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 (Nicotinamide Mononucleotide) is a substance similar to vitamin B3, which can produce NAD+ (a key metabolic intermediate) in the body. Therefore, studies have shown that NMN may help improve aging-related health issues such as metabolism, immunity, cell repair, brain health, and more.
Currently, NMN supplements are mainly used to treat the following diseases:
Aging-related metabolic disorders such as diabetes, obesity, high cholesterol, etc.
Aging-related neurodegenerative diseases, such as Alzheimer's disease.
Aging-associated immune decline.
Aging-related cardiovascular disease.
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
However, these studies were small, and NMN has not been shown to be effective in clinical trials, so further research is needed to determine the effectiveness of NMN supplements.
NMN supplements may cause side effects such as upset stomach, diarrhea, and nausea. There is also research showing that NMN supplements may affect insulin sensitivity and insulin levels, so people with diabetes should consult their doctor before taking them.
NMN supplements have not yet undergone large-scale clinical trials to verify their effectiveness. Currently, research on NMN supplements is mainly focused on animal and in vitro experiments. These studies show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process.
The long-term health effects of NMN supplementation are not well studied. Existing studies mainly focus on animal and in vitro experiments, which show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process. However, the results of these studies do not represent the long-term effects of NMN on human health.
Introduction Oxidized form of nicotinamide adenine dinucleotide (NAD+) and its precursor nicotinamide mononucleotide (NMN) have been uncovered to restore DNA repair and prevent cancer progression via the deleted in breast cancer 1 (DBC1). This research is committed to deciphering the detailed molecular mechanisms. About DBC1 DBC1 is a nuclear protein initially cloned from a human chromosome 8p21 region, which can modulate diversified targets by protein-protein interaction, contributing to various cellular processes such as apoptosis, DNA repair, senescence, transcription, metabolism, circadian cycle, epigenetic regulation, cell proliferation, and tumorigenesis. The affinity and molecular binding mechanisms between NAD+/NMN and DBC1354–396 Under the help of nuclear magnetic resonance (NMR) and Isothermal titration calorimetry (ITC) experiments, it is verified that both NAD+ and NMN have a binding relationship with the NHD domain of DBC1. Specifically, NAD+ interacts with DBC1354-396 through hydrogen bonds, with a binding affinity (8.99 μM) nearly twice that of NMN (17.0 μM) and the key binding sites are primarily residues E363 and D372. The vital roles of E363 and D372 mutagenesis in ligand-protein interaction The N-terminal loop of DBC1354-396 encloses the small ligand within a local space, anchoring NAD+ and NMN to the protein through key amino acid residues E363 and D372 via hydrogen bonding. Conclusion Both NAD+ and its precursor NMN can bind to DBC1's NHD domain (DBC1354–396) at key sites E363 and D372, providing novel clues for the development of targeted therapies and drug research on DBC1-associated disease including tumors. Reference Ou L, Zhao X, Wu IJ, et al. Molecular mechanism of NAD+ and NMN binding to the Nudix homology domains of DBC1. Int J Biol Macromol. Published online February 12, 2024. doi:10.1016/j.ijbiomac.2024.130131 BONTAC NAD 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 consisting of Doctors and Masters. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and its precursors (eg. NMN), with various forms to be selected (eg. endoxin-free IVD-grade NAD, Na-free or Na-containing NAD; NR-CL or NR-Malate). 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 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.
