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.
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.”.
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
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 become the mainstream method owing to the advantages of pollution free, high level of purity and stability.
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NMNH also proved more effective than NMN in raising NAD+ levels in a variety of tissues when administered at the same concentration, confirming the results observed in cell lines. The data presented in this study also corroborate the evidence that NAD+ boosters protect against different models of acute kidney injury, and place NMNH as a great alternative intervention to other NAD+ precursors to reduce tubular damage and accelerate recovery.
To overcome the limitations of the current repertoire of NAD+ enhancers, other molecules with a more pronounced effect on the NAD+ intracellular pool are desired. This has stimulated us to investigate the use of the reduced form of nicotinamide mononucleotide (NMNH) as an NAD+ enhancer. There is very scarce information about the role of this molecule in cells. In fact, only one enzymatic activity has been described to produce NMNH. This is the NADH diphosphatase activity of the human peroxisomal Nudix hydrolase hNUDT1232 and the murine mitochondrial Nudt13.33 It has been postulated that, in cells, NMNH would be converted to NADH via nicotinamide mononucleotide adenylyl transferases (NMNATs).34 However, both NMNH production by Nudix diphosphatases and its use by NMNATs for NADH synthesis have only been described in vitro using isolated proteins, and how NMNH participates in cellular NAD+ metabolism remains unknown.
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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Tailoring Personalized Dosage Regimens of NMN Based on NAD Concentration
Introduction Nicotinamide mononucleotide (NMN), one precursor of nicotinamide adenine dinucleotide (NAD+), has been ascertained to be implicated with multiple biological processes such as cellular redox regulation and metabolism as well as DNA repair. Herein, post-hoc analysis of a double-blinded clinical trial is carried out. On the premise of safety, to optimize NMN utilization, personalized dosage regimen can be developed by monitoring the NAD concentration. Research protocol A total of 80 healthy middle-aged adults (age: 40 to 65) are enrolled in the randomized, double-blinded, controlled clinical trial of NMN supplementation, who are randomly assigned into four groups and administrated with placebo or NMN (300 mg, 600 mg, or 900 mg) for 60 days. The clinical data including age, sex, body mass index (BMI), blood biological age, homeostatic model assessment for insulin resistance (HOMA-IR), blood NAD concentration, 6-minute walk test and 36-item short-form survey (SF-36), along with adverse events, are collected at baseline and after supplement, followed by comparison and correlation analysis. The association of participant clinical data at baseline and after supplement of NMN NAD concentration change (NADΔ) is dose-dependently increased post NMN supplementation, with a large coefficient of variation (29.2–113.3%) within group. Notably, only HOMA-IR has a prominent association with blood baseline NAD. As a whole, NMN supplementation has a positive impact on the physical endurance and general health conditions of healthy adults, as evidenced by the obvious improvement of six-minute walking distance, blood biological age, and SF-36 score. In addition, the increase of about 15 nmol/L in NADΔ is related to clinically improvements in the walking distance of 6-minute walk test and the SF-36 score. The safety oral dose of NMN in clinical trials As demonstrated by the registered clinical trials NCT04823260 and CTRI/2021/03/032421, NMN supplementation can boost blood NAD concentration, which is safe and well tolerated with daily oral administration of 900 mg. Strikingly, clinical efficacy expressed by blood NAD concentration and physical performance reaches highest at a dose of 600 mg daily oral intake. Conclusion Blood NAD concentration is increased by NMN supplement at a dose-dependent manner. Personalized regimen of NMN supplement should be based on the close monitoring of NAD concentration change. In addition to longer follow-up duration and large sample size, future trials on the efficacy of NMN supplement should pay much attention to the factors affecting baseline NAD concentration. Reference [1] Kuerec AH, Wang W, Yi L, et al. Towards personalized nicotinamide mononucleotide (NMN) supplementation: Nicotinamide adenine dinucleotide (NAD) concentration. Mech Ageing Dev. 2024;218:111917. doi:10.1016/j.mad.2024.111917 [2] Song Q, Zhou X, Xu K, Liu S, Zhu X, Yang J. The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update. Adv Nutr. 2023;14(6):1416-1435. doi:10.1016/j.advnut.2023.08.008 BONTAC NMN As David Sinclair, a famous professor of genetics at Harvard University, once pointed out in an interview, NMN has unstable molecular structure, which is easily degraded into nicotinamide if stored in the conventional environment. The satisfactory efficacy of NMN cannot be guaranteed if the quality and purity NMN products are not high. BONTAC is the first choice of NMN raw material suppliers worldwide, who has dedicated to the manufacture of raw material for enzyme and natural products for 12 years, with self-owned factory, 173 patents and professional R&D team. The purity of BONTAC NMN can reach up to 99.5%. Also, BONTAC is the NMN raw material supplier of David Sinclair team, 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. 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 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.
