Introduction – Company Background

GuangXin Industrial Co., Ltd. is a specialized manufacturer dedicated to the development and production of high-quality insoles.

With a strong foundation in material science and footwear ergonomics, we serve as a trusted partner for global brands seeking reliable insole solutions that combine comfort, functionality, and design.

With years of experience in insole production and OEM/ODM services, GuangXin has successfully supported a wide range of clients across various industries—including sportswear, health & wellness, orthopedic care, and daily footwear.

From initial prototyping to mass production, we provide comprehensive support tailored to each client’s market and application needs.

At GuangXin, we are committed to quality, innovation, and sustainable development. Every insole we produce reflects our dedication to precision craftsmanship, forward-thinking design, and ESG-driven practices.

By integrating eco-friendly materials, clean production processes, and responsible sourcing, we help our partners meet both market demand and environmental goals.

Core Strengths in Insole Manufacturing

At GuangXin Industrial, our core strength lies in our deep expertise and versatility in insole and pillow manufacturing. We specialize in working with a wide range of materials, including PU (polyurethane), natural latex, and advanced graphene composites, to develop insoles and pillows that meet diverse performance, comfort, and health-support needs.

Whether it's cushioning, support, breathability, or antibacterial function, we tailor material selection to the exact requirements of each project-whether for foot wellness or ergonomic sleep products.

We provide end-to-end manufacturing capabilities under one roof—covering every stage from material sourcing and foaming, to precision molding, lamination, cutting, sewing, and strict quality control. This full-process control not only ensures product consistency and durability, but also allows for faster lead times and better customization flexibility.

With our flexible production capacity, we accommodate both small batch custom orders and high-volume mass production with equal efficiency. Whether you're a startup launching your first insole or pillow line, or a global brand scaling up to meet market demand, GuangXin is equipped to deliver reliable OEM/ODM solutions that grow with your business.

Customization & OEM/ODM Flexibility

GuangXin offers exceptional flexibility in customization and OEM/ODM services, empowering our partners to create insole products that truly align with their brand identity and target market. We develop insoles tailored to specific foot shapes, end-user needs, and regional market preferences, ensuring optimal fit and functionality.

Our team supports comprehensive branding solutions, including logo printing, custom packaging, and product integration support for marketing campaigns. Whether you're launching a new product line or upgrading an existing one, we help your vision come to life with attention to detail and consistent brand presentation.

With fast prototyping services and efficient lead times, GuangXin helps reduce your time-to-market and respond quickly to evolving trends or seasonal demands. From concept to final production, we offer agile support that keeps you ahead of the competition.

Quality Assurance & Certifications

Quality is at the heart of everything we do. GuangXin implements a rigorous quality control system at every stage of production—ensuring that each insole meets the highest standards of consistency, comfort, and durability.

We provide a variety of in-house and third-party testing options, including antibacterial performance, odor control, durability testing, and eco-safety verification, to meet the specific needs of our clients and markets.

Our products are fully compliant with international safety and environmental standards, such as REACH, RoHS, and other applicable export regulations. This ensures seamless entry into global markets while supporting your ESG and product safety commitments.

ESG-Oriented Sustainable Production

At GuangXin Industrial, we are committed to integrating ESG (Environmental, Social, and Governance) values into every step of our manufacturing process. We actively pursue eco-conscious practices by utilizing eco-friendly materials and adopting low-carbon production methods to reduce environmental impact.

To support circular economy goals, we offer recycled and upcycled material options, including innovative applications such as recycled glass and repurposed LCD panel glass. These materials are processed using advanced techniques to retain performance while reducing waste—contributing to a more sustainable supply chain.

We also work closely with our partners to support their ESG compliance and sustainability reporting needs, providing documentation, traceability, and material data upon request. Whether you're aiming to meet corporate sustainability targets or align with global green regulations, GuangXin is your trusted manufacturing ally in building a better, greener future.

Let’s Build Your Next Insole Success Together

Looking for a reliable insole manufacturing partner that understands customization, quality, and flexibility? GuangXin Industrial Co., Ltd. specializes in high-performance insole production, offering tailored solutions for brands across the globe. Whether you're launching a new insole collection or expanding your existing product line, we provide OEM/ODM services built around your unique design and performance goals.

