99.5% β-Nicotinamide Mononucleotide Powder

β-Nicotinamide Mononucleotide is the product of nicotinamide phosphoribosyltransferase (Nampt) reaction and one of the key precursors of NAD +.
  • Product Name: β-Nicotinamide Mononucleotide
  • Other Names: Beta-Nicotinamide Mononucleotide; MNM; β-MNM; Beta-MNM
  • CAS No.: 1094-61-7
  • Molecular Weight: 334.22
  • Molecular Formula: C11H15N2O8P
  • Purity/ Assay: 99.5%
  • Application: Cosmetics, Food and Pharma
  • Packing Size: 0.1kg, 0.5kg, 1kg, 5kg, 10kg, 25kg
  • MOQ: 0.1kg
  • Description
    β-Nicotinamide Mononucleotide is the product of nicotinamide phosphoribosyltransferase (Nampt) reaction and one of the key precursors of NAD +. In mammals, β-Nicotinamide Mononucleotide is generated by nicotinamide (NAM) under the catalysis of Nampt, and then β-Nicotinamide Mononucleotide generates NAD + under the catalysis of nicotinamide mononucleoside adenosyltransferase (N-mnat). The extracellular β-Nicotinamide Mononucleotide needs to be dephosphorylated and transformed into nicotinamide riboside (NR) to enter the hepatocyte. After entering the hepatocyte, NR phosphorylates to produce β-Nicotinamide Mononucleotide under the action of nicotinamide nucleoside 1 (nrk1), and then combines with ATP to generate NAD +. β-Nicotinamide Mononucleotide plays its physiological function by transforming into NAD +, such as activating NAD + substrate dependent enzyme SIRT1 (histone deacetylase, also known as silencing regulatory protein), regulating cell survival and death, maintaining redox state, etc. Recently, it has been found that β-Nicotinamide Mononucleotide can regulate the level of β-Nicotinamide in vivo, which has a good therapeutic and repairing effect on cardiovascular and cerebrovascular diseases, neurodegenerative diseases and aging degenerative diseases; in addition, β-Nicotinamide Mononucleotide can also protect and repair islet function, increase INS-ULIN secretion, prevent and treat metabolic diseases such as diabetes and obesity by participating in and regulating the endocrine of the body.

    Our company is a professional manufacturer of NMN. We have a 40,000 square meter raw material production plant in mainland China, with an annual output of 100 tons of NMN raw material powder. In addition, we have a food and health care products production factory in Hong Kong, it can produce finished products, such as NMN capsules, NMN tablets, etc. 

    Therapeutic effect
    1. β-Nicotinamide Mononucleotide relieves and improves ischemic heart and brain tissue damage
    1) The therapeutic effect of β-Nicotinamide Mononucleotide on stroke:
    Stroke, an acute cerebrovascular disease caused by cerebral blood circulation disorder, has a high mortality and disability rate, which is a serious threat to human health. It has been found that β-Nicotinamide Mononucleotide can protect the brain nerves and promote the regeneration of blood vessels and nerves by activating the Nampt NAD + defense system. It has a good protective effect on the nerve injury caused by cerebral hemorrhage and the transformation of cerebral hemorrhage. It is a potential anti stroke drug. Park [2] et al. Analyzed the metabolic process of β-Nicotinamide Mononucleotide in brain tissue and found that β-Nicotinamide Mononucleotide can prevent neuronal apoptosis induced by cerebral ischemia and promote nerve regeneration after cerebral ischemia by improving the bioenergy metabolism of ischemic tissue. Therefore, β-Nicotinamide Mononucleotide has a strong protective effect on ischemic brain injury. For hemorrhagic brain injury, increasing the level of β-Nicotinamide Mononucleotide can reduce the content of hemoglobin in infarcted tissue, reduce hemorrhage and edema, and reduce the oxidative toxicity of brain tissue caused by oxidative stress.
    2) The therapeutic effect of β-Nicotinamide Mononucleotide on myocardial ischemia-reperfusion:
    Reperfusion is a kind of life-threatening ischemic injury, which is accompanied by the inevitable death of myocardial cells and severe organ dysfunction. Ischemic precondition (IPC) is an endogenous defense mechanism mediated by SIRT1, which can protect myocardial viability during transient ischemia-reperfusion. Studies have shown that β-Nicotinamide Mononucleotide can protect the heart by simulating the protective effect of IPC. After ischemia, the content of NAD + in the heart decreased. Exogenous β-Nicotinamide Mononucleotide can increase the content of NAD + and NADH in the heart, reduce the infarct area, and the data showed that β-Nicotinamide Mononucleotide can reduce the size of infarct area positively related to the expression level of SIRT1. 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 will affect the biosynthesis of NAD +, destroy the regulatory mechanism of SIRT1 activity, and lead to myocardial cell apoptosis and cardiac compensation loss in pressure overload mice. In the model mice of heart failure, β-Nicotinamide Mononucleotide treatment restored the level of NAD + in myocardial cells, increased the activity of SIRT1 deacetylase and the level of gene expression related to MITO-MYCIN function.
