Tag: Medication

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Molecular Imaging Could Detect Early Kidney Fibrosis

Scientists have developed a new biomarker test that can noninvasively detect kidney fibrosis from a urine sample. A study published today in Science Translational Medicine reports the test could accurately differentiate between mild and severe disease, something that is not yet possible with the diagnostic methods available today. 

“Noninvasive and accurate diagnosis of kidney fibrosis remains unavailable in clinics, limiting effective patient management,” write the authors of the study, led by Zhou Jiaguo, PhD, professor of pharmacology at Sun Yat-sen University in China. “Although biopsy is considered the gold standard for assessing fibrotic progression, this invasive approach is subject to sampling error and interobserver variability, which may bias the diagnosis and is improper for repeated monitoring.”

Chronic kidney disease affects approximately 12% of the global population, with rates steadily rising as the world’s population ages. Characterized by the excessive formation of scar tissue, kidney fibrosis is a hallmark of chronic kidney disease that causes the proggressive impairment of kidney function, eventually leading to end-stage renal disease that requires dialysis or transplantation. 

Diagnosing kidney fibrosis at early stages can be critical for preventing irreversible damage to the kidneys. However, current diagnostic methods present some major limitations. While biopsies are invasive and difficult to accurately interpret, blood biomarker tests cannot distinguish kidney fibrosis from other kidney conditions or from fibrosis in other organs.

To circumvent these limitations, Jiaguo’s team identified two biomarkers that are specific to kidney fibrosis and can accurately differentiate this diagnosis from other related conditions. These are the transglutaminase 2 (TG2) enzyme and its substrate, lysyl oxidase–derived allysine (LysAld), which are both upregulated during the formation of fibrotic kidney tissue. 

The researchers developed a fluorescent reporter that binds to LysAld in the kidney and is then cleaved by TG2, turning on its fluorescence. Higher biomarker levels result in a stronger signal, providing an indication of how advanced fibrosis is in the patient’s kidneys. 

In a small cohort of 35 participants, the molecular imaging test could distinguish patients with kidney fibrosis from healthy controls with 84% sensitivity and 94% specificity. In addition, the test could differentiate mild and severe cases of fibrosis, with results confirmed with histological imaging. In contrast, traditional clinical measurements such as glomerular filtration rate, serum creatinine, and blood urea nitrogen were not able to classify patients according to the severity of the condition. 

Large-scale studies will be needed to establish this novel approach as a diagnostic and prognostic. Going forward, Jiaguo and colleagues are also interested in exploring using this test to monitor disease progression over time as a potential tool to evaluate treatment response and help clinicians make critical decisions to improve patient outcomes. 

“This noninvasive activatable reporter holds translational potential for early identification of renal fibrosis and patient stratification of [chronic kidney disease] to improve clinical management and patient outcome,” write the researchers. “We do not envision the probe as a standalone replacement for current standards; synergistic combinations with other biomarkers could further enhance its clinical utility.”

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Ultra-Short Radiotherapy Schedule for Prostate Cancer Supported by HERMES Trial

U.K. research has shown that condensing prostate cancer radiotherapy into two sessions, but with a higher dose per session, rather than the traditional five sessions does not lead to increased side effects when treatment is delivered using state-of-the-art magnetic resonance imaging (MRI)-guided technology.

Lead researcher Sian Cooper, clinical research fellow at The Royal Marsden NHS Foundation Trust and the Institute of Cancer Research in London, told Inside Precision Medicine that the results of the HERMES trial “point toward a future where prostate radiotherapy is tailored to the disease, to the individual’s anatomy and symptom profile, whilst being mindful of the impact of treatment time on patients’ lives.”

Presenting at the 2026 Congress of the European Society for Radiotherapy and Oncology (ESTRO), Cooper said that the number of people diagnosed with prostate cancer is projected to double by 2040, meaning the demand for effective and efficient treatment has never been greater.

At present, localized prostate cancer is typically treated with stereotactic body radiotherapy over five sessions, but there has been increasing interest delivering the treatment in fewer sessions, with a larger dose each session.

