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COG112 ApoE Mimetic Peptide | Anti-Inflammatory & Neuroprotective Research Peptide

Product Overview:

COG112 is a synthetic Apolipoprotein E (ApoE) mimetic peptide designed by conjugating the receptor-binding domain of ApoE (COG133) with the cell-penetrating peptide (CPP) antennapedia (Antp). This modification significantly enhances the peptide’s anti-inflammatory properties and neuroprotective effects compared to COG133 alone.

Sequence:

acetyl-YRQIKIWFQNRRMKWKKCLRVRLASHLRKLRKRLL-amide

Molecular Formula:

C₂₀₂H₃₄₇N₇₁O₃₈S₂

Molecular Weight:

4460.51 g/mol

Key Features and Uses:

● ApoE mimetic peptide COG112 is extensively studied for its ability to modulate inflammatory responses, primarily by inhibiting the NF-κB signaling pathway.

●Exhibits potent anti-inflammatory properties useful for research into neurodegenerative diseases and inflammatory bowel disease.

● Compared to the original ApoE peptide COG133, COG112 demonstrates enhanced cell penetration and therapeutic efficacy due to the CPP antennapedia conjugation.

● Recent research highlights the role of COG112 in cancer biology by inhibiting the SET-Rac1 interaction, resulting in decreased cancer cell migration and invasion.

● COG112 peptide is widely used in anti-inflammatory uses and ApoE peptide research studies to explore novel therapeutic applications.

Research Insights:

● COG112 vs COG133 ApoE peptide: The addition of the CPP domain in COG112 dramatically improves cellular uptake and anti-inflammatory activity compared to COG133 alone, making it a superior candidate for experimental therapies targeting inflammation and neuroprotection.

●Potential applications include modulation of inflammatory bowel disease, neurodegenerative disorders such as Alzheimer’s disease, and oncology research focused on tumor invasion and metastasis.

Product Applications:

Ideal for scientists and researchers investigating:

● Inflammatory signaling pathways (e.g., NF-κB inhibition)

● Neuroprotection mechanisms

● Cancer cell migration and invasion pathways

● Novel peptide therapeutics development

CAS #: NA

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NAD+ (Nicotinamide Adenine Dinucleotide)

$69.00 $79.99

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Nicotinamide Adenine Dinucleotide (NAD+) is a coenzyme that is present in each living cell in the body. It is produced from the breakdown of nicotinamide riboside (niagen), an alternative form of vitamin B3 (niacin). NAD+ plays an integral role in energy production and regulation of vital cellular processes such as DNA repair, strengthening cells’ defense systems, conversion of food into a usable form of energy, and regulation of circadian rhythm.

How NAD+ Works

NAD+ converts nutrients into adenosine triphosphate, a compound that provides energy to living cells. Aside from this important function, it works together with various forms of proteins to carry out a wide array of biological processes such as DNA repair, calcium signaling, maintenance of cell energy and chromosomal integrity, and gene expression.

Chemical Structure of NAD+

Research on NAD+

A. Extends Lifespan

Aging is associated with progressive restriction in the length of telomeres, which are located at chromosome ends. They play an important role in the preservation of chromosome stability. Studies have shown that individuals with longer telomeres have a longer subsequent lifespan. [1-2] Increasing sirtuin activity is known to stabilize telomeres and attenuate age-related telomere shortening. [3] Since NAD+ activates SIRT1, it can help achieve chromosome stability and longer telomeres – all of these mechanisms can increase longevity.

The natural process of aging is associated with a decline in the quality and activity of the “powerhouse of the cell” known as the mitochondria. As the name implies, the mitochondria produce the energy needed to power the cell’s biochemical reactions – everything from the transmission of signals, digestion, muscle function, and other essential bodily processes. Mitochondrial function is a determinant of lifespan and studies show that mitochondrial dysfunction can shorten lifespan. [4-5]

Another mechanism that can help extend lifespan is through the activation of SIRT1 function in the nucleus of cells. Evidence suggests that boosting NAD+ levels through NAD+ supplementation can dramatically ameliorate mitochondrial dysfunction via activation of sirtuin 1 (SIRT1). [6] SIRT1 is an enzyme that plays an integral role in the regulation of proteins involved in cellular metabolism and processes associated with longevity, inflammation, and stress. SIRT1 activation by NAD+ can increase longevity by promoting mitochondrial biogenesis, a cellular process that involves the production of new mitochondria. [7]

A convincing number of evidence suggests that NAD+ can extend lifespan:

The administration of the NAD+ precursor nicotinamide riboside extended the lifespan of mice without calorie restriction. [8]
In mice with ataxia-telangiectasia (A-T), a rare disease characterized by progressive neurodegeneration that affects movements and speech, NAD+ replenishment improved lifespan and health span by stimulating neuronal DNA repair and improving mitochondrial quality. [9]
In a mouse model of amyotrophic lateral sclerosis (ALS), a medical condition characterized by progressive degeneration of motor neurons, supplementation with a bioavailable NAD+ precursor (nicotinamide riboside, NR) delayed the degeneration of motor neurons, decreased spinal inflammation, and improved survival rate. [10]
In a mouse model of muscular dystrophy, a condition characterized by gradual weakening of the muscles, treatment with the NAD+ precursor nicotinamide riboside (NR) delayed muscle breakdown and increased lifespan. [11]
In a mouse model of chronological aging, the administration of CD38 inhibitor 78c increased NAD+ levels which in turn improved exercise performance, endurance, and metabolic function and increased lifespan. [12]
In Caenorhabditis elegans, a type of worm, NAD+ increased lifespan through the activation of sirtuin (SIR-2). [13-14]
In Saccharomyces cerevisiae, a species of yeast, NAD+ extended the lifespan and ameliorated aging-related conditions. [15]

B. Anti-Aging Benefits

While a decline in the function of the mitochondria has been linked with normal aging, this is also associated with a wide array of age-related medical conditions. Evidence suggests that mitochondrial aging contributes to cellular senescence (also known as biological aging), increased inflammation, decreased stem cell activity, reduced healing rate, and a decline in tissue and organ function. [16] Interestingly, NAD+ can reverse age-related mitochondrial dysfunction via SIRT1 activation.