From small-batch custom orders to full-scale mass production, our flexible insole manufacturing capabilities adapt to your business needs. With expertise in PU, latex, and graphene insole materials, we turn ideas into functional, comfortable, and market-ready insoles that deliver value.

Contact us today to discuss your next insole project. Let GuangXin help you create custom insoles that stand out, perform better, and reflect your brand’s commitment to comfort, quality, and sustainability.

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Custom graphene foam processing Indonesia

Are you looking for a trusted and experienced manufacturing partner that can bring your comfort-focused product ideas to life? GuangXin Industrial Co., Ltd. is your ideal OEM/ODM supplier, specializing in insole production, pillow manufacturing, and advanced graphene product design.

With decades of experience in insole OEM/ODM, we provide full-service manufacturing—from PU and latex to cutting-edge graphene-infused insoles—customized to meet your performance, support, and breathability requirements. Our production process is vertically integrated, covering everything from material sourcing and foaming to molding, cutting, and strict quality control.China pillow ODM development service

Beyond insoles, GuangXin also offers pillow OEM/ODM services with a focus on ergonomic comfort and functional innovation. Whether you need memory foam, latex, or smart material integration for neck and sleep support, we deliver tailor-made solutions that reflect your brand’s values.

We are especially proud to lead the way in ESG-driven insole development. Through the use of recycled materials—such as repurposed LCD glass—and low-carbon production processes, we help our partners meet sustainability goals without compromising product quality. Our ESG insole solutions are designed not only for comfort but also for compliance with global environmental standards.Taiwan insole ODM design and manufacturing factory

At GuangXin, we don’t just manufacture products—we create long-term value for your brand. Whether you're developing your first product line or scaling up globally, our flexible production capabilities and collaborative approach will help you go further, faster.ODM service for ergonomic pillows China

📩 Contact us today to learn how our insole OEM, pillow ODM, and graphene product design services can elevate your product offering—while aligning with the sustainability expectations of modern consumers.Vietnam ergonomic pillow OEM supplier

The study involved 375 budding service dogs from the Canine Companions service dog organization. Credit: Courtesy of Emily Bray/University of Arizona Dogs may have earned the title “man’s best friend” because of how good they are at interacting with people. Those social skills may be present shortly after birth rather than learned, a new study by University of Arizona researchers suggests. Published today in the journal Current Biology, the study also finds that genetics may help explain why some dogs perform better than others on social tasks such as following pointing gestures. Lead study author Emily Bray. Credit: University of Arizona “There was evidence that these sorts of social skills were present in adulthood, but here we find evidence that puppies — sort of like humans — are biologically prepared to interact in these social ways,” said lead study author Emily Bray, a postdoctoral research associate in the UArizona School of Anthropology in the College of Social and Behavioral Sciences. Bray has spent the last decade conducting research with dogs in collaboration with California-based Canine Companions, a service dog organization serving clients with physical disabilities. She and her colleagues hope to better understand how dogs think and solve problems, which could have implications for identifying dogs that would make good service animals. To better understand biology’s role in dogs’ abilities to communicate with humans, Bray and her collaborators looked at how 375 of the organization’s 8-week-old budding service dogs, which had little previous one-on-one interaction with humans, performed on a series of tasks designed to measure their social communication skills. Because the researchers knew each puppy’s pedigree — and therefore how related they were to one another — they were