NMNH: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder. 2. Bontac is a very first manufacture in the world to produce the NMNH powder on the level of high purity, stability. 3. Exclusive “Bonpure” seven-step purification technology, high purity(up to 99%) and stability of production of NMNH powder 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMNH powder 5. Provide one-stop product solution customization service
NADH: 1. Bonzyme whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive Bonpure seven-step purification technology, purity up higher than 98 % 3. Special patented process crystal form, higher stability 4. Obtained a number of international certifications to ensure high quality 5. 8 domestic and foreign NADH patents, leading the industry 6. Provide one-stop product solution customization service
NAD: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Stable supplier of 1000+ enterprises around the world 3. Unique “Bonpure” seven-step purification technology, higher product content and higher conversion rate 4. Freeze drying technology to ensure stable product quality 5. Unique crystal technology, higher product solubility 6. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products
NMN: 1. “Bonzyme”Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive“Bonpure”seven-step purification technology, high purity(up to 99.9%) and stability 3. Industrial leading technology: 15 domestic and international NMN patents 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products 5. Multiple in vivo studies show that Bontac NMN is safe and effective 6. Provide one-stop product solution customization service 7. NMN raw material supplier of famous David Sinclair team of Harvard University
Bontac Bio-Engineering (Shenzhen) Co., Ltd. (hereafter referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales, with enzyme catalysis technology as the core and coenzyme and natural products as main products. There are six major series of products in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates.
As the leader of the global NMN industry, BONTAC has the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 170 invention patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. What’s more, BONTAC has established the first coenzyme engineering technology research center at the provincial level in China which also is the sole in Guangdong Province.
In the future, BONTAC will focus on its advantages of green, low-carbon and high-value-added biosynthesis technology, and build ecological relationship with academia as well as upstream/downstream partners, continuously leading the synthetic biological industry and creating a better life for human beings.
NMN was only considered as a source of cellular energy and an intermediate in NAD+ biosynthesis, currently, the attention of the scientific community has been paid on anti-aging activity and a variety of health benefits and pharmacological activities of NMN which are related to the restoring of NAD+. Thus, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease.
NMN powder in general is typically produced via chemical or enzymatic synthesis, or fermentation biosynthesis. There are pros and cons to all three methods.
Chemical synthesis is expensive and labor intensive, and all raw ingredients used are categorized as “unnatural,” i.e., not from biological systems. There are, however, some advantages from the manufacturer’s perspective. The yield is well suited to mass NMN powder production, and all of those unnatural raw ingredients can be carefully controlled. But there are a number of drawbacks as well. Some of the solvents used in the manufacturing process are seriously bad from an environmental standpoint, and impurities and by-products can be challenging to remove from the finished product – that’s seriously bad for the consumer.
Enzymatic production of NMN powder, on the other hand, is considered a “green preparation method.” Like the chemical route, it’s pricey, but it offers a higher yield and impressively high purity. The finished NMN ticks all the boxes – stable, easily absorbed, lightweight, low density, and a low molecular structure.
Fermentation has also been explored as a method of producing NMN, but yield, though high quality, is pretty abysmal, so many supplement companies quite sensibly look to other, more efficacious processes.
1、“Bonzyme”Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder
2、Exclusive“Bonpure”seven-step purification technology, high purity(up to 99.9%) and stability of production of NMN powder
3、Industrial leading technology: 15 domestic and international NMN patents
4、Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMN powder
5、Multiple in vivo studies show that Bontac NMN powder is safe and effective
6、Provide one-stop product solution customization service
7、NMN raw material supplier of famous David Sinclair team of Harvard University.