New research found that some of the age-related changes in the structures of the mitochondria can be reversed through NAD+ supplementation. [17] In this study, the administration of NMN (nicotinamide mononucleotide), a molecule that boosts NAD+ levels, via injections in elderly mice reversed age-related mitochondrial deterioration. It was observed that declining NAD+ levels were associated with interruptions in the normal signaling between the cell’s nucleus and mitochondria. Interestingly, raising NAD+ levels restored the communication between these cellular structures.

During the normal process of aging, DNA damage occurs continuously on a massive scale. The age-related DNA damage contributes to cell death and a decline in the function of neurons or nerve cells. This creates a domino effect, causing a gradual decline in a number of bodily functions. NAD+ can mitigate these effects since it is connected to the DNA repair precursor poly adenosine diphosphate-ribose polymerase 1 (PARP 1). PARP 1 consumes NAD+ in the presence of DNA damage in order to promote cell survival. This in turn can help slow down the effects of aging.

Preclinical evidence also shows that boosting NAD+ levels can help mitigate age-related functional decline:

In elderly mice, treatment with the NAD+ booster nicotinamide mononucleotide (NMN) improved blood flow and increased endurance via the promotion of SIRT1-dependent increases in capillary density. [18]
In mice with progressive weakness and loss of muscle mass, NAD+ repletion improved muscle and mitochondrial function. [19]
In mice, the administration of the NAD+ booster nicotinamide mononucleotide prevented age-related weight gain and improved physical activity, energy metabolism, lipid profiles, and insulin sensitivity. [20]
In mouse models of retinal dysfunction, NAD+ deficiency caused metabolic dysfunction in the cells of the retina of the eye, suggesting that restoring NAD+ to youthful levels can help age-related vision loss. [21]
In mice with mitochondrial dysfunction, oral administration of nicotinamide riboside (NR), a NAD+ precursor, increased mitochondrial numbers and prevented muscle abnormalities. [22]
In mice, the administration of nicotinamide riboside (NR) prevented noise-induced hearing loss and degeneration of ear cells, suggesting that increasing NAD+ levels can help age-related hearing loss. [23]
In mice fed with a high-fat diet, the administration of the NAD+ booster nicotinamide mononucleotide prevented diet- and age-induced diabetes by enhancing insulin sensitivity. [24]

C. Increases Energy Levels

NAD+ plays an integral role in energy production and regulation of vital cellular processes. This includes the conversion of food into a usable form of energy called adenosine triphosphate.

Studies suggest that increased ATP production caused by NAD+ may help boost energy levels and reduce fatigue:

In old mice, supplementation with a NAD+ precursor improved ovarian mitochondrial energy metabolism. [25]
In obese mice, chronic NAD+ supplementation (1 mg/kg/day for the last 4 weeks) significantly attenuated weight gain and improved diurnal locomotor activity patterns. [26]
In patients with chronic fatigue syndrome, NAD+ supplementation decreased anxiety and improved heart rate. [27]
A study reported that NAD+ may be a promising intervention to overcome symptoms of fatigue and to improve the quality of life of patients with chronic fatigue syndrome. [28]
The use of coenzyme Q10 (CoQ10) plus NAD+ supplementation reduced perceived cognitive fatigue and improved the health-related quality of life in patients with chronic fatigue syndrome. [29-31]
In trained and untrained subjects, NAD+ supplementation was associated with improved exercise endurance. [32]
7. NAD+ treatment was found to be more effective than conventional therapy for chronic fatigue syndrome. [33]

D. Promotes Weight Loss

The ability of NAD+ to induce weight loss can be attributed to its energy-boosting mechanisms. With increased energy expenditure, the body will not store additional fat. Instead, the metabolism is increased, resulting in weight loss.

There’s a great deal of evidence supporting the fat-burning effects of NAD+:

In obese female mice, NAD+ injections reversed glucose intolerance induced by obesity and improved exercise capacity. [34]
In healthy obese participants, NAD+ supplementation reduced weight by 17.1%. [35]
In mammalian cells and mouse tissues, NAD+ protected against oxidative stress and high-fat diet-induced metabolic abnormalities. [36]
In mice, supplementation with NAD+ at 400 mg/kg/day reduced abdominal visceral fat deposition. [37]
In a study of twins, lower NAD+ levels were associated with acquired obesity. [38]
A cell study found that NAD+ can promote weight loss by reducing the number of adipocytes (fat cells). [39]
Several studies have revealed that decreased NAD+ levels in cells were associated with higher fat mass tissues in the skeletal muscles, liver, and brain. [40-43]
In mice, NAD+ protected against obesity by promoting whole-body energy homeostasis. [44]
In mice, long-term administration of NAD+ reduced age-associated body weight gain. [45]
NAD+ supplementation in mice ameliorated maternal obesity. [46]
A cell study found that NAD+ normalized mitochondrial function and whole-body metabolism. [47]
In mice fed with a high-fat diet, NAD+ protected against high-fat diet-induced metabolic abnormalities. [48]

E. Increases Muscle Mass and Strength

The anti-aging effects of NAD+ can also help attenuate the age-related decline in muscle mass and strength. Evidence suggests that NAD+ reverses detrimental age-associated changes in muscle by boosting ATP production, increasing mitochondrial function, and reducing inflammation. [49]

Studies show that NAD+ can help combat loss of muscle mass and strength associated with aging and musculoskeletal disease:

In mice with progressive weakness and loss of muscle mass, NAD+ repletion improved muscle and mitochondrial function. [19]
In mice with mitochondrial dysfunction, oral administration of nicotinamide riboside (NR), a NAD+ precursor, increased mitochondrial numbers and prevented muscle abnormalities. [22]
In older men, NAD+ supplementation increased muscle mass and reduced circulating inflammatory cytokines. [50]
In old mice, restoration of NAD+ levels to normal reversed skeletal muscle aging. [51]
A 2018 study reported that NAD+ is essential in skeletal muscle development and regeneration. [52]
In healthy obese men and women, administration of NAD+ at 1g per day for 6 weeks improved skeletal muscle composition. [53]
A study found that aerobic and resistance exercise training can reverse age-related muscle loss by increasing NAD+ levels. [54]
In a mouse model of Duchene’s muscular dystrophy (DMD), NAD+ supplementation improved muscle function. [55]

F. Improves Cognitive Function

A decline in NAD+ levels is associated with a number of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and other brain disorders that cause cognitive dysfunction. [11] Interestingly, NAD+ has neuroprotective effects and the ability to decrease the production of reactive oxygen species (ROS), which are linked to a wide array of medical maladies including neurodegenerative diseases.

NAD+ can also help prevent cell death by regulating the activity of polyadenosine diphosphate-ribose polymerase 1 (PARP1). [56] PARP1 activity is usually increased in the brain of patients with Alzheimer’s disease and other neurodegenerative disease and is associated with increased deposition of abnormal protein structures in the brain. [57] Basically, NAD+ regulates PARP1 activity so that it will not kill too many cells before they can be repaired.

In addition, NAD+ plays important roles in a wide array of biological processes in the brain such as transmission of nerve signals, learning, and memory. [58] NAD+ helps increase the levels of brain chemicals called neurotransmitters, such as dopamine, serotonin, and norepinephrine, which are involved in a number of cognitive functions including memory, motivation, attention, mood, and emotions.

A number of strong scientific evidence suggests that NAD+ can help improve cognitive health:

In a cell study, researchers found that cells treated with NAD+ were more resistant to stress. [59]
According to a rat study, NAD+ helps protect the brain against oxidative stress. [60]
A rat udy found that NAD+ can significantly decrease brain injury. [61]
In a rat study, researchers found that NAD+ is also essential for altering genes that accelerate aging. [62]
According to a rat study, NAD+ can slow or even reverse the progression of age-related brain diseases. [63]
Studies found that decreased amounts of NAD+ in the cells accelerate the aging process of the brain. [64-67]
A rat study found that NAD+ helps the brain function at optimal levels. [68-72]
Numerous studies suggest that insufficient amounts of NAD+ result in cell breakdown, which in turn accelerates the aging process and causes mitochondrial dysfunction in the brain. [73-77]
Several studies found that NAD+ is important for the continued production of energy (ATP) by the mitochondria in the brain. [78-81]
Studies found that NAD+ helps maintain a healthy neurological system and protects against various neurological diseases. [82-84]
A study found that NAD+ is an essential coenzyme needed for brain function. [85]
Cell studies found that NAD+ can help improve the functions of the neurons in the brain. [86-88]
In a mouse model of Alzheimer’s disease, NAD+ supplementation significantly normalized nerve cell inflammation, synaptic transmission, and DNA damage as well as improved learning, memory, and motor function. [89-95]
A study found that NAD+ may help improve cognitive function through its anti-inflammatory effects. [96]

G. Fights Cancer

Mitochondrial respiration malfunction and increased glucose uptake are usually observed in cancer cells. Interestingly, increasing NAD+ levels has been shown to boost mitochondrial respiration and reduce glucose (blood sugar) uptake. [97] By counteracting these processes, NAD+ can help prevent the growth of cancer cells.

Increased NAD+ levels can also help boost the activity of SIRT1 and SIRT6, both of which inhibit the growth and spread of tumors via alteration of beta-catenin signaling and reduction of glucose uptake. [98-99]

Studies suggest that NAD+ exerts its anti-cancer effects through several mechanisms:

A study found that NAD+ regulates cell cycle arrest and programmed cell death of malignant cells. [100]
In human ovarian tumor tissues, NAD+ enhanced the anti-tumor activities of chemotherapeutic drugs. [101]
A 2018 study published in Frontiers in Oncology found that NAD+ prevented the progression of cancer by stimulating DNA repair. [102]
A 2019 study reported that targeting NAD+ metabolism can enhance radiation therapy responses in cancer patients. [103]
A 2015 study published in the Journal of Molecular & Cellular Oncology found that boosting NAD+ can prevent and treat liver cancer. [104]

H. Improves Cardiovascular Health

NAD+ levels are essential for normal heart function and are associated with improved cardiac recovery from injury. Interestingly, SIRT3, one of the signaling proteins of NAD+, can help improve heart health by preventing enlargement of the heart and scarring. [105-107]

There’s increasing evidence supporting the cardiovascular benefits of NAD+:

In animal models of heart failure, NAD+ improved a multitude of processes needed for cardiovascular function such as the production of energy for cardiomyocytes (heart muscle cells) and reversing vascular dysfunction and oxidative stress. [108-111]

A cell study reported that NAD+ protected rat heart tissues against apoptosis (programmed cell death). [112]

In rats with impaired heart function, NAD+ supplementation improved markers of cardiovascular health. [113-116]
Studies in mice found that NAD+ can stimulate the regeneration of heart muscle cells, reduce left ventricular contractile dysfunction, and prevent heart enlargement. [117-118]
Rat studies found that higher levels of NAD+ were associated with improved cardiac function. [2, 119]
Animal studies also found that lower NAD+ levels were associated with mitochondrial dysfunction in heart muscle cells. [120-121]
A 2015 study published in Nature Reviews found that NAD+ can prevent the progression of obesity through its antioxidant and anti-inflammatory properties. [122]
In patients with heart failure, 5 to 9 days of oral nicotinamide riboside (NR) supplementation increased NAD+ levels, improved respiratory capacity, and decreased proinflammatory cytokines. [123]
Studies found that increasing NAD+ levels can protect against heart injury caused by insufficient blood supply and pressure overload and can help reduce the size of dead heart tissue. [124-127]

I. Lowers Blood Pressure

NAD+ activates SIRT1 which in turn increases the production of nitric oxide, a substance that helps widen blood vessels to allow an increase in blood flow. This process reduces the pressure within the blood vessels.