“For patients, a two-session treatment course would be far less disruptive than the weeks of daily hospital visits that radiotherapy has traditionally required. This convenience comes with clear benefits for work, leisure, family life and travel. For clinicians and health systems, fewer fractions mean faster workflow throughput, and getting patients the right treatment, quicker,” said Cooper.

“We wanted to find out whether giving the equivalent dose in just two treatment sessions could be feasible and safe for patients, and to understand how it might affect the potential side effects patients can experience, such as problems with urinary and bowel function.”

The move toward giving higher radiotherapy doses in fewer sessions has been made possible by improvements in radiotherapy delivery technology over recent years.

“It has allowed us to harness the power of modern computing and discoveries in clinical physics, to create radiotherapy doses which conform very tightly to the edge of the prostate,” Cooper explained. “This results in vastly less dose to the normal, healthy tissues around the cancer.”

The HERMES trial used a Unity MR-Linac (Elekta AB, Sweden) machine, which Cooper describes as “the ultimate evolution of this progress,” to deliver radiotherapy to participants.

The device combines real-time MR scanning with a linear accelerator and is known as MRI-guided adaptive radiotherapy. It allows adaptation of the radiotherapy beam design to changes in patient anatomy on the treatment day as well as moment by moment motion management, meaning that if there are any changes in the target or healthy bystander organs, the radiation beam can be switched off.

“This level of precision was needed to safely deliver the high dose of radiation necessary to maintain the biologically equivalent dose in just two fractions,” Cooper noted.

In all, 46 participants (median age 74 years) with intermediate or lower high-risk prostate cancer were randomly assigned to receive radiotherapy at a dose of 24 Gy in two fractions over 8 days, with a 27 Gy integrated boost to the MRI defined tumor (n=22), or 36.25 Gy in five fractions over two weeks to the planning target volume, with 40 Gy to the prostate and proximal one cm seminal vesicles (n=24). All participants had androgen deprivation treatment for at least six months.

Cooper reported that, at two years, four (18%) participants in the two-fraction arm and six (25%) in the five-fraction arm experienced moderate (grade 2) urinary adverse events (AEs) such as increased frequency or urgency. Grade 2 gastrointestinal AEs occurred in one participant in each arm (5% and 4%, respectively).

There were no grade 3 or worse genitourinary or gastrointestinal events in either group.

The team also showed that quality of life, measured by the International Prostate Symptom Score and the International Index of Erectile Function, showed minimal change up to two years but will continue to be monitored up to five years.

Cooper said that the investigators will present efficacy data, a secondary endpoint, when it matures but she pointed out that as “the cancer control rate for prostate cancer is so high, it often takes many years for failures to appear, whereas trial data for ultra hypofractionation show that the genitourinary adverse event rate is the primary concern after treatment.”

ESTRO president, Matthias Guckenberger, MD, from University Hospital Zurich, Switzerland, who was not involved in the research said: “While the technology used in this trial is currently available in only a limited number of specialist centers worldwide, they are growing rapidly. These results can help guide how they are used and help us understand whether two-session radiotherapy should become a new standard of care.”

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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. 

Continue to STAT+ to read the full story…

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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.”

 

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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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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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Carolina Aguilar: Brain-Computer Interfaces that Heal Neural Circuits

Jonathan D. Grinstein, PhD, North American Editor of Inside Precision Medicine, hosts a new series called Behind the Breakthroughs that features the people shaping the future of medicine. With each episode, Jonathan gives listeners access to his guests’ motivational tales and visions for this emerging, game-changing field.

Brain-computer interfaces have captured global attention in recent years, but most public discussion has focused on assistive technologies—systems designed to help patients control computers, prosthetics, or digital devices through thought alone. Carolina Aguilar, co-founder and CEO of INBRAIN Neuroelectronics, believes the larger opportunity lies elsewhere: using advanced neural interfaces not just to decode the brain but to treat disease directly. Built around graphene-based technology, INBRAIN is developing implantable systems capable of reading and writing neural signals with far greater precision than traditional metal-based devices.