also able to look at whether inherited genes explain differences in dogs’ abilities. Genetics explained more than 40% of the variation in puppies’ abilities to follow human pointing gestures, as well as variation in how long they engaged in eye contact with humans during a task designed to measure their interest in people. “People have been interested in dogs’ abilities to do these kinds of things for a long time, but there’s always been debate about to what extent is this really in the biology of dogs, versus something they learn by palling around with humans,” said study co-author Evan MacLean, assistant professor of anthropology and director of the Arizona Canine Cognition Center at the University of Arizona. “We found that there’s definitely a strong genetic component, and they’re definitely doing it from the get-go.” At the time of the study, the puppies were still living with their littermates and had not yet been sent to live with a volunteer puppy raiser. Therefore, their interactions with humans had been limited, making it unlikely that the behaviors were learned, Bray said. The researchers engaged the puppies in four different tasks. In one task, an experimenter hid a treat beneath one of two overturned cups and pointed to it to see if the puppy could follow the gesture. To ensure that the pups weren’t just following their noses, a treat was also taped to the inside of both cups. In another version of the task, puppies watched as the researchers placed a yellow block next to the correct cup, instead of pointing, to indicate where the puppy should look for the food. The other two tasks were designed to observe puppies’ propensity to look at human faces. In one task, the researchers spoke to the puppies in “dog-directed speech,” reciting a script in the sort of high-pitched voice people sometimes use when talking to a baby. They then measured how long the puppy held a gaze with the human. In the final task — a so-called “unsolvable task” — researchers sealed a treat inside a closed container and presented it to the puppy, then measured how often the puppy looked to the human for help opening the container. While many of the puppies were responsive to humans’ physical and verbal cues, very few looked to humans for help with the unsolvable task. That suggests that while puppies may be born knowing how to respond to human-initiated communication, the ability to initiate communication on their own may come later. “In studies of adult dogs, we find a tendency for them to look to humans for help, especially when you look at adult dogs versus wolves. Wolves are going to persist and try to independently problem solve, whereas dogs are more likely to look to the social partner for help,” Bray said. “In puppies, this help-seeking behavior didn’t really seem to be part of their repertoire yet.” In many ways, that mirrors what we see in human children’s development, Bray said. “If you think about language learning, children can understand what we’re saying to them before they can physically produce the words,” she said. “It’s potentially a similar story with puppies; they are understanding what is being socially conveyed to them, but the production of it on their end is probably going to take a little bit longer, developmentally.” MacLean said the next step will be to see if researchers can identify the specific genes that may contribute to dogs’ capacity to communicate with humans. “We’ve done some previous studies that show that dogs who tend to be successful as service dogs respond to people in different ways than dogs who aren’t successful,” MacLean said. “If you could identify a potential genetic basis for these traits, you might be able to predict, even before the puppy is born, if they are part of a litter that would be good service dog candidates, because they have the right genetic background. It’s a long way down the road, but there is potential to start applying this.” Reference: “Early-emerging and highly heritable sensitivity to human communication in dogs” by Emily E. Bray, Gitanjali E. Gnanadesikan, Daniel J. Horschler, Kerinne M. Levy, Brenda S. Kennedy, Thomas R. Famula and Evan L. MacLean, 3 June 2021, Current Biology. DOI:10.1016/j.cub.2021.04.055 Funding: Office of Naval Research, AKC Canine Health Foundation, National Science Foundation Graduate Research Fellowship Program