A number of studies support the antihypertensive effects of NAD+:

In healthy middle-aged and older adults, NAD+ supplementation for 6 weeks reduced blood pressure and arterial stiffness. [128]
A study found that administration of NAD+-boosting molecules decreased blood pressure in Korean subjects. [129]
In obese men and women, administration of NAD+ at 1-2 g per day for 6-12 weeks significantly reduced blood pressure. [130-131]

J. Improves Blood Sugar Levels

NAD+ can help improve blood sugar levels by reducing glucose (blood sugar) uptake. This in turn prevents sudden spikes in blood sugar which can be detrimental to health. In addition, NAD+ can also help increase the body’s response to insulin, a hormone that regulates blood sugar.

There’s a good deal of evidence supporting the beneficial effects of NAD+ on blood sugar levels:

In prediabetic women, NAD+ increased muscle insulin sensitivity. [132]
In obese mice, increased NAD+ levels improved glucose and lipid homeostasis by increasing the activity of SIRT1 and SIRT3. [133-134]

K. Boosts Immune Function

The age-related shortening of telomeres adversely affects the function of the immune system. These adverse changes can significantly increase the risk for severe infection and even death. Studies suggest that patients with significantly shortened telomeres are at higher risk for different medical conditions such as rheumatoid arthritis and diabetes mellitus (type 1 and type 2). [135-137] Since NAD+ activates SIRT1, it can help achieve longer and more stable telomeres. This has a positive impact on the overall function of the immune system.

Another mechanism that can help improve the immune function is by suppressing or decreasing the inflammatory response. NAD+ has been shown to possess potent anti-inflammatory properties that can help treat or ward off a broad range of inflammatory conditions.

There is a growing body of evidence that NAD+ can help strengthen immune function:

Treatment of 24-month-old mice with the NAD+ precursor nicotinamide mononucleotide for 1 week significantly reduced the levels of inflammatory markers such as TNFα and IL-6 in the skeletal muscle. [49]
Oral nicotinamide has been found to be effective in the management of inflammatory lesions associated with acne vulgaris and acne rosacea. [138]
In mice with brain inflammation, the administration of a NAD+ precursor attenuated the loss of brain cells and improved behavioral deficits. [139]
In men exposed to ultraviolet radiation, topical nicotinamide application prevented immunosuppression. [140-142]
Restoring normal NAD+ levels has been found to decrease the severity of immune reaction in patients with COVID-19 infection. [143]
Studies suggest that NAD+ has significant immunomodulatory effects such as modulation of cytokine action, regulation of the intercellular adhesion molecules, blockage of mast cell degranulation, and inhibition of protease release from leukocytes. [144-146]

L. Improves Liver Health

By activating SIRT1, NAD+ can produce protective effects on the liver. SIRT1 is known to improve liver health by maintaining mitochondrial integrity, improving cholesterol transport, and improving fatty acid homeostasis. [147-149]

Several lines of evidence suggest that NAD+ can help prevent the development of liver diseases:

A 2016 study found that NAD+ deficiency in the liver increases the risk of non-alcoholic fatty liver disease. [150-151]
In mice, NAD+ attenuated alcohol-induced liver injury. [152]
In a mouse model of liver fibrosis, NAD+ prevented liver scarring. [153]
A 2019 study found that NAD+ protected against aging-induced non-alcoholic fatty liver disease-like liver dysfunction in mice. [154]
A 2015 study published in Nature Reviews found that NAD+ can prevent the progression of non-alcoholic fatty liver disease by influencing the oxidative stress response, programmed cell death, and inflammatory response. [155]

M. Improves Kidney Health

Reduced levels of NAD+ also reduce sirtuin activity. This process is largely responsible for the age-related decline in kidney function.

Latest studies indicate that NAD+ is beneficial for kidney health:

A 2019 study published in National Reviews in Nephrology found that NAD+ deficiency could lead to chronic kidney disease. [156]
A 2017 study also found that NAD+ supplementation can help improve kidney function. [157]
A 2017 study also found that lower NAD+ levels were associated with a higher incidence of acute kidney injury. [158]
Studies in mice showed that NAD+ protected against kidney injury caused by chemotherapeutic drugs such as cisplatin and other medications that are toxic to the kidneys. [159-165]

Nicotinamide Adenine Dinucleotide Side Effects

NAD+ side effects are very uncommon. There have been some side effects associated with the use of this drug wherein the patient had one of the issues listed below at some point while being on NAD+. However, these side effects weren’t confirmed to be associated with the treatment and could have been a coincidence and not related to the use of NAD+. Despite this, it was listed as a side effect associated with NAD+ even though these associated side effects are very uncommon.