Aging, as a natural process is identified by downregulation of energy production in mitochondria of various organs such as brain, adipose tissue, skin, liver, skeletal muscle and pancreas due to the depletion of NAD+ . NAD+ levels in the body decrease as a consequence of increasing NAD+ consuming enzymes when aging There are three different biosynthesis pathways to produce NAD+ in mammalian cells including de novo synthesis from tryptophan, salt and Preiss-Handler pathways. Among these three pathways, NMN is an interproduct by is involved in NAD+ biosynthesis through salt and Preiss-Handler pathways. The salvage pathway is the most efficient and the main route for the NAD+ biosynthesis, in which nicotinamide and 5-phosphoribosyl-1-pyrophosphate are converted to NMN with the enzyme of NAMPT followed by conjugation to ATP and conversion to NAD by NMNAT. Furthermore, NAD+ consuming enzymes are responsible for degradation of NAD+ and consequence nt formation of nicotinamide as a by-product.
The safety of NMN powder cannot be assessed since required clinical and toxicological studies have not been completed yet to establish the recommended safe levels for long term administration. Nevertheless, their safety and efficacy are uncertain and unreliable since most of them have not been back by Rigorous scientific preclinical and clinical testing. This issue has been arisen as manufacturers are hesitant to pay for research and clinical trials due to potential lower profit margin, and there is no authorizing agency to regulate NMN products because it is often product sold as functional food than heavily regulated therapeutic drug. Therefore, more strict approval process has been demanded by consumer advocacy groups requesting regulatory agencies to set standard and restrictions for marketing anti-aging health products, considering safety, health and wellbeing of N red besumers. a panacea for the elderly, because boosting NAD levels when not required may yield some detrimental effects. Therefore, the dose and frequency of NMN supplementation should be carefully prescribed depending on the type of age-related deficiency and all other confronting health conditions of the people. Other NAD precursors over have been studied to diverse age-related deficiencies and they are used for particular deficiencies, only after they are proven for effectiveness and safe to use. Therefore, the same principle should be applied to NMN as well
First, inspect the factory. After some screening, NMN companied that directly face consumers pay more attention to brand building. Therefore, for a good brand, quality is the most important thing, and the first thing to control the quality of raw materials is to inspect the factory. Bontac company actually manufacturing NMN powder of high quality with the caterias of SGS. Secondly, the purity is tested. Purity is one of the most important parameters of NMN powder. If high purity NMN cannot be guaranteed, the remaining substances are likely to exceed the relevant standards. As the attached certificates demonstrates that the NMN powder produced by Bontac reach the purity of 99.9%. Finally, a professional test spectrum is needed to prove it. Magnetic Resonance Spectroscopy (NMR) and high-resolution mass spectrometry (HRMS). Usually through the analysis of these two spectra, the structure of the compound ca n be preliminarily determined.
Introduction Wound healing is a sophisticated process responding to tissue damage, which is associated with numbers of interaction of various cell types, cytokines, growth factors, and other molecules. Strikingly, increasing the nicotinamide adenine dinucleotide (NAD) pool by nicotinamide riboside (NR) can accelerate wound healing and macrophage migration, which is partially achieved through PGE2 synthesis and signaling as well as the function of the NAD+-dependent sirtuin, SIRT3. Regulatory effects of NR on the expression of M1 macrophage markers in human MDMs. NR could modulate the expression levels of canonical M1 (inflammatory phenotype) and M2 (reparative phenotype) cell surface markers during macrophage polarization. With a great detail, a significant downregulation in CD64 and a obvious upregulation of CD197/CCR7 are viewed in the polarized M1 cells incubated with NR. Furthermore, NR increases CD197/CCR7-mediated M1 macrophage migration. The significance of chemotaxis mediator PGE2 in NR-regulated macrophage migration NR-mediated upregulation of macrophage migration through CCL19/CCR7 is dependent on the synthesis of PGE2, an inflammatory lipid mediator in the eicosanoid family. Concretely, NR administration increases the PGE2 level in cultured human monocytes, MDMs, and human serum. In addition, NR-mediated increases in CCR7 expression and CCL19-induced migration are attenuated by PGE2 synthesis blockers. NR/SIRT3/migration axis in human M1 MDMs NR facilitates collective cell migration at a SIRT3-dependent manner in human M1 MDMs