Supplementing NAD+ precursors as a promising approach for DPN
1. Introduction Diabetic peripheral neuropathy (DPN) is one of the most frequent complications of diabetes, ans also a major cause of foot ulcers, disability, and eventual amputation. With the prolongation of the diabetes, about 50% of people with diabetes will eventually develop DPN. Notably, supplementing NAD+ precursors could alleviate DPN symptoms by increasing the NAD+ level and activating the sirtuin-1 (SIRT1) protein. 2. The reversal effect of NAD+ precursors on DPN In vitro, the Dorsal Root Ganglion neurons (DRGs) isolated from diabetic mice are exposed to the NAD+ precursor Nicotinamide Riboside (NR) or Nicotinamide Mononucleotide (NMN). It is found that the NAD+ level, the SIRT1 protein, and the deacetylation activity are elevated, followed by the boosted neurite growth, the improved nerve function, and the reversal of IENFD loss. In vivo, supplement of NMN or NR also offsets the neuropathy in C57BL6 mice induced by streptozotocin (STZ) or high fat diet (HFD), as manifested by the improved sensory function, normalized nerve conduction velocities, and restored intraepidermal nerve fibers. 3. The increase of neurite length in a SIRT1-dependent manner post the addition of NMN/NR SIRT1, one of the most unique NAD+ consuming enzymes, can protect against DPN when activated, which may attribute to the improved mitochondrial function and energy homeostasis. Apart from these, SIRT1 activity in the nucleus can deacetylate the transcriptional and co-transcriptional factors that regulate glucose homeostasis and fat oxidation. The activation of SIRT1 is critical for axonal regeneration. NMN/NR treatment or transfection with SIRT1 overexpression vector can directly facilitate the neurite growth in cultured DRG neurons, which however is hindered by the SIRT1 inhibitor EX527, hinting the significance of SIRT1. 4. The association of SARM1 with NMNAT2 in axonal degeneration of DPN Sterile alpha and Toll/interleukin-1 receptor motif-containing 1 (SARM1) controls the axonal degeneration and regeneration via a well-regulated system comprising NAD+ and NMN. NAD and NMNAT2 can boost vesicular glycolysis and axonal transport to maintain the axonal health. The mitochondrial localization of SARM1 complements the coordinated activity of NMNAT2 that promotes axonal survival. 5. Conclusion Supplementing NAD+ precursors may be a promising approach for the treatment of DPN. A SARM1 inhibitor coupled with either NR or NMN may be more effective than a single agent alone in preventing or treating DPN. Reference Chandrasekaran K, Najimi N, Sagi AR, et al. NAD+ Precursors Reverse Experimental Diabetic Neuropathy in Mice. Int J Mol Sci. 2024;25(2):1102. Published 2024 Jan 16. doi:10.3390/ijms25021102 BONTAC NMN and NR BONTAC has dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 160 global patents as well as strong R&D team consisting of Doctors and Masters. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. Both the precursors NMN and NR are available in BONTAC. The high purity and stability 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.
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.