Background: Type 1 diabetes remains an underrecognized and challenging condition across Southeast Asia, where many countries face limited health care infrastructure, shortages of trained health care professionals, inconsistent access to diabetes education, and a lack of culturally appropriate resources in local languages. These barriers contribute to delayed diagnosis, suboptimal self-management, high rates of diabetic ketoacidosis, and inequities in care. During the COVID-19 pandemic, Action4Diabetes, a nonprofit organization working with local health care professionals and diabetes associations across Southeast Asia, developed HelloType1, a multilingual digital educational platform designed to improve awareness, education, and access to credible type 1 diabetes information. The platform was launched sequentially in Cambodia in 2021, Vietnam and Thailand in 2022, and Malaysia in 2023 through formal memorandums of understanding with local partners. Objective: This study aimed to evaluate the reach, platform usage, and online engagement of the HelloType1 digital educational platform across Southeast Asia between 2021 and 2024. Methods: Website analytics from Google Analytics 4 and Meta Business Suite metrics were descriptively analyzed to assess digital reach and engagement across countries. Metrics were compared over time and by country to examine patterns of platform uptake and user engagement. Results: HelloType1 demonstrated substantial growth between 2021 and 2024. Total unique website users increased from 1178 in 2021 to 40,361 in 2024, representing a marked expansion in regional reach. Pageviews rose from 4644 in 2021 to 83,689 in 2024, suggesting increasing content use and user platform engagement. By 2024, most website visits originated from organic search engines. Platform use was predominantly mobile-based, particularly in Vietnam, Thailand, and Malaysia, with the strongest engagement among adults aged 25 to 54 years. Facebook followers increased from 940 to 4553, and average engagement rates rose between 2022 and 2024. Cambodia achieved the highest number of Facebook interactions, whereas Thailand demonstrated the highest engagement rate. Content-level analysis showed that practical self-management topics, including blood glucose monitoring, insulin treatment, nutrition and exercise, complications, and emotional support, generated high levels of reach and interaction. Conclusions: HelloType1 demonstrates strong growth, mobile-first use, search-driven visibility, and engagement with practical self-management content. These findings support the feasibility and potential utility of a low-cost, multilingual digital education model, while future studies should evaluate its effects on knowledge, behavior, and clinical outcomes.
<img src="https://jmir-production.s3.us-east-2.amazonaws.com/thumbs/f42cc3a2c711eb52cb2e1acd2a3dd461" />
STAT+: Eli Lilly to acquire psychedelics-focused biotech AtaiBeckley
Eli Lilly is acquiring AtaiBeckley, the developer of psychedelic treatments for mental health conditions, to expand its portfolio of neuroscience medicines, the company said Thursday.
The AtaiBeckley deal is just the latest in a string of acquisitions by the pharma giant, flush with cash from its booming GLP-1 business.
Lilly is paying $2.8 billion in cash upfront for AtaiBeckley, with the potential for another $1 billion payout contingent on certain development and regulatory milestones.
STAT+: FTC settles lawsuit with CVS Caremark over charges it manipulated insulin prices, impeded access
The Federal Trade Commission settled a lawsuit against CVS Caremark, one of the largest pharmacy benefit managers in the U.S., over allegations that the company artificially inflated the price of insulin and impeded access to the lifesaving diabetes treatment.
As part of the deal, which the agency maintained will save Americans up to $8.5 billion in out-of-pocket costs over 10 years, CVS Caremark, which is owned by CVS Health, must make several changes to its dealings with employers, health plans, and pharmacies. The FTC also estimated the deal will unlock up to $4.5 billion in further savings for patients through pharmacy counter rebates.
In its complaint, the FTC alleged that CVS Caremark — as well as Cigna’s Express Scripts and UnitedHealth’s Optum Rx — created a “perverse” system of rebates that favored insulin, which was then sold at higher list prices in order to “line their pockets” at the expense of patients who were forced to pay more for the medication.
Protein Design’s AI Revolution: Inside David Baker’s “Communal Brain”
“I have this idea of a communal brain.” David Baker, PhD, told me as I sat in his office at the University of Washington (UW) surrounded by colorful and complex figurines of protein structures. It was the one-year anniversary of his Nobel Prize in Chemistry win.
Just outside his doors, a lab of more than 100 researchers was united by the shared ambition to design proteins from scratch (or de novo) for powerful applications across pharmaceuticals, vaccines, biosensors, and more. This “communal brain” housed at the UW Institute for Protein Design (IPD), where Baker led as director, was hard at work developing deep learning methods that could achieve atomic precision.
A small protein composed of 100 amino acids had an astronomical 20¹⁰⁰ possible sequences. Yet, only a vanishingly tiny fraction could fold into stable, functional structures. Misplacing a residue by an angstrom could mean the difference between a drug binding tightly to its target or complete failure.
For the antibody drug market worth hundreds of billions of dollars, Nathaniel Bennett, PhD, former postdoctoral researcher in the Baker lab, says AI-guided antibody design that bypasses the need for time-consuming experimental screens has long been a “holy grail” for a breadth of indications, including cancer and autoimmune disease.
Last November, Bennett and colleagues published a Nature paper demonstrating that full length de novo antibodies could bind user-specified epitopes. AI models could now construct antibody loops, the key region involved in binding that has been historically challenging to design due to its flexible nature.
Despite this technological leap, AI-designed proteins that were manufacturable, remained stable in the body, and avoided unwanted side effects, were still a step away. The gap fueled an industry debate over whether generating de novo medicines was even possible.
When I asked Baker to separate the hype from reality, he didn’t hesitate.
“The reality is that we can now design proteins on a computer,” Baker explained in our video interview. “The hype is that for therapeutics, there’s a lot more than the basic activity of a protein binding or catalyzing a reaction. Whether de novo proteins will revolutionize medicine will require improving our understanding of the biology.”
Nobel guests
Bennett is continuing molecular design research as a co-founder at Xaira Therapeutics. The AI-focused biotech launched in 2024 with over $1 billion in total funding and a star-studded leadership team, including Baker, as a scientific advisor, and Marc Tessier-Lavigne, PhD, former president of Stanford and CSO of Genentech, as CEO. Carolyn Bertozzi, PhD, Nobel laureate in chemistry, Scott Gottlieb, MD, former FDA head, and Alex Gorsky, former CEO of Johnson & Johnson, are among the board of directors.
Xaira is among a staggering list of biotech companies that Baker has co-founded over the past three decades.
“Science all becomes obsolete quickly because the field’s moving!” Baker told me. “The people that you mentor are more important than any science you do. They all go on and do great things.”