    2. β-Nicotinamide Mononucleotide improves oxidative related degenerative diseases and physical dysfunction
    1) Therapeutic effect of β-Nicotinamide Mononucleotide on Alzheimer's disease:
    With the acceleration of the aging trend of society, the incidence rate of Alzheimer's sdisease (AD) is increasing year by year. The disease is a kind of central nervous system disease, which is characterized by cognitive dysfunction and memory impairment. The abnormal structure and function of mitochondria is one of the pathogenic factors of AD, and β-Nicotinamide Mononucleotide promotes the energy metabolism of mitochondria, which plays an important role in improving cognitive function and memory function. It was found that when the β-Nicotinamide Mononucleotide level was increased, the availability of NAD + increased, the oxygen consumption rate (OCR) of mitochondria was increased, the fusion of mitochondria was promoted, the fission tendency was reduced, the longer mitochondria were produced in the hippocampus, and the respiratory function of mitochondria was improved. Amyloid β-oligomer (a β) is considered to be the main neurotoxic agent leading to AD. It was found that β-Nicotinamide Mononucleotide improved the cognitive and memory functions of Alzheimer's rats caused by a β 1-42 oligomer, restored the levels of NAD + and ATP, and reduced the accumulation of ROS (reactive oxygen species) in hippocampal slices of AD mice by improving energy metabolism and inhibiting oxidative stress. It was found that β-Nicotinamide Mononucleotide improved the behavioral cognitive impairment of AD mice by activating c-Jun amino terminal kinase (JNK), inhibited the production of β-amyloid, reduced the load of amyloid plaques, synaptic damage and inflammatory response in the nervous system. The above experiments show that β-Nicotinamide Mononucleotide can be used as a potential drug in the treatment of AD.
    1. The therapeutic effect of β-Nicotinamide Mononucleotide on Parkinson's disease:
    Parkinson's disease (PD) is a kind of degenerative disease of central nervous system, which is mainly manifested by motor symptoms such as slow motion, static tremor, rigidity, abnormal gait and posture, and non motor symptoms such as olfactory decline, anxiety and depression, constipation, etc. The pathogenesis of the disease is complex and unclear, so there is almost no effective treatment. The results show that β-Nicotinamide Mononucleotide can improve the survival rate of neural cells, reduce apoptosis, restore NAD + and ATP levels, inhibit apoptosis, resist energy damage, and improve the energy metabolism disorder induced by mitochondrial inhibitors. Compared with Alzheimer's disease, the effect of β-Nicotinamide Mononucleotide on Parkinson's disease is less studied, and more in vivo experimental data are needed to prove its effectiveness.
    3) Therapeutic effect of β-Nicotinamide Mononucleotide on vascular disorders:
    Another serious threat to health is Cardiovasculardiseases (CVD), which has high incidence rate, high disability rate and wide danger. This kind of disease is mainly due to the imbalance of oxidation system and antioxidant system after aging of the body. It is found that β-Nicotinamide Mononucleotide can reduce oxidative stress of blood vessels, improve atherosclerosis and vascular dysfunction; β-Nicotinamide Mononucleotide can reduce the accumulation of collagen in the whole blood vessels, increase the accumulation of arterial elastin, reduce atherosclerosis, and delay the aging of arteries with the increase of age. β-Nicotinamide Mononucleotide improves endothelial dysfunction and large-scale elastic Arteriosclerosis Caused by aging by increasing the bioavailability of NAD + in the vascular system, restoring the activity of SIRT1 in the artery. β-Nicotinamide Mononucleotide can also maintain glutathione and thioredoxin anti-oxidation system by enhancing the metabolic flux of tricarboxylic acid cycle and electron transport chain, reducing the accumulation of reactive oxygen species in cells, and increasing the level of NADPH (reduced nicotinamide adenine dinucleotide phosphate). In addition, β-Nicotinamide Mononucleotide can also improve the distribution of lipid in plasma and maintain the level of blood glucose, thus improving the vascular function.
