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
We Have The Best Solutions for Your Business
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.
What NMN Supplements Do?
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
However, these studies were small, and NMN has not been shown to be effective in clinical trials, so further research is needed to determine the effectiveness of NMN supplements.
What diseases can NMN supplements treat?
NMN (Nicotinamide Mononucleotide) is a substance similar to vitamin B3, which can produce NAD+ (a key metabolic intermediate) in the body. Therefore, studies have shown that NMN may help improve aging-related health issues such as metabolism, immunity, cell repair, brain health, and more.
Currently, NMN supplements are mainly used to treat the following diseases:
Aging-related metabolic disorders such as diabetes, obesity, high cholesterol, etc.
Aging-related neurodegenerative diseases, such as Alzheimer's disease.
Aging-associated immune decline.
Aging-related cardiovascular disease.
What are the purposes of NMN supplements?
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
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Frequently Asked Question
Do you have any question?
NMN supplements may cause side effects such as upset stomach, diarrhea, and nausea. There is also research showing that NMN supplements may affect insulin sensitivity and insulin levels, so people with diabetes should consult their doctor before taking them.
NMN supplements have not yet undergone large-scale clinical trials to verify their effectiveness. Currently, research on NMN supplements is mainly focused on animal and in vitro experiments. These studies show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process.
The long-term health effects of NMN supplementation are not well studied. Existing studies mainly focus on animal and in vitro experiments, which show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process. However, the results of these studies do not represent the long-term effects of NMN on human health.
Our updates and blog posts
Targeting NAD+ Salvage Pathway as a Potential Approach to Combat Obesity
Introduction Mar 4th is determined as the World Obesity Day. World Obesity Federation, UNICEF and WHO have hosted a global youth-led webinar to talk about obesity & youth. The obesity crisis has gradually attracted much attention. The latest report by the Lancet suggests that one billion people are bothered by obesity (2022), with 650 million adults, 340 million adolescents and 39 million children. Recently, etiological studies and interventions for obesity have been progressively focused on the central nervous system, with an attempt to curb the onset of obesity at its source. Notably, targeting NAD+ salvage pathway in hypothalamic astrocytes may be a potential approach to combat obesity. The association of hypothalamic astrocytes and obesity The hypothalamus functions as the appetite regulation center, which receives and integrates the neuroendocrine factors produced by the central nervous system and peripheral tissues to promote or suppress appetite, so as to affect body weight. Noteworthily, aypothalamic astrocytes can apparently decrease glucose clearance and increase plasma insulin levels, playing an essential role in modulating energy metabolism, which are expected to be a new target for obesity treatment. Alleviation of high-fat diet (HFD)-induced obesity by repressing astrocyte NAD+ salvage pathway Under conditions of excessive fat intake, the NAD+ salvage pathway is specifically activated in hypothalamic astrocytes, which restrains the energy expenditure (EE) and fat oxidation in adipose tissues by downregulating sympathetic nerve innervation, eventually resulting in the accumulation of adipose tissue fat and the development of obesity. CD38 as a downstream mediator of astrocyte inflammation induced by the NAD+ salvage pathway. CD38 functions downstream of the NAD+ salvage pathway in hypothalamic astrocytes burdened with excess fat. CD38 knockdown in arcuate nucleus astrocytes diminishes the weight gain, reduces fat mass, increases EE, and lowers RER during HFD consumption. Cd38 depletion in hypothalamic astrocytes may improve hypothalamic inflammation by increasing NAD+ level. Hypothalamic inflammation can not only lead to energy imbalances, but also exacerbate central insulin resistance and leptin resistance, which can lead to the accumulation of fat in peripheral tissues. The role of nicotinamide phosphoribosyltransferase (NAMPT)–NAD+–CD38 axis in obesity In mammals, the salvage pathway represents the primary means of maintaining cellular NAD+ level. A crucial step in the NAD+ salvage pathway is catalyzed by NAMPT. In response to fat overload, the activation of the astrocytic NAMPT-NAD+-CD38 axis induces pro-inflammatory responses in the hypothalamus, eliciting aberrantly activated basal Ca2+ signals and compromised Ca2+ responses to metabolic hormones such as insulin, leptin, and glucagon-like peptide 1, ultimately resulting in dysfunctional hypothalamic astrocytes and contribute to the development of obesity. Conclusion Mechanically, inhibition of hypothalamic astrocytic NAD+ salvage pathway, along with its downstream CD38, mitigates hypothalamic inflammation and attenuates the development of HFD-induced obesity in male mice. Reference Park, J.W., Park, S.E., Koh, W. et al (2024). Hypothalamic astrocyte NAD+ salvage pathway mediates the coupling of dietary fat overconsumption in a mouse model of obesity. Nat Commun 15, 2102. https://doi.org/10.1038/s41467-024-46009-0 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. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and its precursors (eg. NMN and NR). There are various types of NAD to be selected, encompassing NAD ER Grade (endoxin removal), NAD Grade I (IVD/dietary supplement/cosmetics raw powder), NAD Grade II (API/intermediates) and NAD Grade IV (if any higher requirement on the solubility), which can be provided in the form of lyophilized powder or crystalline powder. The purity of BONTAC NAD can reach above 98%. 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. BONTAC holds no responsibility 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.