2024 Nobel Week was a testament to Baker’s scientific reach. Nearly 200 current and former members of his lab gathered in the Grand Hôtel in Stockholm to celebrate the newly named laureate, who was among a cohort of renowned AI experts who swept the awards ceremony.
Baker shared the Nobel Prize in Chemistry with Google DeepMind duo, CEO Demis Hassabis, PhD, and then-senior research scientist, John Jumper, PhD, whose AI model, AlphaFold, solved the protein structure prediction problem and has become one of the most widely adopted computational tools for drug discovery.
Meanwhile, the Nobel Prize in Physics was jointly awarded to Geoffrey Hinton, PhD, professor emeritus at University of Toronto, and John Hopfield, PhD, professor emeritus at Princeton University, for foundational discoveries that enabled machine learning with neural networks.
Together, the prizes represented a pivotal moment. AI was no longer confined to computer science but had become a transformative force across disciplines, earning recognition as a breakthrough deemed to confer the “greatest benefit to humankind.”
Back at the IPD, Baker’s research group spanned multiple floors. Yet, he knew everyone’s name, where they sat, and moved easily between conversations, bringing together researchers whose expertise might unlock a new direction. In the weeks after receiving the historic Nobel call, Baker chose to remain fully present for his team, implementing a strict “no travel rule,” despite the avalanche of invitations and media attention that accompanied the prize.
“David’s really good at forcing you to break the ice with people,” said Seth Woodbury, a graduate student who is designing metallohydrolases, enzymes that cleave some of the strongest bonds in biology for sustainability applications, including degrading pollutants. “Once you talk to your colleagues at happy hour, it’s not so scary to go ask them a question.”
Woody Ahern, graduate student and co-author of the metallohydrolase Nature paper, adds that Baker has a “very reasonable disdain for hierarchy.”
“Anyone can speak up in meetings. Anyone can question the work. It breeds this culture of staying focused on what matters in an interdisciplinary way,” said Ahern.
When Ria Sonigra was applying to graduate schools in the U.S., every option felt equally far from her home in India. She recalled sending Baker a cold email with questions about the lab. He quickly replied and offered to connect her with another international student who could help her navigate the application process. Today, Sonigra is an IPD graduate student, designing programmable nanopores for molecular sensing and sequencing.
“People outside the lab may think that David can’t pay attention to everyone, which is not true,” Sonigra said. “He knows your project and what he expects of you before the next meeting, even if he has a hundred trainees.”
At one point, Baker waved me over with a smile. “You’re missing chocolate hour!” he said, inviting me to one of many small weekly rituals that embodied the collaborative culture he had built.
Lowest energy search
At GEN’s inaugural virtual event, The State of AI in Drug Discovery, I asked Baker for his initial reactions to winning the Nobel.
“My group was not the first to do protein design,” he said humbly.
The field’s early innings trace back to 1988, when William DeGrado, PhD, demonstrated that sequences not found in nature could achieve stable 3D folds. The work challenged the long-held belief that functional proteins could only arise through evolution.
Steps toward computational design came a decade later, when for the first time, an in silico predicted protein was experimentally validated to adopt a target structure. The work was published in a Science study led by Steve Mayo, PhD.
Baker, alongside then-postdoctoral researcher, Brian Kuhlman, PhD, went a step further in 2003, expanding the design scope to include flexible backbones that represented entirely new folds, making it possible to not only modify natural proteins, but to create new ones from scratch.
“The prize was given because protein design has so much promise now, and that reflects the work of the whole community,” Baker continued.
Today, Degrado, Mayo, and Kuhlman are continuing to advance structural biology as prominent faculty members across University of California, San Francisco (UCSF), California Institute for Technology, and University of North Carolina (UNC) Chapel Hill, respectively.
![Top7 was the first protein created on a computer with a custom amino acid sequence that folds into a never-before-seen structure. When viewed at an angle, the transparent partition allows the two forms to become superimposed, illustrating the beauty of uniting sequence and structure. [UW Institute for Protein Design]](https://www.genengnews.com/wp-content/uploads/2026/07/3D-printed-proteins-IPD-04.jpg)
Decades before OpenAI co-founder, Andrej Karpathy, coined the term “vibe coding,” Baker’s team was writing a program in FORTRAN. Named Rosetta, the molecular modeling suite simulated proteins atom-by-atom based on biophysical properties, from hydrogen bonds to backbone torsion angles. By calculating free energy, Rosetta could estimate which sequences were most likely to achieve a desired structure: the lower the energy, the more stable the predicted fold.
Yet, a protein’s energy landscape is rugged, with countless local minima among an astronomical number of conformations. Success was rare. Researchers were searching for a single grain of sand across the desert.
Still, “Rosetta was impressive,” said Sierin Lim, PhD, an associate professor at Nanyang Technological University, who is among a group of researchers engineering self-assembling nanoscale containers, known as protein cages, for applications across drug discovery, imaging, and materials science. She recalled watching molecules move on her screen in Singapore in the early 2000s. At the time, Rosetta was the only program that could model proteins.
Over the next twenty years, Baker adamantly pushed Rosetta to be openly available, inviting collaborators to not only use the software, but to improve it.
PyRosetta, a user-friendly Python-based implementation developed by Johns Hopkins University researchers led by Jeffrey Gray, PhD, broadened Rosetta’s access for structural biologists without a strong computational background. Meanwhile, progress in generating high affinity and selective ligand binders and epitope scaffolds for vaccine development were bringing computational proteins closer to real-world medicines.
What started as a single lab project grew into the Rosetta Commons, an international collaboration spanning more than 100 laboratories.
“It was a great move making Rosetta open, seeing what it can do now,” Lim said.
CASP14
Then came a seminal 2017 report titled simply, “Attention Is All You Need.”
Researchers from Google introduced the transformer, a neural network architecture that enabled machines to analyze entire sequences at once. By using a “self-attention” mechanism, AI models could now uncover patterns across massive datasets at unprecedented scale. Soon, large language models (LLMs) trained on internet-scale text could not only understand, but converse in eloquent dialogue with humans.
The generative AI era had begun.
While the rest of the world was captivated by chatbots, structural biologists were sitting on a treasure trove of biological data pristine for machine learning.
For over fifty years, researchers had painstakingly deposited hundreds of thousands of experimentally determined structures in the Protein Data Bank (PDB) for public use. This molecular atlas now offered AI a window into the rules of biology.
In 2020, Baker received a phone call from one of the organizers of the Critical Assessment of protein Structure Prediction (CASP) competition, the biannual experiment that assesses the field’s latest state-of-the-art models.
