Tag: Biotech

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Force-Sensing Mobile Microgrippers for Gentle Bioassembly of Spheroids

Spheroids can be useful to model complex human tissues because they can re-create specific cell-to-cell and cell-to-matrix interactions. But spheroids are fragile, and common techniques for moving them manually—via suction—can easily damage them. In tissue engineering, the tiniest bit of improper force can harm a living culture. Now, a force-sensing miniature robot—a mobile microgripper (MMG)—has been developed that can handle spheroids with care.

“Other techniques for cell spheroid bioassembly can affect the tissue construct and/or apply limited manipulation forces,” said David Cappelleri, PhD, professor of mechanical engineering and assistant vice president for Research Innovation School of Mechanical Engineering at Purdue University. “The force-sensing MMG presented here addresses these current issues by allowing the safe bioassembly of different spheroids into a single construct.”

This work is published in APL Bioengineering, in a paper entitled, “Force-sensing mobile microrobotic grippers for gentle and precise bioassembly of cell spheroids.”

Integrating different types of spheroids into one culture is key for tissue engineering. But individual spheroids have to be grown in place and then moved around, introducing the chance of damage to the spheroid.

The MMG is a microscopic robot made of two arms connected by a hinge for a controlled—and gentle—gripping. Also, it is controlled by magnets, which are biocompatible with spheroids, decreasing the risk of collateral damage.

“This was a big part of the design—figuring out a way to use magnetic fields for both locomotion and for controlling the opening and closing of the gripper jaws,” Cappelleri said.

The gripping force is monitored and adjusted in real time, allowing researchers to adapt to the delicate nature of the cells. After simulating the efficacy of the MMG, in vitro testing showed that the device was able to successfully move and organize spheroids into neat patterns.

The researchers also verified that the range of gripping forces exerted by the MMG was compatible with the movement and subsequent survival of the spheroids.

Currently, the robot can successfully assemble the spheroids in a cellular “sheet,” but in the future, the researchers want to use their tiny robots to create full engineered tissues. In addition, the researchers want to take their microgrippers a step further, transitioning from manual control to automated spheroid assembly.

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STAT+: Eli Lilly enlists AI startup for next-generation gene editors

Eli Lilly struck a deal Tuesday to develop new forms of gene editors potentially capable of inserting entire genes into patients. 

The collaboration, with artificial intelligence-focused biotech Profluent, is sparse on details, including the number of programs the two companies would work on, the types of diseases they’ll pursue, or how much Lilly was paying upfront. But if every one of its efforts works out, Lilly would pay Profluent $2.25 billion in milestones payments.

The deal is part of a larger push by Lilly into gene editing. The big pharma, flush with record revenues from its obesity and diabetes drugs, has opened a new genetic medicine center in Boston and bought up a series of gene editing or gene therapy companies over the last few years.

Continue to STAT+ to read the full story…

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Retron-Powered Approach Enables Genome Editing Across Diverse Bacterial Species

For decades, the ability to precisely rewrite bacterial genomes has been largely confined to a single workhorse organism: Escherichia coli. That limitation has slowed efforts to study pathogens, engineer sustainable biomanufacturing strains, and probe how microbes influence human health. While genome editing tools have transformed eukaryotic biology, most high‑efficiency bacterial editors simply haven’t worked outside E. coli.

A new study from the Gladstone Institutes aims to change that. In a large, nine‑lab collaboration, researchers have translated a retron‑based DNA editing system from E. coli into 14 additional bacterial species spanning three major phyla. The work, published in Nature Biotechnology and titled “Genome editing of phylogenetically distinct bacteria using cross-species retron-mediated recombineering,” demonstrates that retrons, bacterial immune elements that continuously produce short DNA strands, can be engineered into portable genome editing modules the authors call recombitrons. “Recombitrons—a genome editing tool created by pairing modified, donor-producing bacterial retrons with single-stranded binding and annealing proteins—have increased the efficiency of recombineering to install flexible, precise edits in the prokaryotic chromosome,” the authors wrote.