during wound healing. Simply put, the degree of wound healing is compared on Day 0 and Day 2 in vehicle- or NR-treated human M1 MDMs. It is found that NR increases the relative degree of migration (relative wound healing) and the rate of wound confluence in the presence of CCL19. Besides, the relative degree of wound density (migration) is blunted by SIRT3 knockdown, while being enhanced by SIRT3 overexpression. Application prospect of NR in wound healing Chronic diabetes is often accompanied with poor wound healing. For instance, diabetic foot ulcers, one of the chief cause of amputations, affect 15% of people with diabetes. Given that NR can drive the macrophage migration to boost chronic wound healing, it may have a broad application prospect in treating the wounds including but not limited to diabetic patients. Conclusion In human macrophages, NR induces surface expression of the chemotaxis CD197/CCR7 receptor and levels of its lipid mediator PGE2 via upregulation of cyclooxygenase 2 and functionally increases macrophage migration and wound healing in a SIRT3-dependent manner. Reference Wu J, Bley M, Steans RS, et al. Nicotinamide Riboside Augments Human Macrophage Migration via SIRT3-Mediated Prostaglandin E2 Signaling. Cells. 2024;13(5):455. Published 2024 Mar 5. doi:10.3390/cells13050455 BONTAC NR BONTAC is one of the few suppliers in China that can launch mass production of raw materials for NR, with self-owned factory and professional R&D team. Up till now, there are 173 BONTAC patents. BONTAC provides one-stop service for customized products. Both malate and chloride salt forms of NR are available. By dirt of unique Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method, the product content and conversion rate can be maintained in a higher level. The purity of BONTAC NR can reach above 97%. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.
Introduction Intervertebral disc degeneration (IDD) is a frequently seen orthopedic disease, which is accompanied with excessive apoptosis of nucleus pulposus cells (NPCs) and degeneration of extracellular matrix (ECM), with main symptoms of pain and numbness in the waist, legs and feet, as well as inflammation on and around the surface of bone tissues. Strikingly, ginsenoside Rg3, the main active ingredient of ginseng, has been attested to exhibit anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs and IDD rats by inactivating the p38 MAPK pathway. The risk factors for IDD IDD is generally associated with risk factors such as aging, excessive exercise, working environment, and genetics. As one ages, the amount of water in the body and in the intervertebral discs will be reduced accordingly. Intervertebral discs that lack moisture will lose their elastic function and become hard. Once there is any stimulation or pressure, the intervertebral disc may crack, leading to intervertebral disc injury. For instance, the mechanical trauma caused by excessive exercise and work may accelerate the fragility of disc and exacerbate IDD. Anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β-treated human NPCs and IDD rats Ginsenoside Rg3 plays an anti-apoptotic role in IL-1β-treated human NPCs and IDD rats, as evidenced by the down-regulation of pro-apoptosis protein Bax and up-regulation of anti-apoptosis protein Bcl-2 in IL-1β-stimulated NPCs and IDD model rats. Besides, ginsenoside Rg3 represses ECM degradation in IL-1β-stimulated NPCs and intervertebral disc tissues of IDD rats, as attested by the decreased expression of ECM degradation-related factors MMPs (MMP2 and MMP3) and ADAMTSs (Adamts4, and Adamts5). Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs. Ginsenoside Rg3 reduces apoptosis and catabolism in IDD rats. Alleviation of ginsenoside Rg3 in IDD via p38 MAPK pathway Ginsenoside Rg3 can alleviate NPC degeneration, recover the arrangement of annulus fibrous, and preserve more proteoglycan matrix via inactivating p38 MAPK pathway. In vitro, the fluorescence intensity of p38 is enhanced in IL-1β-stimulated NPCs, yet ginsenoside Rg3 offsets this promoting effect. In vivo, the phosphorylated p38 level is elevated in NPCs and the intervertebral disc tissues of IDD rats, while ginsenoside Rg3 works inversely. Ginsenoside Rg3 suppresses the IL-1β-stimulated p38 MAPK pathway in human NPCs Ginsenoside Rg3 inactivates the p38 MAPK pathway in IDD rats. Conclusion The anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration are accomplished by inactivating the MAPK pathway, providing new clues on the treatment of IDD. Reference Chen J, Zhang B, Wu L, et al. Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration by inactivating the MAPK pathway. Cell Mol Biol. 2024;70(1):233-238. doi:10.14715/cmb/2024.70.1.32 BONTAC Ginsenosides BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be responsible or liable in any way for any claims, damages, losses, expenses or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.
