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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PU insole OEM production in Vietnam
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 OEM/ODM hybrid insole services
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.Thailand insole ODM service provider
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.Indonesia insole ODM design and production
📩 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.China custom product OEM/ODM services
Researchers discovered that a type of protein misfolding, non-covalent lasso entanglement, can slow the folding process, leading to unexpected patterns. Using simulations and experiments, they confirmed this mechanism in phosphoglycerate kinase (PGK), a protein with unusual folding behavior. Their findings could help inform future treatments for diseases related to protein misfolding. A new study reveals a possible protein misfolding mechanism that may resolve a long-standing mystery of why certain proteins refold into unexpected patterns. Proteins are long molecules that must fold into precise three-dimensional shapes to function properly within cells. However, this process sometimes goes wrong, resulting in misfolded proteins that can contribute to disease if not corrected. A new study by chemists at Penn State explores a possible reason why some proteins refold into unexpected patterns. The researchers identified a specific type of misfolding in which protein segments become improperly intertwined, creating an obstacle to normal folding. Correcting this misfolding requires substantial energy or extensive unfolding, which slows down the process and may explain the unusual folding patterns first observed in the 1990s. “Misfolded proteins can malfunction and lead to disease,” said Ed O’Brien, professor of chemistry in the Eberly College of Science, a co-hire of the Institute for Computational and Data Sciences at Penn State, and leader of the research team. “So, understanding the mechanisms involved in the folding process can potentially help researchers prevent or develop treatments for diseases caused by misfolding.” A research paper published on March 14 in Science Advances examines the folding kinetics of the protein phosphoglycerate kinase (PGK). The study integrates computer simulations with refolding experiments to offer a detailed analysis of the protein’s folding process. A Different Folding Pattern: The Mystery of PGK “For most proteins, we model the folding process as if there are two states, folded or unfolded,” said Yang Jiang, assistant research professor of chemistry in the Eberly College of Science at Penn State and the first author of the paper. “When we track the progression of a protein from unfolded to folded, we see a characteristic time-dependent pattern that we call the folding kinetics of the protein. Usually, the proportion of unfolded proteins goes down exponentially until essentially all of the proteins are folded, but some proteins don’t fit this pattern, and we were interested in the mechanisms that might explain this.” The unusual folding pattern of PGK was first observed experimentally over 25 years ago. Whereas most proteins fit the “two-state” model of exponential folding kinetics, the molecules of PGK followed a different pattern to reach a fully folded state. This new pattern was described as “stretched-exponential refolding kinetics,” but the structural mechanism that explained this difference remained a mystery — until now. The research team hypothesized that a recently described class of misfolding may be responsible for PGK’s deviation from the traditional two-state model of folding. A new study has described a potential mechanism that could help explain why some proteins refold in a different pattern than expected. The research showed that a type of misfolding, called non-covalent lasso entanglement, in which the proteins incorrectly intertwine their segments, can occur and create a barrier to the normal folding process. The image shows the native folded structure of the protein phosphoglycerate kinase (PGK) on the left and one of the misfolded PGK structures predicted in this study on the right, with the entangled regions highlighted in red and blue. Credit: Yang Jiang, Penn State “Non-covalent lasso entanglement is a class of misfolding we recently identified where a loop of the protein traps another segment of the protein, essentially intertwining itself incorrectly,” O’Brien said. “If a protein like PGK is more prone to this type of misfolding, it could help explain why we see the stretched-exponential refolding kinetics.” To test this hypothesis, the research team first built a computer model to simulate the folding process of PGK. Their simulations recapitulated the stretched-exponential kinetics seen in the earlier experiments. They then explored the intermediate stages of the folding process in their simulations to see if there were structural changes that could explain the stretched refolding. Simulations and Experimental Validation “We found several examples of misfolding involving entanglements,” Jiang said. “Sometimes a new entanglement formed and sometimes an entanglement that was part of the protein’s native structure failed to form. In our simulations, we could then remove these misfolding events and saw that the protein folded with the typical two-state exponential pattern.” To confirm the results of their simulation, the research team, which included experimentalist Stephen Fried and lab members at Johns Hopkins University, examined the structural variation of PGK upon refolding in experiments. They found that the misfolded states predicted in the simulations were consistent with the structural signals experimentally observed in the refolded protein. They also found that these misfolded states were long-lived, suggesting that they are a crucial component of the observed stretched-exponential folding kinetics. “Because of the nature of this type of misfolding, the protein gets stuck,” Jiang said. “The protein must backtrack in the folding process to correct the mistake, which takes time and is energetically expensive. The demonstration of this mechanism helps expand our understanding of how proteins are folded and gives an example of how it can go wrong. This is basic research, but it could eventually inform how we develop therapeutics for diseases linked to protein misfolding.” Reference: “Protein misfolding involving entanglements provides a structural explanation for the origin of stretched-exponential refolding kinetics” by Yang Jiang, Yingzi Xia, Ian Sitarik, Piyoosh Sharma, Hyebin Song, Stephen D. Fried and Edward P. O’Brien, 14 March 2025, Science Advances. DOI: 10.1126/sciadv.ads7379 In addition to Jiang, O’Brien and Fried, the research team includes graduate student Ian Sitarik and Assistant Professor of Statistics Hyebin Song at Penn State and co-first author Yingzi Xia and Piyoosh Sharma at Johns Hopkins University. Computer simulations and data analysis were carried using the Roar Collab, a high-performance computing cluster operated by the Institute for Computational and Data Sciences at Penn State. The U.S. National Science Foundation and the U.S. National Institutes of Health funded the research.
