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STAT+: Florida hospitals win $8 billion in extra Medicaid funds

The federal government is sending nearly $8 billion in supplemental Medicaid funds to hospitals in Florida for care they delivered last year, delivering a windfall to facilities in the politically influential state ahead of the imposition of new limits stemming from President Trump’s 2025 tax cut bill.

The extra cash is another victory for hospitals, which now are routinely getting paid much-higher commercial prices to treat Medicaid patients. Florida’s hospitals, which lobbied to get these extra funds approved, could get billions more on top of that once federal Medicaid officials mull over this year’s application.

On April 30, officials with the Centers for Medicare and Medicaid Services approved the money through a mechanism called a state directed payment program. CMS released the approval letters this week. The $8 billion, which also was authorized by state lawmakers, covers Medicaid patients treated from Oct. 1, 2024, through Sept. 30, 2025.

Continue to STAT+ to read the full story…

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STAT+: Scientists track cellular disruptions that lead to type 1 diabetes

The story of type 1 diabetes begins in the pancreas, long seen as a battleground between insulin-producing beta cells and misdirected immune defenders. Scientists have been searching for ways to spot this internal warfare early enough to prevent a lifelong disease that depletes the body’s source of insulin. 

Two new papers published Wednesday in Science Translational Medicine offer new clues to what happens in these beta cells before type 1 diabetes emerges. Experiments in human cells and in mouse models used biosensors and genetic analyses to illuminate this pathway and detect possible ways to halt beta-cell destruction.

In the first study, a team from the Indiana University School of Medicine explored how certain immune cells involved in inflammation, known as signaling cytokine interferon-alpha, normally trigger beta cells to produce other molecules  that play a role in inflammation, cell proliferation, and cell death. These reactive oxygen species, ROS for short, sometimes cause collateral damage. But cells from patients with type 1 diabetes did not have ROS-producing beta cells, suggesting they lacked the cytokines that stimulate their ROS production. That dearth might be useful in flagging the decline of beta cells early on in type 1 diabetes, the study authors surmised. 

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MYC Protein Linked to Tumor Survival Through DNA Repair Pathway

Researchers from Oregon Health & Science University (OHSU) have discovered the the MYC protein, which has long been known to drive cancer growth and development, also helps cancer survive DNA-damaging treatments by repairing the DNA in cancer cells. The research, published in the journal Genes & Development, shows that a form of MYC moves directly to sites of DNA damage to recruit proteins to help cancer cells survive the stress caused by chemotherapy and radiation treatments. The OHSU team’s findings indicate that finding a way to disrupt this repair function could be leveraged to make some tumors more vulnerable to treatment.

“Our work shows that MYC isn’t just helping cancer cells grow—it’s also helping them survive some of the very treatments designed to kill them,” senior author Rosalie Sears, PhD, Krista L. Lake chair in Cancer Research and co-director of the OHSU Brenden-Colson Center for Pancreatic Care said in a press release.

“These insights advance our understanding of MYC’s function beyond transcriptional regulation, highlighting additional contributions to MYC-driven oncogenesis and resistance to cellular stress and DNA-damaging therapies that could be critical for patient outcomes,” Sears told Inside Precision Medicine.

MYC has been studied extensively because of its role in regulating genes involved in cell proliferation, metabolism, and responses to stress. MYC deregulation is found in virtually all human cancers and is associated with chemotherapy resistance and lower patient survival rates. For this new research, the OHSU team focused on how phosphorylation at serine 62 (pS62-MYC) affects the protein’s DNA repair activities.

“Genomic instability is a hallmark of cancer, driving oncogenic mutations that enhance tumor aggressiveness and drug resistance,” the researchers wrote. “[MYC] paradoxically induces replication stress and associated DNA damage while also increasing expression of DNA repair factors and mediating resistance to DNA-damaging therapies.”

The study sought to find out how MYC behaves when DNA double-strand breaks occur. To do this the researchers used DNA double-strand break-specific proximity ligation assay, known as DI-PLA, to determine whether MYC physically associates with damaged DNA. They also used proximity-dependent proteomics to map proteins interacting with MYC and also examined MYC occupancy at chromatin during replication stress.

Their analysis showed that phosphorylation at serine 62 was needed to allow MYC to move to damaged DNA and interact with repair proteins including BRCA1 and RAD51.

