L-Glutathione Reduced
Home > NMN
Products

99% NMN Powder

Product parameters
Trade Name: Cosroma® NMN
Product Name: β-Nicotinamide Mononucleotide
Other Names: Nicotinamide Mononucleotide; β-NMN; NMN
CAS No.: 1094-61-7
Form: Powder
Origin: Enzymatic Method
Assay: 99.0-102.0%
Solid Content: Food Grade
Certification: ISO9001; ISO 14001; ISO 18001
Packing Sizes: 0.1kg, 0.5kg, 1kg, 10kg, 25kg
INQUIRY
Description
NMN is a reaction product of Nicotinamide phosphate ribose transferase (Nampt) and is one of the key precursors of NAD+. In mammals, NMN is produced by Nicotinamide (Nam) under the catalysis of Nampt, and then NMN is produced under the catalysis of Nicotinamide mononucleotide adenosine transferase (Nmnat) to produce NAD+. Extracellular NMN needs to be dephosphorylated and converted to Nicotinamide riboside (NR) before it can enter the liver cell. After entering the cell, NR is phosphorylated under the action of Nicotinamide riboside kinase NRK1) to produce NMN, and then NMN and ATP are combined to produce NAD+. NMN is converted into NAD+ in the human body to exert its physiological functions, such as activating the NAD+ substrate-dependent enzyme Sirt1 (histone deacetylase, also known as sirtuin), regulating cell survival and death, and maintaining redox state. Recent studies have found that by regulating the level of NMN in the organism, it has a better therapeutic and repairing effect on cardiovascular and cerebrovascular diseases, neurodegenerative diseases, and aging degenerative diseases; in addition, NMN can also play a role by participating in and regulating the bodys endocrine. To protect and repair pancreatic islet function, increase insulin secretion, prevent and treat metabolic diseases such as diabetes and obesity.
 
1 Biological activity of NMN
1.1 NMN relieves and improves ischemic heart and brain tissue damage
1.1.1 The therapeutic effect of NMN on stroke. Stroke is an acute cerebrovascular disease caused by blood circulation disorder in the brain. It has a high mortality and disability rate, and seriously threatens human health. Studies have found that NMN can protect brain nerves and promote blood vessel and nerve regeneration by activating the Nampt-NAD+ defense system. It has a good protective effect on cerebral hemorrhage and nerve damage caused by cerebral hemorrhage transformation. It is a potential anti-stroke treatment drug. Park et al. analyzed the metabolic process of NMN in brain tissue and found that NMN prevents neuronal cell apoptosis induced by cerebral ischemia by improving tissue bioenergy metabolism after ischemia, and promotes nerve regeneration after cerebral ischemia. Blood brain injury has a strong protective effect. For hemorrhagic brain injury, increasing the level of NMN can reduce the hemoglobin content in the infarcted tissue, reduce bleeding and edema, and reduce the oxidative toxic damage of brain tissue caused by oxidative stress. In addition, Wei Chunchun and his team further researched that: NMN enhanced the expression of two cytoprotective proteins, namely nuclear factor-erythroid 2 related factor 2 (Nrf2) and heme oxygenase (Heme oxygenase). , HO-1), activates the Nrf2/HO-1 signaling pathway, inhibits cranial nerve inflammation and oxidative stress, and reduces the damage after intracerebral hemorrhage.
 
1.1.2 Therapeutic effect of NMN on cardiac ischemia and reperfusion
Reperfusion after cardiac ischemia is a life-threatening ischemic injury, which is accompanied by inevitable cardiomyocyte death and severe organ dysfunction. Ischemic preconditioning (IPC) is an endogenous defense mechanism mediated by Sirt1 that can protect myocardial viability during transient ischemia and reperfusion. Yamamoto and other studies have shown that NMN can protect the heart by simulating the protective effect of IPC. After ischemia, the NAD+ content in the heart decreases. Exogenous NMN can increase the NAD+ and NADH content in the heart and reduce the infarct size. The data show that the reduction of the infarct size by NMN is positively correlated with the Sirt1 expression level. In addition, the expression level of Nampt in the heart will be down-regulated under pathological conditions, such as ischemia, ischemia-reperfusion and pressure overload, which in turn affects the biosynthesis of NAD+, destroys the regulatory mechanism of Sirt1 activity, and leads to pressure overload mice Cardiomyocyte apoptosis, cardiac decompensation. Studies by Masamichi and others have shown that in model mice of heart failure, NMN treatment restores the NAD+ level in cardiomyocytes, increases the deacetylase activity of Sirt1 and the expression level of genes related to mitomycin function.
 