Retrons normally function as part of a viral defense system, generating DNA fragments that help bacteria detect and respond to infection. Seth Shipman, PhD, a Gladstone Investigator and senior author of the study, has spent years repurposing this machinery. “We’ve been easily editing E. coli genomes using retrons for years now, which has substantially increased the pace of our fundamental biology and our molecular technology development,” he said. “But we kept hearing from the broader field, asking when there would be a version of this technology that could be put to work in other bacterial species that matter for the environment, industrial processes, or human health.”

Shipman’s lab previously showed that retrons can act as cellular DNA-making factories, generating the donor strands needed for genome editing. In bacteria, the resulting editing tool built by pairing modified retrons with single‑stranded DNA–binding and annealing proteins is known as a recombitron. Until now, however, functional recombitrons existed only in E. coli.

To test whether the architecture could travel, the team designed a panel of 10 retron-based editing systems and partnered with other labs specializing in diverse bacterial species. “We designed all the molecular parts at Gladstone, then sent them to the collaborators, where they ran the experiment in their labs,” said first author Alejandro González‑Delgado, PhD. Samples were then returned to Gladstone for centralized analysis.

The results show broad functionality. The recombitrons worked in all 15 species tested, including clinically relevant pathogens such as Klebsiella pneumoniae and Pseudomonas aeruginosa, as well as fast‑growing biotechnology strains like Vibrio natriegens and Pseudomonas putida. Editing efficiencies varied widely—from fractions of a percent to more than 90%—but the team demonstrated that modifying retron structure or other system components could boost performance in lower‑efficiency hosts.

“Each retron worked differently in different bacteria,” González‑Delgado noted. “This reinforces why it’s important to have lots of different retrons, so scientists can choose the ones best suited to their favorite bacterial species.”

The study provides a roadmap for expanding genome editing into species that have historically been difficult to engineer. Researchers studying microbial pathogenesis, gut ecology, or industrial bioproduction can now match retron systems to their organism of interest.

“My lab builds molecular technology, and we want these technologies to be used as broadly as possible to uncover new biology and intervene in disease,” Shipman said. “We hope it will continue to spread from here.”

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Pencil Beam Laser Could Help Researchers Design Brain-Targeted Therapies

Scientists at MIT say they made a finding in optical physics that could enable a new bioimaging method that’s faster and higher-resolution than existing technology. They discovered that, under the right conditions, laser light clutter can spontaneously self-organize into a highly focused “pencil beam.”

Using this self-organized pencil beam, the team captured 3D images of the human blood-brain barrier 25 times faster than the gold-standard method, while maintaining comparable resolution, according to the scientists.

By showing individual cells absorbing drugs in real-time, this technology could help scientists test whether new drugs for neurodegenerative disease like Alzheimer’s or ALS reach their targets in the brain, with greater speed and resolution, they add.

“The common belief in the field is that if you crank up the power in this type of laser, the light will inevitably become chaotic. But we proved that this is not the case. We followed the evidence, embraced the uncertainty, and found a way to let the light organize itself into a novel solution for bioimaging,” says Sixian You, PhD, assistant professor in the MIT department of electrical engineering and computer science (EECS), a member of the research laboratory for electronics.

You is senior author of a paper “Self-localized ultrafast pencil beam for volumetric multiphoton imaging” on this imaging technique in Nature Medicine.

A better beam

When the researchers performed characterization experiments of this pencil beam, it was more stable and high-resolution than many similar beams. Other beams often suffer from “sidelobes,”  blurry halos of light that can distort images.

Their beam was more pristine and tightly focused, according to You. Building on those experiments, the researchers demonstrated the use of this pencil-beam in biomedical imaging of the human blood-brain barrier.

Scientists and clinicians often want to see how drugs flow inside the vasculature of the blood-brain barrier and whether they reach their targets within the brain. But with standard optical settings, the best one can do is capture one 2D section of the vasculature at a time, and then repeat the process multiple times to generate a fuller image, You explains.

Using this new technique, the researchers created an ultrafast, high-precision pencil beam that enabled them to dynamically track how cells absorb proteins in real-time.

“The pharmaceutical industry is especially interested in using human-based models to screen for drugs that effectively cross the barrier, as animal models often fail to predict what happens in humans. That this new method doesn’t require the cells to have a fluorescent tag is a game-changer,” notes Roger Kamm, PhD, the Cecil and Ida Green Distinguished Professor of Biological Science and Mechanical Engineering.

