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
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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.
NADH powder manufacturing method
The main methods of NMNH powder preparation include extraction, fermentation, fortification, biosynthesis and organic matter synthesis. Compared with other preparations, the whole enzyme becomes the mainstream method owing to the advantages of pollution free, high level of purity and
BONTAC NMNH product features and advantages
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
NMNH is more potent than NMN
When applied to cultured cells, the NMNH is shown to be more efficient than NMN as it was able to “significantly increase NAD+ at a ten times lower concentration (5 µM) than that needed for NMN”. Moreover, NMNH shows to be more effective , as at 500 µM concentration, it achieved “an almost 10-fold increase in the NAD+ concentration, while NMN was only able to double NAD+ content in these cells, even at 1 mM concentration.”.
Interestingly, NMNH also appears to act quicker and has a longer-lasting effect compared to NMN. According to the authors, NMNH induces a “significant increase in NAD+ levels within 15 minutes”, and “NAD+ steadily increased for up to 6 hours and remained stable for 24 hours, while NMN reached its plateau after only 1 hour, most likely because the NMN recycling pathways to NAD+ had already become saturated.”.
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Frequently Asked Question
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NADH is synthesized by the body and thus is not an essential nutrient. It does require the essential nutrient nicotinamide for its synthesis, and its role in energy production is certainly an essential one. In addition to its role in the mitochondrial electron transport chain, NADH is produced in the cytosol. The mitochondrial membrane is impermeable to NADH, and this permeability barrier effectively separates the cytoplasmic from the mitochondrial NADH pools. However, cytoplasmic NADH can be used for biologic energy production. This occurs when the malate-aspartate shuttle introduces reducing equivalents from NADH in the cytosol to the electron transport chain of the mitochondria. This shuttle mainly occurs in the liver and heart.
Nicotinamide adenine dinucleotide (NAD+ ) homeostasis is constantly compromised due to degradation by NAD+ -dependent enzymes. NAD+ replenishment by supplementation with the NAD+ precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) can alleviate this imbalance. However, NMN and NR are limited by their mild effect on the cellular NAD+ pool and the need of high doses. Here, we report a synthesis method of a reduced form of NMN (NMNH), and identify this molecule as a new NAD+ precursor for the first time. We show that NMNH increases NAD+ levels to a much higher extent and faster than NMN or NR, and that it is metabolized through a different, NRK and NAMPT-independent, pathway. We also demonstrate that NMNH reduces damage and accelerates repair in renal tubular epithelial cells upon hypoxia/reoxygenation injury. Finally, we find that NMNH administration in mice causes a rapid and sustained NAD+ surge in whole blood, which is accompanied by increased NAD+ levels in liver, kidney, muscle, brain, brown adipose tissue, and heart, but not in white adipose tissue. Together, our data highlight NMNH as a new NAD+ precursor with therapeutic potential for acute kidney injury, confirm the existence of a novel pathway for the recycling of reduced NAD+ precursors and establish NMNH as a member of the new family of reduced NAD+ precursors.
First, inspect the factory. After some screening, NMNH companies that directly face consumers pay more attention to brand building. Therefore, for a good brand, quality is the most important thing, and the first thing to control the quality of raw materials is to inspect the factory. Bontac company actually manufacturing NMNH powder of high quality with the caterias of SGS. Secondly, the purity is tested. Purity is one of the most important parameters of NMN powder. If high purity NMNH cannot be guaranteed, the remaining substances are likely to exceed the relevant standards. As the attached certificates demonstrates that the NMNH powder produced by Bontac reach the purity of 99%. Finally, a professional test spectrum is needed to prove it. Common methods for determining the structure of an organic compound include Nuclear Magnetic Resonance Spectroscopy (NMR) and high-resolution mass spectrometry (HRMS). Usually through the analysis of these two spectra, the structure of the compound can be preliminarily determined.