“We identify a noncanonical role of MYC in DNA damage response (DDR) through its association with DNA breaks,” the researchers wrote, adding that phosphorylation at serine 62 “is crucial for the efficient recruitment of MYC to damage sites, its interaction with repair factors BRCA1 and RAD51, and effective DNA repair to support cell survival under stress.”

These findings help explain why some MYC-driven tumors often are resistant to treatments that are designed to overwhelm cancer cells with DNA damage. Chemotherapy agents and radiation therapy often work by creating DNA lesions that cancer cells cannot repair. The study suggests that tumors with high MYC activity may evade these treatments because MYC enhances repair pathways that restore damaged DNA.

“Cancer therapies often depend on overwhelming tumor cells with DNA damage,” Sears said. “If a cancer cell is very good at fixing that damage, it can survive treatment and keep growing.”

The implications of this may be especially pertinent for finding new methods of treating pancreatic ductal adenocarcinoma (PDAC). The researchers said MYC activity is elevated in a subset of aggressive PDAC tumors characterized by replication stress, liver metastasis, and increased DNA repair signaling. They linked this environment to oncogenic KRAS signaling and loss of tumor suppressors such as p53, both of which contribute to elevated pS62-MYC levels.

“These findings are particularly relevant for aggressive cancers like pancreatic cancer, where MYC activity is often very high,” said first author Gabriel Cohn, PhD, formerly of OHSU and now a postdoctoral researcher at the University of Würzburg, Germany. “Tumor cells in these cancers experience significant DNA damage and replication stress, yet they continue to survive and grow. Our work suggests that MYC helps these cells cope with that stress by actively promoting DNA repair.”

The study built on prior research that showed MYC can contribute to genomic maintenance during transcription and replication stress. Previous work demonstrated that MYC recruits topoisomerases to relieve DNA torsional stress, facilitates repair during transcriptional elongation, and stabilizes stalled replication forks. Other studies had shown that MYC and the related protein MYCN interact with DNA repair proteins, including BRCA1. But the researchers said their research is the first fully explore if MYC has a direct role in mediating DNA repair.

While MYC has long been considered an “undruggable” because its structure is difficult to target without affecting normal cellular functions, uncovering its role in DNA repair could provide a new avenue for selectively influencing its function, as opposed to attempting to block all MYC functions.

“MYC is one of the two most important oncogenes in all of human cancer,” Sears said. “If we can interfere with MYC’s role in DNA repair—without shutting down everything MYC does in healthy cells—we may be able to make cancer cells more vulnerable to treatment.”

At OHSU, investigators are currently studying a first-in-class MYC inhibitor called OMO-103 in a window-of-opportunity trial involving patients with advanced pancreatic cancer. The study includes biopsies collected before and after treatment to evaluate how MYC inhibition affects tumors in patients. Future studies will examine how MYC organizes repair complexes at DNA damage sites and whether blocking pS62-MYC-dependent repair functions can improve responses to DNA-damaging therapies in MYC-driven cancers.

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ctDNA and Immune Signals Reveal Who Benefits Most from Metastasis-Directed Radiation

Analysis of the Phase II EXTEND clinical trial suggests that adding metastasis-directed therapy (MDT)—primarily radiation therapy—to standard systemic treatment can significantly improve progression-free survival in patients with oligometastatic cancer, particularly prostate and pancreatic cancer. The treatment can also trigger measurable systemic immune responses and changes in circulating tumor DNA (ctDNA) that may help refine patient selection and treatment monitoring.

The findings come from the multicenter External Beam Radiation to Eliminate Nominal Metastatic Disease (EXTEND) trial (NCT03599765), one of the largest randomized studies to date examining MDT across multiple tumor types. Investigators reported that patients receiving MDT plus standard of care (SOC) experienced significantly longer progression-free survival compared with patients receiving standard systemic therapy alone. The study also identified histology-specific differences in benefit and uncovered translational biomarkers that could help define which patients are most likely to respond. The results were published in the Journal of Clinical Oncology.

The EXTEND trial enrolled patients with one to five metastatic lesions across six disease-specific “baskets,” including breast, pancreatic, kidney, prostate, and other tumor types. Patients were randomized to receive either standard systemic therapy alone or systemic therapy plus MDT, which consisted overwhelmingly of radiation therapy.

