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 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 (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 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 The gut is a diverse and dynamic microbiotic system. There are about 100 trillion microorganisms in the gut, which is mainly composed of anaerobic, partially anaerobic, and aerobic bacteria. In the process of ageing, the intestinal tract may show an increase in the permeability of the epithelial barrier and impaired tight junction proteins. Notably, supplementing β-Nicotinamide mononucleotide (NMN) to elevate NAD+ level has been proved to prolong life and maintain the colon health in ageing Mice. Research protocol Zmpste24−/− mice are frequently used in the construction of the prematurely ageing model, due to their features of slow weight gain, malnutrition and progressive hair loss, with a short median survival of about 20 weeks. Herein, to fathom out the role of NMN in maintaining the colon health of ageing mice, Zmpste24−/− mice aged 5-7 weeks are orally gavaged with phosphate-buffered saline (PBS), or NMN at 100/300 mg kg−1 every other day until natural death. Likewise, natural ageing C57BL/6 mice aged 10 months old are subjected to the oral gavage of PBS or NMN at 300 mg kg−1, serving as the the control. During experiments, the body weight of mice is recorded, and their frailty index and fecal samples are detected. The life span and frailty indices in Zmpste24-/- mice after NMN treatment NMN extends the healthy and median lifespan of Zmpste24−/−improves the Zmpste24−/− ageing phenotype. Specifically, the median lifespan of the mice is increased from 21.4 weeks to 25.7 weeks post NMN intervention, with more than 20% growth. Also, NMN effectively increases body weight. Meanwhile, mice have better overall health after NMN treatment, as manifested by the slowly increasing trend towards Sinclair’s frailty indices. The role of NMN in the intestinal tract of ageing mice NMN adjusts the activity of genes involved in ageing mice colons. Simply put, in the presence of NMN supplement, the protein level of transcriptional regulator P53 is reduced, while the expression levels of ageing marker Sirt1, NMNAT2 and NMNAT3 are elevated. NMN improves the pathology of intestinal epithelial cells and intestinal permeability, as evidenced by the upregulation of intestinal tight junction protein (Claudin1,) and the number of goblet cells, the elevated release of anti-inflammatory factor (IL-10), and the increasing beneficial intestinal bacteria (Akkermansia muciniphila and Bifidobacterium pseudolongum). Conclusion NMN supplementation exerts a protective effect on colon mucosa by controlling the activity of genes involved in ageing, intestinal stem cell differentiation and improving intestinal flora homeostasis, which may be a viable strategy for maintaining healthy ageing in the gut. Reference Yanrou Gu, Lidan Gao, Jiamin He et al. β-Nicotinamide mononucleotide supplementation prolongs the lifespan of prematurely aged mice and protects colon function in ageing mice. Food Funct., 2024 (15): 3199-3213. DOI: 10.1039/D3FO05221D 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 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 Solute carrier family 25 member 51 (SLC25A51) is perceived as a mammalian transporter, which is capable of importing oxidized nicotinamide adenine dinucleotide (NAD+) into mitochondrial matrix. Remarkably, upregulation of SLC25A51 has correlation with poorer outcomes in patients with acute myeloid leukemia (AML), a clinically aggressive haematological disease with a mortality rate of over 70% within the first 5 years following an initial diagnosis. The association between NAD+/NADH ratio and SLC25A51 in AML cells Both NAD+ (oxidative form) and NADH (reduced form) are essential coenzymes for cellular energy metabolism, and the ratio of NAD+/NADH reflects the metabolic activity and health state, which has a direct impact on cellular rhythms, senescence, carcinogenesis and death. Importing mitochondrial NAD+ by SLC25A51 could be a critical aspect supporting mitochondrial metabolism in AML tumorigenesis. Concretely, the decreased mitochondrial NAD+/NADH ratio and specific loss of reduced ubiquinol are observed post the depletion of SLC25A51 in AML cells U937. SLC25A51 as an NAD+/NADH redox decoupler in AML SLC25A51 functions as an NAD+/NADH redox decoupler in AML tumorigenesis to sustain an oxidative TCA cycle and promote glutaminolysis. Depletion of SLC25A51 results in increased usage of non-glutamine carbon sources to support the TCA cycle, as determined by increased proportions of unlabeled TCA intermediates. SLC25A51 is required for robust glutaminolysis. In the context of SLC25A51 depletion, AML cells are forced to rely more on glutamine for aspartate synthesis. Alleviation of AML by SLC25A51 depletion and 5-azacytidine Loss of SLC25A51 leads to a subcellular redistribution of NAD+ in AML cells to limit proliferation. The combination of SLC25A51 depletion and 5-azacytidine is much effective in repressing the viability of AML cells and prolonging the survival time of mice. Conclusion SLC25A51 can maintain mitochondrial oxidative phosphorylation and boost the proliferation of AML cells by regulating NAD+/NADH ratio in mitochondria, with promising efficacy in treating AML, especially in combination with 5-azacytidine. 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 and NR), 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 Nicotinamide adenine dinucleotide (NAD) has been unveiled to be essential for embryonic development. Patients with genetic variants in the NAD+ de novo synthesis pathway often have congenital NAD deficiency disorder (CNDD), a multisystem condition inherited in an autosomal recessive manner. In the context of NAD+ deficiency, all organs and systems, not just vertebrae, heart, kidneys, and limbs, may be affected. 2. The association between NAD synthetase 1 (NADSYN1) and CNDD Individuals delivering biallelic NADSYN1 variants share similar clinical features to those with CNDD. Up till now, almost all of the identified CNDD cases can be attributed to biallelic loss-of-function variants in any of 3 nonredundant genes of the NAD de novo synthesis pathway, including kynureninase (KYNU), 3-hydroxyanthranilate 3,4-dioxygenase (HAAO), or NADSYN1. Among individuals with CNDD identified to date, those with biallelic pathogenic NADSYN1 variants are the most diverse in phenotype. 3. The impact of NADSYN1 variants upon enzymatic activity and phenotype Specifically, NADSYN1 can catalyse the amidation of nicotinic acid adenine dinucleotide (NaAD) to NAD. Biallelic pathogenic variants in NADSYN1 cause a metabolic block in both the de novo pathway and the Preiss-Handler pathway, leading to NAD deficiency. Biallelic NADSYN1 loss-of-function variants impact the NAD metabolome of humans. Post-birth phenotypes involve feeding difficulties, developmental delay, short stature, etc. 4. Mouse embryogenesis disrupted by the loss of NADSYN1 In NADSYN1-/- mouse embryos, NAD-dependent malformations occur when maternal dietary NAD precursors are limited during gestation. The affected Nadsyn1-/- embryos most frequently present malformations of the kidneys, eyes, and lungs. 5. The preventative effect of amidated NAD precursor supplementation against CNDD NADSYN1-dependent embryo loss and malformation in mice are preventable by dietary supplementation of amidated NAD precursors (NMN and NAM) during pregnancy. Maternal diet–derived NAD precursors primarily determine the development of healthy embryos. 6. Conclusion NAD-boosting supplements are essential for individuals with biallelic loss-of-function variants in NADSYN1. Maternal NAD precursor supplementation, to some extent, can reduce the risk of developing CNDD. Reference Szot JO, Cuny H, Martin EM, et al. A metabolic signature for NADSYN1-dependent congenital NAD deficiency disorder. J Clin Invest. 2024;134(4):e174824. Published 2024 Feb 15. doi:10.1172/JCI174824 About BONTAC 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 and NR), 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 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.