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.

🔗 Learn more or get in touch:
🌐 Website: https://www.deryou-tw.com/
📧 Email: shela.a9119@msa.hinet.net
📘 Facebook: facebook.com/deryou.tw
📷 Instagram: instagram.com/deryou.tw

Thailand OEM/ODM hybrid insole services

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.Taiwan OEM insole and pillow supplier

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.PU insole OEM production in Vietnam

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.China OEM/ODM hybrid insole services

📩 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.Taiwan foot care insole ODM development factory

Researchers have discovered that mutation of a neuronal gene can have a positive effect: higher IQ in humans. Researchers found that a gene mutation linked to blindness can also increase intelligence. When genes mutate, it can result in severe diseases of the human nervous system. Neuroscientists at Leipzig University and the University of Würzburg have now used fruit flies to demonstrate how, apart from the negative effect, the mutation of a neuronal gene can have a positive effect – namely higher IQ in humans. They have published their findings in the prestigious journal Brain. Synapses are the contact points in the brain via which nerve cells ‘talk’ to one another. Disruptions in this communication lead to nervous system diseases, since altered synaptic proteins, for example, can impair this complex molecular mechanism. This can cause mild symptoms, but also very severe disabilities in those affected. Mutation Linked to Above-Average Intelligence The interest of the two neurobiologists Professor Tobias Langenhan and Professor Manfred Heckmann, from Leipzig and Würzburg respectively, was aroused when they read in a scientific publication about a mutation that damages a synaptic protein. At first, the affected patients attracted scientists’ attention because the mutation caused them to go blind. However, doctors then noticed that the patients were also of above-average intelligence. “It’s very rare for a mutation to lead to improvement rather than loss of function,” says Langenhan, professor and holder of a chair at the Rudolf Schönheimer Institute of Biochemistry at the Faculty of Medicine. Research on fruit flies helps to better understand diseases of the human nervous system. Credit: Swen Reichhold/Leipzig University The two neurobiologists from Leipzig and Würzburg have been using fruit flies to analyze synaptic functions for many years. “Our research project was designed to insert the patients’ mutation into the corresponding gene in the fly and use techniques such as electrophysiology to test what then happens to the synapses. It was our assumption that the mutation makes patients so clever because it improves communication between the neurons which involve the injured protein,” explains Langenhan. “Of course, you can’t conduct these measurements on the synapses in the brains of human patients. You have to use animal models for that.” “75 percent of genes that cause diseases in humans also exist in fruit flies” First, the scientists, together with researchers from Oxford, showed that the fly protein called RIM looks molecularly identical to that of humans. This was essential in order to be able to study the changes in the human brain in the fly. In the next step, the neurobiologists inserted mutations into the fly genome that looked exactly as they did in the diseased people. They then took electrophysiological measurements of synaptic activity. “We actually observed that the animals with the mutation showed a much increased transmission of information at the synapses. This amazing effect on the fly synapses is probably found in the same or a similar way in human patients, and could explain their increased cognitive performance, but also their blindness,” concludes Professor Langenhan. Prof. Tobias Langenhan in his laboratory at the Rudolf Schönheimer Institute for Biochemistry. Credit: Swen Reichhold Molecular Insights into Enhanced Synaptic Transmission The scientists also found out how the increased transmission at the synapses occurs: the molecular components in the transmitting nerve cell that trigger the synaptic impulses move closer together as a result of the mutation effect and lead to increased release of neurotransmitters. A novel method, super-resolution microscopy, was one of the techniques used in the study. “This gives us a tool to look at and even count individual molecules and confirms that the molecules in the firing cell are closer together than they normally are,” says Professor Langenhan, who was also assisted in the study by Professor Hartmut Schmidt’s research group from the Carl Ludwig Institute in Leipzig. “The project beautifully demonstrates how an extraordinary model animal like the fruit fly can be used to gain a very deep understanding of human brain disease. The animals are genetically highly similar to humans. It is estimated that 75 percent of the genes involving disease in humans are also found in the fruit fly,” explains Professor Langenhan, pointing to further research on the topic at the Faculty of Medicine: “We have started several joint projects with human geneticists, pathologists and the team of the Integrated Research and Treatment Center (IFB) AdiposityDiseases; based at Leipzig University Hospital, they are studying developmental brain disorders, the development of malignant tumors and obesity. Here, too, we will insert disease-causing mutations into the fruit fly to replicate and better understand human disease.” Reference: “The human cognition-enhancing CORD7 mutation increases active zone number and synaptic release” by Mila M. Paul, Sven Dannhäuser, Lydia Morris, Achmed Mrestani, Martha Hübsch, Jennifer Gehring, Georgios N. Hatzopoulos, Martin Pauli, Genevieve M. Auger, Grit Bornschein, Nicole Scholz, Dmitrij Ljaschenko, Martin Müller, Markus Sauer, Hartmut Schmidt, Robert J. Kittel, Aaron DiAntonio, Ioannis Vakonakis, Manfred Heckmann and Tobias Langenhan, 12 January 2022, Brain. DOI: 10.1093/brain/awac011