Before founding INBRAIN, Aguilar spent 13 years at Medtronic, including a decade leading the company’s global neuromodulation business. During that time, she saw both the extraordinary potential of brain stimulation therapies and the limitations of incremental innovation inside large medical technology companies. Her background in neuroscience research, including early work studying the relationship between pesticides and Parkinson’s disease, shaped a long-term interest in circuit modulation and neurotherapeutics. That experience eventually converged with the emergence of graphene as a promising material for next-generation neural interfaces.

In this conversation, Aguilar discusses why INBRAIN chose to focus on therapeutic BCI applications rather than assistive computing, how graphene may enable higher-resolution neural decoding and stimulation, and why Parkinson’s disease became the company’s first major target. She also outlines INBRAIN’s broader vision for personalized neurotechnology, AI-driven therapies, and future applications ranging from epilepsy and memory restoration to bioelectronic treatments for cardiometabolic disease.

This interview has been edited for length and clarity.

 

IPM: You spent more than a decade at Medtronic before founding INBRAIN. What made you realize that incremental innovation was no longer enough, and why did graphene feel like the right breakthrough technology at the right time?

Aguilar: INBRAIN is a graphene-based brain-computer interface (BCI) company developing the most intelligent and adaptive interface between the neural system and AI to solve health for billions.

I started my career in consumer goods, but then I spent 13 years at Medtronic, where, for ten of those 13 years, I was leading the brain stimulation, or neuromodulation, business globally. I was always extremely impressed by what the company vision was and the number of disease areas and patients that we could help. However, I saw that every year we were innovating, but it was a bit incremental versus breakthrough. It’s normal for big companies to prioritize preserving shareholder value and revenue opportunities.

Investing in breakthroughs is harder; they usually just acquire those breakthroughs and then integrate them. And, of course, they revitalized their innovation. So I thought at that point that I could be one of those breakthrough innovators that could take a little bit more risk but then bring much bigger value into the field.

When the right opportunity presented itself to us, after the European Union put €1 billion into bringing graphene to market and after having gone through different speeds as pieces, we realized that it was the time to build INBRAIN and make that breakthrough a step instead of the incremental innovation of the past.

It’s interesting because I actually studied neuroscience at Virginia Tech, and at Virginia Tech, I had to define my thesis to study for my master’s degree. I picked up a combination of pesticides in the study. The study focused on the effects of pesticides and their combinations on brain chemistry in Parkinson’s disease. Right. So it was already quite oriented toward what we are solving today. And I got a grant award for the best vision on circuit modulation. So it was not about targeting the brain. It was about the circuit that was actually managing some of these dynamics of Parkinson’s disease.

At that early stage, I was already very attracted to the problem we are solving today, even though I did not know I would have a company dedicated to that field and to this innovation. However, it was always driving me in that direction. Medtronic was the company that turned that ambition into a real product and broad platform, which I also helped launch globally. So I guess it was always there. It was the seed that had been growing over time.

 

IPM: Medtronic exposed you to commercial, upstream product development, and engineering challenges. What did you learn that prepared you to build INBRAIN, and how did graphene change your engineering perspective?

Aguilar: It also evolves over time. So we start with a problem, such as pesticides in the development of Parkinson’s. Then I think I stepped into Medtronic as a solution to the problem that existed at that time. I was like, great. Now we have a problem. We have a solution. Let’s fix Parkinson’s disease.

At Medtronic, I was exposed to new experiences even while working in a commercial role, as I became a global director. I was exposed to the upstream. At Medtronic, there is a downstream process from which all employees receive their compensation. Then there’s the upstream piece, which is the product development and the planning of the next platforms. I was not in charge of that, but I was exposed to the process, the thinking, what is coming next, how we can make it happen, and where the constraints are. And that intrigued me a lot.

I discovered that I had a little bit of an engineering part inside of me that I never exploited. When the right opportunity came, I received a call from an investor friend of mine, who sometimes asked me to do some small due diligence. And he said, “Hey, there are some guys who have some graphene technology here that you might understand better than me. Do you want to come to the pitch?” I said, “Perfect.”

