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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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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.
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Metabolites of Rg3 are Expected to Increase the Anti-cancer Properties of Rg3
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.
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.
Health Upgrade: Focus on the Therapeutic Effect of Ginsenoside Rh2
1. Introduction Ginseng has always been highly perceived as a valuable traditional Chinese medicine in China. Currently, much attention also has been paid to ginsenosides, the main active ingredients extracted from ginseng. Strikingly, ginsenoside Rh2, one of the most representative bioactive ginsenosides in Panax ginseng, has immunomodulatory, anti-inflammatory, and anti-tumor activities, showing a therapeutic role in numerous diseases. 2. The therapeutic effect of ginsenoside Rh2 * Enhance the immune function of the human body Ginsenoside Rh2 has the effect of enhancing the immune function of the patient's body. Notewothily, it can effectively reduce the toxicity left by chemotherapy in the human body by improving immunity. *Ameliorate neuropathic pain Intrathecal administration of ginsenoside Rh2 significantly attenuates SNI-induced mechanical allodynia and thermal hyperalgesia. The antinociceptive effect of Rh2 continued until 10 days after SNI surgeryn, showing a potential application value in pain therapy. Figure 1 Intrathecal injection of Rh2 inhibits neuropathic pain in mice * Suppress the inflammation Previous studies have revealed that ginsenoside Rh2 can inhibit spared nerve injury (SNI)-induced increase of proinflammatory cytokines (tumor necrosis factor-α, interleukin-1 and interleukin-6), and significantly inhibit lipopolysaccharide (LPS)-induced activation of BV2 cells. Figure 2 Intrathecal injection of Rh2 reduced expression of proinflammatory cytokines IL-1, IL-6 and TNF-α in SNI mice * Promote the synthesis of albumin Ginsenoside Rh2 acts as an immune regulator to promote the synthesis of albumin, which can provide heat for the human body, protect and stabilize the immunoglobulin in the blood. * Inhibit the growth of tumor cells Ginsenoside Rh2 exhibits a chemical structure similar to that of dexamethasone. In in vitro studies, it can suppress the growth and viability of various cancer cells, induce tumor cell cycle arrest and cellular apoptosis, trigger necrosis and autophagy in cancer cells, inhibit metastasis, and suppress angiogenesis. * Reversal of abnormal tumor differentiation Ginsenoside Rh2 has a differentiation-inducing effect on tumor cancer cells, and can effectively enhance the melanin production ability in cancer cells, thereby causing cancer cells to transform into normal cells in morphology. Table 1 Anticancer effects and mechanisms of ginsenoside‑Rh2 in in vivo studies 3. The difference between ginsenoside Rg3 and ginsenoside Rh2 Figure 3 Molecular struction of ginsenoside Rg3 and ginsenoside Rh2 Both ginsenoside Rg3 and ginsenoside Rh2 have been attested to achieve antitumor effects by strengthening the immune function of the body. Despite their similar mechanisms of action, differences still exist between ginsenoside Rg3 and ginsenoside Rh2. In terms of the molecular structure, ginsenoside Rh2 has only one glycosyl group, whereas ginsenoside Rg3 has two. In addition, ginsenoside Rh2 has a higher bioavailability than ginsenoside Rg3. Ginsenoside Rg3 is easy to be excreted from the body after being taken, and won't make much difference to the body. With regard to the intestinal absorption, ginsenotone Rh2 is about 5 times of ginsenotone Rg3. 4. Conclusion The monosaccharide ginsenoside Rh2 can effectively improve human immunity, enhance disease resistance, and reduce the risk of cancer. Relative to ginsenoside Rg3, ginsenoside Rh2 shows higher cost-efficiency in the intestinal absorption, application scope and efficacy, providing an upgraded health support. Product Features and advantages of BONTAC Ginsenoside Rh2 One-stop product solution customization service Multiple patents and strict third-party self-inspection The first national mass production of ginsenosides by enzymatic synthesis Unique Bonzyme enzymatic synthesis technology Reference [1] Fu, Yuan-Yuan et al. Ginsenoside Rh2 Ameliorates Neuropathic Pain by inhibition of the miRNA21-TLR8-mitogen-activated protein kinase axis. Molecular pain. 2022;18:17448069221126078. doi:10.1177/17448069221126078 [2] He XL, Xu XH, Shi JJ, et al. Anticancer Effects of Ginsenoside Rh2: A Systematic Review. Curr Mol Pharmacol. 2022;15(1):179-189. doi:10.2174/1874467214666210309115105 Disclaimer BONTAC shall hold no responsibility for any claims arising directly or indirectly from your reliance on the information and material on this website.