1.2 NMN improves oxidation-related degenerative diseases and physical dysfunction
1.2.1 The therapeutic effect of NMN on Alzheimer's disease With the acceleration of social aging, the incidence of Alzheimer's disease (AD) is increasing year by year. The disease is a central nervous system disease, characterized by cognitive dysfunction and memory impairment. Abnormality of mitochondrial structure and function is one of the pathogenesis factors of AD, and NMN promotes the energy metabolism of mitochondria and plays an important role in improving cognitive function and memory function. Long Aaron et al. found that when the level of NMN in the body is increased, the availability of NAD+ increases immediately, which increases the mitochondrial oxygen consumption rate (OCR), promotes mitochondrial fusion, reduces the tendency of fission, and makes mitochondria produce longer mitochondria in the hippocampal subregion. Thereby improving the respiratory function of mitochondria. β-amyloid protein oligomer (Amyloidβprotein, Aβ) is considered to be the main neurotoxic agent that causes AD. XiaonanWang et al. found that NMN improves the cognitive and memory functions of Alzheimers disease rats caused by Aβ1-42 oligomers, restores NAD+ and ATP levels, and reduces The accumulation of ROS (reactive oxygen species) in hippocampal slices of AD mice. Zhiwen Yaos research found that NMN improves the behavioral cognitive impairment of AD mice by activating c-Jun N-terminal kinase (JNK), inhibits the production of β-amyloid, and reduces the nervous system Amyloid plaque burden, synaptic damage and inflammation. The above experiments show that NMN can be used as a potential drug for the treatment of AD.
 
1.2.2 The therapeutic effect of NMN on Parkinson's disease
Parkinson's disease (PD) is characterized by motor symptoms such as bradykinesia, resting tremor, rigidity, abnormal gait and posture, as well as non-motor symptoms such as hypoosmia, anxiety and depression, and constipation. It is a kind of disease that usually occurs in the elderly. Degenerative diseases of the human central nervous system. The pathogenesis of the disease is relatively complicated and is still unclear, so there is almost no effective treatment. LEI LU and other studies have shown that: NMN can increase the survival rate of nerve cells, reduce cell apoptosis, restore NAD+ and ATP levels, inhibit cell apoptosis, resist energy damage, and improve energy metabolism disorders induced by mitochondrial inhibitors. Compared with Alzheimer's disease, there are fewer studies on the effect of NMN on Parkinson's disease, and more in vivo experimental data are needed to prove its effectiveness.
 
1.2.3 The therapeutic effect of NMN on vascular disorders
Another serious health-threatening disease related to aging is cardiovascular disease (CVD), which has the characteristics of high morbidity, high disability, and widespread harm to the population. This type of disease is mainly due to the imbalance between the oxidation system and the antioxidant system after the body ages, and the accumulation of superoxide in the blood vessels causes the body's oxidative damage. Picciotto and other studies have found that supplementation of NMN can reduce vascular oxidative stress, improve aortic sclerosis and vascular dysfunction; supplementation of NMN can reduce the accumulation of collagen in the entire blood vessel, increase the accumulation of arterial elastin, reduce arterial stiffness, and delay the progression with age Artery aging due to growth. NMN mainly increases the bioavailability of NAD+ in the vascular system, restores the activity of Sirt1 in the arteries, and improves endothelial dysfunction and large elastic arteriosclerosis caused by aging. NMN can also increase the level of NADPH (reduced nicotinamide adenine dinucleoside phosphate) to maintain glutathione and sulfur by enhancing the metabolic flux of the tricarboxylic acid cycle and the electron transport chain, reducing the accumulation of reactive oxygen species in the cell, and increasing the level of NADPH (reduced nicotinamide adenine dinucleoside phosphate). Oxidation protein antioxidant system. In addition, NMN can also improve lipid distribution in plasma and maintain blood sugar levels, thereby improving vascular function.
 
1.2.4 The therapeutic effect of NMN on acute kidney injury
The morbidity and mortality of acute kidney injury (Acute kidney injury, AKI) have been increasing year by year, which has attracted more and more attention. Yi Guan and other studies have shown that the levels of Sirt1 and NAD+ decrease with age; the reduction of NAD+ and Sirt1 in the kidneys of elderly organisms will lead to an increase in the susceptibility of AKI; supplementation of NMN can protect mice from cisplatin (which can be used to inhibit DNA replication) induced AKI; the mechanism of NAD+/Sirt1 protecting the kidney involves the epigenetic regulation of the JNK pathway; in vitro, Sirt1 attenuates the stress response by regulating the JNK signaling pathway. In the elderly, endogenous NAD+ is considered to be a potential therapeutic target of AKI. Supplementing the intermediate NMN of NAD+ is a good treatment strategy.
 