“This is probably the largest trial published to date in which we randomized patients to radiation versus not,” said lead investigator Chad Tang, MD, of MD Anderson Cancer Center. “We found that overall, if you add all the baskets together, there was a progression-free survival benefit with metastasis-directed therapy.”

Of 350 randomized patients, 334 were included and randomized to either standard of care SOC or SOC/MDT. Radiotherapy was used for 98% of treated metastases. After a median follow-up of 53 months, investigators found that MDT plus standard therapy reduced the risk of progression or death by 46% compared with standard therapy alone.

Not all tumor types responded equally, however.

“Some baskets, like the prostate baskets or the pancreas basket, had a big benefit for progression-free survival with metastasis-directed therapy,” Tang said. “Other baskets, like breast and kidney, there was no benefit.”

The investigators say the variability highlights the biological complexity of oligometastatic disease and underscores the need for more precise biomarkers beyond conventional imaging.

To improve disease characterization, the researchers incorporated ctDNA analyses using a methylation-based assay designed to detect molecular residual disease (MRD). The team found that detectable ctDNA at baseline was associated with significantly shorter progression-free and overall survival across tumor types. Conversely, patients whose ctDNA cleared within three months after enrollment experienced improved survival outcomes.

“If you were to clear your ctDNA—you go from MRD positive to negative—you also did much better for overall survival,” Tang said. “That may be an early endpoint showing that something positive happened for these patients.”

The findings suggest ctDNA could eventually help physicians determine which patients are appropriate candidates for MDT. “If your ctDNA is really high, maybe you shouldn’t do metastasis-directed therapy,” Tang said. “Maybe you should be changing your drug therapy.”

The study also revealed substantial differences in ctDNA shedding between tumor types. Pancreatic cancers showed the highest detection rates, while prostate cancers demonstrated relatively low ctDNA shedding, likely reflecting differences in tumor biology and treatment context.

Beyond ctDNA, the investigators conducted extensive immune profiling to better understand how radiation-based MDT might produce systemic effects. The team analyzed cytokines, flow cytometry markers, and T cell receptor (TCR) sequencing data collected before and after treatment.

One longstanding hypothesis in radiation oncology is that localized radiation can stimulate broader antitumor immune responses—sometimes referred to as the “abscopal effect.” Previous attempts to harness this phenomenon, particularly in combination with immunotherapy, have produced inconsistent clinical results. Tang believes the EXTEND findings may point to a different and potentially more clinically relevant mechanism.

“Here we’re radiating all the sites, and there’s only microscopic disease left,” he said. “The thinking is that we’re trying to turn the immune system on to control microscopic disease, which may not yet have developed a strongly immunosuppressive environment.”

Patients receiving MDT demonstrated substantially greater immune activation than those receiving systemic therapy alone. One of the strongest signals involved TCR remodeling—expansion and contraction of specific T cell clones following treatment.

“That means the T cells are getting channeled toward some antigen,” Tang explained. “Patients who had those T cell receptor modifications seemed to do better for overall survival.”

Notably, the most pronounced TCR changes occurred in pancreatic and prostate cancer baskets—the same groups that demonstrated progression-free survival benefits. By contrast, breast and kidney cancer cohorts showed minimal TCR changes and did not demonstrate clear clinical benefit from MDT.

The researchers also identified another potentially important immune biomarker: induction of proliferating CD8-positive, PD-1-positive T cells following MDT. Patients exhibiting this immune signature experienced improved progression-free survival.

“These two phenomena—TCR modification and induction of this proliferating T-cell population—were associated with good outcomes,” Tang said.

The findings may help inform future combination strategies involving radiation and immunotherapy, as well as the development of biomarkers to guide treatment intensification.

Tang said the broader message of the study is that oligometastatic disease likely represents a biologically heterogeneous state rather than a simple lesion count.

“The effect of metastasis-directed therapy seems to be very variable,” he said. “ctDNA may help us understand whether we’re actually treating the right patients, and the immune data suggest there may be ways to further enhance these responses.”

 

The post ctDNA and Immune Signals Reveal Who Benefits Most from Metastasis-Directed Radiation appeared first on Inside Precision Medicine.

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Standardizing Cell Therapy Production with Technology Facelift

From a manufacturing standpoint, cell therapies are a disparate group of products, each requiring different starting materials and unique production processes. And, for an industry looking to standardize, this diversity is proving to be a challenge.

So says Marta Costa, PhD, a principal scientist at Portugal-based R&D non-profit, IBET, and co-author of a new study looking at efforts to make cell therapy production more time and cost efficient.

