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
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.
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.”.
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.
Introduction Rare ginsenoside Rg3, an active extract from Panax ginseng, is reported to possess a wide range of pharmacological properties including anti-angiogenesis and anti-cancer, with high lipophilicity (estimated log P4) and a low water solubility at pH7.4. Nevertheless, its permeability and bioavailability are relatively low, and production procedures are complex. Remarkably, the metabolites of Rg3 have similar and even stronger activity than Rg3, opening up new opportunities for future adjuvant cancer therapy. The association of ginsenoside Rg3 and its metabolites There are two epimers of ginsenoside Rg3, which can be subsequently deglycosylated into epimers of ginsenoside Rh2 (S-Rh2 and R-Rh2) and protopanaxadiol (S-PPD and R-PPD). The anti-cancer properties of Rg3 metabolites Angiogenesis and tumor cell proliferation are both interdependent factors in tumor progression. In terms of anti-proliferation, Rg3 metabolites, who induce S-phase arrest and necroptosis in a human triple negative breast cancer cell line MDA-MB-231 as well as G0/G1 arrest and apoptosis in human umbilical vein endothelial cells (HUVECs), are more potent than Rg3. The clinically relevant target of Rg3 metabolites are the endothelial cells. Anti-angiogenic effects are evaluated using loop formation assay. Among Rg3 metabolites, S-Rh2 is the most potent inhibitor of loop formation. VEGFR2 and AQP1 as the targets of Rh2 According to the prediction by in silico molecular docking, there is a good binding score between Rh2/PPD and the ATP-binding pocket of VEGFR2, a dominant regulator controlling both physiological and pathological angiogenesis. Through VEGF bioassay, it is discovered that S-Rh2 is a most potent anti-angiogenic candidate with allosteric modulatory action on VEGFR2 function. In addition, Rh2 and PPD have the potential of blocking AQP1 and AQP5, two members of the aquaporin family with vital roles in proliferation, migration, invasion and angiogenesis. Moreover, Rg3 is more selective for AQP1 and does not show a good binding score with AQP5. In light of this, blocking the water channel function of AQP1 may have an immediate role in inhibition of loop formation and anti-angiogenic effects of Rh2. Conclusion Metabolites of Rg3 could potentially increase the anti-cancer properties of Rg3. The application of these molecules alone or together may be potent alternatives for future adjuvant cancer therapy. Reference Nakhjavani M, Smith E, Yeo K, et al. Differential antiangiogenic and anticancer activities of the active metabolites of ginsenoside Rg3. J Ginseng Res. 2024;48(2):171-180. doi:10.1016/j.jgr.2021.05.008 BONTAC Ginsenosides 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. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. 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, 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 (NAD) compartmentalized in adipocytes can modulate adipocyte differentiation and gene expression, in addition to controlling glucose metabolism. White adipose tissue (WAT), one major adipose tissue, may be one of the direct target for NAD supplementation. 2. About WAT In contrast to brown adipose tissue (BAT), WAT contains a single lipid droplet and few mitochondria. WAT, once thought to be morphologically and functionally unremarkable, is in fact highly dynamic, with plasticity and heterogeneity, which is widely distributed in the subcutaneous tissues and around the internal organs. WAT plays a key role in a range of biological processes, such as maintenance of energetic homeostasis, processing and handling of glycans and lipids, blood pressure control, and host defence, with tight relationship with metabolic disorders such as diabetes. 3. The tissue-specific roles of NAD NMN is synthesized from NAM and NR by NAMPT and NRK, respectively. The synthesized NAD+ from NMN is used as a SIRT1 substrate, which leads to the recycling of NAD+ via the salvage pathway. In this process, NAD+ can exert different effects depending on the tissue. Remarkably, NAD precursors can control metabolic stress particularly via focusing on adipose tissue. 