Side effects associated with NAD+ may include the following:

Decreased blood levels of phosphorus
Decreased insulin sensitivity
Decreased platelets
Dizziness
Frontal dull headaches
Nausea

Reference

Monaghan, P., & Haussmann, M. F. (2006). Do telomere dynamics link lifestyle and lifespan?. Trends in ecology & evolution, 21(1), 47–53. https://doi.org/10.1016/j.tree.2005.11.007.
Monaghan P. (2010). Telomeres and life histories: the long and the short of it. Annals of the New York Academy of Sciences, 1206, 130–142. https://doi.org/10.1111/j.1749-6632.2010.05705.x.
Palacios, J. A., Herranz, D., De Bonis, M. L., Velasco, S., Serrano, M., & Blasco, M. A. (2010). SIRT1 contributes to telomere maintenance and augments global homologous recombination. The Journal of cell biology, 191(7), 1299–1313. https://doi.org/10.1083/jcb.201005160.
Wang, Y., Oxer, D., & Hekimi, S. (2015). Mitochondrial function and lifespan of mice with controlled ubiquinone biosynthesis. Nature communications, 6, 6393. https://doi.org/10.1038/ncomms7393.
Lanza, I. R., & Nair, K. S. (2010). Mitochondrial function as a determinant of life span. Pflugers Archiv: European journal of physiology, 459(2), 277–289. https://doi.org/10.1007/s00424-009-0724-5.
Imai S, Guarente L. NAD+ and sirtuins in aging and disease. Trends Cell Biol. 2014;24(8):464-471. doi:10.1016/j.tcb.2014.04.002.
Tang B. L. (2016). Sirt1 and the Mitochondria. Molecules and cells, 39(2), 87–95. https://doi.org/10.14348/molcells.2016.2318.
Belenky, P., Racette, F. G., Bogan, K. L., McClure, J. M., Smith, J. S., & Brenner, C. (2007). Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+. Cell, 129(3), 473–484. https://doi.org/10.1016/j.cell.2007.03.024.
Fang, E. F., Kassahun, H., Croteau, D. L., Scheibye-Knudsen, M., Marosi, K., Lu, H., Shamanna, R. A., Kalyanasundaram, S., Bollineni, R. C., Wilson, M. A., Iser, W. B., Wollman, B. N., Morevati, M., Li, J., Kerr, J. S., Lu, Q., Waltz, T. B., Tian, J., Sinclair, D. A., Mattson, M. P., … Bohr, V. A. (2016). NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair. Cell metabolism, 24(4), 566–581. https://doi.org/10.1016/j.cmet.2016.09.004.
Harlan, B. A., Killoy, K. M., Pehar, M., Liu, L., Auwerx, J., & Vargas, M. R. (2020). Evaluation of the NAD+ biosynthetic pathway in ALS patients and effect of modulating NAD+ levels in hSOD1-linked ALS mouse models. Experimental neurology, 327, 113219. https://doi.org/10.1016/j.expneurol.2020.113219.
Zhang, H., Ryu, D., Wu, Y., Gariani, K., Wang, X., Luan, P., D’Amico, D., Ropelle, E. R., Lutolf, M. P., Aebersold, R., Schoonjans, K., Menzies, K. J., & Auwerx, J. (2016). NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science (New York, N.Y.), 352(6292), 1436–1443. https://doi.org/10.1126/science.aaf2693.
Peclat, T. R., Thompson, K. L., Warner, G. M., Chini, C., Tarragó, M. G., Mazdeh, D. Z., Zhang, C., Zavala-Solorio, J., Kolumam, G., Liang Wong, Y., Cohen, R. L., & Chini, E. N. (2022). CD38 inhibitor 78c increases mice lifespan and healthspan in a model of chronological aging. Aging cell, 21(4), e13589. https://doi.org/10.1111/acel.13589.
Hashimoto, T., Horikawa, M., Nomura, T., & Sakamoto, K. (2010). Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16. Biogerontology, 11(1), 31–43. https://doi.org/10.1007/s10522-009-9225-3.
Mouchiroud, L., Houtkooper, R. H., Moullan, N., Katsyuba, E., Ryu, D., Cantó, C., Mottis, A., Jo, Y. S., Viswanathan, M., Schoonjans, K., Guarente, L., & Auwerx, J. (2013). The NAD(+)/Sirtuin Pathway Modulates Longevity through Activation of Mitochondrial UPR and FOXO Signaling. Cell, 154(2), 430–441. https://doi.org/10.1016/j.cell.2013.06.016.
Odoh, C. K., Guo, X., Arnone, J. T., Wang, X., & Zhao, Z. K. (2022). The role of NAD and NAD precursors on longevity and lifespan modulation in the budding yeast, Saccharomyces cerevisiae. Biogerontology, 23(2), 169–199. https://doi.org/10.1007/s10522-022-09958-x.
Sun, N., Youle, R. J., & Finkel, T. (2016). The Mitochondrial Basis of Aging. Molecular cell, 61(5), 654–666. https://doi.org/10.1016/j.molcel.2016.01.028.
Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., White, J. P., Teodoro, J. S., Wrann, C. D., Hubbard, B. P., Mercken, E. M., Palmeira, C. M., de Cabo, R., Rolo, A. P., Turner, N., Bell, E. L., & Sinclair, D. A. (2013). Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624–1638. https://doi.org/10.1016/j.cell.2013.11.037.
Das, A., Huang, G. X., Bonkowski, M. S., Longchamp, A., Li, C., Schultz, M. B., Kim, L. J., Osborne, B., Joshi, S., Lu, Y., Treviño-Villarreal, J. H., Kang, M. J., Hung, T. T., Lee, B., Williams, E. O., Igarashi, M., Mitchell, J. R., Wu, L. E., Turner, N., Arany, Z., … Sinclair, D. A. (2018). Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging. Cell, 173(1), 74–89.e20. https://doi.org/10.1016/j.cell.2018.02.008.