Recent study findings suggest that inhibiting a protein called transforming growth factor beta 1 (TGFβ1) could enhance hematopoiesis in acute myeloid leukemia (AML) patients. Bone marrow failure due to acute myeloid leukemia (AML) is a significant factor behind the disease’s high rate of morbidity and mortality. Previous studies in mice suggest that AML cells inhibit healthy hematopoietic (blood) stem and progenitor cells (HSPC). A study released in STEM CELLS adds to this extent of knowledge by showing how secreted cell factors, in particular a protein called transforming growth factor beta 1 (TGFβ1), leads to a breakdown in the production of healthy blood cells (a process called hematopoiesis) in humans. The study’s findings indicate that blocking TGFβ1 could improve hematopoiesis in AML patients. Although AML makes up only about 1 percent of all cancers, it is the second most common type of leukemia diagnosed, according to the American Cancer Society. AML affects the blood and bone marrow — the spongy tissue inside bones where blood cells are made. The mortality rate is high — for those aged 20 and older, the five-year survival rate is a dismal 26 percent. Thomas Schroeder, MD, PhD, corresponding author of the study. Credit: AlphaMed Press The mechanisms by which AML develops are not completely understood, but it is generally believed to begin in the hemopoietic stem cells or progenitors, which develop into myeloid cells and in turn go on to become red blood cells, white blood cells or platelets. This latest study, by researchers at Heinrich-Heine-University Düsseldorf, was designed to investigate what role fluids secreted by leukemic cells might play in inhibiting the growth of healthy hematopoietic stem and HSPC. “Experiments using conditioned media (CM) from AML cells to address secretory mechanisms have been performed before, but mainly in mice. In order to gain new insights into how this plays out in humans, we focused on the interaction between leukemic cells and healthy HSPC using an in vitro system modeling the in vivo situation of bone marrow infiltration by AML cells,” said the study’s corresponding author, Thomas Schroeder, M.D., Ph.D., Department of Hematology, Oncology and Clinical Immunology. This was accomplished by exposing healthy bone marrow-derived CD34+ HSPC to supernatants derived from AML cell lines and newly diagnosed AML patients. (CD34 is a marker of human HSC, while supernatants are the products secreted by cells.) “Our findings revealed that exposure to AML-derived supernatants significantly inhibited proliferation, cell cycling, colony formation, and differentiation of healthy CD34+ HSPC,” Dr. Schroeder reported. “Further experiments determined that leukemic cells induce functional inhibition of healthy HSPC, at least in part through TGFβ1. “Blocking the TGFβ1 pathway is something that could be pharmacologically accomplished with a TGFβ1 inhibitor such as SD208. Our data indicate this could be a promising approach to improve hematopoiesis in AML patients.” Dr. Jan Nolta, Editor-in-Chief of STEM CELLS, said, “Finding factors for possible intervention in the perplexing issue of suppression of normal hematopoiesis by AML cells is highly important. The possibility of targeting TGFβ1 in order to allow the normal stem and progenitor cells to expand is a promising lead toward future treatments.” Reference: “Acute myeloid leukemia-induced functional inhibition of healthy CD34+ hematopoietic stem and progenitor cells” by Paul Jäger, Stefanie Geyh, Sören Twarock, Ron-Patrick Cadeddu, Pablo Rabes, Annemarie Koch, Uwe Maus, Tobias Hesper, Christoph Zilkens, Christina Rautenberg, Felix Bormann, Karl Köhrer, Patrick Petzsch, Dagmar Wieczorek, Beate Betz, Harald Surowy, Barbara Hildebrandt, Ulrich Germing, Guido Kobbe, Rainer Haas and Thomas Schroeder, 20 May 2021, Stem Cells. DOI: 10.1002/stem.3387

