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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.
NMN supplement is a nutritional supplement, a metabolite naturally occurring in plants and animals, which mainly consists of the precursor of the coenzyme NAD+. NMN is a substance that can be supplemented to increase NAD+ levels. NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. NMN supplementation is thought to increase NAD+ levels, improve metabolic disease, and delay aging.
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Further Discussion on the Potential Mechanism of NMN Affecting Neuromuscular Junction
1. Introduction In mammalian cells, the majority of NAD+ is produced from metabolites entering the NAD+ salvage pathway. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme of the salvage pathway, which can convert nicotinamide (NAM) into nicotinamide mononucleotide (NMN). Neuronal NAMPT is important for pre-/post-synaptic NMJ function, and maintaining skeletal muscular function and structure. 2. The involvement of NAMPT in NAD+ salvage pathway NAMPT activity has a pivotal role in energy metabolism and homeostasis. NAMPT can condense nicotinamide (NAM) and 5-phosphoribosyl pyrophosphate (PRPP) into nicotinamide mononucleotide (NMN). NMN is subsequently synthesized into NAD+ by nicotinamide mononucleotide adenylyltransferase (NMNAT), the enzyme immediately after NAMPT. 3. The effect of NMN on partially reversing the NMJ impairments in NAMPT-/- cKO mice In the presence of NMN treatment, vesicle endocytosis/exocytosis is improved and endplate morphology is restored in Thy1-NAMPT-/-conditional knockout (cKO) mice. Also, loss of NAMPT in projection neurons impairs the endocytosis and exocytosis of synaptic vesicles at NMJs, but NMN can largely prevent these impairments. Furthermore, NMN treatment restores sarcomere alignment rather than mitochondrial morphology. 4. The underlying mechanism of NMN affecting NMJs The ameliorating effects of NMN on NMJs may be realized via NAMPT-mediated NAD+ salvage pathway, and this speculation is confirmed by the ameliorated synaptic vesicle cycling, endplate morphology, and muscle fiber structure and function post 2-week administration of the NAD+ precursor, NMN. 5. Conclusion Mechanically, the effects of NMN improving NMJ function, endplate morphology and muscular structure and contractility possibly involves NAMPT-mediated NAD+ salvage pathway. NMN holds a great promise as a therapeutic agent for skeletal muscle diseases. Reference Lundt S, Zhang N, Wang X, Polo-Parada L, Ding S. The effect of NAMPT deletion in projection neurons on the function and structure of neuromuscular junction (NMJ) in mice. Sci Rep. 2020;10(1):99. Published 2020 Jan 9. doi:10.1038/s41598-019-57085-4 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 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 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.
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.
Delving into the Function of Ginsenoside Rh2 in the Develpoment of Breast Cancer
1. Introduction According to the 2020 report of World Health Organization (WHO), there are approximately 2.3 million cases with breast cancer worldwide. Breast cancer has emerged as one of the most malignant tumor in females with significant incidence rate. Although great progress has made in improving the cure rate of early-stage breast cancer in recent years, advanced breast cancer is still hard to be cured. How to reduce the risk of recurrence and metastasis of early-stage breast cancer as well as prolong the survival of patients with advanced breast cancer is still a challenge in the clinical treatment of breast cancer. Notably, ginsenoside Rh2 (GRh2) exerts prominent impacts on retarding the progression of breast cancer via strengthening the immune surveillance of natural killer (NK) cells, a kind of cytotoxic innate lymphocytes critical for tumor immune response. 2. The repressive role of GRh2 in the progression of breast cancer GRh2 hinders the growth, proliferation and metastasis of breast cancer. Simply put, the body weight and tumor volume of model mice are markedly reduced post treatment of GRh2 (10 mg/kg and 20 mg/kg). In addition, the proliferating rate of breast cancer cells is repressed by GRh2 in a dose-dependent manner (5, 10 and 20 mg/kg). Upon the treatment of GRh2 (20 mg/kg), the loss of lung capacity is obviously reduced and the lung metastases formed by MDA-MB-231 tumor cells are strikingly mitigated as well, with no apparent liver metastatic nodules. 3. The enhanced killing effect of NK cells on breast cancer cells following GRh2 treatment GRh2 exerts remarkable effects on retarding the progression of breast cancer via improving the killing ability of NK92MI cells. In a nutshell, the mRNA expression levels of killing mediators perforin and IFN-γ in NK92MI cell-breast cancer cell co-culture system are explicitly upregulated post GRh2 treatment. Strikingly, the reduced lung metastasis of breast cancer by GRh2 is almost counteracted upon the depletion of NK cells. Relative to that of the vehicle control, the amount of CD107a, a degranulation marker of NK cells, is overtly elevated in the presence of GRh2 (20 mg/kg), verifying the enhanced killing activity of NK cells on breast cancer. 4. The underlying molecular mechanism of GRh2 on potentiating the NK cell activity against breast cancer Breast cancer cells reduce the recognition by NKG2D through proteolytic shedding MICA mediated by ERp5 to escape NK cell surveillance. GRh2 interferes with the formation of soluble MICA (sMICA) by suppressing the expression of ERp5 to increase the contents of killing mediators from NK cells, thereby exerting striking effects on fighting against breast cancer. 5. Conclusion GRh2 potentiates the cytotoxic effect of NK cells and enhances the immune surveillance function of NK cells to fight against breast cancer, which may be a potent drug candidate for the prevention and treatment of breast cancer. Reference [1] Sung H, Ferlay J, Siegel RL, et al. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin. 2021;71(3):209-249. doi:10.3322/caac.21660 [2] Yang C, Qian C, Zheng W, et al. Ginsenoside Rh2 enhances immune surveillance of natural killer (NK) cells via inhibition of ERp5 in breast cancer. Phytomedicine. 2024;123:155180. doi:10.1016/j.phymed.2023.155180 Product advantages of BONTAC ginsenoside Rh2 BONTAC is the first enterprise worldwide that can provide national mass production of ginsenosides (Rh2) by enzymatic synthesis, 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 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.