“The first thing he said was, ’David somebody has done amazingly well this year, and it isn’t you!’” Baker recalled during his Nobel banquet speech. “That was how I first learned about the work of Demis and John.”
Instead of relying on human-defined biophysical rules, AlphaFold quickly learned decades of biochemistry from the PDB, uncovering the hidden instructions governing an amino acid sequence to fold into its 3D shape. At CASP14, the model remarkably predicted structures that were indistinguishable from real-world proteins. Months of laboratory work turned into a computational task completed in minutes.
Hassabis was quick to translate the breakthrough into medicine, taking the helm of DeepMind’s drug discovery spinout, Isomorphic Labs, as CEO a year later.
Today, the company’s IsoDD (Isomorphic Labs Drug Design Engine) platform, expands the druggable landscape by probing previously inaccessible biology, including predicting induced-fit interactions, where proteins change shape upon ligand binding, and identifying hidden binding pockets for drug targeting.
Isomorphic was betting, not on single therapeutic assets, but on a general discovery engine applicable across any disease area. That vision has since secured major pharma partnerships with Novartis, Eli Lilly, and Johnson & Johnson.
“I’ve always believed the No.1 application of AI should be to improve human health,” wrote Hassabis on LinkedIn when announcing Isomorphic’s whopping $2.1 billion funding raise in May.
Diffusion evolution
Concurrently, Baker’s team began applying deep learning to de novo design, drawing inspiration from AI’s emerging ability to generate realistic images. These diffusion models could operate on atomic coordinates and create entirely new protein backbones. Designs were conditioned for desired structural and functional constraints, opening the door to programmable biology.
When Baker’s team presented de novo design model, RFdiffusion (RoseTTAFold diffusion), in Nature in 2023, Mohammed AlQuraishi, PhD, assistant professor of systems biology at Columbia University, described the advance as “a really big deal.”
‘‘Prior to the ‘diffusion evolution’, the success rates were probably on the order of 1 to 10,000, if you’re lucky,’’ AlQuraishi told me shortly after RFdiffusion’s publication. ‘‘With diffusion models, the success rates are closer to the single percentages when you get into the laboratory. It’s a huge magnitude improvement of what it used to be.”
Donald Hilvert, PhD, professor emeritus at ETH Zurich, met Baker twenty years ago while working on enzyme design with Defense Advanced Research Projects Agency (DARPA). Traditional Rosetta methods would carve out binding pockets in existing proteins and install a new catalytic apparatus.
“But the activities were not very good,” Hilvert recalled. Designing catalysis, where success depended on precisely positioning chemical groups to stabilize fleeting transition states, proved far more difficult than engineering a stable protein fold. Rosetta struggled to achieve that level of accuracy, prompting much of the field, including Baker, to turn attention elsewhere.
“Two years ago, David called me and said, ‘Why don’t you come and visit? All these new AI-driven techniques are really changing the game!’” Hilvert told me.
Hilvert has spent the past two summers at the IPD, collaborating with Woodbury, Ahern, and IPD postdoctoral researcher, Donghyo Kim, PhD, to design metallohydrolases using RFdiffusion. He “hardly knew how to turn on a computer,” yet was reading Python scripts and generating his first computational designs within weeks. To his amazement, experiments quickly yielded five or six promising hits.
“There is this common purpose of people helping one another,” Hilvert said. “David sets the tone from the top.”
Application generalist
As I walked through the halls of the IPD, I saw the extraordinary reach of protein design applications firsthand. Desks were intermingled across fields. The proximity was deliberate for ideas to travel as far as possible.
Florence Hardy, PhD, is a postdoctoral researcher tackling a new enzyme design project for global health applications, including streamlining the manufacturing process for therapeutics.
“I always say that I can only think in a ten angstrom sphere at a time,” she chuckled. “That’s just as big as the active site.”
“Most medicines focus on inhibitors,” Xinru Wang, PhD, explained when describing her postdoctoral research developing insulin agonists, or binders that lead to activation, to address metabolic disease. In contrast to blocking activity, “turning on” a signaling complex required precise structural tuning that was a natural fit for the IPD’s expertise.
Last November, Wang and colleagues published a study in Molecular Cell, demonstrating that de novo designed insulin receptor (IR) agonists could extend glucose-lowering effects. The findings offered a therapeutic alternative to escalating insulin doses, which is a known contributor to resistance. Notably, these engineered agonists avoided triggering cancer proliferation that is often associated with excessive insulin activation. Wang is currently an assistant professor at Northeastern University.
Tabitha Tcheau designs DNA binding proteins inducible with small molecules that can recognize novel pathogens and trigger the plant immune system. The highlight of her project, she says, is the ability to span interdisciplinary subgroups, from conformational dynamics, small molecules, and nucleic acids.
“One thing that blew me away here is that people are extremely supportive,” Tcheau told me. “Everyone you ask is super eager to help.”
Enisha Sehgal is among a team of researchers designing sequence specific DNA binding proteins that can power programmable transcription factors, targeted gene regulation, and new genome engineering tools.
“Being in this lab allows you to be a specialist in protein design, but a generalist in all the applications,” Sehgal said. “You get answers faster. You can iterate faster. Science moves faster.”
Visiting researcher and machine learning scientist, Kieran Didi, reiterates how the IPD’s interdisciplinary team enables rapid experimental validation of models. “I’m not going to spend two months in this fantasy world of computational benchmarks,” he said. “In the next week, I know if the model is actually working. Someone will quickly put it to the reality test.”
Postdoctoral researcher and chemist, Declan Evans, PhD, concurs and sees himself as the Alpha tester.
“I can go straight to the developer and say, ‘this is not how computational chemists would use this software,’” Evans said. “You can see changes being made in real time.”
Back in Baker’s office, he told me about his regular weekend escape to the mountains, one of the benefits of living in Seattle. Skiing and hiking were activities he valued highly. When asked to contribute an item to the Nobel Prize Museum, Baker chose a broken ski pole as a symbol that progress often comes through overcoming setbacks.
“But I don’t think people get ideas on top of mountains,” Baker tempered. “If you’re going to be a [principal investigator], you have to really like mentoring. For me, it’s super fun!”
Baker’s most enduring creation may not be any single protein, but rather the network he built—the diverse, inviting, and interconnected communal brain.
The post Protein Design’s AI Revolution: Inside David Baker’s “Communal Brain” appeared first on GEN – Genetic Engineering and Biotechnology News.