1.Introduction Mitochondria, a type of highly plastic organelle, can maintain a relatively stable dynamic equilibrium state towards the morphology, structure, quantity, volume, quality, and function under normal physiological conditions. This dynamic equilibrium state is generally called mitochondria homeostasis. Replenishment of nicotinamide mononucleotide (NMN) to boost intracellular NAD+ level can regulate mitochondrial homeostasis. 2.The amelioration of mitochondrial dysfunction and senescence post NMN treatment Typically, NAD+ level determines the rate and extent of senescence. The NAD+ pool experienced by cells and tissues presents a declined tendency with age, which may lead to a loss of mitochondrial homeostasis and senescent phenotypes in CD8+ T cells. Following NMN (100 μM) supplementation, NAD+ level is restored and the NAD+/NADH ratio is elevated in senescent CD8+ T cells, by which the mitochondrial functions are obviously improved and the cytoplasmic mtDNA is reduced. 3.The prevention of neuroinflammation and senescence in CD8+ T cells via NMN supplement Post NMN supplementation, the senescence and neuroinflammation are correspondingly repressed. With a great detail, NMN supplementation decreases the ROS and mitochondrial membrane potential in CD8+ T cells, while increasing the intracellular ATP. Furthermore, NMN suppresses the inflammation-associated markers (IL-1β, IL-6, TNF-α and IFN-γ) in the supernatant and the mRNA of senescent CD8+ T cells. 4. The inhibitory effect of NMN on the senescence-related pathway STING The activation of STING can launch a robust proinflammatory response and senescence, which is closely related to the deficient health span in model mice. Strikingly, NMN can prominently improve the senescent state of T cells and reduce the secretion of senescence-related inflammatory factors via inhibition of the STING pathway. 5. Conclusion Upregulation of NAD+ level by NMN supplementation can regulate the mitochondrial homeostasis to prevent STING-induced senescence in CD8+ T cells. Reference Ye B, Pei Y, Wang L, et al. NAD+ supplementation prevents STING-induced senescence in CD8+ T cells by improving mitochondrial homeostasis. J Cell Biochem. 2024;1-17. doi:10.1002/jcb.30522 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 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 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.
1. Introduction Acute lung injury comprises a uniform response of the lung to inflammatory or chemical insults which is commonly caused by systemic illness including sepsis or trauma, infection with pathogens, and toxic gas inhalation. Sepsis-induced acute lung injury is a leading cause of morbidity and mortality worldwide, imposing substantial economic, social, and health burdens. Despite advances in knowledge of septic pulmonary pathologies over the years, efficient targeted therapies are still lacking. Notably, NMN administration has been uncovered to be effective in alleviating sepsis-induced acute lung injury, which can reduce cellular inflammation, oxidative stress, and apoptosis. 2. The impact of NMN upon macrophage polarization in LPS-induced MH-S cells In mouse alveolar macrophage cell line MH-S treated by lipopolysaccharide (LPS), NMN can facilitate the transformation of macrophages from pro-inflammatory M1 phenotype towards the anti-inflammatory M2 phenotype to promote inflammatory resolution and tissue repair, as evidenced by the downregulation of M1 phenotype-associated markers (iNOS and CD86+ F4/80+) and pro-inflammatory cytokines (IL-1β, TNF-α and IL-6) as well as the upregulation of M2 phenotype-related markers (Arg1 and CD86+ F4/80+) and anti-inflammatory mediators (IL-10) post NMN administration. 3. The alleviation of LPS-induced lung injury post NMN administration In vitro, NMN represses the apoptosis and production of pro-inflammatory factors in LPS-stimulated MH-S cells. In vivo, NMN explicitly ameliorates LPS-induced pathological alterations, encompassing thickened alveolar wall, inflammatory cell infiltration, septa swelling, and erythrocyte exudation, in a murine septic model. 4. The association of SIRT1/NF-κB signaling activation with NMN-mediated macrophage polarization SIRT1/NF-κB signaling pathway is involved in the lung protection of NMN, as manifested by the elevated expression of SIRT1 as well as the reduced acetylation and phosphorylation of NF-κB-p65 post NMN treatment. Repression of SIRT1/NF-κB signaling offsets NMN-mediated M2 macrophage polarization. SIRT1 inhibitor EX-527 decreases the expression of SIRT1, yet increases the expression of acetylated and phosphorylated NF-κB-p65 in septic mice pretreated with NMN. In contrast to NMN, EX-527 overtly promotes the expression levels of M1 macrophage-associated markers (iNOS and CD86) while inhibiting those of M2 phenotype-related markers (Arg1 and CD206). 5. Conclusion NMN can effectively ameliorate LPS-induced acute lung injury through modulating macrophage polarization via SIRT1/NF-κB signalling pathway, providing a novel therapeutic direction for sepsis-induced acute lung injury. 6. Reference He, Simeng et al. “Nicotinamide mononucleotide alleviates endotoxin-induced acute lung injury by modulating macrophage polarization via the SIRT1/NF-κB pathway.” Pharmaceutical biology vol. 62,1 (2024): 22-32. doi:10.1080/13880209.2023.2292256 BONTAC NMN BONTAC is the leader of the global NMN industry, with 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 160 invention patents including 15 NMN patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. Both the high-quality product and excellent service can be better ensured in BONTA. BONTAC has 12 years of industry experience, which is worthy of your trust. 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.