1.2.5 The anti-aging effect of NMN,
The study by Mills found that NMN can significantly improve the age-related physiological decline in mice, such as inhibiting age-related weight gain, enhancing energy metabolism, improving insulin sensitivity and lipid distribution in plasma, and improving Eye function; NMN prevents age-related gene expression changes in a tissue-specific manner, and enhances the oxidative metabolism of mitochondria in skeletal muscle, at least partially mediating its anti-aging effects. Kawamura and other studies have shown that in rats, NMN, which is a candidate compound for anti-aging, has a longer retention time than Nam. Because Nampt is inhibited by NAD+, Nam is not converted to NAD+ through the NamNMNNAD+ pathway, but through Namnicotinic acid (NiA)nicotinic acid mononucleotide (NaMN)nicotinic acid adenine dinucleotide (NaAD) )NAD+ pathway to produce NAD+; on the other hand, NAD+ synthesis from NMN is not regulated by cellular NAD+ levels, so it is easier to increase NAD+. According to the metabolic control mechanism and many reports on NMN, NMN may be more effective than Nam as a precursor of NAD+. Because Sirt1 is an NAD+-dependent enzyme, supplementation of NMN accelerates the turnover of NAD+ salvage biosynthesis, thereby activating the Sirt1 reaction. Sirt1 can induce DNA silencing, helping to fight aging and prolong life. In addition to mammals, studies have also shown that enhancing NAD+ biosynthesis can extend the lifespan of yeast, worms and flies.
 
1.2.6 The therapeutic effect of NMN on degenerative diseases of vision
The causes of visual impairment are complex and diverse, but photoreceptor death is the end point of many blinding diseases. Photoreceptors constitute an important part of the neurosensory retina, which is one of the most metabolically active tissues in the body. Research by Lin et al. showed that multiple mouse models of retinal dysfunction (light-induced degeneration, streptozotocin-induced diabetic retinopathy, and age-related retinal dysfunction) all show early retinal NAD+ deficiency, and NAD+ is not only in Each step of the tricarboxylic acid cycle and glycolysis performs the function of coenzyme, and can maintain the best Sirt3 activity. Sirt3 and Sirt5 play an important role in retinal homeostasis. The lack of NAD+ causes a variety of metabolic dysfunctions (such as glycolytic dysfunction and mitochondrial dysfunction), and the inability to respond appropriately to metabolic stress, which ultimately leads to Death of photoreceptors and retinal degeneration. The researchers found that supplementation of NMN can restore normal basic glycolysis, mitochondrial function and the ability to adapt to metabolic stress in mice, reduce photoreceptor cell death, and significantly improve dark vision and retinal function. These conclusions support the possibility of using NAD+intermediate NMN to treat retinal degenerative diseases, establish a unified therapeutic target for ophthalmic degenerative diseases, and provide a powerful treatment approach. Because it can be implemented for multiple diseases with multiple pathogenic mechanisms, once it is successfully implemented, the impact of this treatment strategy will be far-reaching.
 
1.3 The therapeutic effect of NMN on metabolic diseases
1.3.1 The therapeutic effect of NMN on type 2 diabetes
Chronic inflammation is an important factor in causing pancreatic β-cell failure in Type 2 diabetes mellitus (T2DM). Exposure to pro-inflammatory cytokines such as Interleukin 1β (IL1β); Tumor necrosis factor α (Tumor necrosis factor α) , TNFα), can cause the death of pancreatic β cells and inhibit insulin secretion. Since the pancreas lacks iNAMPT (intracellular Nampt), the pancreatic islets rely on circulating eNAMPT (extracellular Nampt) to stimulate insulin secretion. NMN can restore eNampt levels, re-verse the state of impaired insulin secretion, and protect pancreatic islets from the negative effects of pro-inflammatory factors. Caton et al. found that NMN can improve islet dysfunction in high fructose (FRD) mice, re-verse FRD and pro-inflammatory cytokine-mediated changes in the expression of islet marker genes, reduce the expression of pro-inflammatory factors, and restore insulin secretion. Improve cytokine Nampt-mediated islet dysfunction. Taken together, NMN improves pancreatic islet function in FRD mice, which is related to beneficial changes in gene expression involved in glucose metabolism, anti-inflammatory and apoptosis processes.
 