Fertility Treatment May Not Drive Cancer Risk
Women who undergo medically assisted reproduction (MAR) may have a slightly higher risk of developing certain hormone-related cancers, but a large Australian study suggests much of that increase is likely explained by underlying infertility, greater medical surveillance, and other patient characteristics rather than the fertility treatments themselves.
The findings, published in JAMA Network Open, analyzed data from nearly 1.75 million Australian women and represent one of the largest investigations to date of cancer risk following fertility treatment. Using an emulated target trial design—a statistical approach intended to better approximate the conditions of a randomized clinical trial—the researchers examined whether three common forms of MAR were associated with later cancer diagnoses.
The study included 1,748,927 women aged 18 to 55 years between 1991 and 2018, including 396,661 who had received some form of MAR. Treatments evaluated included assisted reproductive technology (ART), intrauterine insemination (IUI) or ovarian stimulation, and ovulation induction with clomiphene citrate.
Researchers found modest increases in the relative risk of several hormone-related cancers—including breast, ovarian, uterine, thyroid, colorectal cancers, and melanoma—after some fertility treatments. However, the absolute increase in risk was small.
For any individual invasive cancer, the investigators estimated that treated women experienced fewer than 20 additional cancers per 100,000 women per year compared with women who had not undergone MAR.
The authors emphasized that the observed associations should not be interpreted as evidence that fertility treatment causes cancer. “Although we observed increased relative risk for most hormone-related cancers following MAR, this corresponded to only small increases in estimated absolute excess risk,” the authors wrote.
To better distinguish treatment effects from other influences, the investigators incorporated several bias analyses rarely included in previous studies. They calculated E-values to estimate the impact of unmeasured confounding and analyzed cancers not believed to be hormonally driven—including pancreatic, lung, and hematologic cancers—as negative controls.
Those analyses suggested that underlying infertility-related conditions, such as endometriosis and polycystic ovary syndrome, as well as factors including obesity, anovulation, and demographic differences, could account for much of the increased risk observed for ovarian, uterine, and thyroid cancers.
The researchers also found that cancer diagnoses tended to cluster during the first few years after fertility treatment. According to the investigators, “Several emulated trials suggested a greater likelihood of incident cancer shortly after first treatment.” They noted that this pattern could reflect either accelerated growth of preexisting cancers or increased medical monitoring during fertility treatment and pregnancy.
After examining the data, the authors concluded that enhanced surveillance was the more likely explanation. “We believe detection bias is the more likely explanation for these results. This finding is the first empirical indication using a negative control that medical surveillance may be responsible for an increased risk of cancer following MAR,” they wrote.
Women pursuing fertility treatment often undergo repeated medical evaluations and may also be more likely to participate in cancer screening programs, increasing the likelihood that existing cancers are detected earlier than they otherwise would be.
Overall, the researchers concluded that while associations between MAR and hormone-related cancers were observed, the evidence does not support a simple causal relationship.
The investigators said the findings should reassure patients while also encouraging careful counseling and follow-up. They recommend that clinicians discuss the possibility of a small increase in cancer risk but explain that the excess risk “may be partially or fully due to the health and sociodemographic profile of women who receive MAR and increased surveillance during treatment.”
The authors added that routine surveillance after fertility treatment remains appropriate, but they cautioned that observed increases in cancer diagnoses should be interpreted within the broader context of infertility-related health conditions and differences in healthcare utilization rather than being attributed solely to fertility medications themselves.
The post Fertility Treatment May Not Drive Cancer Risk appeared first on Inside Precision Medicine.
GLP-1 Treated Patients with Diabetes Have Raised Risk for Eye Condition
A large study of people with type 2 diabetes suggests that those who started treatment with a glucagon‑like peptide (GLP)‑1 receptor agonist after diagnosis had slightly increased risk of developing a serious eye condition called ischemic optic neuropathy than people with diabetes treated with other medications.
As reported in the Annals of Internal Medicine, the risk for patients given GLP-1 drugs was about twice that of those given a sodium–glucose cotransporter (SGLT)‑2 inhibitor or a dipeptidyl peptidase (DPP)-4 inhibitor although the absolute risk was still low in all groups.
Ischemic optic neuropathy occurs when the optic nerve sustains damage caused by reduced or blocked blood flow, leading to loss of nerve tissue and vision. The main symptom is sudden, usually painless vision loss in one eye, often with missing areas of the visual field that are frequently permanent. It is a rare condition, with 4-10 cases per 100,000 people per year in the U.S., with some factors like age and conditions like type 2 diabetes increasing risk.
In this study, Chintan Dave, PhD, a researcher at Rutgers University, and colleagues included claims data from 161,489 adults aged 18 to 65 years with type 2 diabetes who were newly prescribed a GLP-1 receptor agonist, 122,114 who started a SGLT‑2 inhibitor, and 86,047 who started a DPP‑4 inhibitor.
They excluded anyone who had previously used these drugs or previously had ischemic optic neuropathy. They approximated randomization by balancing more than 80 characteristics across groups. They then collected follow up data for up to 18 months to see who was later diagnosed with ischemic optic neuropathy.
Over 18 months, about nine out of every 10,000 people in the GLP-1 group were diagnosed with ischemic optic neuropathy, compared with about six out of 10,000 in the GLT‑2 inhibitor group and about four out of 10,000 in the DPP‑4 inhibitor group. Essentially there were three to four extra cases of ischemic optic neuropathy per 10,000 patients in the GLP-1 compared with the other groups.
The researchers note that the apparent excess risk was concentrated in older adults, men, and people with more advanced diabetes or eye or cardiovascular conditions.
GLP-1 receptor agonists are now widely used, both in lower doses for treatment of type 2 diabetes and in higher doses to treat obesity. “Despite the very low absolute risk for ischemic optic neuropathy, the rapidly expanding use of GLP-1 receptor agonists in patients with and without type 2 diabetes increases the clinical and public health importance of any potential association,” conclude the authors.
“Given that type 2 diabetes itself is a risk factor for nonarteritic anterior ischemic optic neuropathy [which constitutes approximately 75% of ischemic optic neuropathy cases] the potential for GLP-1 receptor agonists to further augment this risk has relevant implications for clinical decision making.”
The post GLP-1 Treated Patients with Diabetes Have Raised Risk for Eye Condition appeared first on Inside Precision Medicine.
Targeting Microglia Could Help Extend the Recovery Window After Stroke
Stroke care has advanced most clearly in the acute phase: rapid reperfusion, prevention of edema, secondary prevention, and early rehabilitation. Yet for many patients, the most difficult clinical reality begins after stabilization. Neurological recovery often improves over weeks to months, then plateaus. Once that spontaneous recovery window closes, residual motor, language, or cognitive deficits may become permanent.
A study published in Nature now identifies a molecular mechanism that may help explain why this window narrows. Researchers led by Jun Tsuyama and Takashi Shichita, PhD, at the Institute of Science Tokyo found that microglia, the brain’s resident immune cells, can remain in the post-stroke brain after losing their reparative function. The team identified ZFP384 as a transcriptional regulator that suppresses the microglial repair program and showed that blocking it with an antisense oligonucleotide improved long-term recovery in mouse models of ischemic stroke.
A repair program that fades too soon
Microglia are often discussed in the context of neuroinflammation, but their role after stroke is not uniformly harmful. In the acute phase, activated myeloid cells contribute to inflammatory injury. During recovery, however, microglia can shift toward a reparative state, producing neurotrophic and tissue-supportive factors that contribute to remyelination, synaptic remodeling, and functional improvement.
One of the key markers in this study was insulin-like growth factor 1, or IGF1, a neurotrophic factor produced by reparative microglia. IGF1 has known roles in synaptogenesis, oligodendrocyte function, and myelin repair. The researchers used IGF1 expression to track microglia involved in the recovery phase after ischemic stroke.
“We aimed to identify the molecular mechanism responsible for diminishing microglial reparative functions,” Tsuyama said in the press release.
The central observation was clinically relevant: reparative microglia did not simply disappear. Instead, lineage-tracing experiments showed that cells which had once expressed repair-associated genes persisted in the peri-infarct region but later lost that gene-expression program. In mice, recovery-associated gene expression rose after stroke and then declined toward baseline by around day 28. The cells remained, but their reparative identity faded.
ZFP384 as a brake on microglial repair
To identify what shuts down this repair state, the researchers combined RNA sequencing, single-cell RNA sequencing, ATAC-seq, and transcription-factor analysis. A protein known as ZFP384 emerged as a candidate regulator whose expression increased as the microglial repair program declined.
Functionally, ZFP384 acted as a brake. Overexpression of Zfp384 reduced Igf1 expression in microglial cells, while genetic deletion of Zfp384 in microglia sustained recovery-associated gene expression after stroke. Mice lacking Zfp384 specifically in microglia showed better long-term neurological outcomes on behavioral tests, without significant differences in infarct volume, cerebral blood flow, or survival.
That distinction is important. The intervention did not appear to reduce the initial ischemic injury. Instead, it improved the recovery phase, suggesting a therapeutic concept distinct from acute neuroprotection.
Mechanistically, the study links ZFP384 to disruption of YY1-mediated chromatin interactions. YY1 helped maintain enhancer–promoter contacts required for recovery-associated gene expression, including at the Igf1 locus. As ZFP384 increased, it displaced this repair-permissive chromatin organization, shifting microglia toward a dysfunctional state.
The authors describe this as a strategy to “prevent the loss of reparative immunity,” preserving beneficial immune-cell functions rather than broadly suppressing inflammation.
Antisense therapy improved recovery in mice
The translational component of the study used antisense oligonucleotides (ASO) designed to reduce Zfp384 expression. After intracerebroventricular administration, the ASO was taken up by microglia and reduced Zfp384 mRNA expression.
When ASO-Zfp384 was administered on days 8 and 22 after stroke onset, mice showed improved neurological recovery compared with controls. Notably, benefit was also observed when treatment began on day 29, suggesting that the approach may influence the chronic recovery phase in this mouse model rather than only early repair.
The biological readouts supported the behavioral findings. ASO-Zfp384 sustained microglial recovery-associated gene expression, increased IGF1-positive microglia in peri-infarct tissue, and promoted broader neural repair signatures in oligodendrocyte precursor cells, excitatory neurons, and astrocytes. Treated mice showed improved myelination, enhanced white matter conduction, and increased synaptic markers including synaptophysin and PSD95.
Neutralizing IGF1 or SPP1 reduced the recovery benefit, strengthening the conclusion that microglial neurotrophic factors were functionally involved.
Human tissue supports the pathway
The researchers also examined human post-mortem brain tissue from patients who had experienced ischemic stroke. In peri-infarct regions, IGF1-positive IBA1-positive cells were more abundant early after stroke and declined later. ZNF384, the human orthologue of mouse ZFP384, showed the opposite pattern, increasing later in the recovery period.
The inverse relationship between IGF1 and ZNF384 supports the relevance of the pathway in human stroke biology, although it remains correlative. The human samples do not show that ZNF384 inhibition would improve patient outcomes, but they indicate that the same molecular pattern observed in mice may also occur in the human post-stroke brain.
Implications for rehabilitation medicine
The findings point to a therapeutic space that remains underdeveloped: enhancing recovery after the acute phase. Rehabilitation depends on plasticity, remyelination, and circuit remodeling, but current pharmacological options to extend or potentiate this biology are limited.
A therapy that sustains reparative microglia could, in principle, complement rehabilitation by keeping the peri-infarct environment more permissive for repair. That would represent a different clinical goal from thrombolysis, thrombectomy, or anti-inflammatory intervention. Rather than rescuing threatened tissue in the first hours, the aim would be to improve the quality and duration of recovery over subsequent weeks.
The study remains preclinical. Delivery route, dose, safety, timing, durability, and patient selection all require further work. The mouse model cannot capture the full heterogeneity of human stroke, including lesion location, age, comorbidities, vascular risk, rehabilitation intensity, and medication use. Sustaining immune-mediated repair also needs careful safety evaluation, because prolonged activation of tissue-resident immune cells could have context-dependent risks.
Still, the concept is compelling. Microglia are not merely inflammatory cells to inhibit; they can be repair partners whose beneficial state may be actively preserved. If ZFP384-targeted approaches prove safe and effective in larger models, they could open a new class of post-stroke recovery therapies focused on extending the brain’s own repair window.
As Tsuyama put it, “sustaining the brain’s endogenous repair program” may create opportunities to reduce permanent neurological symptoms during rehabilitation.
The post Targeting Microglia Could Help Extend the Recovery Window After Stroke appeared first on Inside Precision Medicine.
