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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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Application Value of Ginsenoside Rg3 in Targeting BCSCs to Treat Breast Cancer
Introduction Ginsenoside Rg3 is Panaxanediol type tetracyclic triterpenoid saponin monomer extracted from the root of Panax ginseng, which has a wide range of pharmacological effects including anti-tumor, neuroprotection, cardiovascular protection, anti-fatigue, anti-oxidation, hypoglycemia, and enhancement of immune function. This research unveils the potential value of ginsenoside Rg3 in targeting breast cancer stem cells (BCSCs) to treat breast cancer, one of the most common tumor worldwide with significant morbidity and mortality. Ginsenoside Rg3 as anticancer adjuvant Ginsenoside Rg3 can promote the apoptosis of tumor cells, and inhibit tumor growth, infiltration, invasion, metastasis and neovascularization. At the same time, it has the effect of reducing toxicity, increasing efficacy in the joint application with chemotherapeutic drugs, improving immunity of the organism, and reversing multi-drug resistance of tumor cells. Shenyi capsule, a new anticancer drug with ginsenoside Rg3 monomer as the main component, was approved by China FDA and marketed in 2003, which is mainly used in the adjuvant treatment of various tumors. About BCSCs Breast cancer stem cells (BCSCs) are a group of undifferentiated cells with strong ability of self-renewal and differentiation, which is the main reason for poor clinical outcomes and poor efficacy. BCSCs can clonally proliferate under serum-free three-dimensional culture conditions and form mammospheres. BCSCs have specific surface markers (CD44, CD24, CD133, OCT4 and SOX2) or enzymes (ALDH1). BCSCs function as potential drivers of breast cancer, which are resistant to conventional breast cancer clinical treatments such as radiotherapy, leading to breast cancer recurrence and metastasis. The suppressive effect of ginsenoside Rg3 in the progression of breast cancer Ginsenoside Rg3 exerts inhibitory effects on the viability and clonogenicity of breast cancer cells in a time- and dose-dependent manner. In addition, it suppresses mammosphere formation, as evidenced by the spheroid number and diameter. Furthermore, ginsenoside Rg3 reduces the expression of stem cell-related factors (c-Myc, Oct4, Sox2, and Lin28), and decreases the ALDH (+) subpopulation breast cancer cells. Ginsenoside Rg3 as an accelerator of MYC mRNA degradation Ginsenoside Rg3 depresses BCSCs mainly through downregulating the expression of MYC, one of the main cancer stem cell reprogramming factors with a pivotal role in tumor initiation. Its regulatory effect on MYC mRNA stability is chiefly achieved by promoting the microRNA let-7 cluster. Under normal conditions, the let7 family is expressed at low levels in cancer cells, resulting in stable MYC mRNA expression and high c-Myc expression. However, Rg3 treatment leads to the upregulation of let-7 cluster, impairment of MYC mRNA stability, downregulation of c-Myc expression and inhibition of breast cancer stem-like properties. Conclusion The traditional Chinese herbal monomer ginsenoside Rg3 has the potential to suppress breast cancer stem-like properties by destabilizing MYC mRNA at the post-transcriptional level, showing great promise as adjuvant for the treatment of breast cancer. Reference Ning JY, Zhang ZH, Zhang J, Liu YM, Li GC, Wang AM, Li Y, Shan X, Wang JH, Zhang X, Zhao Y. Ginsenoside Rg3 decreases breast cancer stem-like phenotypes through impairing MYC mRNA stability. Am J Cancer Res. 2024 Feb 15;14(2):601-615. PMID: 38455405; PMCID: PMC10915333. 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 for any claims, damages, losses, expenses, or costs whatsoever resulting or arising directly or indirectly from your reliance on the information and material on this website.
The Prospect of the NAD+ Precursors in Age-related Diseases
1. Introduction Age-related NAD+ depletion affects physiological functions and contributes to various aging-related diseases. NAD+ precursors can significantly elevate NAD+ level in murine tissues, effectively mitigate metabolic syndrome, enhance cardiovascular health, protect against neurodegeneration, and boost muscular strength, with broad prospect in the anti-aging-related field. 2. The synthesis and metabolism of NAD+ in age-related pathologies NAD+ is synthesized from NAD+ precursors and amino acids tryptophan via three main pathways: De novo, Preiss-Handler, and Salvage. Supplementation of NAD+ precursors can be advantageous in maintaining normal cellular metabolism regulated by NAD+ and NAD+-dependent enzymes such as Sirtuins, PARP, CD38, and SARM1. NAD+ intermediates require conversion into NA to elevate NAD+ level. NAD+ and its metabolism-related enzymes have very important roles in biological processes such as cellular metabolic processes, gene expression, apoptosis and carcinogenesis. NAD+ repletion is drawing attention as an anti-aging intervention. NAD+ precursors, such as NA, NAM, NR, and NMN, provide beneficial effects in various preclinical disease models of age-induced deficits, including metabolic disorders, cardiovascular, neurodegenerative diseases, and musculoskeletal diseases. 3. Comparison on the efficacy of replenishing NAD precursors in pre-clinical studies and clinical studies in age-related pathologies The downregulation of NAD+ level in cells and tissues is not a universal phenomenon for aging-related pathologies. NAD+ merely decreases with age in certain tissues. The efficacy of NAD+ precursors in clinical studies has been limited in comparison with that in the pre-clinical studies. Noteworthily, this issue can be addressed as long as much attention has been paid to the metabolism of NAD. With regards to the oral supplementation of NAD+ precursors, there is obvious link between NAD metabolism and gut microbes. Specifically, oral consumption of NMN is converted into NAMN through interaction with the gut microbiome. In addition, dietary NAM and NR are converted into NA through gut microbiota. 4. Future research directions regarding the NAD+ metabolism It is fundamental to consider how the gut microbiome affects NAD+ metabolism, and changes in microbiome composition may affect the availability of NAD+ precursors. Future studies also require the comparative analysis of different precursors, and the role of gut microbiomes regarding various intermediaries needs to be investigated. Assessment of how NAD+ precursors affect microbiota and how their interaction with NAD+ metabolism benefits the physiological condition is essential for future preclinical and clinical studies. 5. Conclusion Supplementation of suitable NAD+ precursors or intervening in NAD+ metabolism can restore the body's NAD+ level, which is of great practical significance for effectively improving aging-related diseases and prolonging healthy life span is of great practical significance for effectively improving aging-related diseases and prolonging healthy life span. NAD metabolism involves gut microbiome, and in-depth research on their interaction is possibly an important breakthrough in the future to combat aging-related pathologies. Reference Iqbal T, Nakagawa T. The therapeutic perspective of NAD+ precursors in age-related diseases. Biochem Biophys Res Commun. Published online February 2, 2024. doi:10.1016/j.bbrc.2024.149590 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 160 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. BONTAC holds no responsibility for any claims, damages, losses, expenses, costs or liabilities whatsoever 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.