1. Introduction Atherosclerosis is a chronic progressive inflammatory disease, which is featured by the accumulation of lipids in the intima of the arteries with yellow appearance. This disease is dominated by coronary artery atherosclerosis and cerebrovascular atherosclerosis, representing the fundamental cause of most cardiovascular diseases, with over 15 million deaths worldwide in 2019. By virtue of its potent anti-inflammatory and anti-oxidative properties, nicotinamide mononucleotide (NMN), an effective NAD+ booster, has promising potential in hampering the progression of atherosclerosis. 2. Establishment of mouse atherosclerotic model and NMN treatment The atherosclerotic model is constructed by feeding ApoE−/− mice with high-fat diet (HFD) for 10 weeks until the plaque formation and accumulation in the middle arteries. Subsequently, the model mice are subjected to daily intraperitoneal injection of saline (100 μL) or NMN (500mg/kg) for 8 consecutive weeks (6 days a week). Strikingly, it is found that the weight and food consumption of mice are barely affected post NMN intraperitoneal injection. 3. The alleviation of atherosclerotic burden by NMN intraperitoneal injection possibly via anti-oxidant property NMN greatly dampens the progression of atherosclerosis, as evidenced by the overtly diminished size of atherosclerotic plaque (36 %) and necrotic core (48 %) in aortic sinus, as well as the decreased lipid area (43 %) and increased collagen content (51 %) in atherosclerotic lesions. Noteworthily, the anti-atherosclerotic effect of NMN may be partially achieved by its anti-oxidative property. In a nutshell, NMN lessens the level of malondialdehyde (MDA), a major biomarker of lipid peroxidation and oxidative stress, yet elevates the levels of anti-oxidant markers superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in serum. 4. The involvement of macrophages in the repression of plaque inflammation by NMN NMN regulates macrophages to repress plaque inflammation. There are two main polarization phenotypes for macrophages, where M1 type contributes to pro-inflammatory cytokines production and are deemed to be atherogenic, while the M2 type produces anti-inflammatory cytokines and exerts a preventive effect on the progression of atherosclerosis. NMN promotes the polarization of macrophages to the anti-inflammatory M2 phenotype, as manifested by the downregulation of M1-associated markers (Tnf-α, Il-6, Il-1β and Mcp-1) and upregulation of M2-related markers (Arg-1, Mrc-1, Retlna and Irf-4) in aortic samples. 5. Conclusion NMN produces anti-atherosclerotic effects possibly via suppressing oxidative stress and inflammatory response in HFD-fed ApoE−/− mice, hinting its promising potential in the treatment of atherosclerosis. Reference [1] Vaduganathan M, Mensah GA, Turco JV, et al. The Global Burden of Cardiovascular Diseases and Risk: A Compass for Future Health. J Am Coll Cardiol. 2022;80(25):2361-2371. doi:10.1016/j.jacc.2022.11.005 [2] Wang Z, Zhou SH, Hao YL, et al, Nicotinamide mononucleotide protects against high-fat-diet-induced atherosclerosis in mice and dampens aortic inflammation and oxidative stress. J Functional Foods. 2024 (112): 1756-4646, doi: 10.1016/j.jff.2023.105985. BONTAC NMN BONTAC is the pioneer of NMN industry and the first manufacturer to launch NMN mass production, with the first whole-enzyme catalysis technology around the world. At present, BONTAC has become the leading enterprise in niche areas of coenzyme products. Notably, BONTAC is the NMN raw material supplier of famous David Sinclair team at the Harvard University, who uses the raw materials of BONTAC in a paper titled “Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging”. Our services and products have been highly recognized by global partners. Furthermore, BONTAC has the first national and the only provincial independent coenzyme engineering technology research center in Guangdong, China. The coenzyme products of BONTAC are widely used in fields such as nutritional health, biomedicine, medical beauty, daily chemicals and green agriculture. Disclaimer This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC.