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
We Have The Best Solutions for Your Business
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.
What are the purposes of NMN supplements?
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
What diseases can NMN supplements treat?
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.
What NMN Supplements Do?
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.
User Reviews
What users say about BONTAC
Frequently Asked Question
Do you have any question?
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.
Our updates and blog posts
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.
NMN Administration: a Novel Therapeutic Direction for Sepsis-induced Acute Lung Injury
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.
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.