The 93-year-old Xerces blue butterfly specimen used in this study. Credit: Field Museum The Xerces blue butterfly was last seen flapping its iridescent periwinkle wings in San Francisco in the early 1940s. It’s generally accepted to be extinct, the first American insect species destroyed by urban development, but there are lingering questions about whether it was really a species to begin with, or just a sub-population of another common butterfly. In a new study in Biology Letters, researchers analyzed the DNA of a 93-year-old Xerces blue specimen in museum collections, and they found that its DNA is unique enough to merit being considered a species. The study confirms that yes, the Xerces blue really did go extinct, and that insect conservation is something we have to take seriously. “It’s interesting to reaffirm that what people have been thinking for nearly 100 years is true, that this was a species driven to extinction by human activities,” says Felix Grewe, co-director of the Field’s Grainger Bioinformatics Center and the lead author of the Biology Letters paper on the project. “There was a long-standing question as to whether the Xerces blue butterfly was truly a distinct species or just a population of a very widespread species called the silvery blue that’s found across the entire west coast of North America,” says Corrie Moreau, director of the Cornell University Insect Collections, who began work on the study as a researcher at Chicago’s Field Museum. “The widespread silvery blue species has a lot of the same traits. But we have multiple specimens in the Field Museum’s collections, and we have the Pritzker DNA lab and the Grainger Bioinformatics Center that has the capacity to sequence and analyze lots of DNA, so we decided to see if we could finally solve this question.” A collections drawer of extinct Xerces blue butterflies. Credit: Field Museum To see if the Xerces blue really was its own separate species, Moreau and her colleagues turned to pinned butterfly specimens stored in drawers in the Field’s insect collections. Using forceps, she pinched off a tiny piece of the abdomen of a butterfly collected in 1928. “It was nerve-wracking, because you want to protect as much of it as you can,” she recalls. “Taking the first steps and pulling off part of the abdomen was very stressful, but it was also kind of exhilarating to know that we might be able to address a question that has been unanswered for almost 100 years that can’t be answered any other way.” Once the piece of the butterfly’s body had been retrieved, the sample went to the Field Museum’s Pritzker DNA Laboratory, where the tissues were treated with chemicals to isolate the remaining DNA. “DNA is a very stable molecule, it can last a long time after the cells it’s stored in have died,” says Grewe. Even though DNA is a stable molecule, it still degrades over time. However, there’s DNA in every cell, and by comparing multiple threads of DNA code, scientists can piece together what the original version looked like. “It’s like if you made a bunch of identical structures out of Legos, and then dropped them. The individual structures would be broken, but if you looked at all of them together, you could figure out the shape of the original structure,” says Moreau. Study authors Felix Grewe and Corrie Moreau working in the Field Museum’s Pritzker DNA Lab. Credit: Field Museum Grewe, Moreau, and their colleagues compared the genetic sequence of the Xerces blue butterfly with the DNA of the more widespread silvery blue butterfly, and they found that the Xerces blue’s DNA was different, meaning it was a separate species. The study’s findings have broad-reaching implications. “The Xerces blue butterfly is the most iconic insect for conservation because it’s the first insect in North America we know of that humans drove to extinction. There’s an insect conservation society named after it,” says Moreau. “It’s really terrible that we drove something to extinction, but at the same time what we’re saying is, okay, everything we thought does in fact align with the DNA evidence. If we’d found that the Xerces blue wasn’t really an extinct species, it could potentially undermine conservation efforts.” DNA analysis of extinct species sometimes invites questions of bringing the species back, à la Jurassic Park, but Grewe and Moreau note in their paper that those efforts could be better spent protecting species that still exist. “Before we start putting a lot of effort into resurrection, let’s put that effort into protecting what’s there and learn from our past mistakes,” says Grewe. Moreau agrees, noting the urgent need to protect insects. “We’re in the middle of what’s being called the insect apocalypse– massive insect declines are being detected all over the world,” says Moreau. “And while not all insects are as charismatic as the Xerces blue butterfly, they have huge implications for how ecosystems function. Many insects are really at the base of what keeps many of these ecosystems healthy. They aerate the soil, which allows the plants to grow, and which then feeds the herbivores, which then feed the carnivores. Every loss of an insect has a massive ripple effect across ecosystems.” In addition to the study’s implications for conservation, Grewe says that the project showcases the importance of museum collections. “When this butterfly was collected 93 years ago, nobody was thinking about sequencing its DNA. That’s why we have to keep collecting, for researchers 100 years in the future.” Reference: “Museum genomics reveals the Xerces blue butterfly (Glaucopsyche xerces) was a distinct species driven to extinction” by Felix Grewe, Marcus R. Kronforst, Naomi E. Pierce and Corrie S. Moreau, 21 July 2021, Biology Letters. DOI: 10.1098/rsbl.2021.0123

