Advantages of NMNH
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
Advantages of NADH
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
Advantages of NAD
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
Advantages of MNM
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
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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.
NAD powder manufacturing method
The preparation methods utilized by manufacturers worldwide of NAD powder are mainly divided into chemical synthesis method and biocatalytic method, among which biocatalytic method includes biological fermentation method and enzyme catalysis method. Enzyme catalysis method has gradually become the mainstream direction because of its advantages of green, environmental protection and pollution-free. And then the purity of NAD powder will reach 99% after the procedure of further purifying. But some NAD manufacturers tend to choose the multiple methods to develop the producing of NAD.
BONTAC NAD product features and advantages
1、As an advanced technology NAD manufacturer, BONTAC choose the Enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder
2、High purity（up to 99%) and stability of production of NAD powder
3、Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NAD powder
4、Multiple in vivo studies show that Bontac NAD powder is safe and effective
5、Provide one-stop product solution customization service
NAD powder efficacy in health
Molecules that can be taken in supplement form to increase NAD levels in the body are referred to by some as “NAD boosters.” Studies conducted over the past six decades suggest that the following are some of the many benefits associated with taking an NAD supplement:
Can Help Restore Mitochondrial Function
Helps Repair Blood Vessels —A 2018 mice study found that supplementation could aid in repair and growth of aged blood vessels. There’s also some evidence it can help manage heart disease risk factors like high blood pressure and high cholesterol.
May Improve Muscle Function — One animal study conducted in 2016 found that degenerative muscles had improved muscle function when supplemented with NAD+ precursors.
Potentially Helps Repair Cells and Damaged DNA — Some studies have found evidence that NAD+ precursor supplementation leads to an increase in DNA damage repair. NAD+ is broken down into two component parts, nicotinamide and ADP-ribose, which combine with proteins to repair cells.
May Help Improve Cognitive Function — Several studies conducted on mice have found that mice treated with NAD+ precursors experienced improvements in cognitive function, learning and memory. Findings have led researchers to believe that NAD supplement may help protect against cognitive decline/Alzheimer’s disease.
May Help Prevent Age-Related Weight Gain — A 2012 study showed that when mice fed a high-fat diet were given an NAD supplement, they gained 60 percent less weight than they did on the same diets without the supplement. One reason this may be true is that nicotinamide adenine dinucleotide helps regulate production of stress- and appetite-related hormones, thanks to its effects on circadian rhythms.
Precursors are molecules used in chemical reactions inside the body to create other compounds. There are a number of precursors of NAD+ that result in higher levels when you consume enough of them.
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1.Prevention and treatment of viral-induced inflammatory storms
Scientists have found after extensive research that neo-coronavirus has a mechanism similar to SARS virus to activate inflammatory vesicles NLRP3. and the activation of NLRP3 produces more inflammatory factors, generating excessive inflammation and thus triggering a deadly cytokine storm. This problem can be well addressed by NAD+, which inhibits the activity of NF-κB inflammatory pathway and NLRP3 inflammasome by increasing the activity of sirtuins (SIRT1, SIRT2 and SIRT3), thus preventing cytokine storm caused by excessive inflammation. Therefore, Sinclair and other scientists believe that increasing the concentration of NAD+ may play an important role in the prevention and treatment of neocoronavirus and other viral infections.
2.Restoration of virus-induced metabolic disorders
NAD+ is an essential coenzyme for many cellular energy metabolic pathways, present in every cell of the body, involved in thousands of reactions, and an important player in maintaining cellular viability. In the COVID-19 infection model, NAD+ and NMN supplementation was found to be effective in alleviating cell death and protecting the lung.
First, inspect the factory. After some screening, NAD manufactures 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 NAD powder of high quality with the caterias of SGS. Secondly, the purity is tested. Purity is one of the most important parameters of NAD powder. If high purity NAD cannot be guaranteed, the remaining substances are likely to exceed the relevant standards. As the attached certificates demonstrates that the NAD powder produced by Bontac reach the purity of 99.9%. Finally, a professional test spectrum is needed to prove it. Common methods for determining the structure of an organic compound include Nuclear Magnetic Resonance Spectroscopy (NMR) and high-resolution mass spectrometry (HRMS). Usually through the analysis of these two spectra, the structure of the compound can be preliminarily determined.
In the international market, NAD+ food supplements are in production in the United States, the Australian Food and Drug Administration has approved NAD+ products for sale, and Japanese NAD+ manufactures are devoted to extend the market share in China. Li Ka-shing invested HK$200 million in the US NAD manufacturer, whose NAD+ products are being sold by Watsons in Hong Kong! Then Mclane, a company owned by Warren Buffett also joined the NAD market.
