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.
It is a naturally occurring substance in humans and organisms. Judging from the fact that breast milk contains NMN, it can be said to be one of the nutrients that humans ingest at the beginning of life. Yellow and green vegetables also contain NMN, so it is different from medicine. NMN is a food of natural origin and is safe.
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.
1. Introduction Mitochondria are the center of energy metabolism in cardiomyocytes, which are necessary for maintaining normal myocardial contractility and cardiac function. Typically, the development of cardiovascular disease is usually accompanied by mitochondrial dysfunction. Impaired autophagy is known to cause mitochondrial dysfunction and heart failure, in part due to altered mitophagy and protein quality control. Notably, external replenishment of nicotinamide adenine dinucleotide (NAD+) precursors can enhance autophagy and mitochondrial quality control to maintain metabolic health, thereby regulate mitochondrial and cardiac function. 2. NAD+ metabolism in mitochondrial and cardiac function Cardiomyocytes accumulate NAD+ mostly within their mitochondria, where the bulk of cellular oxidation-reduction reactions occur. However, NAD+ is also present in the cytosol and nucleus, in which NAD+-derived metabolites and NAD+-dependent enzymes contribute to various cellular functions. 3. Mitochondrial and cardiac dysfunction induced by NAD+ deficiency Mitochondrial and cardiac dysfunction triggered by NAD+ deficiency is alleviated in cAtg3-KO mouse hearts post the administration of β-nicotinamide mononucleotide (NMN), as evidenced by the restoration of citrate synthase (CS) activity, partial normalization of ATP level and NPPB mRNA expression in cAtg3-KO mice as well as upregulation of ADP level in WT mouse hearts. Besides, NNMT inhibition can rescue mitochondrial and cardiac dysfunction in cAtg3-KO mice by restoring NAD+ level. 4. The impact of autophagic flux upon cardiac and mitochondrial function Autophagy is an intracellular degradation pathway that recycles subcellular components, playing a critical in modulating metabolic homeostasis. Autophagic flux, a central homeostatic mechanism that degrades materials toxic to cardiomyocytes, can mediate SQSTM1-NF-κB-NNMT signal transduction to control the cellular level of NAD+, thereby maintaining the mitochondrial and cardiac function. 5. Conclusion Autophagic flux may be a potential way to maintain the cellular level of NAD to regulate mitochondrial and cardiac fiunction. . Reference [1] Abdellatif M, Sedej S, Kroemer G. NAD+ Metabolism in Cardiac Health, Aging, and Disease. Circulation. 2021;144(22):1795-1817. doi:10.1161/CIRCULATIONAHA.121.056589 [2] Zhang Q, Li Z, Li Q, et al. Control of NAD+ homeostasis by autophagic flux modulates mitochondrial and cardiac function. EMBO J. Published online January 11, 2024. doi:10.1038/s44318-023-00009-w About BONTAC BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and NMN. Bonzyme whole-enzymatic method is adopted, which is environmental-friendly, with no harmful solvent residues. The purity of products can reach up to 95%, which is benefited from the exclusive Bonpure seven-step purification technology. BONTAC has self-owned factories and has obtained a number of international certifications, where high quality and stable supply of products can be ensured. BONTAC has over 160 domestic and foreign patents, leading the industry of coenzyme and natural products. In the future, BONTAC will actively expand the international market, and work with global partners to promote the prosperous development of synthetic biology industry. In this era full of challenges and opportunities, BONTAC is confident to make greater contributions to the cause of human health. 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.
1. Introduction Heart failure is a serious condition in the development of cardiovascular disease. In particular, diastolic heart failure, as one of the most common manifestations of heart failure in the elderly, has always been viewed as a classic aging-related terminal illness due to its high prevalence and lack of effective treatment. Nicotinamide mononucleotide (NMN) raises the hope for the treatment of this illness. NMN can restore the functions of heart and blood vessels, protect the heart from damage after a heart attack, prevent heart failure by promoting the health of the mitochondria, and restore cardiovascular, cognitive, and metabolic decline. This study is dedicated to deciphering another mechanism of action for NMN administration, namely improving lysosomal ferroptosis to prevent heart failure. 2. The key pathogenesis of diastolic heart failure The effect of NMN on improving cardiac function is mainly realized by elevating the level of myocardial nicotinamide adenine dinucleotide (NAD+), an important coenzyme in the tricarboxylic acid cycle. The mitochondrial dysfunction and decreased ability of NAD+ biosynthesis are the key pathogenesis of diastolic heart failure. 3. Restoration of lysosomal function and autophagic function by NMN administration Lysosomal function is impaired owing to decreased NAD+ biosynthesis in vivo. NMN administration improves lysosomal function and activates amino acid metabolism in the mice with cardiomyocyte-specific knockout of p32 (p32cKO), yet barely affects the lysosomal morphology. Additionally, NMN administration improves the degradation mechanism of autophagy, as evidenced by the restoration of autophagic function post NMN administration. 4. The detailed mechanism of action for NMN administration on heart failure NMN administration does not restore functional mitochondrial damage caused by the inhibition of mitochondrial translation. These findings suggest that NMN administration improves heart failure by improving lysosomal function without improving mitochondrial function. 5. The involvement of ferroptosis in heart-specific mitochondrial translation defect The suppression of ferroptosis ameliorates heart failure. The expression levels of ferroptosis-related factors (Chac1, GPX4, and Ho1) are also diminished by NMN, indicating that ferroptosis in the p32cKO heart is improved by NMN administration. 6. The improvement of mitochondrial dysfunction-induced ferroptosis by NMN administration The ferroptosis is induced in the p32 knockdown cells, as attested by the mitochondrial translation defect and the downregulation of intracellular NAD+ and NADH levels. The induction of ferroptosis in lysosome is closely related to the amount of NAD+ biosynthesis. When intracellular NAD+ level is lowered, the intracellular iron deposition and lipid peroxide are induced, which however are ameliorated by NMN administration. 7. Conclusion Mechanically, NMN administration can prevent heart failure by improving lysosomal ferroptosis, opening up new insight for the treatment of this illness. Reference Yagi, Mikako et al. “Improving lysosomal ferroptosis with NMN administration protects against heart failure.” Life science alliance vol. 6,12 e202302116. 4 Oct. 2023, doi:10.26508/lsa.202302116 BONTAC NMN product features and advantages * “Bonzyme” Whole-enzymatic method (environmental-friendly; no harmful solvent residues) * Exclusive “Bonpure” seven-step purification technology, with high purity (up to 99.9%) and stability * Industrial leading technology: 15 domestic and international NMN patents * Self-owned factories and a number of international certifications to ensure high quality and stable supply of products * One-stop customized service for product solution * NMN raw material supplier of famous David Sinclair team of Harvard University 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.