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.
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
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.”.
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.
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.
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.
On March 20~22, 2024, Personal Care & Home Ingredients Shanghai (PCHi) will be held in Shanghai World Expo Exhibition & Convention Center. BONTAC’s active raw materials for high-end cosmetics will be displayed at Booth No. 3A53 in 2024 PCHi, including but not limited to NMN, Pro-Xylane, Rare Ginsenoside Rh2/Rg3, Ergothioneine, Salidroside and Type III Recombinant Collagen. BONTAC has been dedicated to provide high-quality raw materials of coenzymes and natural products for 12 years. Looking forward to seeing you at site. BONTAC Product List Niche Area Products Application Scope NMN (CAS No.: 1094-61-7) Healthcare products; Cosmetics; Medicine NAD (CAS No.: 53-84-9) Healthcare products; Cosmetics; Diagnostic reagents Raw materials for enzyme catalysis; Animal health Coenzyme Endotoxin-free grade NADH (CAS No.: 606-68-98) Functional food and drink; Biomedical research and development Healthcare product; Diagnostic reagents NADP (CAS No.: 24292-60-2/1184-16-3) Raw materials for medicine or enzyme catalysis; Diagnostic reagents; In vitro diagnostic reagents (GR); Biomedical research and development S-NAD (CAS No.: 4090-29-3) Biochemical diagnostic reagents NR (CAS No.: 23111-00-4) Healthcare products; Cosmetics; Diagnostic reagent Natural products Ginsenoside Rh2(CAS No.:78214-33-2) Healthcare products; Cosmetics; Drink; Alcohol; Medicine; Functional food Ginsenoside Rg3(Cas No. : 38243-03-7) Salidroside (Cas No.: 10338-51-9) Healthcare products; Scientific research experiment; New drug development Stevia Sweetener (RD)(Cas No.: 63279-13-0 ) Food; Drink; Daily chemical industry; Brewing Raw materials for cosmetics Pro-Xylane (CAS No.: 439685-79-7) Cosmetics Erythrothioneine Cosmetics Dietary supplements L-Glutathione Reduced Healthcare products; Cosmetics Resveratrol Healthcare products; Cosmetics Phosphatidylserine Healthcare products; Biochemical diagnostic reagent Medicine and intermediate Ursodeoxycholic acid(CAS No.: 128-13-2) Healthcare products; Biochemical diagnostic reagent Chenodeoxycholic acid Healthcare products; Biochemical diagnostic reagent Cholic acid Healthcare products; Biochemical diagnostic reagents BONTAC profile Bontac Bio-Engineering (Shenzhen) Co., Ltd. (also referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales. There are six major series of product in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates. BONTAC is the pioneer of NMN industry. By virtue of the first whole-enzyme catalysis technology in China, BONTAC takes the industry lead in its niche field of coenzyme. 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. BONTAC has undertaken a number of provincial and national science projects in China, with the only approved "coenzyme engineering technology research center" in Guangdong China. In the future, BONTAC will continue to build ecological relationship with academia, and upstream/downstream partners, lead the synthetic biological industry and create a better life for human beings.
Introduction Cigarettes containing nicotine (Nic) and sugar-sweetened beverages (SSBs) with high fructose corn syrup (HFCS) have been uncovered to induce hepatic steatosis, which are the risk factors for the development of metabolic diseases including non-alcoholic fatty liver disease (NAFLD). Noteworthily, nicotinamide riboside (NR) can elevate mitochondrial nicotinamide adenine dinucleotide (NAD+) to exert a protect role against hepatic steatosis in NAFLD. About NAFLD NAFLD, which is marked by excessive neutral fat accumulation in the liver, is a frequent chronic liver disease unrelated to alcohol and other well-defined liver-damaging factors, with a global prevalence of 25%. With the epidemic trend of obesity and metabolism-associated syndromes worldwide, NAFLD has been regarded as a type of metabolic stress liver injury with tight association with insulin resistance and genetic predisposition. The association between Nic/Coke and hepatic steatosis in NAFLD Nic plus Coke administration causes hepatic steatosis. In addition, Nic plus Coke also leads to a striking increase in lipid accumulation and mitochondrial swelling as well as loss of the mitochondrial cristae (arrowhead), with a decrease in the amount of endoplasmic reticulum (arrow) and glycogen deposition (asterisk). The preventive role of NR against hepatic steatosis in NAFLD NR leads to a decrease in the calorie intake to reduce hepatic steatosis through the increased of the NAD+ concentration, and triggers the downstream signaling of NAD+, with a reduction in oxidative stress markers and mitochondrial damage. Underpinned mechanism of NR in ameliorating Nic plus Coke-induced hepatic steatosis Nic plus Coke consumption reduces the protein levels of the NAMPT, diminishing NAD+-dependent enzyme Sirt1 and downstream PGC1α. This combined treatment also enhances SREBP1c and ACC activity, increasing intracellular triglyceride deposits and reducing AMPK phosphorylation. The decline in PGC1α can result in the retention of damaged mitochondria with increased oxidative stress, indicated by higher MDA and HO1 levels as well as lower SOD2 level. Importantly, the reduced hepatic NAD+ level is a risk factor to develop NAFLD. NR is a precursor of NAD+ that reduces plasma triglycerides and total cholesterol levels, in turn preventing hepatic lipid accumulation in mice and humans. Sirt1, an NAD+-dependent enzyme, has a protective effect in NAFLD. Sirt1 promotes mitochondrial biogenesis through PGC1α. NR supplementation activates Sirt1 signaling to repress the progression of NAFLD. Conclusion NR supplement has the potential to mitigate oxidative stress and mitochondrial abnormalities, and prevent hepatic steatosis induced by Nic plus Coke, which may be promissory candidates for the management of NAFLD. Reference Rivera JC, Espinoza-Derout J, Hasan KM, et al. Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR). Front Endocrinol (Lausanne). 2024;15:1282231. Published 2024 May 2. doi:10.3389/fendo.2024.1282231 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 170+ 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 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.