    4) Therapeutic effect of β-Nicotinamide Mononucleotide on acute renal injury:
    The incidence rate and mortality of Acutekidneyinjury (AKI) have been increasing year by year, which has attracted more and more attention. The results showed that the levels of Sirt1 and NAD+ decreased with the increase of age; the decrease of NAD+ and Sirt1 in the kidney of the aged organism increased the susceptibility to AKI; β -Nicotinamide was supplemented Mononucleotide can protect mice from AKI induced by CISPL-ATIN (which can be used to inhibit DNA replication); the mechanism of NAD + / SIRT1 protecting kidney involves the epigenetic regulation of JNK pathway; in vitro, SIRT1 attenuates stress response by regulating JNK signaling pathway. Endogenous NAD + is considered to be a potential therapeutic target of AKI in the elderly. β-Nicotinamide Mononucleotide, an intermediate of NAD +, is a good therapeutic strategy.
    5) Anti aging effect of β-Nicotinamide Mononucleotide:
    It was found that β-Nicotinamide Mononucleotide could significantly improve the age-related physiological decline of mice, such as inhibiting age-related weight gain, enhancing energy metabolism, improving INS-ULIN sensitivity and lipid distribution in plasma, and improving eye function Mononucleotide can prevent age-related gene expression changes in a tissue-specific manner, enhance the oxidative metabolism of mitochondria in skeletal muscle, and at least partially mediate its anti-aging effect. Studies have shown that in rats, beta -Nicotinamide Mononucleotide as an anti-aging candidate compound has longer retention time than Nam. Because Nampt is inhibited by NAD +, Nam is not transformed into NAD + through the Nam β-Nicotinamide Mononucleotide → NAD + pathway, but prepared through the Nam niacin (NIA) nicotinate mononucleotide (namn) nicotinate adenine dinucleotide (naad) NAD + pathway; on the other hand, from β-Nicotinamide The synthesis of NAD + in mononucleotide is not regulated by the level of NAD +, so the increase of NAD + is easier. According to the metabolic control mechanism and many reports on β-Nicotinamide Mononucleotide, β-Nicotinamide Mononucleotide may be more effective as NAD + precursor than Nam. Because SIRT1 is a NAD + dependent enzyme, β-Nicotinamide Mononucleotide can accelerate the turnover of NAD + remediation biosynthesis, thus activating SIRT1 reaction. SIRT1 can induce DNA silencing, contribute to anti-aging and prolong life. In addition to mammals, studies have also shown that enhancing NAD + biosynthesis can prolong the life span of yeast, worms and flies.
    6) Therapeutic effect of β-Nicotinamide Mononucleotide on visual degenerative diseases:
    The causes of visual impairment are complex and varied, 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 active tissues in the body. Studies have shown that several mouse models of retinal dysfunction (photo induced degeneration, streptozotocin induced diabetic retinopathy and age-related retinal dysfunction) all show early retinal NAD + deficiency, and NAD + not only performs coenzyme function in each step of tricarboxylic acid cycle and glycolysis, but also maintains the best SIRT3 activity. SIRT3 and sirt5 play an important role in retinal homeostasis, and the lack of NAD + causes many obstacles), and they can not respond to metabolic stress properly, which eventually leads to photoreceptor death and retinal degeneration. The researchers found that β-Nicotinamide Mononucleotide can restore the normal basic glycolysis function, mitochondrial function and the ability to adapt to metabolic stress in mice, reduce the death of photoreceptor cells, and significantly improve the dark vision and retinal function. These conclusions support the possibility of using β-Nicotinamide Mononucleotide, an intermediate of NAD +, to treat retinal degenerative diseases, and provide a unified treatment target for ophthalmic degenerative diseases and a powerful treatment approach. Because it can be applied to a variety of diseases with a variety of pathogenic mechanisms, once successfully implemented, the impact of this treatment strategy will be far-reaching.
    3. Therapeutic effect of β-Nicotinamide Mononucleotide on metabolic diseases
    1) The therapeutic effect of β-Nicotinamide Mononucleotide on type 2 diabetes mellitus:
    chronic inflammation is an important factor that causes the failure of islet β cells in type 2 diabetes mellitus (T2DM). Exposure to proinflammatory cytokines such as interleukin 1 β (IL1 β), tumor necrosis factor α (TNF α) can lead to the death of islet β cells and inhibit INS-ULIN secretion. Due to the lack of inampt in the pancreas, the islets rely on circulating enampt to stimulate INS-ULIN secretion. β-Nicotinamide Mononucleotide can restore the level of enampt, rever-se the impaired state of INS-ULIN secretion, and protect the islets from the negative effects of proinflammatory factors. It was found that β-Nicotinamide Mononucleotide could improve the islet dysfunction of mice in high fructose group, rever-se the expression of FRD and proinflammatory cytokines mediated gene encoding islet, reduce the expression of proinflammatory factors, restore INS-ULIN secretion, and improve the islet dysfunction mediated by cytokines Nampt. In conclusion, β-Nicotinamide Mononucleotide can improve the islet function of FRD mice, which is related to the beneficial changes of gene expression involved in glucose metabolism, anti-inflammatory and apoptosis.