“For the first time, we can now visualize the time-dependent entry of drugs into the brain and even identify the rate at which specific cell types internalize the drug.”

“Importantly, however, this approach is not limited to the blood-brain barrier but enables time-resolved tracking of diverse compounds and molecular targets across engineered tissue models, providing a powerful tool for biological engineering,” points out postdoctoral fellow Sarah Spitz, PhD.

The team reports that it captured cellular-level 3D images that were higher quality than with other methods, and generated these images about 25 times faster.

“Usually, you have a tradeoff between image resolution and depth of focus—you can only probe so far at a time. But with our method, we can overcome this tradeoff by creating a pencil-beam with both high resolution and a large depth of focus,” You says.

In the future, the researchers want to better understand the fundamental physics of the pencil-beam and the mechanisms behind its self-organization. They also plan to apply the technique to other scenarios, such as imaging neurons in the brain, and work toward commercializing the technology.

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Sun Pharma Aims for Top 3 in Women’s Health with $11.75B Organon Purchase

Sun Pharmaceutical Industries has agreed to acquire Organon, the women’s health drug developer spun out of Merck & Co., for $11.75 billion in a deal intended to catapult the buyer into a top 25 global biopharma—top three in women’s health—by growing its innovative medicines business and expanding its product offerings into biosimilar drugs, the companies said today.

Headquartered in Jersey City, NJ, Organon was spun out of Merck in 2021 and has since then grown its portfolio to more than 70 women’s health and general medicines products, including biosimilars, that have been commercialized in the U.S. and some 140 countries worldwide. In addition to the U.S., Organon’s largest markets include Brazil, Canada, China, and the countries of the European Union. Organon said it has six manufacturing facilities across the EU and emerging markets.

Sun Pharma said the combined company created by the deal will have annual revenue of $12.4 billion, a figure the company said would propel it into a top 25 global pharma—though the company was ranked No. 14 in GEN’s most recent A-List of Top 25 Biotech Companies Heading Into 2026, compiled last December, based on its market capitalization (share price times the number of outstanding shares) of INR 4.31 trillion ($50.8 billion).

Sun Pharma said Organon’s portfolio was similar to its own, and that the acquisition of Organon was aligned with its strategies of growing its Innovative Medicines business (to a 27% revenue share) and expanding into biosimilars as a Top 10 global company.

The combined company, Sun Pharma and Organon said, would be top three in global women’s health, creating a commercial platform for future growth; the seventh largest global biosimilar player; and a presence in 150 countries worldwide, with 18 large markets that would each generate more than $100 million in revenues.

“This transaction represents a significant opportunity for Sun Pharma to build on its vision of Reaching People and Touching Lives,” Sun Pharma executive chairman Dilip Shanghvi said in a statement. “Organon’s portfolio, capabilities, and global reach are highly complementary to our own, and we believe that bringing the two organizations together can create a stronger and more diversified platform. We have deep respect for Organon’s mission and look forward to building on its legacy while driving sustainable long‑term growth.”

Deal speculation

The deal ends two weeks of speculation that began with an April 10 report in the Indian news outlet The Economic Times stating that Sun Pharma had submitted a $12 billion all-cash offer for Organon. On Friday, the news outlet followed up with a report stating that Sun Pharma had submitted a revised $13 billion offer.

Investors appeared to support the deal, as Sun Pharma shares on India’s National Stock Exchange rose about 7% to INR 1,733.50 ($18.41) at the close of trading today.

Sun Pharma has agreed to acquire 100% of Organon’s issued and outstanding shares for cash. Sun said it planned to fund the acquisition through a combination of available cash resources and committed financing from banks.

“Together, we will become a partner of choice for acquiring and launching new products,” stated Kirti Ganorkar, managing director of Sun Pharma. “Our immediate priorities will be business continuity, disciplined integration, and responsible value creation. We see strong potential in leveraging Organon’s talent pool. In addition, there is a scope for synergies including significant revenue upside opportunities to be realized over the coming years.”

Those synergies were later quantified by Sun Pharma as approximately $350 million within two to four years of the deal’s completion.

Sun Pharma did say, however, that the acquisition of Organon will strengthen its generation of cash, with its earnings before interest, taxes, depreciation, and amortization (EBITDA) and cash flow set to nearly double, supporting future efforts to reduce the net debt/EBITDA of 2.3x resulting from the deal.

