of industrial bioreactors, but in a compact, implantable form. It supplies nutrients and oxygen to the cells, supports their viability, and allows for controlled production of therapeutic molecules.
One of the key technological innovations lies in how HAMMR generates oxygen. Using electrolysis—a well-established chemical engineering process—the device splits water molecules into hydrogen and oxygen. This hybrid oxygenation bioelectronics system for implanted therapy (HOBIT) component provides a steady, localized oxygen supply to sustain the embedded cells. “We’ve got a way to do electrolysis with low power and in a safe manner that actually allows this to be viable for the engineered cells,” Veiseh explained.
Real-time, feedback-controlled medicine
The device also incorporates electronic controls and sensors. Electrical signals can activate or deactivate the cells, effectively turning drug production on or off. Meanwhile, onboard sensors monitor pharmacokinetic and pharmacodynamic data.
This data is transmitted wirelessly to an external interface, enabling clinicians to adjust dosing in real time. Veiseh said, “The implanted device also communicates with an app that allows us to control dosing and get a lot of data from the patient as far as their physiological conditions, meaning the impact the drug is having on the body.”
One of the most transformative aspects of HAMMR is its potential to enable feedback-controlled drug delivery. Rather than administering fixed doses on a set schedule, clinicians could tailor therapy dynamically based on continuous biological data. “For the first time ever, we can create feedback drug delivery systems where you can dose to a pKa level or, better yet, to a pharmacodynamic level, which allows for that precise dosing for every patient,” said Veiseh.
This capability could be especially impactful in oncology, where patients often receive complex combinations of biologics. Current regimens may involve multiple drugs administered on different schedules, requiring frequent clinic visits and careful coordination.
Veiseh described a typical scenario: patients receiving checkpoint inhibitors such as ipilimumab and nivolumab, along with additional biologics like bevacizumab. These therapies often require weekly infusions over extended periods. “The vast majority of patients are getting IV infusions weekly and they are living longer, which is great,” he said. “But now you have patients that are on this regimen for three years.”
HAMMR aims to replace this model with a single implanted device capable of producing multiple drugs, with dosing adjusted digitally rather than through repeated clinical visits. “We’re moving away from physical prescriptions to a world of digital prescriptions,” Veiseh said.
The convergence of components
The idea of implantable bioreactors has been explored for years, but only recently have the necessary technologies matured enough to make it feasible. According to Veiseh, advances in several fields have converged: electronic miniaturization, wireless power transfer, synthetic biology, and biomaterials engineering. Together, these innovations enable the integration of complex functionalities into a small, biocompatible device.
By leveraging established technologies and adapting them for medical use, the team aims to reduce development risk and accelerate regulatory approval.
Wotton, a seasoned biotech executive working with the team, emphasized that many of the underlying components are not entirely new; they are adapted from existing technologies. “One of the advantages here is that these guys have been really intelligent when they’ve taken off-the-shelf technologies,” Wotton told Inside Precision Medicine. “The oxygen technology is lifted from what’s already used in submarines… The battery charging work is being done… The RPE cell lines that we work with… have successfully gotten into the clinic.”
Looking ahead, the team envisions integrating artificial intelligence into the platform. With continuous data collection from implanted devices, machine learning algorithms could identify patterns in treatment response and optimize therapy over time. “You can imagine… this device could now cycle through different therapies, and as it starts seeing efficacy responses, it starts learning,” Veiseh said.
Such a system could enable highly personalized medicine, adapting treatment strategies based on real-time data and accumulated experience across patients.
The HAMMR platform is built around the preparation of polymer-encapsulated cells, obtained from the human immortalized retinal pigment epithelia (RPE) cell line ARPE-19, which has already been used to generate cytokines for treating intraperitoneal tumors with oversight from the U.S. Food and Drug Administration (FDA). This provides a regulatory advantage, as the cells have an established safety profile. These preparations of ARPE-19 cells can be engineered to produce a wide range of biologics beyond cytokines.
A cost-cutting catalog
Veiseh noted that there are more than 300 FDA-approved biologics in the United States, and his team has already created versions of over 150 within this system. “This platform has the potential to really disrupt the biotech market as it exists today,” he said.
The implications extend beyond oncology. Wotton highlighted potential applications in autoimmune diseases, infectious diseases, and metabolic disorders. “There are so many applications of this technology,” he said. “Whether it’s in oncology… or… delivering antibodies like Humira to treat chronic diseases… there are applications where you can treat type two diabetes… HIV.” In each case, the goal is the same: replace repeated injections or infusions with a long-lasting implant that continuously produces therapeutic proteins.
HAMMR could have significant implications for the cost and accessibility of biologic therapies. Biologics are among the most expensive treatments in medicine, with some costing hundreds of thousands of dollars per year. Much of this cost stems from manufacturing, purification, and distribution. By producing drugs directly inside the body, HAMMR could dramatically reduce these costs. “The cost of goods is actually quite low relative to manufacturing today,” Veiseh said. “This is like one-tenth of the price.”