    1. The therapeutic effect of β-Nicotinamide Mononucleotide on obesity:
    Obesity is closely related to the development of type 2 diabetes. Type 2 diabetes is mainly due to the insufficiencies of islets of Langerhans and the decrease of INS-ULIN sensitivity of glucose metabolism tissue. Obesity leads to dysfunction of adipose tissue, increased release of pro-inflammatory cytokines, and increased secretion of fat synthetase, all of which contribute to the damage of islet β cells. β-Nicotinamide Mononucleotide can improve islet dysfunction and restore INS-ULIN secretion by catalyzing the biosynthesis of NAD + in mammals. It was found that Nampt and β-Nicotinamide Mononucleotide had no direct effect on the activity of human islet β cells and did not cause apoptosis, but they could enhance glucose stimulated INS-ULIN secretion and improve the level of NAD +. Exercise is an effective way to resist obesity, which is due to the increase of NAD + level and the enhancement of mitochondrial energy metabolism. And β-Nicotinamide Mononucleotide can also improve the level of NAD +, so theoretically using β-Nicotinamide Mononucleotide can achieve the same weight loss effect as exercise.
    1. Application of β-Nicotinamide Mononucleotide in medical care
    In view of the above biological activity of β-Nicotinamide Mononucleotide, the development of drugs with β-Nicotinamide Mononucleotide as the active ingredient has become a medical hotspot. Huizenga of the United States has invented a group of compositions containing NAD +, β-Nicotinamide Mononucleotide, NR and other active ingredients, which can be used for anti-aging and anti-oxidation treatment. Akihiro of Yoshida University and others invented β-Nicotinamide Mononucleotide and NR and their salts as raw materials, which can be used to treat corneal disorders. Imai of the University of Washington has developed treatment methods to improve age-related obesity, hyperlipidemia and type 2 diabetes, as well as drug Douglas with β-Nicotinamide Mononucleotide as the active ingredient, which has developed methods to evaluate and treat vascular endothelial disorders and drugs with β-Nicotinamide Mononucleotide as the active ingredient. Michael et al. Developed β-Nicotinamide Mononucleotide (a neuroprotective drug) for the treatment of neurodegenerative diseases.
    2. Application of β-Nicotinamide Mononucleotide in food
    β-Nicotinamide Mononucleotide is widely found in natural foods. β-Nicotinamide Mononucleotide is found in vegetables, fungi, meat and shrimp. It was also found that β-Nicotinamide Mononucleotide was present in human milk and donkey milk through the new enzyme coupling technology, and the content of β-Nicotinamide Mononucleotide was higher in human milk. It was found that the activity of β-Nicotinamide Mononucleotide was stable when it was treated in water or milk at 75 for 5min, and the loss of activity was about 20% when it was treated at 95 for 5min, which indicated that adding β-Nicotinamide Mononucleotide to pasteurized milk had theoretical feasibility. In addition, oral experiments showed that β-Nicotinamide Mononucleotide with low concentration could be absorbed rapidly within 30 minutes, effectively transported to the blood circulation, and immediately transformed into NAD + in the main metabolic tissues. In addition, during the intervention period lasting for 12 months, β-Nicotinamide Mononucleotide showed no significant toxicity and mortality rate, and no serious side effects, with high food safety. At present, Megumi in Japan has developed a food composition of β-Nicotinamide Mononucleotide and resveratrol. Resveratrol is a kind of natural polyphenol compound, which can act as estrogen. It has the functions of antioxidation, antibacterial, inhibition of tyrosinase activity, improvement of metabolic syndrome and prolongation of life span. The experiment proved that the food composition can reduce the total cholesterol content in the blood, reduce the incidence rate of myocardial infarction, reduce the content of low density lipoprotein, reduce the uric acid content in blood and the content of neutral fat, such as triglyceride. The functional food with β-Nicotinamide Mononucleotide as the active ingredient has great development potential, but the human experimental data of β-Nicotinamide Mononucleotide are few, and the maximum tolerance dose and tolerance time of human body are rarely reported. Therefore, the human safety of β-Nicotinamide Mononucleotide needs further exploration.
    In the aspect of health food, with β-Nicotinamide Mononucleotide as the active ingredient, Fu Rongzhao invented health products that can be used to improve arteriosclerosis and cardiovascular disease, Parkinson's disease and anti-aging. At present, the application of β-Nicotinamide Mononucleotide in China is still concentrated in medicine, and the application in food is in a blank stage. With the further disclosure of the safety of β-Nicotinamide Mononucleotide, it is believed that more β-Nicotinamide Mononucleotide food or health products will be added in the future to benefit human life.