Ryu, D., Zhang, H., Ropelle, E. R., Sorrentino, V., Mázala, D. A., Mouchiroud, L., Marshall, P. L., Campbell, M. D., Ali, A. S., Knowels, G. M., Bellemin, S., Iyer, S. R., Wang, X., Gariani, K., Sauve, A. A., Cantó, C., Conley, K. E., Walter, L., Lovering, R. M., Chin, E. R., … Auwerx, J. (2016). NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation. Science translational medicine, 8(361), 361ra139. https://doi.org/10.1126/scitranslmed.aaf5504.
Mills, K. F., Yoshida, S., Stein, L. R., Grozio, A., Kubota, S., Sasaki, Y., Redpath, P., Migaud, M. E., Apte, R. S., Uchida, K., Yoshino, J., & Imai, S. I. (2016). Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell metabolism, 24(6), 795–806. https://doi.org/10.1016/j.cmet.2016.09.013.
Lin, J. B., Kubota, S., Ban, N., Yoshida, M., Santeford, A., Sene, A., Nakamura, R., Zapata, N., Kubota, M., Tsubota, K., Yoshino, J., Imai, S. I., & Apte, R. S. (2016). NAMPT-Mediated NAD(+) Biosynthesis Is Essential for Vision In Mice. Cell reports, 17(1), 69–85. https://doi.org/10.1016/j.celrep.2016.08.073.
Khan, N. A., Auranen, M., Paetau, I., Pirinen, E., Euro, L., Forsström, S., Pasila, L., Velagapudi, V., Carroll, C. J., Auwerx, J., & Suomalainen, A. (2014). Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO molecular medicine, 6(6), 721–731. https://doi.org/10.1002/emmm.201403943.
Brown, K. D., Maqsood, S., Huang, J. Y., Pan, Y., Harkcom, W., Li, W., Sauve, A., Verdin, E., & Jaffrey, S. R. (2014). Activation of SIRT3 by the NAD⁺ precursor nicotinamide riboside protects from noise-induced hearing loss. Cell metabolism, 20(6), 1059–1068. https://doi.org/10.1016/j.cmet.2014.11.003.
Yoshino, J., Mills, K. F., Yoon, M. J., & Imai, S. (2011). Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell metabolism, 14(4), 528–536. https://doi.org/10.1016/j.cmet.2011.08.014.
Yang, Q., Cong, L., Wang, Y., Luo, X., Li, H., Wang, H., Zhu, J., Dai, S., Jin, H., Yao, G., Shi, S., Hsueh, A. J., & Sun, Y. (2020). Increasing ovarian NAD+ levels improve mitochondrial functions and reverse ovarian aging. Free radical biology & medicine, 156, 1–10. https://doi.org/10.1016/j.freeradbiomed.2020.05.003.
Roh, E., Myoung Kang, G., Young Gil, S., Hee Lee, C., Kim, S., Hong, D., Hoon Son, G., & Kim, M. S. (2018). Effects of Chronic NAD Supplementation on Energy Metabolism and Diurnal Rhythm in Obese Mice. Obesity (Silver Spring, Md.), 26(9), 1448–1456. https://doi.org/10.1002/oby.22263.
Alegre, J., Rosés, J. M., Javierre, C., Ruiz-Baqués, A., Segundo, M. J., & de Sevilla, T. F. (2010). Nicotinamida adenina dinucleótido (NADH) en pacientes con síndrome de fatiga crónica [Nicotinamide adenine dinucleotide (NADH) in patients with chronic fatigue syndrome]. Revista clinica espanola, 210(6), 284–288. https://doi.org/10.1016/j.rce.2009.09.015.
Dehhaghi, M., Panahi, H., Kavyani, B., Heng, B., Tan, V., Braidy, N., & Guillemin, G. J. (2022). The Role of Kynurenine Pathway and NAD+ Metabolism in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Aging and disease, 13(3), 698–711. https://doi.org/10.14336/AD.2021.0824.
Castro-Marrero, J., Segundo, M. J., Lacasa, M., Martinez-Martinez, A., Sentañes, R. S., & Alegre-Martin, J. (2021). Effect of Dietary Coenzyme Q10 Plus NADH Supplementation on Fatigue Perception and Health-Related Quality of Life in Individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial. Nutrients, 13(8), 2658. https://doi.org/10.3390/nu13082658.
Castro-Marrero, J., Sáez-Francàs, N., Segundo, M. J., Calvo, N., Faro, M., Aliste, L., Fernández de Sevilla, T., & Alegre, J. (2016). Effect of coenzyme Q10 plus nicotinamide adenine dinucleotide supplementation on maximum heart rate after exercise testing in chronic fatigue syndrome – A randomized, controlled, double-blind trial. Clinical nutrition (Edinburgh, Scotland), 35(4), 826–834. https://doi.org/10.1016/j.clnu.2015.07.010.
Castro-Marrero, J., Cordero, M. D., Segundo, M. J., Sáez-Francàs, N., Calvo, N., Román-Malo, L., Aliste, L., Fernández de Sevilla, T., & Alegre, J. (2015). Does oral coenzyme Q10 plus NADH supplementation improve fatigue and biochemical parameters in chronic fatigue syndrome?. Antioxidants & redox signaling, 22(8), 679–685. https://doi.org/10.1089/ars.2014.6181.
Mach, J., Midgley, A. W., Dank, S., Grant, R. S., & Bentley, D. J. (2010). The effect of antioxidant supplementation on fatigue during exercise: potential role for NAD+(H). Nutrients, 2(3), 319–329. https://doi.org/10.3390/nu2030319.
Santaella, M. L., Font, I., & Disdier, O. M. (2004). Comparison of oral nicotinamide adenine dinucleotide (NADH) versus conventional therapy for chronic fatigue syndrome. Puerto Rico health sciences journal, 23(2), 89–93.
Stein LR, Imai S. The dynamic regulation of NAD metabolism in mitochondria. Trends EndocrinolMetab. 2012;23(9):420-428. doi:10.1016/j.tem.2012.06.005.