“Manufacturing cell therapies depends heavily on the cell type, therapeutic modality, and the clinical application, which makes production quite diverse. Different cell types have distinct requirements for cell sourcing, expansion, genetic engineering, and downstream processing,” she tells GEN.

Costa cites the differences between patient-specific autologous therapies—where cells are collected, modified, and reinfused—and allogeneic therapies—which are made from donor-derived or stem cell banks for multiple patients.

“Autologous manufacturing is individualized and tends to be decentralized, while allogeneic manufacturing explores scaled bioprocesses to produce larger cell batches in often centralized operations. Besides, even within the same therapeutic class, manufacturing can vary according to disease indication, donor material, genetic engineering strategy, and quality requirements,” she says.

Technology

Despite these challenges, industry’s ever-present desire for efficiency means standardization efforts continue. The current focus is on using closed, automated, and modular platforms to create reproducible workflows, Costa adds.

“Key enabling technologies of next-generation cell therapies will likely explore automated and closed platforms to reduce the risk of variability introduced by manual operations, reduce labor intensity, and, overall, improve consistency in operations that range from the initial cell isolation and selection of starting material up to fill-and-finish.

“In addition, tools like bioreactors, particularly when combined with process analytical technologies, provide tighter control over culture conditions and offer the opportunity to not only monitor but also adjust operations to ensure final cell quality,” she says.

Digital standardization

Digital technologies, such as electronic batch records, are also changing production, according to Costa, who says, “These strategies contribute not only to improve efficiency but also to enhance reproducibility, decrease COGs, and ensure compliance.”

In the future, artificial intelligence will also have a role to play, Costa says, as cell therapy firms will use the technology to make production more reproducible and data-driven.

“Although AI is unlikely to eliminate biological variability, its value probably lies in increasing process understanding and control. Examples of strategies already in place exploring AI are in predictive process control to optimize conditions before failures occur and in cell quality prediction, reducing reliance on end-point testing,” she said.

AI could also help manufacturers determine which quality attributes have the biggest impact on therapeutic efficacy, according to Costa.

“Identification of critical quality attributes is also another capability where AI could play a significant role, helping manufacturers understand which variables most strongly affect therapeutic performance.

“And, of course, automation is already viewed as a practical pathway toward standardization because it reduces operator-to-operator variation, contamination risk, and batch failures,” she says.

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Mutating Antibodies for Easier Drug-Conjugate Manufacturing

Scientists in the United States have developed a general-purpose antibody that they hope will help revolutionize antibody-drug conjugate (ADC) manufacturing. The team, from Johns Hopkins University, says they mutated the fragment crystallizable (FC) region, the part of an antibody that modulates immune response. The aim was to create new sites to attach molecules, including nanoparticle drugs or fluorescent markers for quality assurance.

According to Jamie Spangler, PhD, associate professor of biomedical engineering and chemical & biomolecular engineering, the new antibodies could—in the future—lead to more effective and easier-to-manufacture drug conjugates.

“The chemistry of antibody drug conjugates is so heterogeneous. It can be hard to characterize the drug-to-antibody ratio and to [do things like] maintain consistency in formulations.”

To get around this problem, Spangler’s team installed six mutations on the FC region of an antibody that can act as attachment sites for a variety of molecules. The team was able to attach a dye to quantify how many sites were available and discovered the best productivity was found when using up to four sites.

They emphasize that the sites can be used for many purposes.

“You can attach whatever you want,” Spangler explains. “You could use [them] to make an antibody-dye conjugate or even a drug conjugate.”

According to Spangler, the team has already shown that the mutations can be used to conjugate with nanoparticles. “We encapsulate the protein we want to deliver within the nanoparticle, and then we coat the surface with an antibody. The nanoparticle we’re carrying, in this case, contains some GFP [green fluorescent protein], which is a fluorescent readout, but we can attach that to an antibody.”

After the antibody binds to a cell expressing the target, it’s internalized, and the nanoparticle can release its cargo, she explains. This system can be used for any number of purposes.

“The sky’s the limit for how people want to use this in their own research and their own work,” she says. “It’s a fully tuneable and generalisable system, and we’d encourage people to think broadly and creatively about the different attachments they can use.”