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Protective Role of NAD+ Against MI-induced HF in Sprague-Dawley Rats and Beagles
1. Introduction Disrupted nicotinamide adenine dinucleotide (NAD+) metabolism is increasingly deemed to be one of risk factor for amendable cardiovascular disorders. A substantial evidence has mirrored that restoring NAD+ stock and energy metabolism may be effective in alleviating the symptoms of patients with heart failure (HF), one of the typical cardiovascular disease after myocardial infarction (MI). 2. About HF HF has dominant clinical features of ventricular filling or ejection impairment, concomitant with abnormalities in cardiac structure/function. This disorder afflicts about 38 million patients across the world, and the number of HF patients is on the rise with the age, posing a great threat to the life of patients and bringing huge economic burden on the patient family and society. In terms of drug therapies of HF, the "golden triangle" of beta blockers, ACEI/ARB, and aldosterone receptor antagonists has long been the preferred option. Despite significant improvement on the survival of patients, the 5-year mortality rate remains at 50%. Hence, it is of great significance to seek novel way with high efficacy and safety. NAD supplements may be an effective choice for alleviating HF. 3. Research protocol For further verification of the efficacy of NAD+, MI-induced HF models are constructed in male Sprague-Dawley rats and beagles herein. Subsequently, the left anterior descending arteries of MI-induced HF animals are ligated for 1 week, followed by 4-week treatment with or without low/medium/high dose of NAD+ and the positive control drug LCZ696, an angiotensin receptor blocker-neprilysin inhibitor with an cardioprotective effect after MI. 4. The efficacy of NAD on rats and beagles with MI-induced HF NAD+ shows the equivalent efficacy as LCZ696 in the treatment of MI-induced HF, or even better than LCZ696 at the medium and high doses. In rat/beagle HF models, the heart mass index, heart function, and myocardial fibrosis in the infarct marginal zone are dose-dependently improved post administration of NAD or LCZ696, as manifested by decreased end-systolic volume, end-systolic dimension, creatine kinase and lactic dehydrogenase, as well as the increased ejection fractions, fractional shortening, cardiac output, and stroke volume. In addition, the downregulation of left ventricular blood pressure in the HF model animals is ameliorated post administration of NAD or LCZ696. 5. Conclusion In rat and beagle MI-induced HF models, NAD+ conspicuously alleviates myocardial hypertrophy and cardiac function, represses myocardial fibrosis, and reduces the myocardial infarction, laying a theoretical foundation for the clinical application of energy metabolism therapy with NAD+. Reference Pei Z, Yang C, Guo Y, Dong M, Wang F. The Role of NAD+ in Myocardial Ischemia-induced Heart Failure in Sprague-Dawley Rats and Beagles. Curr Pharm Biotechnol. Published online February 13, 2024. doi:10.2174/0113892010275059240103054554 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.
The Miraculous Potency of NR-CL on Mitigating Ischemia-induced Hippocampal Damage and Maintaining Cognitive Function
1 Introduction Nicotinamide riboside (NR), a derivative of vitamin B3, is a new type of bioactive substance, which can be generated by binding a carbohydrate molecular ribose with nicotinamide (also known as niacin or vitamin B3). Nicotinamide riboside chloride (NRC/NR-CL) is a chloride salt form of NR. In daily life, NR-CL can be taken from NR supplements and food such as meat, fish and cereals. A recent study has revealed that NR-CL protects the hippocampus and ultimately promotes the recovery of cognitive function after brain ischemia. 2. The ameliorating impact of NRC upon ischemia-induced cognitive deficits Ischemia-induced cognitive deficits are ameliorated post NRC treatment. Specifically, NRC treatment improves the learning ability of mice, as evidenced by the shorter latency and the decreased path length. The hippocampal protection provided by NRC contributes to the recovery of spatial learning and memory after the ischemic insult. Figure 1 Acute NRC treatment potentiates cognitive recovery after ischemia 3. Reduction of the infarct volume in the hippocampus post acute NRC treatment After ischemia, there are deformed cell bodies, condensed nuclear chromatin, increased intracellular cell gaps, loosened cell arrangements and blurred visible staining in the damaged pyramidal neurons. NRC treatment partially offsets these morphological changes. Figure 2 Acute NRC treatment reduces the hippocampal infarct volume. 4. Recovery of neuronal damage in the hippocampus post acute NRC treatment After ischemia, brain damage emerges due to energy crisis-induced mitochondrial dysfunction, followed by the cell loss and neuronal apoptosis. NRC treatment leads to an increase in the number of positive cells, signifying the recovery of local neuronal loss. Figure 3 Acute NRC treatment attenuates neuronal loss in the hippocampus. 5. Upregulation of NAD and ATP levels in the hippocampus post acute NRC treatment By repleshing the production of NAD, acute treatment with NRC, to some extent, can salvage the energy supply in the hippocampus, which conspicuously enhances the recovery of ATP level. 6. Conclusion Collectively, acute NRC treatment increases the energy supply and reduces the neuronal loss to protect the hippocampus, thereby facilitating the recovery of cognitive function. NR-CL (ie. NRC) is a very promising component of health care products and has a wide range of application prospects. Before use, one should follow the guidance of professionals. At the same time, attention should be paid to reasonable intake and safe use to avoid the adverse effects of excessive use. References Cheng, Yin-Hong et al. “Acute Treatment with Nicotinamide Riboside Chloride Reduces Hippocampal Damage and Preserves the Cognitive Function of Mice with Ischemic Injury.” Neurochemical research vol. 47,8 (2022): 2244-2253. doi:10.1007/s11064-022-03610-3 Product advantages and features of BONTAC NR-CL * Bonzyme Whole-enzymatic method (environmental-friendly; no harmful solvent residues) * Unique Bonpure seven-step purification technology, with higher product content and higher conversion rate * Self-owned factories and a number of international certifications to ensure high quality and stable supply of products * One-stop customized service for product solution 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.
