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 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.
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.
BONTAC NAD product features and advantages
1、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
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What users say about BONTAC
Frequently Asked Question
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Nicotinamide adenine dinucleotide (NAD) has several essential roles in metabolism. It acts as a coenzyme in redox reactions, as a donor of ADP-ribose moieties in ADP-ribosylation reactions, as a precursor of the second messenger molecule cyclic ADP-ribose, as well as acting as a substrate for bacterial DNA ligases and a group of enzymes called sirtuins that use NAD+ to remove acetyl groups from proteins. In addition to these metabolic functions, NAD+ emerges as an adenine nucleotide that can be released from cells spontaneously and by regulated mechanisms, and can therefore have important extracellular roles.
First, inspect the factory. After some screening, NAD 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 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.
The difference all comes down to the charge of these coenzymes. NAD+ is written with a superscript + sign because of the positive charge on one of its nitrogen atoms. It is the oxidized form of NAD. It’s considered “an oxidizing agent” because it accepts electrons from other molecules.
Although they are different chemically, these terms are mostly used interchangeably when discussing their health benefits. Another term you may come across is NADH, which stands for nicotinamide adenine dinucleotide (NAD) + hydrogen (H). This is also used interchangeably with NAD+ for the most part. Both are nicotinamide adenine dinucleotides that function as either hydride donors or hydride acceptors. The difference between these two is that that NADH becomes NAD+ after it donates an electron to another molecule.
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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.
How to Maintain NAD+ Homeostasis to Regulate Mitochondrial and Cardiac Function
1. Introduction Mitochondria are the center of energy metabolism in cardiomyocytes, which are necessary for maintaining normal myocardial contractility and cardiac function. Typically, the development of cardiovascular disease is usually accompanied by mitochondrial dysfunction. Impaired autophagy is known to cause mitochondrial dysfunction and heart failure, in part due to altered mitophagy and protein quality control. Notably, external replenishment of nicotinamide adenine dinucleotide (NAD+) precursors can enhance autophagy and mitochondrial quality control to maintain metabolic health, thereby regulate mitochondrial and cardiac function. 2. NAD+ metabolism in mitochondrial and cardiac function Cardiomyocytes accumulate NAD+ mostly within their mitochondria, where the bulk of cellular oxidation-reduction reactions occur. However, NAD+ is also present in the cytosol and nucleus, in which NAD+-derived metabolites and NAD+-dependent enzymes contribute to various cellular functions. 3. Mitochondrial and cardiac dysfunction induced by NAD+ deficiency Mitochondrial and cardiac dysfunction triggered by NAD+ deficiency is alleviated in cAtg3-KO mouse hearts post the administration of β-nicotinamide mononucleotide (NMN), as evidenced by the restoration of citrate synthase (CS) activity, partial normalization of ATP level and NPPB mRNA expression in cAtg3-KO mice as well as upregulation of ADP level in WT mouse hearts. Besides, NNMT inhibition can rescue mitochondrial and cardiac dysfunction in cAtg3-KO mice by restoring NAD+ level. 4. The impact of autophagic flux upon cardiac and mitochondrial function Autophagy is an intracellular degradation pathway that recycles subcellular components, playing a critical in modulating metabolic homeostasis. Autophagic flux, a central homeostatic mechanism that degrades materials toxic to cardiomyocytes, can mediate SQSTM1-NF-κB-NNMT signal transduction to control the cellular level of NAD+, thereby maintaining the mitochondrial and cardiac function. 5. Conclusion Autophagic flux may be a potential way to maintain the cellular level of NAD to regulate mitochondrial and cardiac fiunction. . Reference [1] Abdellatif M, Sedej S, Kroemer G. NAD+ Metabolism in Cardiac Health, Aging, and Disease. Circulation. 2021;144(22):1795-1817. doi:10.1161/CIRCULATIONAHA.121.056589 [2] Zhang Q, Li Z, Li Q, et al. Control of NAD+ homeostasis by autophagic flux modulates mitochondrial and cardiac function. EMBO J. Published online January 11, 2024. doi:10.1038/s44318-023-00009-w About BONTAC BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and NMN. Bonzyme whole-enzymatic method is adopted, which is environmental-friendly, with no harmful solvent residues. The purity of products can reach up to 95%, which is benefited from the exclusive Bonpure seven-step purification technology. BONTAC has self-owned factories and has obtained a number of international certifications, where high quality and stable supply of products can be ensured. BONTAC has over 160 domestic and foreign patents, leading the industry of coenzyme and natural products. In the future, BONTAC will actively expand the international market, and work with global partners to promote the prosperous development of synthetic biology industry. In this era full of challenges and opportunities, BONTAC is confident to make greater contributions to the cause of human health. 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.
Supplementing NMN to Protect Osteoblasts Against LPS-Induced Inflammation
Introduction It has been reported that infection with Gram-negative bacteria can disrupt the osteogenic differentiation. Notably, nicotinamide mononucleotide (NMN) protects against osteogenesis from inflammation caused by Gram-negative bacterial infections possibly via regulating the Wnt/β-catenin signaling pathway. About osteogenic differentiation Osteogenic differentiation refers to the formation process of osteoblasts from bone marrow mesenchymal stem/stromal (a.k.a. skeletal stem) cells and bone progenitor cells, which is a key event in bone formation during development, fracture repair, and tissue maintenance. Abnormalities in the process of osteogenic differentiation may disrupt physiological bone homeostasis, which is strongly associated with a variety of bone-related diseases such as osteoporosis, bone tumors, and osteoarthritis, making negative impacts upon fracture healing and repair of bone tissue defects. LPS-induced suppression of osteogenesis Lipopolysaccharide (LPS) is a component of the cell wall in Gram-negative bacteria, which is intensively applied to mimic Gram-negative bacterial infections in cell and animal models. LPS can hamper osteogenic differentiation of pre-osteoblasts MC3T3-E1 by diminishing the expression of mRNA markers (Alp1, Bglap, Runx2, and Sp7), ALP activity, and mineralization. Partial protection of NMN against the LPS-induced suppression of osteogenesis LPS-induced inhibition of osteogenic differentiation in MC3T3-E1 cells is partially offset by 1 mM of NMN. Concretely, the mRNA levels of Alp1, Bglap, and Sp7 in cells co-treated with NMN and LPS are relatively higher than those in cells treated solely with LPS. Furthermore, ALP activity and mineralization repressed by LPS are restored in the presence of NMN (1 mM). Potential involvement of the Wnt/β-catenin signaling pathway in NMN's effect on osteogenesis Wnt/β-catenin signaling pathway has been attested to play a vital role in osteogenesis by promoting bone formation and inhibiting bone resorption. In cells treated with LPS, β-catenin is localized in the cytoplasm rather than the nucleus. Following NMN treatment, β-catenin is translocated to the nucleus, similar to what occurred in response to the treatment of osteogenic induction medium (OIM). Meanwhile, the fluorescence intensity of β-catenin is restored upon NMN treatment. Conclusion NMN has a protective role against LPS-induced osteogenesis disruption, which is potentially achieved by the Wnt/β-catenin signaling pathway. NMN may function as a viable therapeutic strategy to preserve bone homeostasis in elderly and immunocompromised patients. Reference Kang I, Koo M, Jun JH, Lee J. Effect of nicotinamide mononucleotide on osteogenesis in MC3T3-E1 cells against inflammation-induced by lipopolysaccharide. Clin Exp Reprod Med. Published online April 11, 2024. doi:10.5653/cerm.2023.06744 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. 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 BOMNTAC 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 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.