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Mixed-Reality Fermentation Simulator Preps Workforce

Hands-on biomanufacturing training is expensive, regardless of whether that training occurs in manufacturing facilities where training may take production units offline, or in community colleges and universities where the availability of equipment and consumables may limit training time.

A mixed-reality fermentation training platform dubbed BioSuite Virtual solves much of that challenge.

Developed by Prism Immersive with funding from BioMADE and expertise from an industry consortium, BioSuite Virtual immerses learners in a world in which they interact with a virtual bioreactor in their physical space. Conversely, the perhaps more familiar augmented reality lets learners interact with physical objects with virtual overlays.

BioSuite Virtual consists of more than 40 different modules across 12 chapters, starting with a short introduction to the biomanufacturing space, followed by content-specific modules.

“It’s end-to-end fermentation training,” Jared DeCoste, PhD, CEO and co-founder of Prism Immersive, tells GEN. “Learners gain vital skills along the way as they assemble a bioreactor, sterilize it, inoculate it, add the media, set the controls, and perform a run. They monitor the run by taking samples and observing the fermentation conditions, making necessary adjustments throughout.” As a learner, “you can do things multiple times if you need to. You can start and stop. You can go at your own pace, all the way through the run.”

Shaped by fermentation SMEs

Training is based on best practices from industry subject matter experts—especially Amyris, which shared its processing best practices and expertise with Prism early on—and partners at Bioscience Core Skills Institute (BCSI), Northeastern University, and Harford Community College who shaped and piloted the software. Prism made these connections with the support of BioMADE’s member network.

This lets all users learn from what Dan Beaupré, COO and co-founder of Prism, calls “the best of the best” in precision fermentation. “BioSuite Virtual is informed by dozens of subject matter experts [from industry],” he stresses.

“BioSuite Virtual isn’t meant to completely supplant in-person training,” Beaupré adds. “It’s a precursor, where users can obtain literacy and develop operational familiarity with precision fermentation workflows before they touch real equipment.” Because they have this foundation, trainers can then focus on teaching more complex processes and scenarios.

Prism’s first clients, community colleges, began using the virtual training tool this spring, and “about a dozen others” from Massachusetts to Hawaii are licensing it for use in the next academic year. DeCoste reports interest from contract development and manufacturing organizations and biopharma companies, too. “One of the great things about software is that you can modify it for the exact procedures utilized within [a specific] environment.”

Going forward, Prism Immersive plans to create new modules in such areas as biosafety cabinet operations and aseptic training, “because that’s what industry is calling for,” Beaupré says.

“All sorts of things are possible in XR [mixed, augmented, or virtual reality], as long as they’re well-designed,” Beaupré emphasizes. “Everything we do is intentional,” and knowledge checks are built in to reinforce and validate learning. After successfully completing the course, learners have the option to be credentialed through BCSI.

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Biomanufacturing Could Reshape Organ Transplantation

A persistent global shortfall has long defined the organ transplantation landscape, but a new generation of biofabrication and biomanufacturing technologies is positioning the field for a shift from scarcity to scale. As Boyang Wang, founder and CEO of Immortal Dragons, puts it bluntly, “There is a structural shortage,” even as transplant numbers reach record highs.

In 2024, approximately 174,000 solid-organ transplants were performed worldwide, yet nearly 668,000 patients remained on waitlists, Wang says. The mismatch is stark—and deadly. “We have a therapy that works, but the input—organs—is fundamentally scarce and cannot be scaled,” Wang says, underscoring the central limitation of modern transplantation systems.

This imbalance is driving a paradigm shift toward what Wang describes as a “replacement strategy” for medicine. Rather than attempting to repair every failing biological pathway, the idea is to replace entire organs. “The human body has hundreds of ways to fail, but only one way to work correctly,” he explains. “Trying to patch every individual failure mode is inherently inefficient.”

At the center of this shift lies bioprocessing. The challenge is no longer just proving that engineered tissues can work, but manufacturing them reproducibly at scale. Early progress is evident in simpler tissues. Bioengineered vascular grafts, for example, have already demonstrated that “engineered tissues can be manufactured, regulated, and used in real patients,” marking an inflection point for the field, Wang notes.

Scaling up to full organs, however, remains a formidable engineering problem. “The main blockers are vascularization and hierarchy,” Wang says, referring to the difficulty of building thick tissues with complex, multi-scale blood vessel networks. Without this architecture, engineered organs cannot sustain long-term function in vivo.

