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 Amyotrophic lateral sclerosis (ALS) is a progressive fatal neurodegenerative disease that affects the motion-related nerve cells in the brain and spinal cord. The disease is featured by the death of upper and lower motor neurons (MNs) and manifested by progressive muscle atrophy and weakness, culminating in immobility to paralysis, with the body gradually frozen as if by ice. Patients with this disorder generally have a low survival rate and life quality. At present, there is no effective way to cure this disease, but early invention has a positive significance in improving the symptoms of patients and delaying the progression of disease. Remarkably, dietary NMN supplementation has been uncovered to be beneficial against ALS, which can enhance the motor and function of neuromuscular junctions (NMJs) in ALS, bringing a glimpse of hope for ALS patients. 2. The improved healthspan and reduced motor dysfunction in ALS mice post dietary NMN supplementation The median lifespan of ALS mice administrated with or without NMN is 143 days and 138 days, respectively, hinting that NMN supplementation in diet has a modest effect on lifespan extension. Relative to those without dietary NMN supplementation, NMN-treated ALS mice shows a slower motor impairment in both rotarod and hanging wire tests, with a two-week delay in dysfunction, despite no difference in body weight loss during testing period. When compared with those in the absence of dietary NMN supplementation, ALS mice administrated with NMN are more active, with increased travel distance, elevated mean speed and reduced immobile time. In addition, NMN diet prevents ALS-induced gait impairments, as manifested by the improved forelimb and hindlimb stride length in NMN-treated ALS mice. 3. The alleviating effect of NMN on the function of NMJs in ALS NMJs are one of the earliest affected site in ALS, which are benefited greatly from NMN diet. In addition to improving the length and breadth of the motor endplate, dietary NMN supplementation also ameliorates the impairment of NMJ function and reduce the semitendinosus muscle mass in ALS mice. Furthermore, NMN conspicuously elevates the innervation ratio of NMJs in ALS mice. Dietary NMN supplementation strengthens synaptic function at NMJ in ALS, while diminishing NMJ and intermyofibrillar (IMF) mitochondrial abnormalities. With a great detail, NMN prominently increases Feret's diameter of mitochondria and restores mitochondria circularity in ALS mice. 4. Conclusion Dietary NMN supplementation can modestly extend lifespan and significantly enhance healthspan by improving motor performance and NMJ function in ALS mice, opening up new opportunities for the future treatment of ALS. Reference Lundt S, Zhang N, Polo-Parada L, et al. Dietary NMN supplementation enhances motor and NMJ function in ALS. Exp Neurol. Published online January 22, 2024. doi:10.1016/j.expneurol.2024.114698 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. 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 phosphate hydrogen (NADPH), also known as reduced coenzyme II, is a critical cofactor in cellular antioxidant systems and lipid synthesis, which links insulin resistance and ferroptosis of pancreatic β cells in the context of metabolic disorders such as diabetes mellitus, playing a central role in maintaining metabolic homeostasis. 2. Biological role of NADPH NADPH functions as a coenzyme essential to cellular metabolism, playing pivotal roles in various critical biological processes, such as ROS scavenging, ROS production, fatty acid synthesis and cholesterol synthesis. 3. Biosynthetic pathway of NADPH Cellular production of NADPH is facilitated through several pathways, including the pentose phosphate pathway, the citric acid cycle, and fatty acid metabolism. The dynamic equilibrium between NADPH synthesis and consumption is essential for preserving cellular redox balance and enabling a host of biosynthetic reactions. 4. The role of NADPH in insulin secretion from pancreatic β-Cells Both redox reaction and metabolic signaling can modulate insulin secretion from pancreatic β-cells, where NADPH plays a central role. It can not only serves as a metabolic coupling factor, but also acts as a custodian of β-cell integrity, delicately managing the interplay between metabolic inputs and insulin output. 5. The interaction between insulin resistance and NADPH A substantial body of evidence reveals that NADPH is critical for the regulation of oxidative stress and inflammatory responses, the main contributors to the pathogenesis of insulin resistance. Specifically, NADPH is implicated in ROS production via NOX and is also utilized in the synthesis of new fatty acids, which contributes to the development of insulin resistance, particularly in the context of obesity-induced chronic inflammation. 6. The impact of NADPH upon the ferroptosis in the context of diabetes In pancreatic β cells, the elevated blood sugar and pro-inflammatory cytokines can trigger oxidative stress and iron accumulation to promote lipid peroxidation, thereby facilitating the ferroptosis. In return, the ferroptosis can reduce insulin secretion and beta cell mass, which is contributive to the progression of diabetes. In general, NADPH plays a dual role in ferroptosis. On the one hand, it can promote ROS generation via NOX. On the other hand, it can support antioxidant defense through glutathione regeneration. In the context of diabetes, NADPH may predominantly fuel processes leading to ferroptosis, mainly due to the enhanced activity and affinity of NOX, which however requires further research for verification. 