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Why Choose BONTAC?
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.
NAD Drip: Materials, NAD Powder, and Effectiveness Explained
NAD Drip therapy, also known as IV NAD therapy, is gaining attention for its potential health benefits. In this comprehensive guide, we delve into the essential components of NAD Drip, including the standards for NAD drip materials, the role of NAD powder in the process, and its effectiveness in promoting overall well-being.
- NAD Drip Materials Standards
- Quality Assurance in Material Selection:
For an effective NAD Drip, ensuring the highest standards in material selection is paramount. IV bags, tubing, and other equipment must meet stringent quality standards to guarantee patient safety and the proper administration of NAD.
- Sterilization and Safety Protocols:
Safety protocols, including sterilization, must be rigorously maintained. The materials involved in the NAD Drip process should adhere to industry best practices for cleanliness and patient safety.
- Professional Administration:
Trained healthcare professionals are essential for administering NAD Drip safely and effectively. Adequate training and certification of personnel are part of the materials standard.
- NAD Powder in NAD Drip
- The Role of NAD Powder:
NAD (Nicotinamide Adenine Dinucleotide) powder is a crucial component of NAD Drip therapy. It is a bioavailable form of NAD that is dissolved in a sterile saline solution for intravenous infusion.
- Purity and Quality:
The quality and purity of NAD powder are vital. The best NAD powder is produced using high-quality raw materials and rigorous manufacturing standards to ensure the absence of impurities or contaminants.
- Dosage and Customization:
NAD Drip therapy can be tailored to individual needs through the precise control of NAD powder dosage. Customized dosages can be formulated based on a patient's specific requirements.
- NAD Drip Effectiveness
- Boosting Cellular Energy:
NAD Drip therapy is believed to enhance cellular energy production by increasing NAD levels in the body. This has potential benefits for overall vitality and performance.
- Anti-Aging Properties:
NAD Drip therapy is also associated with potential anti-aging effects, as NAD plays a key role in DNA repair and cell rejuvenation.
- Support for Wellness:
Many individuals turn to NAD Drip therapy to support general wellness, particularly in conditions related to fatigue, oxidative stress, and age-related health concerns.
NAD Drip therapy is a promising avenue for those seeking to optimize their well-being. Ensuring the highest standards for NAD Drip materials, the quality of NAD powder, and understanding its potential effectiveness is essential for a safe and successful therapy experience.
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Frequently Asked Question
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Nicotinamide adenine dinucleotide (NAD) has several essential roles in metabolism. It acts as a coenzyme in redox reactions, as a donor of ADP-ribose moieties in ADP-ribosylation reactions, as a precursor of the second messenger molecule cyclic ADP-ribose, as well as acting as a substrate for bacterial DNA ligases and a group of enzymes called sirtuins that use NAD+ to remove acetyl groups from proteins. In addition to these metabolic functions, NAD+ emerges as an adenine nucleotide that can be released from cells spontaneously and by regulated mechanisms, and can therefore have important extracellular roles.
First, inspect the factory. After some screening, NAD companied that directly face consumers pay more attention to brand building. Therefore, for a good brand, quality is the most important thing, and the first thing to control the quality of raw materials is to inspect the factory. Bontac company actually manufacturing NAD powder of high quality with the caterias of SGS. Secondly, the purity is tested. Purity is one of the most important parameters of NAD powder. If high purity NAD cannot be guaranteed, the remaining substances are likely to exceed the relevant standards. As the attached certificates demonstrates that the NAD powder produced by Bontac reach the purity of 99.9%. Finally, a professional test spectrum is needed to prove it. Common methods for determining the structure of an organic compound include Nuclear Magnetic Resonance Spectroscopy (NMR) and high-resolution mass spectrometry (HRMS). Usually through the analysis of these two spectra, the structure of the compound can be preliminarily determined.
The difference all comes down to the charge of these coenzymes. NAD+ is written with a superscript + sign because of the positive charge on one of its nitrogen atoms. It is the oxidized form of NAD. It’s considered “an oxidizing agent” because it accepts electrons from other molecules.
Although they are different chemically, these terms are mostly used interchangeably when discussing their health benefits. Another term you may come across is NADH, which stands for nicotinamide adenine dinucleotide (NAD) + hydrogen (H). This is also used interchangeably with NAD+ for the most part. Both are nicotinamide adenine dinucleotides that function as either hydride donors or hydride acceptors. The difference between these two is that that NADH becomes NAD+ after it donates an electron to another molecule.
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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.
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.
Deciphering Another Mechanism of Action for NMN Administration: Improving Lysosomal Ferroptosis to Prevent Heart Failure
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.