New research uncovers how human retinas, grown in labs, demonstrate that retinoic acid, rather than thyroid hormones, determines the development of color-sensing cells crucial for human vision. This discovery advances our understanding of color blindness, vision loss, and the genetic basis of how we see color, offering promising avenues for future treatments of vision disorders. Researchers have cultivated human retinas in a laboratory setting, unveiling the process by which a derivative of vitamin A produces the unique cells responsible for humans’ capacity to perceive a vast spectrum of colors. This visual capability is absent in dogs, cats, and various other mammals. “These retinal organoids allowed us for the first time to study this very human-specific trait,” said author Robert Johnston, an associate professor of biology. “It’s a huge question about what makes us human, what makes us different.” The findings, published in PLOS Biology, increase understanding of color blindness, age-related vision loss, and other diseases linked to photoreceptor cells. They also demonstrate how genes instruct the human retina to make specific color-sensing cells, a process scientists thought was controlled by thyroid hormones. Mechanism of Color Sensing By tweaking the cellular properties of the organoids, the research team found that a molecule called retinoic acid determines whether a cone will specialize in sensing red or green light. Only humans with normal vision and closely related primates develop the red sensor. Scientists for decades thought red cones formed through a coin toss mechanism where the cells haphazardly commit to sensing green or red wavelengths—and research from Johnston’s team recently hinted that the process could be controlled by thyroid hormone levels. Instead, the new research suggests red cones materialize through a specific sequence of events orchestrated by retinoic acid within the eye. Retinal organoid marked to show blue cones in cyan and green/red cones in green. Cells called rods that help the eye see in low-light or dark conditions are marked in magenta. Credit: Sarah Hadyniak/Johns Hopkins University The team found that high levels of retinoic acid in early development of the organoids correlated with higher ratios of green cones. Similarly, low levels of the acid changed the retina’s genetic instructions and generated red cones later in development. “There still might be some randomness to it, but our big finding is that you make retinoic acid early in development,” Johnston said. “This timing really matters for learning and understanding how these cone cells are made.” Green and red cone cells are remarkably similar except for a protein called opsin, which detects light and tells the brain what colors people see. Different opsins determine whether a cone will become a green or a red sensor, though the genes of each sensor remain 96% identical. With a breakthrough technique that spotted those subtle genetic differences in the organoids, the team tracked cone ratio changes over 200 days. “Because we can control in organoids the population of green and red cells, we can kind of push the pool to be more green or more red,” said author Sarah Hadyniak, who conducted the research as a doctoral student in Johnston’s lab and is now at Duke University. “That has implications for figuring out exactly how retinoic acid is acting on genes.” Variability and Vision The researchers also mapped the widely varying ratios of these cells in the retinas of 700 adults. Seeing how the green and red cone proportions changed in humans was one of the most surprising findings of the new research, Hadyniak said. A section of a human retina. Dotted lines depict an individual green cone in blue and a red cone in pink. Credit: Sarah Hadyniak/Johns Hopkins University Scientists still don’t fully understand how the ratio of green and red cones can vary so greatly without affecting someone’s vision. If these types of cells determined the length of a human arm, the different ratios would produce “amazingly different” arm lengths, Johnston said. To build an understanding of diseases like macular degeneration, which causes loss of light-sensing cells near the center of the retina, the researchers are working with other Johns Hopkins labs. The goal is to deepen their understanding of how cones and other cells link to the nervous system. “The future hope is to help people with these vision problems,” Johnston said. “It’s going to be a little while before that happens, but just knowing that we can make these different cell types is very, very promising.” Reference: “Retinoic acid signaling regulates spatiotemporal specification of human green and red cones” by Sarah E. Hadyniak, Joanna F. D. Hagen, Kiara C. Eldred, Boris Brenerman, Katarzyna A. Hussey, Rajiv C. McCoy, Michael E. G. Sauria, James A. Kuchenbecker, Thomas Reh, Ian Glass, Maureen Neitz, Jay Neitz, James Taylor and Robert J. Johnston Jr, 11 January 2024, PLOS Biology. DOI: 10.1371/journal.pbio.3002464 Other Johns Hopkins authors include: Kiara C. Eldred, Boris Brenerman, Katarzyna A. Hussey, Joanna F. D. Hagen, Rajiv C. McCoy, Michael E. G. Sauria, and James Taylor; as well as James A. Kuchenbecker, Thomas Reh, Ian Glass, Maureen Neitz, Jay Neitz of the University of Washington.