Then I saw that some of these constraints that we were dealing with in Medtronic in terms of miniaturization, higher-resolution interfaces, charge injection limits, and many of these engineering problems, partially, we could also solve by going graphene and going a different kind of electronics and a different kind of platform. When these consolidated and we created INBRAIN, I had to put a huge amount of effort into understanding semiconductors, microelectronics, mechanical configurations, and data architectures. So it’s been a huge learning journey for me.

 

IPM: INBRAIN appears to be building a platform strategy across multiple applications and devices. What are the product verticals and why does graphene offer capabilities that traditional neural interfaces cannot?

Aguilar: So it’s effectively a platform with three product verticals. When Morgan Stanley released the BCI industry report, it stated that the market was a $400 billion opportunity. We already knew that with one device, you could not capture all that immense market. So we were already working on a stepwise approach to the biggest opportunity. And this is what we have today on the table in the sense that we have a first product. The first product I can show you is a cortical interface. Starting with about 100 contacts, we can grow to a thousand. But in this case, it was not necessary.

It’s made of graphene. So it’s not about the number of contacts but the quality of what these contacts can decode. What is the precision of anatomy and the resolution of disease-related biomarkers that we can decode at high resolution in a way that that resolution is superior to a standard medical technology?

In some cases, standard platinum and iridium are used; in some cases, iridium oxide. We decided to create this first product for use for less than 30 days once it’s approved. It’s not yet approved, but we are getting closer, and it is the one that we actually took first-in-human. The results of those three reports are being generated using this device to demonstrate both the safety of graphene and its decoding superiority compared to metal technology. And, of course, within that first-in-human study, we also decoded speech at the phoneme level.

It was about creating the first step toward making graphene and consolidating advanced materials in clinical practice. So from there, the second product is actually an implantable platform that uses some of that configuration. So we use a cortical and subcortical interface to actually decode a circuit.

In our case, the microcircuit that is involved in Parkinson’s disease. And that is the second one. And the third product is actually the same platform, where instead of these two cortical and subcortical interfaces, we put in the central nervous system. We are truly connected to a vagus nerve interface that decodes the fibers within the vagus nerve, which go into the different modulations of the different organs of the body.

We go from reading the brain to reading the body. This sequence of product verticals opens up the immense possibility of a $400 billion opportunity. But even more important is the number of patients we could actually touch and improve therapeutically with such a platform.

 

IPM: Many BCI companies focus on assistive applications like computer and prosthetic control. INBRAIN appears to be therapeutic. Why did you choose direct disease treatment, and what makes it harder?

Aguilar: People say “invasive” or “noninvasive.” I call them implantable and non-implantable. And within the implantable, there might be different levels of invasiveness, but we were looking at the problem to solve, and especially coming from the field we come from and having experience for ten years, the use cases we saw are assistive BCI, meaning I transfer thought to action in the computer as solving a very important problem, but actually in a small population because, at the end, paraplegia and ALS. They are very important disease areas, but compared to other areas, there are smaller populations.

There were many people and companies, great companies, already aiming to solve that. So Neuralink and Synchron and Paradromics were always positioned there. And we thought, well, we have a similar approach, but maybe with a material that is much better suited to actually read and write bidirectionally, therapeutically. In assistive BCI, you do a ton of decoding. So, you read it and then transfer it to the computer. On the therapeutic side, where we are doing it, you have to read, write, and do that computing already within the implanted system.

It’s a much more complex architecture and a harder problem to solve. Now the benefit is solving the disease for as long as the system is active. And Parkinson’s was only the beginning. We are currently examining the validation of this program. We’re looking at memory restoration. We are looking at a set of disease areas on the cardiometabolic side that I cannot disclose without an NDA that we are developing with Merck KGaA. Those deals were unexplored or suboptimally explored by some of the low-resolution companies in the field.

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An AI framework for multi-disease detection via retinal imaging

Nature Medicine, Published online: 20 May 2026; doi:10.1038/s41591-026-04424-4

Using large-scale retinal images from community and tertiary hospitals, we developed Reti-Pioneer, a quality-aware, multi-task framework for multi-disease detection. Diverse external validation confirmed its generalizability. Furthermore, a prospective silent trial and clinical pilot study demonstrated its time efficiency, real-world feasibility, and potential for integration into clinical workflows.