Wotton echoed this point, suggesting that the platform could replace expensive annual treatment regimens with lower-cost implantable devices. “Imagine what you could do if you could replace the $250,000 a year injectable schedule,” Wotton said.
This cost reduction could be particularly impactful in low-resource settings. Veiseh noted that the Gates Foundation has supported the project in part because of its potential to expand access to biologics in developing countries. “Biologics are way too expensive for sub-Saharan Africa,” he said. “But a device that can produce HIV treatments… once yearly… now it becomes… practical for that world too.”
Houston, we have clinical liftoff
Backed by more than a decade of research funding exceeding $100 million from agencies and organizations including DARPA, ARPA-H, the NIH, and the Gates Foundation, Duracyte is preparing to bring its first device into clinical trials. Duracyte plans to initiate a Phase I clinical trial this year evaluating patients with recurrent ovarian cancer. The company has already held multiple meetings with the FDA and completed a pre-IND (Investigational New Drug) meeting. “We have a clear plan as to what it takes to file an IND,” Veiseh said. “We’re on track to actually file… before the end of this year.”
If all goes as planned, the first patients could receive the implant by late this year or early next year. The trial will be conducted in Houston, leveraging partnerships with leading medical institutions, including the renowned MD Anderson Cancer Center. “Our partners at MD Anderson… will be running the first clinical trial,” Wotton said. “Taking advantage of the ecosystem down in Houston.” The proximity of Veiseh’s lab to the clinical site has helped accelerate development, enabling close collaboration between researchers and clinicians.
Despite its promise, the HAMMR platform faces significant challenges. Integrating multiple complex technologies into a single device is inherently difficult, and clinical validation will be critical. Execution risk remains high, particularly in selecting initial indications and navigating regulatory pathways. “We can’t do everything all at once,” Veiseh said. “It’s really thinking about what the value creation is at early stages.”
Prioritization will be key, given the platform’s broad potential. With hundreds of possible biologics and numerous disease targets, choosing the right starting point could determine the company’s trajectory. Wotton emphasized this challenge as well. “What are the challenges we have? Making the right choices with respect to where we go next,” Wotton said.
If successful, HAMMR could mark a fundamental shift in how medicines are delivered and even defined. Instead of prescribing drugs as physical products, physicians could prescribe programmable devices that manufacture therapies on demand. In this model, the distinction between drug and device blurs, giving rise to a new category of therapeutics. “This is so different than what pharma does,” Veiseh said. “I think it’s really interesting to see whether they are also eager to imagine a future of medicine, which gets away from the injectables.”
For now, that future remains speculative. But with clinical trials imminent and a strong foundation of research behind it, Duracyte’s “living pharmacy” is poised to test whether the idea can move from concept to clinical reality.
As Wotton put it, “This is just the tip of the iceberg.”
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Effects of an Exercise-Assisting Mobile App (Osteoarthritis-Rehabilitation Assistant [O-RA]) on Rehabilitation Outcomes in Older Adults: Randomized Controlled Parallel Clinical Trial
Background: Mobile apps and biofeedback using motion analysis have both been used separately to increase compliance with exercise programs. We developed a mobile app, Osteoarthritis-Rehabilitation Assistant (O-RA), that uses motion analysis technology in the mobile app to assist older adults with performing a knee exercise program. Objective: This study aimed to evaluate the effects of the O-RA app on the compliance and correctness of the exercise program by older adults. Methods: We conducted an assessor-blind, parallel-design, randomized controlled trial with 40 older adults (aged 60 years or older) who had no symptoms and no diagnosis of knee osteoarthritis. Participants were divided into 2 groups: O-RA app (intervention) group and standard treatment (control) group. Both groups were taught 4 types of exercise programs by a physical therapist for 15 minutes and were instructed to do exercises at home every day for 1 week. The number of exercises, the percentage between observed and prescribed exercises, the correctness of exercises, and overall pain during the program were assessed in both groups. Results: The control group had significantly higher compliance with the exercise program than the intervention group (=3.5044, =.001). There was no statistically significant difference in the correctness of the exercise program between the intervention and control groups. The difficulty of use and satisfaction were 47 and 59, respectively, out of the full score of 100. The main problems were the instability and the difficulty using the app. Conclusions: In older adults without knee osteoarthritis symptoms or diagnosis, the O-RA app was not a facilitator but a barrier to the lower extremity exercise program. An updated version, aiming to increase the stability and make it more user-friendly, should be developed; however, more comprehensive data, including qualitative user feedback and standardized usability metrics, will be needed to effectively guide its design. Trial Registration: Thai Clinical Trial Record TCTR20240923002; https://www.thaiclinicaltrials.org/export/pdf/TCTR20240923002
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