Sun Pharma finished the first nine months of its fiscal year ending March 31, 2026, with a net profit of INR 87.654 billion ($931.5 million) and EBITDA of INR 137.772 billion ($1.464 billion; up 19.2% from the year-ago period), on sales of INR 436.604 billion ($4.64 billion), up 11.3% year over year.

During its fiscal year ending March 31, 2025, Sun Pharma reported adjusted net profit (excluding one-time items) of INR 119.844 billion ($1.274 billion), up 19% from a year earlier, on sales of INR 520.412 billion (about $5.53 billion). Reported net profit for FY 2025 was INR 109.290 billion ($1.161 billion), vs. Rs. 95.764 billion ($1.017 billion) during FY 2024.

Organon finished last year with adjusted EBITDA of $1.9 billion on revenue of $6.2 billion. The company reported debt of $8.64 billion—down from the $9.5 billion in debt it reported when it separated from Merck—and a cash balance of $574 million.

Planned sale

In November, Organon announced plans to sell its JADA® System, designed to control and treat abnormal postpartum uterine bleeding or hemorrhage, to Laborie Medical Technologies for up to $465 million—$440 million to be paid at closing, subject to adjustments, and up to $25 million tied to achieving 2026 revenue targets. Net proceeds from the divestiture will contribute to Organon’s cash balance as of March 31, 2026.

Organon will merge with a subsidiary of Sun Pharma, with Organon surviving the merger. The transaction is expected to close in early 2027 subject to customary conditions, including regulatory approvals and Organon stockholder approval.

The boards of both Sun Pharma and Organon have approved the deal.

“Following a comprehensive review of strategic alternatives, our Board determined that this all‑cash transaction offers compelling and immediate value to Organon stockholders,” stated Carrie Cox, executive chair of Organon. “We believe Sun Pharma is well positioned to support Organon’s businesses, employees, and patients globally, and to further advance our commitment to delivering impactful medicines and solutions.”

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Anticancer Strategy Targets Defense Mechanism in Senescent Cells

Scientists headed by a team at MRC Laboratory of Medical Sciences (LMS) and Imperial College London have found that a new set of drugs can exploit a recently-revealed weakness in senescent—or ‘zombie-like’—cells, a finding that could lead to new treatments for cancer and age-associated diseases.

Senescent cells walk a tightrope, risking cell death with high levels of iron and other damaging agents, but compensating for this by overproducing a protective protein, GPX4, which staves off death. The team showed that targeting this defense mechanism removes the shield and could be used to treat diseases that are associated with senescence, including cancer. Tests showed that combining anticancer therapies with GPX4 inhibitors eliminated senescent tumor cells in models of melanoma, prostate and ovarian cancer. This approach, they say, could complement existing treatments to bring much-needed improvements for cancer patients.

Mariantonietta D’Ambrosio, PhD, a postdoctoral researcher at the LMS, is first author of the international research team’s published paper in nature cell biology, titled “Electrophilic compound screening identifies GPX4-dependent ferroptosis as a senescence vulnerability.”

Cancers grow as a result of unconstrained cell division. But within most tumors, there is a portion that does not divide at all: senescent cells. Chemotherapy often increases the proportion of senescent cells in a tumor as it aims to stem the rapid proliferation, the team explained. However, while these senescent cells don’t directly increase the size of a tumor, they can wreak havoc in their own way.

Senescent cells, which are also a defining feature of aging conditions such as fibrosis, influence neighboring cells by secreting molecules that increase proliferation, the spread of the cancer, and unwanted immune system activity. “Senescent cells drive aging and age-related pathologies, including cancer,” the team wrote. There is therefore an increasing interest in developing drugs that directly target and kill senescent cells, in cancer and beyond. “Consequently, senolytics, drugs that selectively kill senescent cells, have broad therapeutic appeal,” they continued. “Compounds that selectively kill senescent cells (senolytics) can treat different age-related pathologies.”