Neurons in Drosophila fruit flies were studied by The Picower Institute for Learning and Memory to understand the diversity in neuronal communication. They found that a protein, complexin, plays a vital role in controlling neurotransmitter release. The study showed that RNA editing of complexin results in different versions of the protein, affecting how neurons communicate and grow synapses. Credit: SciTechDaily.com Neurons stochastically generated up to eight different versions of a protein-regulating neurotransmitter release, which could vary how they communicate with other cells. Neurons are talkers. They each communicate with fellow neurons, muscles, or other cells by releasing neurotransmitter chemicals at “synapse” junctions, ultimately producing functions ranging from emotions to motions. But even neurons of the exact same type can vary in their conversational style. A new open-access study published in the journal Cell Reports by neurobiologists at The Picower Institute for Learning and Memory highlights a molecular mechanism that might help account for the nuanced diversity of neural discourse. The scientists made their findings in neurons that control muscles in Drosophila fruit flies. These cells are models in neuroscience because they exhibit many fundamental properties common to neurons in people and other animals, including communication via the release of the neurotransmitter glutamate. In the lab of Troy Littleton, Menicon Professor in MIT’s departments of Biology and Brain and Cognitive Sciences, which studies how neurons regulate this critical process, researchers frequently see that individual neurons vary in their release patterns. Some “talk” more than others. In a new study of a key protein that regulates how neurons communicate via the release of neurotransmitters, scientists tracked how RNA editing affected the protein’s distribution and performance. Here three different edits of complexin (yellow) resulted in different distributions of the protein in segments of motor neurons as well as different degrees of function. The left panel shows distribution of unedited complexin while the right two panels show distribution of two different edited variants. Credit: Littleton Lab/Picower Institute Complexin’s Role in Neuronal Communication In more than a decade of studies, Littleton’s lab has shown that a protein called complexin has the job of restraining spontaneous glutamate chatter. It clamps down on fusion of glutamate-filled vesicles at the synaptic membrane to preserve a supply of the neurotransmitter for when the neuron needs it for a functional reason, for instance to simulate a muscle to move. The lab’s studies have identified two different kinds of complexin in flies (mammals have four) and showed that the clamping effectiveness of the rare but potent 7B splice form is regulated by a molecular process called phosphorylation. How the much more abundant 7A version is regulated was not known, but scientists had shown that the RNA transcribed from DNA that instructs the formation of the protein is sometimes edited in the cell by an enzyme called ADAR. In the new study from Littleton’s team, led by Elizabeth Brija PhD ’23, the lab investigated whether RNA editing of complexin 7A affects how it regulates glutamate release. What she discovered was surprising. Not only does RNA editing of complexin 7A have a significant impact on how well the protein prevents glutamate release, but also this can vary widely among individual neurons because they can stochastically mix and match up to eight different editions of the protein. Some edits were much more common than others on average, but 96 percent of the 200 neurons the team examined had at least some editing, which affected the structure of an end of the protein called its C-terminus. Experiments to test some of the consequences of this structural variation showed that different complexin 7A edits can dramatically affect the level of electrical current measurable at different synapses. That varying level of activity can also affect the growth of the synapses the neurons make with muscle. RNA editing of the protein might therefore endow each neuron with fine degrees of communication control. “What this offers the nervous system is that you can take the same transcriptome and by alternatively editing various RNA transcripts, these neurons will behave differently,” Littleton says. Expanding the Scope: Editing of Other Proteins Additionally, Littleton and Brija’s team found that other key proteins involved in synaptic glutamate release, such as synapsin and Syx1A, are also sometimes edited at quite different levels among the same population of neurons. This suggests that other aspects of synaptic communication might also be tunable. “Such a mechanism would be a robust way to change multiple features of neuronal output,” Brija, Littleton, and colleagues wrote. The team tracked the different editing levels by meticulously extracting and sequencing RNA from the nuclei and cell bodies of 200 motor neurons. The work yielded a rich enough dataset to show that any of three adenosine nucleotides encoding two amino acids in the C-terminus could be swapped for another, yielding eight different editions of the protein. A slim majority of complexin 7A went unedited in the average neuron, while the seven edited versions composed the rest with widely varying degrees of frequency. To investigate the functional consequences of some of the different editions, the team knocked out complexin and then “rescued” flies by adding back in unedited or two different edited versions. The experiments showed a stark contrast between the two edited proteins. One, which occurs more commonly, proved to be a less effective clamp than unedited complexin, barely preventing spontaneous glutamate release and upticks in electrical current. The other turned out to be more effective at clamping than the unedited version, keeping a tight lid on glutamate release and synaptic output. And while both of the edited versions showed a tendency to drift away from synapses and into the neuron’s axon, the long branch that extends from the cell body, the edition that clamped well prevented any overgrowth of synapses while the one that clamped poorly provided only a meager curb. Because multiple editions are often present in neurons, Brija and the team did one more set of experiments in which they “rescued” complexin-less flies with a combination of unedited complexin and the weak-clamping edition. The result was a blend of the two: reduced spontaneous glutamate release than with just the weakly clamping edition alone. The findings suggest that not only does each edition potentially fine-tune glutamate release, but that combinations among them can act in a combinatorial fashion. Reference: “Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release” by Elizabeth A. Brija, Zhuo Guan, Suresh K. Jetti and J. Troy Littleton, 17 September 2023, Cell Reports. DOI: 10.1016/j.celrep.2023.113152 In addition to Brija and Littleton the paper’s other authors are Zhuo Guan and Suresh Jetti. The National Institutes of Health, The JPB Foundation, and The Picower Institute for Learning and Memory supported the research.

DVDV1551RTWW78V