The Effects of Lumateperone on Obesity and Physiologic Aging and Their Association With Antidepressant Response in Bipolar Depression
Conditions: Bipolar Depression Depressed Phase; Obesity & Overweight
Interventions: Drug: Lumateperone 42 mg
Sponsors: Massachusetts General Hospital; Johnson and Johnson Medical
Not yet recruiting
Interventions: Drug: Lumateperone 42 mg
Sponsors: Massachusetts General Hospital; Johnson and Johnson Medical
Not yet recruiting
HALO-TRIAL: High, Medium And LOw Intensity Psychotherapy for Binge Eating Disorder
Conditions: Binge Eating Disorder; Binge Eating Episodes; Binge Eating/Loss of Control Eating; Binge Eating Disorders; Binge Eating; Binge Eating Behaviour; Binge Eating Disorder Associated With Obesity; Eating Disorder Binge; Eating Disorders
Interventions: Behavioral: Cognitive Behavioral Therapy Enhanced – Individual; Behavioral: Cognitive Behavioral Therapy Enhanced – Group; Behavioral: Cognitive Behavioral Therapy – Guided Self Help; Behavioral: Systemic Narrative Therapy – Group
Sponsors: Herlev and Gentofte Hospital; Jascha Fonden; BETA-HEALTH Foundation; Mental Health Centre Ballerup; Region Capital Denmark; University of Copenhagen
Recruiting
Interventions: Behavioral: Cognitive Behavioral Therapy Enhanced – Individual; Behavioral: Cognitive Behavioral Therapy Enhanced – Group; Behavioral: Cognitive Behavioral Therapy – Guided Self Help; Behavioral: Systemic Narrative Therapy – Group
Sponsors: Herlev and Gentofte Hospital; Jascha Fonden; BETA-HEALTH Foundation; Mental Health Centre Ballerup; Region Capital Denmark; University of Copenhagen
Recruiting
StockWatch: Insilico Projects Profit, Revenue Leaps as AI-Developed Lead Candidate Moves to Phase III
Insilico Medicine (Hong Kong Exchange: 3696), an AI-based drug developer whose profile within biopharma has risen with its recent collaborations with industry giants, has offered investors an upbeat revenue and profit forecast for the first half of 2026, driven by its series of partnerships and a wide-ranging pipeline whose first program has reached late-stage development this past week.
Insilico said it expects to finish the first half of 2026 in the black, with “net profit” or net income ranging from approximately $33.5 million to $39.5 million, compared with its $19.2 million net loss in January–June 2025. Insilico also released adjusted non-International Financial Reporting Standards (IFRS) net profit forecasts in the range of approximately $45.5 million to $51.5 million for H1 2026. Non-IFRS metrics exclude one-time costs, such as restructuring charges and asset sales.
The company is additionally forecasting record first-half revenue ranging from approximately $102.5 million to $106.5 million, up approximately 272.7% to 287.3% from a year ago.
By contrast, Insilico finished all of 2025 with $56.239 million in revenue, down 34% from $85.834 million a year earlier, as a 69% slide in pipeline development revenue (to $23.885 million) outpaced the company’s nearly eight-fold increase in drug discovery revenue, to $24.952 million.
Notably, Insilico last year incurred a $352.5 million net loss, more than 20 times the company’s $17.1 million net loss in 2024, a jump the company attributed to the revenue drop as well as a $296.7 million loss from changes in the fair value of financial liabilities at fair value through profit or loss. That loss stemmed from Insilico converting the preferred shares issued in previous financings into ordinary shares when the company went public in December, raising HKD 2.277 billion (about $292.3 million at the time; now worth $283.9 million) on the Hong Kong Exchange.
Yet just as notably, Insilico’s cash and cash equivalents more than tripled last year, to $393.338 million.
“We look forward to achieving sustained profitability,” Alex Zhavoronkov, PhD, Insilico’s founder and CEO, said in a statement.
The forecasts continued the small but noticeable rise in Insilico’s stock price since Wednesday when the company announced that its lead candidate rentosertib, a drug designed to treat idiopathic pulmonary fibrosis (IPF), has advanced to a Phase III trial, the first drug within the company’s expansive 40+ program pipeline to reach that clinical milestone.
“Full arc of our mission”
“Rentosertib is a very important program for Insilico because it represents the full arc of our mission: using AI not only to move faster, but to originate new biology, new chemistry, and new therapeutic opportunities in aging and disease,” Zhavoronkov stated.
That news sparked a mini surge that sent Insilico’s shares climbing 19% over three days. Shares rose 2.7% from HKD$36.02 ($4.49) Tuesday to HKD$37 ($4.61) Wednesday, followed by a 7.7% gain Thursday as the stock rose to HKD$39.84 ($4.97)—then a 7.5% jump Friday, with Insilico closing the week at HKD42.82 ($5.34).
At least one investment firm started coverage of Insilico’s Hong Kong-traded stock with positive commentary: Cui Cui, an equity analyst with Jefferies, initiated the firm’s coverage with a “Buy” rating and 12-month price target of HK$100 ($12.47).
Jefferies’ endorsement capped a year in which Insilico escalated its partnership activity with pharma giants and smaller biotechs, adding roughly up to $7 billion to a potential haul that could exceed $10 billion.
The largest of these collaborations is its up-to-$2.75 billion collaboration ($115 million upfront) with Eli Lilly (NYSE: LLY), under which Insilico granted Lilly an exclusive global license to develop, manufacture, and commercialize “potentially best-in-class, novel oral therapeutics in preclinical development for certain indications,” according to an announcement that didn’t specify the therapeutic areas where the companies plan to partner. The alliance expanded from an “over $100 million” R&D partnership inked last November, which in turn grew from a 2023 licensing agreement allowing Lilly to access Insilico’s Pharma.AI software suite.
“Combining first-mover advantage, wet-lab validation, deep medical science, and in-house clinical expertise to train and refine AI, plus LLY’s endorsement, Insilico looks well positioned for scalable BD [business development] and LT [long-term] monetization,” Cui wrote in a research note.
“As AI-driven productivity cont[inues] to scale PCC [preclinical candidate] output, Insilico is positioned to expand its pool of proprietary assets, enhancing the likelihood of future out-licensing opp[ortunity] and strengthening LT monetization potential,” Cui added.
Zhavoronkov highlighted the research note on his LinkedIn feed, adding: “I think that in many ways the analysts know the industry and the company even better than some of the insiders. Definitely worth a read.”
Phase III plans
Cui’s comments followed Insilico announcing its Phase III plans for rentosertib (formerly ISM001-055), which is designed to treat IPF by targeting Traf2- and NCK-interacting kinase (TNIK), a serine/threonine kinase whose activation plays a crucial role in cellular processes that include signal transduction pathways essential for fibrosis development.