Frontier Dynamics on the Molecular Mechanism of Ginsenoside Rh2 Against Tumor
Introduction Ginsenoside Rh2, one protopanaxadiol (PPD)-type rare ginsenoside in Panax ginseng, is uncovered to possibly have broad-spectrum pharmacological activity in diversified tumors. It is utilized as an adjuvant drug for preoperative neoadjuvant chemotherapy, postoperative adjuvant chemotherapy, and rescue treatment of advanced cancer, which has been a research hotspot in recent years. Current states on cancer therapies Cancer has emerged as the second largest cause for death across the world, with approximately 9.6 million cancer-related deaths in 2018, in accordance with the statistical report by World Health Organization (WHO). Radiotherapy, chemotherapy and surgery are the preferred option for cancer, whose efficacy is however limited by the tumor relapse and drug resistance, requiring a patch such as adjuvant drugs to fix the bug. For anticancer treatment, over 60% of the approved and pre-new drug application candidates are natural products or synthetic molecules based upon natural product molecular skeletons. Strikingly, ginsenosides act as a promising therapeutic target by virtue of its pharmacological activities such as immune adjustment, anti-tumor, anti-oxidation, and protection of the heart and cerebral vessels. 20(S) ginsenoside Rh2 vs. 20(R) ginsenoside Rh2 There are two stereoisomeric forms of ginsenoside Rh2, namely 20(S) ginsenoside Rh2 and 20(R) ginsenoside Rh2. Relative to the (20R) ginsenoside Rh2, (20S) ginsenoside Rh2 has higher cytotoxic activity towards cancer cells. In a previously reported study, the half maximal inhibitory concentration values of 20(S) ginsenoside Rh2 and 20(R) ginsenoside Rh2 in A549 cells are 45.7 and 53.6 µM, respectively. The underlying mechanisms of ginsenoside Rh2 against tumor Mechanically, the anti-tumor effects of ginsenoside Rh2 are realized by enhancing the body’s immune activity to regulate microenvironment, inhibiting differentiation, angiogenesis, proliferation, invasion, and metastasis of tumor cells, inducing the apoptosis, cell cycle arrest, autophagy, superoxide and reactive oxygen species, and reversing the drug resistance via regulating a series of important tumor-related signaling pathway. For instance, ginsenoside Rh2 can activate CD4+ and CD8a+ T lymphocytes, promote their invasion, and enhance the killing effect of lymphocytes on B16-F10 melanoma cells in a concentration-dependent manner. Besides, the number of tumor cells in the G0/G1 phase is increased significantly post treatment with ginsenoside Rh2 and 5-FU, by which the expansion and migration of tumor cells are effectively hampered. Additionally, the ginsenoside Rh2 downregulates the levels of drug-resistance-related genes (eg. MRP1, MDR1, LRP and GST), making colorectal cancer cells more sensitive to 5-FU. Conclusion Ginsenoside Rh2 plays multifunctional roles in both tumor treatment and tumor microenvironment immunomodulation, which may become a promising choice of medication for patients with tumors in the future. Reference [1] Xiaodan S, Ying C. Role of ginsenoside Rh2 in tumor therapy and tumor microenvironment immunomodulation. Biomed Pharmacother. 2022;156:113912. doi:10.1016/j.biopha.2022.113912 [2] Yang L, Chen JJ, Sheng-Xian Teo B, Zhang J, Jiang M. Research Progress on the Antitumor Molecular Mechanism of Ginsenoside Rh2. Am J Chin Med. Published online January 31, 2024. doi:10.1142/S0192415X24500095 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. BONTAC holds no responsibility for any claims, damages, losses, expenses, costs or liabilities resulting or arising directly or indirectly from your reliance on the information and material on this website.
SLC25A51 Functions as an NAD+/NADH Redox Decoupler in AML
Introduction Solute carrier family 25 member 51 (SLC25A51) is perceived as a mammalian transporter, which is capable of importing oxidized nicotinamide adenine dinucleotide (NAD+) into mitochondrial matrix. Remarkably, upregulation of SLC25A51 has correlation with poorer outcomes in patients with acute myeloid leukemia (AML), a clinically aggressive haematological disease with a mortality rate of over 70% within the first 5 years following an initial diagnosis. The association between NAD+/NADH ratio and SLC25A51 in AML cells Both NAD+ (oxidative form) and NADH (reduced form) are essential coenzymes for cellular energy metabolism, and the ratio of NAD+/NADH reflects the metabolic activity and health state, which has a direct impact on cellular rhythms, senescence, carcinogenesis and death. Importing mitochondrial NAD+ by SLC25A51 could be a critical aspect supporting mitochondrial metabolism in AML tumorigenesis. Concretely, the decreased mitochondrial NAD+/NADH ratio and specific loss of reduced ubiquinol are observed post the depletion of SLC25A51 in AML cells U937. SLC25A51 as an NAD+/NADH redox decoupler in AML SLC25A51 functions as an NAD+/NADH redox decoupler in AML tumorigenesis to sustain an oxidative TCA cycle and promote glutaminolysis. Depletion of SLC25A51 results in increased usage of non-glutamine carbon sources to support the TCA cycle, as determined by increased proportions of unlabeled TCA intermediates. SLC25A51 is required for robust glutaminolysis. In the context of SLC25A51 depletion, AML cells are forced to rely more on glutamine for aspartate synthesis. Alleviation of AML by SLC25A51 depletion and 5-azacytidine Loss of SLC25A51 leads to a subcellular redistribution of NAD+ in AML cells to limit proliferation. The combination of SLC25A51 depletion and 5-azacytidine is much effective in repressing the viability of AML cells and prolonging the survival time of mice. Conclusion SLC25A51 can maintain mitochondrial oxidative phosphorylation and boost the proliferation of AML cells by regulating NAD+/NADH ratio in mitochondria, with promising efficacy in treating AML, especially in combination with 5-azacytidine. 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.