Potential Treatment for Glaucoma: NAD+ Precursor NR
Introduction Glaucoma is regarded as the second dominant cause of blindness across the world. With the amounting number and proportion of elderly people, it is estimated that 111.8 million people will have glaucoma by 2040. Nicotinamide riboside (NR) has been attested to protect retinal ganglion cells from the stress of elevated intraocular pressure and optic nerve crush. Glaucoma patients can protect their optic nerves by oral administration of NR at a dose of 300 mg (approximately 1.18 mM). The abovementioned protective effects of NR may be achieved by its antioxidant and antifibrotic properties. About glaucoma Glaucoma is a typical ocular disease characterized by atrophy and depression of the optic nerve head, visual field defects, and diminution of vision. The pathologically increased intraocular pressure and insufficient blood supply to the optic nerve are deemed as the primary risk factors for the development of the disease. In addition to those with family history of glaucoma, people with severe myopia/hyperopia, hypertension, hyperlipidemia, hyperglycemia and long-term use of corticosteroid medications, especially eye drops, are at high risk for glaucoma. Extraordinary role of NR in protecting HTMs against oxidative stress In glaucoma, oxidative stress can trigger TM degeneration, thereby resulting in intraocular hypertension. Herein, an oxidative damage model is established in vitro by incubation of human trabecular meshwork (HTM) cells with 200 μM H2O2 for 24 h. As expected, NR hampers H2O2-induced apoptosis in HTM cells, as evidenced by the upregulation of the anti-apoptotic protein Bcl-2 and downregulation of apoptotic protein Bax. Conversely, NR boosts the viability of oxidative-damaged HTM cells. In addition, NR can shield HTM cells from oxidative stress by lowering ROS and superoxide anion levels. Apart from this, NR overtly improves the H2O2-induced decrease in the mitochondrial membrane potential (MMP) in HTM cells, hinting its antioxidant effect possibly achieved by maintaining mitochondrial homeostasis. Underlying mechanism regarding the antioxidant role of NR in HTM cells MAPK and JAK2/Stat3 pathways are related to NR-alleviated HTM cell apoptosis during oxidative stress. In the MAPK pathway, H2O2 leads to the downregulation of p-P38/P38 ratio and upregulation of p-ERK1/2 protein expression, which are offset by intervention with NR. In the JAK2/Stat3 pathway, H2O2 induces downregulation of p-JAK2 protein expression, while NR runs oppositely. Potential antifibrotic role of NR in HTM cells Considering that transforming growth factor-beta 2 (TGF-β2), a profibrotic cytokine, is also a major contributor to glaucomatous HTM dysfunction, an HTM cell model of fibrosis is constructed by induction of TGF-β2 at 10 ng/mL for 48 h. Remarkably, NR prevents TGF-β2-induced fibrosis by reducing extracellular matrix (ECM) deposition in HTM cells. Concretely, the mRNA and protein levels of fibronectin (FN) are elevated in the TGF-β2-treated HTM cells, which however are counteracted by NR. Conclusion NR can boost the viability, proliferation and MMP oxidative damage in H2O2-induced HTM cells, and hamper TGF-β2-induced fibrosis, which is linked to the MAPK and JAK2/Stat3 pathways. NR may be a potential therapeutic agent for glaucoma by inhibiting oxidative damage and fibrosis in HTM cells. Reference Zeng Y, Lin Y, Yang J, et al. The Role and Mechanism of Nicotinamide Riboside in Oxidative Damage and a Fibrosis Model of Trabecular Meshwork Cells. Transl Vis Sci Technol. 2024;13(3):24. doi:10.1167/tvst.13.3.24 BONTAC NR BONTAC is one of the few suppliers in China that can launch mass production of raw materials for NR, with self-owned factory and professional R&D team. Up till now, there are 173 BONTAC patents. BONTAC provides one-stop service for customized products. Both malate and chloride salt forms of NR are available. By dirt of unique Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method, the product content and conversion rate can be maintained in a higher level. The purity of BONTAC NR can reach above 97%. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. 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, or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.