Insilico said its planned Phase III trial (NCT07687459) will be a randomized, double-blind, placebo-controlled, parallel-group study that is expected to enroll 320 participants across 47 centers in China. The trial’s primary endpoint will be the annual rate of decline in forced vital capacity (FVC) over 52 weeks, with a key secondary endpoint of time to first occurrence of any disease progression event.
The Phase III trial aims to assess whether rentosertib can provide clinically meaningful benefit in a larger patient population and over a longer treatment period than its two 12-week Phase IIa studies.
Rentosertib has completed a Phase IIa trial (NCT05938920) in China, published in Nature Medicine last year, and is in a separate Phase II trial (NCT05975983) in the United States. In the Chinese trial, rentosertib met its primary endpoint of safety and tolerability across all dose levels, as well as positive secondary endpoint data, namely dose-dependent FVC improvement with a mean FVC change of +98.4 mL at 12 weeks in patients dosed at 60 mg once daily, vs. -20.3 mL for placebo.
During the BIO International Convention in San Diego, Zhavoronkov hinted at the Phase III, highlighting a planned “next step” for the program “in the second half, but maybe closer to the earlier second half,” he told GEN.
At the convention, Zhavoronkov led Insilico in celebrating its latest big-money collaboration, an up-to-$2.5 billion partnership with SK Biopharmaceuticals to discover new AI-based drug candidates for disorders affecting the neuroimmune area of the central nervous system (CNS). Insilico agreed to apply its Pharma.AI platform, which addresses target validation, generative chemistry, and molecule optimization, along with its preclinical drug discovery expertise, to discover, design, and optimize candidates for neuroimmune indications against targets that will originate with SK.
SK is part of a privately held, family-owned chaebol or conglomerate whose parent holding company is public, SK Inc. (Korea Exchange: 034730). Another SK-owned company—SK Hynix (Nasdaq: SKHY), a supplier of high-bandwidth memory chips that power the AI processors of Nvidia and AMD—went public Friday, raising a staggering $26.5 billion by pricing its U.S. American depositary shares (ADS) at $149 each.
Potentially lucrative partnerships
In addition to SK and Lilly, Insilico also has potentially lucrative partnerships with Sanofi (Euronext Paris: SAN), with which Insilico plans to advance up to six targets (up to $1.2 billion); privately held Menarini Group, to which it has outlicensed Phase I cancer treatments targeting KAT6 and KIF18A (up to $1.05 billion in collaborations launched 2024 and 2025); privately held, French-based Servier, also cancer focused (up to $888 million); and Takeda Pharmaceutical (Tokyo Stock Exchange: 4502), drug discovery across its therapeutic areas (up to $600 million).
Also among Insilico’s collaboration partners: Exelixis (Nasdaq: EXEL), to which Insilico outlicensed in 2023 a Phase I BRCA-mutated cancer drug targeting USP1 (“close to” $1 billion plus royalties), Fosun Pharma (Shanghai Stock Exchange: 600196; Hong Kong Exchange: 02196), which is joining Insilico on R&D for four biological targets plus co-development of Insilico’s QPCTL program (up to $82 million, including $13 million upfront and a $15 million equity investment); Fosun-backed but privately held Hygtia Therapeutics, which is co-developing with Insilico ISM8969, a Phase I oral brain penetrant NLRP3 inhibitor, in CNS disorders (up to $66 million, including $10 million upfront and milestones); and Taipei-based TaiGen Biotechnology (Taipei Exchange: TWD), which holds Greater China rights to an oral PHD1/2 inhibitor in anemia of chronic kidney disease (milestones and royalties totaling “two-digit million dollars”).
Rounding out the list of Insilico’s disclosed collaboration partners are Chinese-based Qilu Pharmaceutical Group, which is partnering to jointly develop small molecule inhibitors for specific targets in cardiometabolic disease management (up to “near” $120 million, including milestones and single-digit royalties); China Medical System Holdings (CMS; Hong Kong Exchange: 867 and Singapore Exchange: 8A8), which is teaming up with Insilico on discovering drugs for central nervous system and autoimmune diseases (up to “tens of millions in Hong Kong dollars per project in R&D support”); and Tenacia Biotechnology, a Bain Capital-backed, privately held Sanghai-based drug developer which in March joined Insilico to expand a year-old R&D collaboration aimed at developing therapies for “underserved” neurological disorders (up to $94.75 million in near-term and milestone payments).
Insilico has out-licensed to undisclosed partners rights to a GLP-1R-targeting program designed to treat obesity and metabolic diseases; and Greater China rights to a Nav1.8-targeting program designed to treat pain.
Vaxart takes a double dose of good news
Settlement ends threat of proxy war; COVID-19 pill aces Phase IIb trial
This week’s annual shareholder meeting had threatened to be anything but routine for Vaxart (Nasdaq: VXRT) after its current executive team and three of its six nominees for board seats had been challenged by an activist shareholder through a proxy campaign.
Since last fall, shareholder Daniel P. Houle and allies have offered persistent criticism of Vaxart’s management—led by CEO Steven Lo and Sean Tucker, PhD, senior vice president and CSO—and the company’s board, whose operations and independent oversight are led by a lead independent director, W. Mark Watson, rather than a traditional chair.
But earlier this month, the threat of a proxy war over Vaxart’s direction ended when Houle and five allies signed a cooperation agreement with the company. Vaxart agreed to begin a search for an additional independent director to be conducted within 90 days of the conclusion of the 2026 annual meeting. Vaxart also agreed to work with Houle and allies to identify a “mutually agreeable” candidate for appointment to the board.
In return, the stockholder group consisting of Houle and his allies—Mark Silverberg, MD; Matthew M. Wallace, MD; Patrice Raffy; Marc Eustace Pereira; and Q3 Nominees Pty Ltd.—agreed to withdraw their board nominations for Houle, Silverberg, and Wallace.
The cooperation agreement also calls for:
- Creation of a Stockholder Engagement Committee and a Clinical and Regulatory Affairs Committee
- A revamp or “refreshment” of board committee chairs, including the selection of new chairs for the Nominating and Governance and Compensation Committees
- Adoption of director stock ownership and resignation policies
- Customary standstill, voting, engagement, and other provisions
“Vaxart is approaching a series of important value-inflection milestones, and these actions enable the company to move forward with a unified focus on executing its strategy,” Watson said in a statement. “We appreciate the constructive dialogue with the stockholder group toward our shared goal of creating value and are pleased to resolve our proxy contest so we can dedicate our full resources and attention to advancing our pipeline with stockholder interests in mind.”