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Exploring the New Role of NAD as a Central Regulator of Axonal Health
1.Introduction A series of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, are accompanied with bioenergetic maladaptations and axonopathy with the increasing age. As a key coenzyme in energy metabolism, nicotinamide adenine dinucleotide (NAD) plays a critical role in maintaining axonal health in central neural system. 2.NMNAT2 as the major source of NAD in cortical neurons NAD is mainly synthesized by nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2). NMNAT2 is pivotal for maintaining NAD redox potential in distal axons, where it provides the adenosine triphosphate (ATP) required for fast axonal transport. Furthermore, NMNAT2 is the main source of NAD in cortical neurons, as evidenced by the reduction of NAD + and NADH levels by approximately 50% in the absence of NMNAT2. 3. The restoring effect of NAD+ supplementation on APP transport via glycolysis in the absence of NMNAT2 Exogenous NAD+ supplementation to NMNAT2-deficient neurons restores glycolysis and resumes fast axonal transport, as manifested by the diminished percentage of stationary/dynamic pause events, the elevated percentage of anterograde and retrograde events, and the restored anterograde and retrograde velocities of APP transport. 4. The molecular mechanism of NAD in protecting axonal health Remarkably, reducing the activity of SARM1, an NAD degradation enzyme, can reduce axonal transport deficits and suppress axon degeneration in NMNAT2-deficient neurons. SARM1 knockdown prevents the reduction in NAD+/NADH ratio normally caused by NMNAT2 loss. Blocking NAD+ degradation by reducing SARM1 abundance protects axons during NMNAT2 loss in vivo and in vitro. 5. Conclusion NAD+ supplementation or repressing the level of SARM1, an NAD + hydrolase, can effectively restore fast axonal transport and prevent the neurodegeneration commonly observed in NMNAT2-deficient axons both in vitro and in vivo, shedding a light on the treatment of neurodegenerative disorders of aging. Reference Yang S, Niou ZX, Enriquez A, et al. NMNAT2 supports vesicular glycolysis via NAD homeostasis to fuel fast axonal transport. Preprint. Res Sq. 2023;rs.3.rs-2859584. Published 2023 May 19. doi:10.21203/rs.3.rs-2859584/v1 About BONTAC BONTAC has dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 160 global patents as well as strong R&D team consisting of Doctors and Masters. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD. High quality and stable supply of products can be better ensured here with the exclusive Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method. 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. 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.
The Significance of NAD+ in Intestinal Senescence Caused by Elevated mtDNA Mutations
1.Introduction The senescence in mammals is generally concomitant with the dysregulation of intestinal homeostasis and the accumulation of mitochondrial DNA (mtDNA) mutations. High-burden mtDNA mutations lead to NAD+ depletion and activate the transcription factor ATF5-dependent UPRmt, which in turn promotes and exacerbates the intestinal senescence phenotype. By supplementation with the NAD+ precursor NMN, this intestinal senescence phenotype can be rescued to some extent, as evidenced by the recovery of intestinal organoid differentiation and the increased number of intestinal stem cells. 2. NAD+ depletion during intestinal senescence caused by mtDNA mutations There is impairment of NADH/NAD+ redox in Mut/Mut*** intestines, as manifested by the enriched NADH dehydrogenase complex assembly pathway. Through transfection of intestinal crypt cells with SoNar (a NADH/NAD+ sensor), a higher NADH/NAD+ ratio is observed in Mut/Mut*** mice, hinting the perturbed redox potential. Likewise, following transfection of intestinal crypt cells with FiNad (a NAD+ sensor), less NAD+ content is discovered in the Mut/Mut*** cells. All of these findings mirror NAD+ depletion in the intestinal senescence triggered by mtDNA mutations. Note: mtDNA mutations are classified into four types: negligible (WT/WT), low (WT/WT*), moderate (WT/Mut**) and high (Mut/Mut***). 3. The link between mtDNA mutation content and physiological intestinal senescence The small intestine of aged mouse intestine is characterized by decreased intestinal crypt number, increased villus length, higher expression of CDKN1A/p21 (a well-known senescence marker) and shorter telomere length, which is accompanied by accumulation of mtDNA mutations, primarily low-frequency (less than 0.05) point mutations. 4. LONP1 protein as a candidate marker for intestinal senescence caused by accumulated mtDNA mutations Mitochondrial unfolded protein response (UPRmt) is activated by a variety of mitochondrial stresses, including protein imbalances between mitochondria and the nucleus as well as impaired mitochondrial protein transport. The hallmarks of UPRmt are increased protein expression levels of LONP1, HSP60 and ClpP. Noteworthily, only LONP1 protein is specifically upregulated in senescent UPRmt activation triggered by accumulated mtDNA mutations, which may be a candidate biomarker for intestinal senescence. 