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.
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.
1. Introduction Atherosclerosis is a chronic progressive inflammatory disease, which is featured by the accumulation of lipids in the intima of the arteries with yellow appearance. This disease is dominated by coronary artery atherosclerosis and cerebrovascular atherosclerosis, representing the fundamental cause of most cardiovascular diseases, with over 15 million deaths worldwide in 2019. By virtue of its potent anti-inflammatory and anti-oxidative properties, nicotinamide mononucleotide (NMN), an effective NAD+ booster, has promising potential in hampering the progression of atherosclerosis. 2. Establishment of mouse atherosclerotic model and NMN treatment The atherosclerotic model is constructed by feeding ApoE−/− mice with high-fat diet (HFD) for 10 weeks until the plaque formation and accumulation in the middle arteries. Subsequently, the model mice are subjected to daily intraperitoneal injection of saline (100 μL) or NMN (500mg/kg) for 8 consecutive weeks (6 days a week). Strikingly, it is found that the weight and food consumption of mice are barely affected post NMN intraperitoneal injection. 3. The alleviation of atherosclerotic burden by NMN intraperitoneal injection possibly via anti-oxidant property NMN greatly dampens the progression of atherosclerosis, as evidenced by the overtly diminished size of atherosclerotic plaque (36 %) and necrotic core (48 %) in aortic sinus, as well as the decreased lipid area (43 %) and increased collagen content (51 %) in atherosclerotic lesions. Noteworthily, the anti-atherosclerotic effect of NMN may be partially achieved by its anti-oxidative property. In a nutshell, NMN lessens the level of malondialdehyde (MDA), a major biomarker of lipid peroxidation and oxidative stress, yet elevates the levels of anti-oxidant markers superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in serum. 4. The involvement of macrophages in the repression of plaque inflammation by NMN NMN regulates macrophages to repress plaque inflammation. There are two main polarization phenotypes for macrophages, where M1 type contributes to pro-inflammatory cytokines production and are deemed to be atherogenic, while the M2 type produces anti-inflammatory cytokines and exerts a preventive effect on the progression of atherosclerosis. NMN promotes the polarization of macrophages to the anti-inflammatory M2 phenotype, as manifested by the downregulation of M1-associated markers (Tnf-α, Il-6, Il-1β and Mcp-1) and upregulation of M2-related markers (Arg-1, Mrc-1, Retlna and Irf-4) in aortic samples. 5. Conclusion NMN produces anti-atherosclerotic effects possibly via suppressing oxidative stress and inflammatory response in HFD-fed ApoE−/− mice, hinting its promising potential in the treatment of atherosclerosis. Reference [1] Vaduganathan M, Mensah GA, Turco JV, et al. The Global Burden of Cardiovascular Diseases and Risk: A Compass for Future Health. J Am Coll Cardiol. 2022;80(25):2361-2371. doi:10.1016/j.jacc.2022.11.005 [2] Wang Z, Zhou SH, Hao YL, et al, Nicotinamide mononucleotide protects against high-fat-diet-induced atherosclerosis in mice and dampens aortic inflammation and oxidative stress. J Functional Foods. 2024 (112): 1756-4646, doi: 10.1016/j.jff.2023.105985. 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 BONTAC 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.
Introduction Replenishing nicotinamide mononucleotide (NMN) to raise the availability of nicotinamide adenine dinucleotide (NAD+) has been deemed as effective approach to prevent neurodegeneration in aging and pathological conditions including ALS, a fatal progressive neurodegenerative disorder with no known way to cure. The association of SOD1 and TDP-43 with ALS Cu/Zn-superoxide dismutase (SOD1) is the first identified protein associated with familial ALS. In most ALS cases, Transactive Response DNA Binding Protein 43 (TDP-43) pathology is frequently observed. Both SOD1 and TDP-43 have tight association with motor neuron degeneration in patients with ALS. Mutant SOD1 could affect the solubility/insolubility of TDP-43 through physical interactions. Mutant SOD1G93A and the fragment form of TDP-43 can exert synergistic effect to mediate toxic events in apoptosis. The protective effect of NMN on motor neurons NMN can increase the neurite length and complexity in mouse motor neurons and iPSC-derived human motor neurons overexpressing wild-type TDP-43/mutant hSOD1G93A. Meanwhile, it prevents the neuronal death and increased nitro-tyrosine immunoreactivity induced by trophic factor deprivation. In motor neurons overexpressing mutant hSOD1G93A, the neuroprotection conferred by NMN supplementation is mediated by a mechanism that involves an increase in glutathione content. However, this neuroprotective effect does not involve the alteration of glutathione content in non-transgenic or TDP-43 overexpressing motor neurons. The involvement of TDP-43 pathology in ALS NMN supplementation can confer axonal protection in motor neurons isolated from two dissimilar models of ALS, with and without involvement of TDP-43 pathology. Besides, NMN treatment correct the morphological changes induced by TDP-43 overexpression in motor neurons and boost the nuclear localization of TDP-43 and phosphorylated TDP-43, which favors its nuclear localization and averts the detrimental effects of TDP-43 overexpression on neurite length and complexity. Conclusion Supplementation of NAD+ precursor NMN can modulate neurite complexity and survival in motor neurons, showing great therapeutic potential in the context of ALS pathology. Reference [1] Hamilton HL, Akther M, Anis S, Colwell CB, Vargas MR, Pehar M. NAD+ precursor supplementation modulates neurite complexity and survival in motor neurons from ALS models. Antioxid Redox Signal. Published online March 19, 2024. doi:10.1089/ars.2023.0360 [2] Jeon GS, Shim YM, Lee DY, et al. Pathological Modification of TDP-43 in Amyotrophic Lateral Sclerosis with SOD1 Mutations. Mol Neurobiol. 2019;56(3):2007-2021. doi:10.1007/s12035-018-1218-2 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. .