7. Conclusion NADPH has a critical role in the complex landscape of metabolic disorders, particularly insulin resistance and ferroptosis. Regulating NADPH-related pathways may open up new opportunities for the treatment of metabolic disorders. Reference Moon, Dong-Oh. “NADPH Dynamics: Linking Insulin Resistance and β-Cells Ferroptosis in Diabetes Mellitus.” International journal of molecular sciences vol. 25,1 342. 26 Dec. 2023, doi:10.3390/ijms25010342 Production advantages and features of BONTAC NADPH BONTAC has rich R&D experience and advanced technology in the biosynthesis of NADPH. Bonzyme whole-enzymatic method is adopted, which is environmental-friendly, with no harmful solvent residues. The purity of NADPH 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 four domestic and foreign NADPH patents, leading the industry. 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 The NAD precursor nicotinamide mononucleotide (NMN) shows a beneficial effect on ageing, yet excessive NMN accumulation may lead to axon degeneration. How to make the anti-ageing effect of NMN compatible with axonal degeneration caused by NMN accumulation is still a challenge. A preliminary discussion on this issue is conducted in this study. 2. The definition and pathological changes of axonal degeneration Axonal degeneration refers to degenerative changes in the axon as a result of direct damage to the primary or as a result of diseases such as neuronal metabolic disorders, which is a common pathological change of the nervous system. The pathological changes after axonal injury include axonal swelling, fracture, retraction and atrophy. 3. The relationship between NMN and sterile alpha and TIR motif–containing 1 (SARM1) SARM1 is a multi-functional enzyme with base exchange activity, which can cleave nicotinamide adenine dinucleotide (NAD) into adenosine diphosphate ribose (ADPR), cyclic adenosine diphosphate ribose (cADPR) and nicotinamide (NAM). A substantial body of evidence mirrors that the degenerative enzyme SARM1 will be bound to and be activated by NMN. Hence, failed conversion of sufficient NMN into NAD may give rise to toxic NMN accumulation and axon degeneration. 4. The specific pathway of axon degeneration NMN only induces axon degeneration in the presence of SARM1, placing the toxic accumulation on a common pathway of axon death. Notably, nicotinamide mononucleotideadenylyltransferases (NMNATs) has a broader, compartment-specific regulatory role in SARM1 activity. For instance, NMNAT2 depletion is associated with SARM1 activation in axons. In a nutshell, NMNAT2 depletion can give rise to NMN accumulation. Next, NMN binds to and activates the pro-degenerative protein SARM1, leading to rapid NAD consumption and axon degeneration. 5. The impacts of NAD precursors upon axonal health NAD precursors are likely to be safe for most people, but there is a risk for people with compromised NMNAT activity, as these supplements could cause SARM1 activation and neurodegeneration. In healthy individuals, rapid conversion from NMN into NAD can be accomplished by NMNAT2, which is conductive to the prevention of NMN toxic accumulation and maintenance of healthy neurons and axons. Yet, downregulation of NMNAT2 level or activity may result in the upregulation of NMN, thereby leading to SARM1 activation, increased axonal vulnerability and/or axon degeneration. 6. The factors for SARM1 activity SARM1 activity is regulated by a ratio between NMN and NAD. When NMN rises, partial inhibition of SARM1 is only seen at high concentrations of NAD. Inefficient conversion of NMN into NAD because of compromised NMNAT activity is the most likely scenario in which NMN can become toxic. The change in NMN level close to the physiological concentration has a much more significant impact on SARM1 activity than NAD level. A twofold increase in NAD level is not sufficient to delay axon degeneration after injury, and even higher NAD level only temporarily delays axon degeneration. 7. The interaction between SARM1 activation and ageing effect of NMN Sub-lethal/chronic SARM1 activation could increase axonal vulnerability or have a significant impact upon NAD homeostasis and important intracellular signalling pathways in neurons.It is pivotal for life to preserve NAD homeostasis. Maintaining NAD homeostasis could be a viable anti-ageing strategy. Similarly, NMNAT2 depletion increases axon vulnerability and the level of the NMNAT2 is declined with ageing. These findings signify that SARM1 and NMNAT2 may be the key factor to reconcile the axonal degeneration caused by the accumulation of the NAD precursor NMN and ageing effect of NMN. 8. Conclusion Efficient conversion of NMN into NAD is key to preventing SARM1 activation and neurotoxicity. SARM1 and NMNAT2 may be the intersection factors between axon degeneration and anti-ageing therapy. Reference Loreto, Andrea et al. “NMN: The NAD precursor at the intersection between axon degeneration and anti-ageing therapies.” Neuroscience research vol. 197 (2023): 18-24. doi:10.1016/j.neures.2023.01.004 BONTAC NMN product features and advantages * Industrial leading technology: 15 domestic and international NMN patents * Self-owned factories and a number of international certifications to ensure high quality and stable supply of products * NMN raw material supplier of famous David Sinclair team of Harvard University Disclaimer BONTAC shall hold no responsibility for any claims arising directly or indirectly from your reliance on the information and material on this website.