A study led by Harvard Medical School researchers has discovered how bacteria break through the brain’s protective layers to cause meningitis, a highly fatal disease. The researchers found that bacteria exploit nerve cells in the meninges to suppress the immune response, allowing the infection to spread. The study identified a chemical released by nerve cells and an immune cell receptor that, when blocked, can interrupt the cascade and prevent bacterial invasion. If replicated through further research, these findings could lead to therapies for this hard-to-treat condition. The treatments would target the early stages of infection before bacteria can spread deep into the brain. Study shows bacteria hijack crosstalk between nerve and immune cells to cause meningitis. A new study led by researchers at Harvard Medical School details the step-by-step cascade that allows bacteria to break through the brain’s protective layers — the meninges — and cause brain infection, or meningitis, a highly fatal disease. The research, conducted in mice and published recently in the journal Nature, shows that bacteria exploit nerve cells in the meninges to suppress the immune response and allow the infection to spread into the brain. “We’ve identified a neuroimmune axis at the protective borders of the brain that is hijacked by bacteria to cause infection — a clever maneuver that ensures bacterial survival and leads to widespread disease,” said study senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at HMS. Scientists have identified the maneuvers bacteria use to invade the brain and cause meningitis. Shown here are pain receptors (in red) in the brain’s protective layers, known as meninges. When activated by bacteria, pain receptors release a chemical that disables the normal protective functions of immune cells known as macrophages (in blue), weakening the brain’s defenses. Credit: Chiu Lab/Harvard Medical School The study identifies two central players in this molecular chain of events that leads to infection — a chemical released by nerve cells and an immune cell receptor blocked by the chemical. The study experiments show that blocking either one can interrupt the cascade and thwart the bacterial invasion. If replicated through further research, the new findings could lead to much-needed therapies for this hard-to-treat condition that often leaves those who survive with serious neurologic damage. Such treatments would target the critical early steps of infection before bacteria can spread deep into the brain. “The meninges are the final tissue barrier before pathogens enter the brain, so we have to focus our treatment efforts on what happens at this border tissue,” said study first author Felipe Pinho-Ribeiro, a former post-doctoral researcher in the Chiu lab, now an assistant professor at Washington University in St. Louis. A Recalcitrant Disease in Need of New Treatments More than 1.2 million cases of bacterial meningitis occur globally each year, according to the U.S. Centers for Disease Control and Prevention. Untreated, it kills seven out of 10 people who contract it. Treatment can reduce mortality to three in 10. However, among those who survive, one in five experience serious consequences, including hearing or vision loss, seizures, chronic headache, and other neurological problems. Current therapies — antibiotics that kill bacteria and steroids that tame infection-related inflammation — can fail to ward off the worst consequences of the disease, particularly if therapy is initiated late due to delays in diagnosis. Inflammation-reducing steroids tend to suppress immunity, weakening protection further and fueling infection spread. Thus, physicians must strike a precarious balance: They must rein in brain-damaging inflammation with steroids, while also ensuring that these immunosuppressive drugs do not further disable the body’s defenses. The need for new treatments is magnified by the lack of a universal meningitis vaccine. Many types of bacteria can cause meningitis, and designing a vaccine for all possible pathogens is impractical. Current vaccines are formulated to protect against only some of the more common bacteria known to cause meningitis. Vaccination is recommended only for certain populations deemed at high risk for bacterial meningitis. Additionally, vaccine protection wanes after several years. Chiu and colleagues have long been fascinated by the interplay between bacteria and the nervous and immune systems and by how the crosstalk between nerve cells and immune cells may either precipitate or ward off disease. Previous research led by Chiu has shown that the interaction between neurons and immune cells plays a role in certain types of pneumonia and in flesh-destroying bacterial infections. This time around, Chiu and Pinho-Ribeiro turned their attention to meningitis — another condition in which they suspected the relationship between nervous and immune systems plays a role. The meninges are three membranes that lie atop one another, wrapping the brain and spinal cord to shield the central nervous system from injury, damage, and infection. The outermost of the three layers — called dura mater — contains pain neurons that detect signals. Such signals could come in the form of mechanical pressure — blunt force from impact or toxins that make their way into the central nervous system through the bloodstream. The researchers focused precisely on this outermost layer as the site of initial interaction between bacteria and protective border tissue. Recent research has revealed that the dura mater also harbors a wealth of immune cells, and that immune cells and nerve cells reside right next to each other — a clue that captured Chiu’s and Pinho-Ribeiro’s attention. “When it comes to meningitis, most of the research so far has focused on analyzing brain responses, but responses in the meninges — the barrier tissue where infection begins — have remained understudied,” Ribeiro said. What exactly happens in the meninges when bacteria invade? How do they interact with the immune cells