Groundbreaking research reveals that 7-dehydrocholesterol (7-DHC) serves as an antioxidant, protecting cells from ferroptosis. This challenges prior assumptions about 7-DHC and could significantly impact cancer treatment and our understanding of related diseases. Credit: SciTechDaily.com Recent research shows that 7-dehydrocholesterol is an antioxidant that protects cells from ferroptosis, offering new avenues for cancer treatment and disease understanding. In a groundbreaking study, a team led by Würzburg Professor José Pedro Friedmann Angeli has shown that the cholesterol precursor 7-dehydrocholesterol (7-DHC) plays a crucial role as an antioxidant: it integrates into the cell membranes and protects the cells by preventing a certain type of cell death, known as ferroptosis. “Until now, the accumulation of 7-DHC was only associated to neurodevelopmental defects, now we show that it actually increases cellular fitness and could promote a more aggressive behavior in cancers such as Burkitt’s lymphoma and neuroblastoma,” says Friedmann Angeli. The newly discovered protective function of 7-DHC opens up exciting prospects for further improving the treatment of cancer and other diseases associated with ferroptosis: “It gives us new opportunities to test potential inhibitors that target cholesterol biosynthesis and are already established in medical practice.” Teams From Würzburg, Dresden, Munich and Heidelberg Involved The researchers report this in the journal Nature. In addition to the Würzburg team from the Rudolf Virchow Zentrum – Center for Integrative and Translational Bioimaging, the following scientists contributed to the study: Dr. Maria Fedorova (Dresden University of Technology), Marcus Conrad (Helmholtz Munich), Derek Pratt (University of Ottawa), and Andreas Trumpp and Hamed Alborzinia (German Cancer Research Center, DKFZ Heidelberg). Observing Changes in 7-DHC Levels High cholesterol levels are associated with health problems such as heart disease and diabetes. Most studies focus on how cholesterol contributes directly to these diseases. In this area, the discovery of the cholesterol precursor 7-DHC as an antioxidant opens up new possibilities: Studies on changes in 7-DHC levels could provide crucial new insights into the diseases. In addition, drugs that specifically block 7-DHC production should be researched in combination with other drugs — this could have a positive effect in the treatment of some cancers. Possible Effects on Tumour Development “Our next research goal is to investigate the effects of 7-DHC accumulation during tumor development,” says Würzburg ferroptosis expert José Pedro Friedmann Angeli. The team responsible for the publication in Nature also calls for further epidemiological studies. Background: There are drugs authorized by the US Food and Drug Administration (FDA) that can inhibit the DHCR7 enzyme. These include trazodone, which is prescribed around 20 million times a year in the USA, sometimes even for off-label use to treat insomnia. “Studies have shown that people taking this drug have elevated plasma levels of 7-DHC. Epidemiological studies are crucial to better understand possible effects here,” says Friedmann Angeli. These studies would help to find out whether there is a connection between patient groups who regularly take ferroptosis-modulating drugs such as trazodone and cancer incidence, the occurrence of metastases, or other critical aspects of public health. Reference: “7-Dehydrocholesterol is an endogenous suppressor of ferroptosis” by Florencio Porto Freitas, Hamed Alborzinia, Ancély Ferreira dos Santos, Palina Nepachalovich, Lohans Pedrera, Omkar Zilka, Alex Inague, Corinna Klein, Nesrine Aroua, Kamini Kaushal, Bettina Kast, Svenja M. Lorenz, Viktoria Kunz, Helene Nehring, Thamara N. Xavier da Silva, Zhiyi Chen, Sena Atici, Sebastian G. Doll, Emily L. Schaefer, Ifedapo Ekpo, Werner Schmitz, Aline Horling, Peter Imming, Sayuri Miyamoto, Ann M. Wehman, Thiago C. Genaro-Mattos, Karoly Mirnics, Lokender Kumar, Judith Klein-Seetharaman, Svenja Meierjohann, Isabel Weigand, Matthias Kroiss, Georg W. Bornkamm, Fernando Gomes, Luis Eduardo Soares Netto, Manjima B. Sathian, David B. Konrad, Douglas F. Covey, Bernhard Michalke, Kurt Bommert, Ralf C. Bargou, Ana Garcia-Saez, Derek A. Pratt, Maria Fedorova, Andreas Trumpp, Marcus Conrad and José Pedro Friedmann Angeli, 31 January 2024, Nature. DOI: 10.1038/s41586-023-06878-9
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