Garten A, Schuster S, Penke M, Gorski T, de Giorgis T, Kiess W. Physiological and pathophysiological roles of NAMPT and NAD metabolism. Nat Rev Endocrinol. 2015;11(9):535-546. doi:10.1038/nrendo.2015.117.
Uddin GM, Youngson NA, Sinclair DA, Morris MJ. Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice. Front Pharmacol. 2016;7:258. Published 2016 Aug 19. doi:10.3389/fphar.2016.00258.
Rappou E, Jukarainen S, Rinnankoski-Tuikka R et al (2016) Weight loss is associated with increased NAD+/SIRT1 expression but reduced PARP activity in white adipose tissue. J ClinEndocrinolMetab 101(3):1263–1273. https://doi.org/10.1210/jc.2015-3054.
Cantó C, Houtkooper RH, Pirinen E, et al. The NAD(+) precursor nicotinamideriboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metab. 2012;15(6):838-847. doi:10.1016/j.cmet.2012.04.022.
Crisol BM, Veiga CB, Lenhare L, et al. Nicotinamideriboside induces a thermogenic response in lean mice. Life Sci. 2018;211:1-7. doi:10.1016/j.lfs.2018.09.015.
Jukarainen S, Heinonen S, Rämö JT, et al. Obesity Is Associated With Low NAD(+)/SIRT Pathway Expression in Adipose Tissue of BMI-Discordant Monozygotic Twins. J ClinEndocrinolMetab. 2016;101(1):275-283. doi:10.1210/jc.2015-3095.
Yamaguchi S, Yoshino J. Adipose tissue NAD+ biology in obesity and insulin resistance: From mechanism to therapy. Bioessays. 2017;39(5):10.1002/bies.201600227. doi:10.1002/bies.201600227.
Yoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD (+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011;14(4):528–536. doi: 10.1016/j.cmet.2011.08.014.
Trammell SA, Weidemann BJ, Chadda A, Yorek MS, Holmes A, Coppey LJ, Obrosov A, Kardon RH, Yorek MA, Brenner C. Nicotinamideriboside opposes type 2 diabetes and neuropathy in mice. Sci Rep. 2016;6:26933. doi: 10.1038/srep26933.
Frederick DW, Davis JG, Davila A, Jr, Agarwal B, Michan S, Puchowicz MA, Nakamaru-Ogiso E, Baur JA. Increasing NAD synthesis in muscle via nicotinamidephosphoribosyltransferase is not sufficient to promote oxidative metabolism. J Biol Chem. 2015;290(3):1546–1558. doi: 10.1074/jbc.M114.579565.
Sasaki T, Kikuchi O, Shimpuku M, Susanti VY, Yokota-Hashimoto H, Taguchi R, Shibusawa N, Sato T, et al. Hypothalamic SIRT1 prevents age-associated weight gain by improving leptin sensitivity in mice. Diabetologia. 2014;57(4):819–831. doi: 10.1007/s00125-013-3140-5.
Yamaguchi S, Franczyk MP, Chondronikola M, et al. Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice. ProcNatlAcadSci U S A. 2019;116(47):23822-23828. doi:10.1073/pnas.1909917116.
Mills, K. F., Yoshida, S., Stein, L. R., Grozio, A., Kubota, S., Sasaki, Y., et al. (2016). Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice. Cell Metab. 24, 795–806. doi: 10.1016/j.cmet.2016.09.013.
Cantó, C., Houtkooper, R. H., Pirinen, E., Youn, D. Y., Oosterveer, M. H., Cen, Y., Fernandez-Marcos, P. J., Yamamoto, H., Andreux, P. A., Cettour-Rose, P., Gademann, K., Rinsch, C., Schoonjans, K., Sauve, A. A., & Auwerx, J. (2012). The NAD(+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell metabolism, 15(6), 838–847. https://doi.org/10.1016/j.cmet.2012.04.022.
Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., White, J. P., Teodoro, J. S., Wrann, C. D., Hubbard, B. P., Mercken, E. M., Palmeira, C. M., de Cabo, R., Rolo, A. P., Turner, N., Bell, E. L., & Sinclair, D. A. (2013). Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624–1638. https://doi.org/10.1016/j.cell.2013.11.037.
Yaku K, Okabe K, Hikosaka K, Nakagawa T. NAD Metabolism in Cancer Therapeutics. Front Oncol. 2018;8:622. Published 2018 Dec 12. doi:10.3389/fonc.2018.00622.
Lewis JE, Singh N, Holmila RJ, et al. Targeting NAD+ Metabolism to Enhance Radiation Therapy Responses. SeminRadiatOncol. 2019;29(1):6-15. doi:10.1016/j.semradonc.2018.10.009.
Djouder N. Boosting NAD(+) for the prevention and treatment of liver cancer. Mol Cell Oncol. 2015;2(4):e1001199. Published 2015 Feb 3. doi:10.1080/23723556.2014.1001199.
Elhassan YS, Kluckova K, Fletcher RS, et al. NicotinamideRiboside Augments the Aged Human Skeletal Muscle NAD+ Metabolome and Induces Transcriptomic and Anti-inflammatory Signatures. Cell Rep. 2019;28(7):1717-1728.e6. doi:10.1016/j.celrep.2019.07.043.
Mendelsohn AR, Larrick JW. Partial reversal of skeletal muscle aging by restoration of normal NAD⁺ levels. Rejuvenation Res. 2014;17(1):62-69. doi:10.1089/rej.2014.1546.
Goody MF, Henry CA. A need for NAD+ in muscle development, homeostasis, and aging. Skelet Muscle. 2018;8(1):9. Published 2018 Mar 7. doi:10.1186/s13395-018-0154-1.
Lautrup, S., Sinclair, D. A., Mattson, M. P., & Fang, E. F. (2019). NAD+ in Brain Aging and Neurodegenerative Disorders. Cell metabolism, 30(4), 630–655. https://doi.org/10.1016/j.cmet.2019.09.001.
Mao, K., & Zhang, G. (2022). The role of PARP1 in neurodegenerative diseases and aging. The FEBS journal, 289(8), 2013–2024. https://doi.org/10.1111/febs.15716.