1.3.2 The therapeutic effect of NMN on obesity
Obesity is closely related to the development of type 2 diabetes. Type 2 diabetes is mainly due to the inability of pancreatic islets to produce enough insulin and the decreased sensitivity of glucose metabolism tissues to insulin. Obesity leads to adipose tissue dysfunction, increased release of pro-inflammatory cytokines, and increased secretion of fat synthase, all of which promote the damage of pancreatic β-cells. NMN can improve the islet dysfunction and restore insulin secretion by catalyzing the biosynthesis of mammalian NAD+. Spinnler et al. found that Nampt and NMN have no direct effect on the viability of human pancreatic β cells, nor will they cause apoptosis, but they can enhance glucose-stimulated insulin secretion and increase the level of NAD+. Exercise is an effective means to fight against obesity. This is because exercise leads to an increase in NAD+ levels and enhances mitochondrial energy metabolism. NMN can also increase the level of NAD+, so theoretically applying NMN can achieve the same weight loss effect as exercise. Stromsdorfer et al. compared mice with intraperitoneal injection of NMN and exercised mice, and the results showed that supplementation of NMN increased fat catabolism and increased the level of NAD+ in the liver, while exercise mainly increased the level of NAD+ in the muscle, suggesting that it is based on NAD+ precursors. NMN is used to treat obesity-related liver diseases such as non-alcoholic fatty liver disease.
 
2 Application status of NMN
2.1 Application of NMN in medical care
In view of the above-mentioned biological activity of NMN, the development of drugs with NMN as the active ingredient has become a medical hot spot. Huizenga in the United States invented a set of compositions containing NAD+, NMN, NR and other active ingredients, which can be used for anti-aging and antioxidant treatment. Akihiro of Yoshida University and others have invented NMN, NR and their salts as raw materials, which can be used to treat corneal disorders. Imai of the University of Washington has developed treatments to improve age-related obesity, high fat, and type 2 diabetes, and drugs that use NMN as the active ingredient. Douglas et al. invented methods for evaluating and treating vascular endothelial disorders and drugs with NMN as the active ingredient. Michael et al. developed NMN modulators (a neuroprotective drug), which can be used to treat neurodegenerative diseases.
 
2.2 Application of NMN in food
NMN is widely found in natural foods. NMN is found in vegetables, fungi, meat and shrimp. Ummarino et al. also found that NMN exists in human milk and donkey milk through a new enzyme coupling technology, and the content of human milk is higher. The study of processing characteristics found that the activity of NMN was stable after treatment at 75°C for 5 min in water or milk; the activity loss was about 20% after treatment at 95°C for 5 min, which indicated that it is theoretically feasible to add NMN to pasteurized milk. Another oral experiment] showed that taking a lower concentration of NMN, NMN can be quickly absorbed within 30 minutes, effectively transported to the blood circulation, and immediately converted into NAD+ in the main metabolic tissues. In addition, in the anticipation of continuous 12 months, NMN did not show any obvious toxicity and lethality, nor did it have serious side effects, and has high food safety].
 
Currently, Megumi of Japan has developed a food composition of NMN and resveratrol. Resveratrol is a natural polyphenol compound, which can act as estrogen. It has antioxidant, antibacterial, inhibiting tyrosinase activity, improving metabolic syndrome, and prolonging lifespan. Experiments have shown that the food combination can reduce the total cholesterol content in the blood, reduce the incidence of myocardial infarction; reduce the low-density lipoprotein content; reduce the blood uric acid content and neutral fat such as triglyceride content. Functional foods with NMN as the active ingredient have great potential for development, but there are few human experimental data about NMN, and there are few reports on the human body's maximum tolerated dose and tolerable time. Therefore, the human safety of NMN still needs to be further explored. . In terms of health food, NMN is an active ingredient, which can be used for health products for improving arteriosclerosis and cardiovascular diseases, health products for improving Parkinson's disease, and health products for aging. The application of NMN in China is still concentrated in medicine at this stage, and the application in food is at a blank stage. As the safety of NMN is further revealed, it is believed that there will be more foods or health products added with NMN to benefit human life in the future.
 
3 Outlook
As an intermediate in the NAD+ salvage pathway, NMN has the effect of anti-oxidation and reducing oxidative stress. It is used in the treatment of some specific diseases, such as stroke, cardiac ischemia reperfusion, Alzheimer's disease, Parkinson's disease, acute kidney injury, retinal degenerative diseases, type 2 diabetes, etc. also have good performance. Especially in terms of anti-aging, NMN can slow down the physiological decline of organisms, enhance energy metabolism, and prolong lifespan. In view of the fact that NMN is a human endogenous substance with high safety and good thermal stability, NMN as an active substance has broad prospects in the development of functional foods. However, the synthesis of NMN is difficult, time-consuming, high-cost, and low-yield. It is difficult to realize large-scale factory production, which limits the application of NMN. In addition, most of the research on the function of NMN stays on animal experiments, and there are few data on human experiments. The safety of adding NMN health products cannot be fully guaranteed. In particular, the safety of long-term human intake requires more experiments. prove.