4. The effects of boosting NAD+ on WAT Supplementation of NMN and NR has been shown to reduce body weight and enhance insulin sensitivity in regular chow-fed aged wild-type mice and diet-induced obese mice, respectively. NAM supplementation diminishes fat accumulation in diet-induced obese mice. Additionally, both NMN and NR supplementation prevent inflammation even with different treatment duration. NAM administration boosts mitochondrial biogenesis and glutathione synthesis in WAT. Similarly, it is evidenced that NMN treatment in high fat diet-induced type 2 diabetes mouse model facilitates the recovery of Glutathione S-transferase Alpha 2 (Gsta2) gene expression in the liver. 5. The adipose-specific effects of nicotinamide phosphoribosyltransferase (NAMPT) NAMPT, one NAD regulator in WAT, is a promising therapeutic target for the treatment of metabolic disorders. NAMPT plays a potential role in maintaining adipose tissue homoeostasis, as evidenced by the explicitly blocked adipocyte differentiation and lipid synthesis in vitro post treatment of NAMPT inhibitor FK866. For some reasons such as differences in sex, age, and/or basal levels of cellular NAD+ availability, there are various inconclusive results regarding the impacts of NAD+ metabolism on adipocytes in the adipocyte-specific NAMPT-deficient mouse model or in vitro cell models. Further investigation on the effects of NAD+ supplementation and the distinct functions of NAMPT in adipocytes is still needed. 6. Conclusion The importance of NAD metabolism in WAT has been highlighted. NAD has tissue-specific roles. Specifically, WAT may be one of the direct target for NAD supplementation. Supplementation with NAD+ precursors can reduce fat accumulation and inflammation in adipose tissue. Reference Kwon SY, Park YJ. Function of NAD metabolism in white adipose tissue: lessons from mouse models. Adipocyte. 2024;13(1):2313297. doi:10.1080/21623945.2024.2313297 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.
Introduction It has been reported that infection with Gram-negative bacteria can disrupt the osteogenic differentiation. Notably, nicotinamide mononucleotide (NMN) protects against osteogenesis from inflammation caused by Gram-negative bacterial infections possibly via regulating the Wnt/β-catenin signaling pathway. About osteogenic differentiation Osteogenic differentiation refers to the formation process of osteoblasts from bone marrow mesenchymal stem/stromal (a.k.a. skeletal stem) cells and bone progenitor cells, which is a key event in bone formation during development, fracture repair, and tissue maintenance. Abnormalities in the process of osteogenic differentiation may disrupt physiological bone homeostasis, which is strongly associated with a variety of bone-related diseases such as osteoporosis, bone tumors, and osteoarthritis, making negative impacts upon fracture healing and repair of bone tissue defects. LPS-induced suppression of osteogenesis Lipopolysaccharide (LPS) is a component of the cell wall in Gram-negative bacteria, which is intensively applied to mimic Gram-negative bacterial infections in cell and animal models. LPS can hamper osteogenic differentiation of pre-osteoblasts MC3T3-E1 by diminishing the expression of mRNA markers (Alp1, Bglap, Runx2, and Sp7), ALP activity, and mineralization. Partial protection of NMN against the LPS-induced suppression of osteogenesis LPS-induced inhibition of osteogenic differentiation in MC3T3-E1 cells is partially offset by 1 mM of NMN. Concretely, the mRNA levels of Alp1, Bglap, and Sp7 in cells co-treated with NMN and LPS are relatively higher than those in cells treated solely with LPS. Furthermore, ALP activity and mineralization repressed by LPS are restored in the presence of NMN (1 mM). Potential involvement of the Wnt/β-catenin signaling pathway in NMN's effect on osteogenesis Wnt/β-catenin signaling pathway has been attested to play a vital role in osteogenesis by promoting bone formation and inhibiting bone resorption. In cells treated with LPS, β-catenin is localized in the cytoplasm rather than the nucleus. Following NMN treatment, β-catenin is translocated to the nucleus, similar to what occurred in response to the treatment of osteogenic induction medium (OIM). Meanwhile, the fluorescence intensity of β-catenin is restored upon NMN treatment. Conclusion NMN has a protective role against LPS-induced osteogenesis disruption, which is potentially achieved by the Wnt/β-catenin signaling pathway. NMN may function as a viable therapeutic strategy to preserve bone homeostasis in elderly and immunocompromised patients. Reference Kang I, Koo M, Jun JH, Lee J. Effect of nicotinamide mononucleotide on osteogenesis in MC3T3-E1 cells against inflammation-induced by lipopolysaccharide. Clin Exp Reprod Med. Published online April 11, 2024. doi:10.5653/cerm.2023.06744 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. 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.