Reproducibility presents another major hurdle. Moving from bespoke, lab-built constructs to standardized, GMP-grade products requires precise control over every step of the manufacturing process. “We need reproducible, GMP-grade biofabrication processes that can deliver organs as ‘products,’ not artisanal one-offs,” Wang emphasizes.

Parallel advances in xenotransplantation are helping to expand supply in the near term. Gene-edited pig organs have shown increasing promise, with recent cases demonstrating months of sustained function in human recipients, Wang points out. These efforts, combined with advances in immunomodulation, could extend organ lifespans and broaden clinical applicability.

Still, biology remains a constraint. “Even when you get an organ, it’s not a generic spare part,” Wang notes, pointing to immune rejection, compatibility challenges, and the burden of lifelong immunosuppression. These factors limit both access and long-term outcomes.

Logistics also impose hard limits. Traditional donor organs degrade quickly, creating tight time windows for transplantation. “Organs can only stay viable for a very short cold ischemia window,” Wang says, underscoring how geography and coordination directly impact patient survival.

Despite these challenges, momentum is building. “We’re past the sci-fi stage and into early clinical reality,” Wang observes, pointing to both engineered tissues and xenotransplants entering human trials.

The road ahead will require advances not only in science but also in infrastructure. A future of scalable organ replacement will demand new regulatory pathways, reimbursement models, and healthcare delivery systems.

If successful, biomanufacturing could fundamentally reshape transplantation—transforming it from a donor-limited procedure into a scalable, industrialized therapy. Wang envisions a world where life-saving organs are not found, but made.

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<![CDATA[Digital gaming, gambling, and AI reliance drive emerging behavioral addictions, affecting mood and cognition.]]>
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Anti-Inflammatory Drug Could Help Some People with Depression

Research led by the University of Bristol suggests treatment with an anti-inflammatory drug, already approved to treat arthritis, could help some people with depression.

The study, published in JAMA Psychiatry,  was small but showed gradual improvement in the severity of depression and physical symptoms like fatigue, as well as a lowering of anxiety in those treated with tocilizumab versus placebo.

“Low-grade systemic inflammation is a putative causal factor in depression, present in approximately 30% of patients,” write co-lead author Golam Khandakar, MD, PhD, a professor and researcher at the University of Bristol, and colleagues.

“Individuals with difficult-to-treat depression have higher cytokine, e.g., interleukin 6 (IL-6) and C-reactive protein (CRP) levels, than treatment-responsive patients and controls.”

Tocilizumab is a humanized monoclonal antibody that blocks the IL‑6 receptor and is used as an immunosuppressive drug in several inflammatory and cytokine‑driven conditions. For example, it is approved by the FDA to treat rheumatoid arthritis and cytokine release syndrome in patients with severe COVID-19.

To test whether IL-6 inhibition could help people with depression, the authors carried out a small randomized controlled trial as a proof-of-concept study. Overall, 14 participants were given a tocilizumab infusion, and 16 participants were randomly assigned to receive a saline placebo infusion.

Adults were eligible to be in the study if they had moderate‑to‑severe, difficult‑to‑treat depression despite antidepressants, showed persistent low‑grade inflammation on repeat CRP tests, and had prominent physical depressive symptoms like fatigue.

After receiving a single infusion, the participants were followed up for four weeks with evaluations at one week, two weeks and four weeks. All were taking anti-depressants when enrolled and continued them during the trial.

The trial was not large enough or long enough to show a statistically significant improvement, but it did show a consistent pattern of greater, clinically sized improvement with tocilizumab by the end of the follow-up period, especially in patients with higher baseline CRP.

No real differences were seen at one or two weeks, but at four weeks people given tocilizumab showed bigger improvements in overall depression scores, fatigue, energy levels, anxiety and quality of life than those in the placebo group. Around 54% of participants in the tocilizumab went into remission at four weeks versus 31% of the placebo group.

“This work represents an important milestone in the development of new treatments for depression especially difficult-to-treat depression, which affects millions of people in the U.K. alone,” said Khandakar in a press statement.

“This is one of the first randomized controlled trials to test immunotherapy for depression, the first to test the IL-6 receptor as the treatment target, and the first to use a targeted approach to select patients most likely to benefit, and to show that it works.”

The researchers now want to carry out a larger randomized trial to assess if the effects they saw are significant in a bigger treatment population.

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