Houle and allies insisted they believe “deeply” in the promise of Vaxart’s oral vaccine platform and resulting commercial opportunities—but took issue with the company’s declining stock price, capital raises that they said diluted the value of existing shareholders’ stock, and with what they termed insufficient oversight by the board.
In February, Houle launched his campaign to persuade shareholders to elect himself, Silverberg, and Wallace to Vaxart’s board. Silverberg is founder and CIO of Heatjac, a manufacturer of heated medical garments. Wallace is a double board-certified dermatologist and Mohs micrographic surgeon, and managing partner of a medical specialty practice focused on dermatology, dermatologic surgery, and oncology.
“We believe Vaxart possesses a unique technology platform with the potential to reshape vaccine delivery and transform global public health. Yet despite this promise, stockholder value has remained significantly compromised,” Houle and allies, calling themselves the Concerned Vaxart Shareholders, wrote in a June 9 letter to shareholders. “Despite these strengths, stockholders have endured years of disappointing performance, declining market value, and insufficient engagement from those entrusted to represent our interests.”
They also took issue with Vaxart’s two workforce reductions last year. The first was a 10% cut after Advanced Technology International, a nonprofit R&D collaboration manager acting on behalf of the U.S. Biomedical Advanced Research and Development Authority (BARDA), issued the first of two stop-work orders on the company’s Phase IIb trial assessing its government-funded COVID-19 oral pill vaccine. The second was a 21% cut in May–June 2025 intended to lower operating costs and better align Vaxart’s resources with higher-priority clinical programs.
“This election is not about creating conflict. It is about restoring confidence,” the Concerned Vaxart Shareholders added. “It is about restoring accountability, increasing transparency, and ensuring that stockholder interests are once again placed at the center of the company’s decision-making process.
Concerned Shareholders owned 1,515,343 shares of Vaxart stock—including 15,622 owned by Houle himself—as of a May 6 regulatory filing.
In an interview at the recent Biotechnology Innovation Organization (BIO) International Convention in San Diego, Lo and Tucker defended the company-endorsed board nominees as possessing greater biotech-related experience.
Lo defended the workforce cuts: “You want to be at the right size. You want to extend your runway. And we’re very careful with shareholder money. We don’t want to exhaust our funds. The reduction in the workforce was not only to extend our cash runway, but also make sure that this company had the right people to fulfill its mission.”
“Our case is, we have a very experienced management team. We have to stay the course,” Lo added. “We are in a great situation where we have good relationships with the U.S. government, as evidenced by being one of the only companies that has survived stop-work orders. We also have good relationships with pharma, as evidenced by our deal with Dynavax.”
Following a second stop-work order issued in August 2025, Vaxart and BARDA agreed to reduce funding for the Phase IIb trial to about $345 million from up to $453 million, but maintain the study at the estimated 5,485 patients recruited by Vaxart. In November 2025, Vaxart signed an up-to-$700 million global exclusive license for the oral COVID-19 vaccine with Dynavax Technologies, with Vaxart allowed to run the trial. Dynavax was acquired by Sanofi (Euronext Paris: SAN) for $2.2 billion, in a deal completed in February.
The cooperation agreement was one of two positive announcements Vaxart shared on July 6. The other was good clinical news: positive topline data from the approximately 400-participant sentinel safety cohort of its Phase IIb trial (NCT06672055) assessing the company’s oral pill COVID-19 vaccine candidate against an undisclosed approved mRNA vaccine comparator. Among key findings:
- No vaccine-related serious adverse events (SAEs) or sustained Grade 3 or higher AEs were reported in either the oral pill vaccine or mRNA arms of the trial.
- The most common AEs for oral vaccine patients were malaise/fatigue (20.9%), headache (18.9%), and anorexia (10.0%). Fewer than 10% of participants experienced any other AE.
- By contrast, the most common AEs in participants receiving the mRNA vaccine were injection site pain (60.3%), injection site tenderness (40.2%), malaise/fatigue (35.2%), myalgia/muscle pain (33.2%), and headache (28.6%). Arthralgia, chills, anorexia, nausea, diarrhea, and induration/swelling at the injection site were experienced by between 10–15% of participants. Fewer than 10% of participants experienced any other AE.
- Thirty-three participants in Vaxart’s oral pill vaccine arm and 30 in the mRNA vaccine arm had symptomatic COVID-19. Asymptomatic COVID-19 cases were reported in 12 participants in each of the trial arms.
“These topline safety data are encouraging and are consistent with the safety profile observed to date in other studies of our oral pill vaccine constructs,” stated James Cummings, MD, Vaxart’s chief medical officer.
Vaxart shares, which trade under $1, rose 16% from 55 cents on June 25 to 64 cents on July 2, the day of the filing disclosing the cooperation agreement. Since then, shares have given back the entire gain, sliding back to 55 cents at Friday’s close.
Leaders and laggards
- Chemomab Therapeutics (Nasdaq: CMMB) shares tumbled 29% from $2.77 to $1.97 Wednesday after the developer of therapeutics for immune-fibrotic diseases with high unmet need said it agreed to merge with precision medicine developer Scipher Medicine through an all-stock merger. The combined company plans to operate under the Scipher Medicine name and trade on Nasdaq under the ticker symbol SCIP. Upon completion of the merger, the combined company plans to focus initially on advancing nebokitug, a first-in-class clinical-stage anti-CCL24 antibody, into a Phase II trial for the treatment of rheumatoid arthritis, Chemomab said. The combined company is valued at $150 million before a concurrent $30 million private placement from a syndicate of current Scipher investors led by Northpond Ventures, with participation from Khosla Ventures, Blue Owl Healthcare Opportunities, funds managed by Neuberger, and other leading investors, and is expected to have cash runway into the second half of 2028.
- Forte Biosciences (Nasdaq: FBRX) shares rocketed 78% from $20.38 to $36.70 Thursday after the developer of treatments for autoimmune and autoimmune-related diseases announced positive results from the FB102 double-blind placebo-controlled Phase Ib study in vitiligo. FB102 achieved a 29.6% mean Facial Vitiligo Area Scoring Index (FVASI) improvement from baseline at week 24 (p-value = 0.020). Response to FB102 was seen early, Forte said, with statistically significant improvements observed by the day 64 visit (p=0.023), continuing through week 24, after completion of the 12-week treatment period. FB102 achieved 43.2% mean FVASI improvement from baseline at week 24 (p-value = 0.006) in subjects with greater disease involvement having baseline FVASI ≥0.75 (approximately one-quarter of face depigmented), including FVASI50 (58.8%) and FVASI75 (23.5%). Forte shares continued climbing Friday, rising another 20% to $43.92.
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