residing there? These questions remain poorly understood, the researchers said. How Bacteria Break Through the Brain’s Protective Layers In this particular study, the researchers focused on two pathogens —Streptococcus pneumoniae and Streptococcus agalactiae, leading causes of bacterial meningitis in humans. In a series of experiments, the team found that when bacteria reach the meninges, the pathogens trigger a chain of events that culminates in disseminated infection. First, researchers found that bacteria release a toxin that activates pain neurons in the meninges. The activation of pain neurons by bacterial toxins, the researchers noted, could explain the severe, intense headache that is a hallmark of meningitis. Next, the activated neurons release a signaling chemical called CGRP. CGRP attaches to an immune-cell receptor called RAMP1. RAMP1 is particularly abundant on the surface of immune cells called macrophages. Once the chemical engages the receptor, the immune cell is effectively disabled. Under normal conditions, as soon as macrophages detect the presence of bacteria, they spring into action to attack, destroy, and engulf them. Macrophages also send distress signals to other immune cells to provide a second line of defense. The team’s experiments showed that when CGRP gets released and attaches to the RAMP1 receptor on macrophages, it prevented these immune cells from recruiting help from fellow immune cells. As a result, the bacteria proliferated and caused widespread infection. To confirm that the bacterially induced activation of pain neurons was the critical first step in disabling the brain’s defenses, the researchers checked what would happen to infected mice lacking pain neurons. Mice without pain neurons developed less severe brain infections when infected with two types of bacteria known to cause meningitis. The meninges of these mice, the experiments showed, had high levels of immune cells to combat the bacteria. By contrast, the meninges of mice with intact pain neurons showed meager immune responses and far fewer activated immune cells, demonstrating that neurons get hijacked by bacteria to subvert immune protection. To confirm that CGRP was, indeed, the activating signal, researchers compared the levels of CGRP in meningeal tissue from infected mice with intact pain neurons and meningeal tissue from mice lacking pain neurons. The brain cells of mice lacking pain neurons had barely detectable levels of CGRP and few signs of bacterial presence. By contrast, meningeal cells of infected mice with intact pain neurons showed markedly elevated levels of both CGRP and more bacteria. In another experiment, the researchers used a chemical to block the RAMP1 receptor, preventing it from communicating with CGRP, the chemical released by activated pain neurons. The RAMP1 blocker worked both as preventive treatment before infection and as a treatment once infection had occurred. Mice pretreated with RAMP1 blockers showed reduced bacterial presence in the meninges. Likewise, mice that received RAMP1 blockers several hours after infection and regularly thereafter had milder symptoms and were more capable of clearing bacteria, compared with untreated animals. A Path to New Treatments The experiments suggest drugs that block either CGRP or RAMP1 could allow immune cells to do their job properly and increase the brain’s border defenses. Compounds that block CGRP and RAMP1 are found in widely used drugs to treat migraine, a condition believed to originate in the top meningeal layer, the dura mater. Could these compounds become the basis for new medicines to treat meningitis? It’s a question the researchers say merits further investigation. One line of future research could examine whether CGRP and RAMP1 blockers could be used in conjunction with antibiotics to treat meningitis and augment protection. “Anything we find that could impact treatment of meningitis during the earliest stages of infection before the disease escalates and spreads could be helpful either to decrease mortality or minimize the subsequent damage,” Pinho-Ribeiro said. More broadly, the direct physical contact between immune cells and nerve cells in the meninges offers tantalizing new avenues for research. “There has to be an evolutionary reason why macrophages and pain neurons reside so closely together,” Chiu said. “With our study, we’ve gleaned what happens in the setting of bacterial infection, but beyond that, how do they interact during viral infection, in the presence of tumor cells, or the setting of brain injury? These are all important and fascinating future questions.” Reference: “Bacteria hijack a meningeal neuroimmune axis to facilitate brain invasion” by Felipe A. Pinho-Ribeiro, Liwen Deng, Dylan V. Neel, Ozge Erdogan, Himanish Basu, Daping Yang, Samantha Choi, Alec J. Walker, Simone Carneiro-Nascimento, Kathleen He, Glendon Wu, Beth Stevens, Kelly S. Doran, Dan Levy and Isaac M. Chiu, 1 March 2023, Nature. DOI: 10.1038/s41586-023-05753-x Co-authors included Liwen Deng, Dylan Neel, Himanish Basu, Daping Yang, Samantha Choi, Kathleen He, Alec Walker, Glendon Wu, and Beth Stevens of Harvard Medical School; Ozge Erdogan, of the Harvard School of Dental Medicine; Kelly Doran of the University of Colorado; Dan Levy and Simone Carneiro-Nascimento of Beth Israel Deaconess Medical Center. This work was supported by National Institutes of Health (NIH) grants R01AI130019, R01DK127257, 2R01NS078263, 5R01NS115972, P50MH112491, R01NS116716, T32GM007753; by the Burroughs Wellcome Fund, the Kenneth Rainin Foundation, the Food Allergy Science Initiative, the Fairbairn Lyme Initiative; with additional support from the Harvard Medical School Immunology Undergraduate Summer Program. Chiu and Ribeiro are inventors on U.S. patent application 2021/0145937A1, “Methods and Compositions for Treating a Microbial Infection,” which includes targeting CGRP and its receptors to treat infections. The Chiu lab receives research support from Abbvie/Allergan and Moderna, Inc.

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