The study by D’Ambrosio and colleagues has identified a new approach to killing senescent cells in cancer.  “Senescence was considered for a long time to be positive, because senescent cells don’t proliferate, which is the core feature of cancer,” D’Ambrosio explained. “Normal chemotherapy induces senescence blocking the proliferation of cancer cells, so the tumor doesn’t get bigger. But with time you also see the negative side of the senescent cells, because they secrete a lot of factors that influence neighboring cells and induce even more proliferation, metastasis, and recruitment of bad parts of the immune system that will provoke even more aggressiveness in the tumor.  For this reason, we tried to find some drugs that were able to kill the senescent cells.”

The researchers cast a broad net in their search for new drugs that might kill senescent cells. Together with collaborators at the Department of Medicinal Chemistry at Imperial, they decided to examine covalent compounds, a class of inhibitors that can form a covalent bond with their target, which can result in the inhibition of proteins previously considered undruggable. The investigators introduced 10,000 different covalent compounds to both senescent cells and normal cells, looking for the ones that preferentially killed senescent cells and classing the drug as “senolytic,” or senescent-killing.

They narrowed their results down to just four promising compounds and found that three of them affected a particular protein, GPX4, which has a protective role in cells, helping stave off ferroptosis, a type of cell death associated with high levels of iron and destructive reactive oxygen species. To protect themselves against the high levels of iron and other ferroptosis-causing agents, senescent cells have high levels of GPX4. It is like proactively taking a painkiller so a person can keep running on an ankle. The damage and danger remains, but the immediate risks are bypassed. Removing the painkiller makes the pain unbearable.

“Senescent cells are primed for ferroptosis and upregulate GPX4 as a protective mechanism,” the team noted. Ferroptosis had only recently been revealed as a potential weakness of senescent cells. D’Ambrosio commented, “recent papers have shown this predisposition of senescent cells to ferroptosis, but it’s a new senescence vulnerability. That creates an opportunity for us to exploit. So now there is research to find senolytic drugs to kill cells through ferroptosis.”

The researchers found that blocking the activity of GPX4 removes the shield, making fatal ferroptosis unavoidable. The authors further commented, “We concentrated our studies on four chloroacetamides displaying senolytic activity in different models of senescence … GPX4 was a target of three of the four senolytic chloroacetamides. GPX4 is a glutathione peroxidase that prevents ferroptosis by reducing lipid peroxidation.”

The team tested their drugs with three different mouse models of cancer and saw improved outcomes as a result of senescent cell death in each case. Translating this to patients could be a huge asset to cancer treatments. “In mouse models we saw that these drugs reduced tumor size, and improved survival,” noted professor Jesus Gil, PhD, senior author and head of the senescence group at the LMS. “Now we need to see the effect on the immune system. Is the improvement also awakening the ‘good side’ of the immune system (T cells, natural killer cells) that helps to kill the tumor? … Once we know more, the next step is to understand which cancer cell types or specific patients might better respond to this treatment. For example, if a patient undergoing chemotherapy overexpressed GPX4 then you could use this approach in combination with existing drugs to improve efficacy.”

This approach offers a much-needed new perspective on cancer therapy, pinpointing senescent cells as an underexploited target. D’Ambrosio says it has potential to transform treatment. “Targeting senescence is a huge opportunity for cancer treatments, and ultimately it can play a supporting role in addition to chemotherapy and immunotherapy.”

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The missing step between hype and profit

This story originally appeared in The Algorithm, our weekly newsletter on AI. To get stories like this in your inbox first, sign up here.

In February, I picked up a flyer at an anti-AI march in London. I can’t say for sure whether or not its writers meant to riff on South Park’s underpants gnomes. But if they did, they nailed it: “Step 1: Grow a digital super mind,” it read. “Step 2: ? Step 3: ?”

Produced by Pause AI, an international activist group that co-organized the protest, it ended with this plea to the reader: “Pause AI until we know what the hell Step 2 is.” 

In the South Park episode “Gnomes,” which first aired in 1998, Kenny, Kyle, Cartman, and Stan discover a community of gnomes that sneak out at night to steal underpants from dressers. Why? The gnomes present their pitch deck. “Phase 1: Collect underpants. Phase 2: ? Phase 3: Profit.”

The gnomes’ business plan has since become one of the greats among internet memes, used to satirize everything from startup strategies to policy proposals. Memelord in chief Elon Musk once invoked it in a talk about how he planned to fund a mission to Mars. Right now, it captures the state of AI. Companies have built the tech (Step 1) and promised transformation (Step 3). How they get there is still a big question mark.