5. The role of NAD+ in intestinal senescence induced by elevated mtDNA mutations. NAD+ repletion in vivo alleviates the small intestine senescent phenotypes caused by mtDNA mutation burden, and rescues the decreased colony formation efficiency in Mut/Mut*** intestinal organoids. NAD+-dependent UPRmt triggered by mtDNA mutations regulates intestinal senescence. These data further indicate that NAD+ depletion functions as a key mediator of the intestinal senescence induced by accumulated mtDNA mutations. 6. The role of NAD+ in the signal pathways regulating intestinal senescence caused by increased mtDNA mutations NAD+ repletion rescues the Foxl1 downregulation and Notch1 upregulation in Mut/Mut*** mice, suggesting that mtDNA mutation burden can regulate the function or number of niche cells through NAD+ depletion. In addition, NAD+ depletion caused by increased mtDNA mutation burden induces the decline of LGR5-positive intestinal cells via impairment of the Wnt/β-catenin pathway. 7. Conclusion NAD+ repletion is significant for the regulation of intestinal homeostasis, playing a critical role in rescuing the intestinal senescence phenotype caused by accumulated mtDNA mutations. Reference Yang, Liang et al. “NAD+ dependent UPRmt activation underlies intestinal aging caused by mitochondrial DNA mutations.” Nature communications vol. 15,1 546. 16 Jan. 2024, doi:10.1038/s41467-024-44808-z About BONTAC 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. BONTAC has over 160 domestic and foreign patents, leading the industry of coenzyme and natural products. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and NMN. High quality and stable supply of products can be ensured here. 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.
Amelioration of Myocardial I/R Injury with NR via Autophagy and Oxidative Stress
Introduction Myocardial ischemia-reperfusion (I/R) injury has emerged as an urgent clinical issue that may offset the benefits of reperfusion therapy and even worsen the prognosis of acute myocardial infarction, a severe cardiovascular disease with significant mortality and morbidity. Nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) intermediate, has been unveiled to hold great therapeutic potential in myocardial I/R injury. About myocardial I/R injury Myocardial I/R injury refers to the damaging effects on cardiomyocytes or heart tissues following ischemia and the regaining of blood perfusion or oxygen supply, with characteristics of cell swelling, contracture of myofibrils, and disruption of the sarcolemma in myocardium. The mechanisms of myocardial I/R injury are extremely complex, chiefly involving cellular and molecular biological events such as cellular oxidative stress, intracellular calcium overload, mitochondrial dysfunction, inflammatory response, apoptosis and autophagy. Strikingly, autophagy and oxidative stress have been perceived as vital factors in the treatment of myocardial I/R injury. The alleviating effects of NR on myocardial I/R injury in mice NR can improve the cardiac function of mice with myocardial I/R injury, and reduce the generation of myocardial injury- and oxidative stress-associated biomarkers. Herein, the optimal concentration of NR for protection against H/R injury is 10 mM. In vivo, NR diminishes the area of myocardial ischemic infarction, alleviates pathological myocardial changes, decreases inflammatory cell infiltration, and attenuates the levels of mitochondrial reactive oxygen species (ROS) as well as creatine kinase myocardial band (CK-MB). In vitro, NR pretreatment lessens the levels of lactate dehydrogenase, CK-MB, malondialdehyde, superoxide dismutase and ROS, as well as the mortality of H9c2 cells after the induction of hypoxia/reoxygenation (H/R) injury. The significance of Sirt 1 pathway in the regulation of autophagy by NR Excessive autophagy can exacerbate I/R injury, giving rise to an increase in cardiomyocyte apoptosis and greater cardiac dysfunction. Noteworthily, NR can lead to the activation of Sirt 1, an NAD+-dependent enzyme, to protect the H9c2 cells against excessive autophagy, thereby alleviating the myocardial I/R injury. Post NR pre-treatment, the levels of autophagy-related proteins (Beclin 1, P62 and LC3II/LC3I) are apparently downregulated in the H9c2 cells challenged with H/R. Remarkably, the supplement of Sirt 1 inhibitor EX527 overtly attenuates NR-induced reduction in the expression levels of autophagy-related proteins under H/R conditions, hinting the significance of Sirt 1 in the regulation of autophagy by NR. Conclusion The myocardial I/R injury can be ameliorated by regulating the autophagy and oxidative stress with NR. On the one hand, NR can directly participate in oxidative reduction to lessen the level of oxidative stress in cardiomyocytes. On the other hand, NR can protect cardiomyocytes against excessive autophagy, which is possibly accomplished by increasing the NAD+ content in the body via the Sirt 1 pathway. Reference Yuan C, Yang H, Lan W, et al. Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress. Exp Ther Med. 2024;27(5):187. doi:10.3892/etm.2024.12475 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.