As far as Pause AI is concerned, Step 2 must involve some kind of regulation. But exactly what it will call for and who will enforce it are up for debate.

AI boosters, on the other hand, are convinced that Step 3 is salvation and tend to glaze over the middle bit. They see us racing toward sunny uplands on the back of an “economically transformative technology,” as OpenAI’s chief scientist, Jakub Pachocki, put it to me a few weeks ago. They know where they want to go—more or less: It’s hazy up there and still some way off. But everyone’s taking a different route. Will they all make it? Will anyone?

For every big claim about the future, there is a more sober assessment of how the rubber meets the road—one that quells the hype. Consider two recent studies. One, from Anthropic, predicted what types of jobs are going to be most affected by LLMs. (A takeaway: Managers, architects, and people in the media should prepare for change; groundskeepers, construction workers, and those in hospitality, not so much.) But their predictions are really just guesses, based on what kinds of tasks LLMs seem to be good at rather than how they really perform in the workplace.   

Another study, put out in February by researchers at Mercor, an AI hiring startup, tested several AI agents powered by top-tier models from OpenAI, Anthropic, and Google DeepMind on 480 workplace tasks frequently carried out by human bankers, consultants, and lawyers. Every agent they tested failed to complete most of its duties.   

Why is there such wide disagreement? There are a number of factors. For a start, it’s crucial to consider who is making the claims (and why). Anthropic has skin in the game. What’s more, most of the people telling us that something big is about to happen have reached that conclusion largely on the basis of how fast AI coding tools are getting. But not all tasks can be hacked with coding. Other studies have found that LLMs are bad at making strategic judgment calls, for example.

What’s more, when they’re deployed, the tools aren’t just dropped into a cleanroom. They need to work in places contaminated with people and existing workflows. And sometimes adding AI will make things worse. Sure, maybe those workflows need to be torn up and refashioned around the new technology for it to achieve transformative status, but that will take time (and guts).  

That big hole? It’s right where Step 2 should be. The lack of agreement on exactly what’s about to happen—and how—creates an information vacuum that gets filled by the latest wild claim of the week, evidence be damned. We’re so unmoored from any real understanding of what’s coming and how it will be deployed that a single social media post can (and does) shake markets.

We need fewer guesses and more evidence. But that’s going to require transparency from the model makers, coordination between researchers and businesses, and new ways to evaluate this technology that tell us what really happens when it’s rolled out in the real world.

The tech industry (and with it the world’s economy) rests on the held-out promise that AI really will be transformative. But that is not yet a sure bet. Next time you hear bold claims about the future, remember that most businesses are still figuring out what to do with their underpants.

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Monoclonal Antibodies: Unlocking Cost and Efficiency Gains in Downstream Processing



Image of Kristina Pleitt

Kristina Pleitt

Senior Staff Scientist
Thermo Fisher Scientific

Panelist

Image of Kristina Pleitt

Kristina Pleitt

Kristina Pleitt is a senior staff scientist at Thermo Fisher Scientific with 15 years of experience in biopharmaceutical process development and manufacturing. Her expertise includes downstream process development, process scale-up, integrated continuous processing, and clinical and commercial production, with a particular focus on advancing intensified downstream strategies that improve process efficiency, performance, and manufacturability.



Broadcast Date: 

  • Time: 

Analytical developers and downstream scientists are under constant pressure to improve process efficiency while maintaining product quality for monoclonal antibodies (mAbs). Yet, many platform purification processes still leave untapped opportunities for optimization, cost reduction, and simplification.

In this webinar, our speaker will explore a series of practical, chromatography-focused strategies designed to enhance mAb purification performance while reducing cost of goods (COGs). Using real-world examples and process scenarios, attendees will gain insight into:

  • Identifying opportunities to simplify traditional mAb purification workflows

  • Improving Protein A performance and lifetime to drive cost savings

  • Enabling efficient two-step downstream processes through better impurity management

  • Addressing difficult HCP and aggregate clearance challenges with advanced polishing strategies

A live Q&A session will follow the presentation, offering you a chance to engage directly with our expert and discuss how these approaches can be applied to your own processes.

Produced with support from:

Thermo Fisher logo

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