Ying W. (2007). NAD+ and NADH in brain functions, brain diseases and brain aging. Frontiers in bioscience: a journal and virtual library, 12, 1863–1888. https://doi.org/10.2741/2194.
Lloret, A., & Beal, M. F. (2019). PGC-1α, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All. Neurochemical research, 44(10), 2423–2434. https://doi.org/10.1007/s11064-019-02809-1.
Yang H, Yang T, Baur JA, et al. Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. Cell. 2007;130(6):1095-1107. doi:10.1016/j.cell.2007.07.035.
Verdin E. NAD⁺ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208-1213. doi:10.1126/science.aac4854.
Ying W. NAD+ and NADH in brain functions, brain diseases and brain aging. Front Biosci. 2007;12:1863-1888. Published 2007 Jan 1. doi:10.2741/2194.
Belenky P, Racette FG, Bogan KL, McClure JM, Smith JS, Brenner C. Nicotinamideriboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+. Cell. 2007 May 4;129(3):473-84.
Rajman L, Chwalek K, Sinclair DA. Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metab. 2018;27(3):529-547. doi:10.1016/j.cmet.2018.02.011.
Massudi H, Grant R, Braidy N, Guest J, Farnsworth B, Guillemin GJ. Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLoS One. 2012;7(7):e42357. doi:10.1371/journal.pone.0042357.
Braidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. ExpGerontol. 2020;132:110831. doi:10.1016/j.exger.2020.110831.
Schultz MB, Sinclair DA. Why NAD(+) Declines during Aging: It’s Destroyed. Cell Metab. 2016;23(6):965-966. doi:10.1016/j.cmet.2016.05.022.
Yaku K, Okabe K, Nakagawa T. NAD metabolism: Implications in aging and longevity. Ageing Res Rev. 2018;47:1-17. doi:10.1016/j.arr.2018.05.006.
Cantó C, Menzies KJ, Auwerx J. NAD(+) Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus. Cell Metab. 2015;22(1):31-53. doi:10.1016/j.cmet.2015.05.023.
Zhang N, Sauve AA. Regulatory Effects of NAD+ Metabolic Pathways on Sirtuin Activity. ProgMolBiolTransl Sci. 2018;154:71-104. doi:10.1016/bs.pmbts.2017.11.012.
Connell, N.J., Houtkooper, R.H. &Schrauwen, P. NAD+ metabolism as a target for metabolic health: have we found the silver bullet?.Diabetologia 62, 888–899 (2019). https://doi.org/10.1007/s00125-019-4831-3.
Elhassan YS, Philp AA, Lavery GG. Targeting NAD+ in Metabolic Disease: New Insights Into an Old Molecule. J Endocr Soc. 2017;1(7):816-835. Published 2017 May 15. doi:10.1210/js.2017-00092.
Okabe K, Yaku K, Tobe K, Nakagawa T. Implications of altered NAD metabolism in metabolic disorders. J Biomed Sci. 2019;26(1):34. Published 2019 May 11. doi:10.1186/s12929-019-0527-8.
Prolla TA, Denu JM. NAD+ deficiency in age-related mitochondrial dysfunction. Cell Metab. 2014;19(2):178-180. doi:10.1016/j.cmet.2014.01.005.
Seo KS, Kim JH, Min KN, et al. KL1333, a Novel NAD+ Modulator, Improves Energy Metabolism and Mitochondrial Dysfunction in MELAS Fibroblasts. Front Neurol. 2018;9:552. Published 2018 Jul 5. doi:10.3389/fneur.2018.00552.
Goody MF, Henry CA. A need for NAD+ in muscle development, homeostasis, and aging. Skelet Muscle. 2018;8(1):9. Published 2018 Mar 7. doi:10.1186/s13395-018-0154-1.
Lightowlers RN, Chrzanowska-Lightowlers ZM. Salvaging hope: Is increasing NAD(+) a key to treating mitochondrial myopathy?. EMBO Mol Med. 2014;6(6):705-707. doi:10.15252/emmm.201404179.
Srivastava S. Emerging therapeutic roles for NAD(+) metabolism in mitochondrial and age-related disorders. ClinTransl Med. 2016;5(1):25. doi:10.1186/s40169-016-0104-7.
Yang Y, Sauve AA. NAD(+) metabolism: Bioenergetics, signaling and manipulation for therapy. BiochimBiophysActa. 2016;1864(12):1787-1800. doi:10.1016/j.bbapap.2016.06.014.
Liu D, Pitta M, Mattson MP. Preventing NAD(+) depletion protects neurons against excitotoxicity: bioenergetic effects of mild mitochondrial uncoupling and caloric restriction. Ann N Y Acad Sci. 2008;1147:275-282. doi:10.1196/annals.1427.028.
Brennan AM, Connor JA, Shuttleworth CW. NAD(P)H fluorescence transients after synaptic activity in brain slices: predominant role of mitochondrial function. J. Cereb. Blood Flow Metab. 2006;26:1389–1406.
Yaku, K., Okabe, K., Gulshan, M. et al. Metabolism and biochemical properties of nicotinamide adenine dinucleotide (NAD) analogs, nicotinamide guanine dinucleotide (NGD) and nicotinamide hypoxanthine dinucleotide (NHD). Sci Rep 9, 13102 (2019). https://doi.org/10.1038/s41598-019-49547-6.
Fricker RA, Green EL, Jenkins SI, Griffin SM. The Influence of Nicotinamide on Health and Disease in the Central Nervous System. Int J Tryptophan Res. 2018;11:1178646918776658. Published 2018 May 21. doi:10.1177/1178646918776658.
Grant R, Berg J, Mestayer R, et al. A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ MetabolomeDuring a 6 Hour Intravenous Infusion of NAD. Front Aging Neurosci. 2019;11:257. Published 2019 Sep 12. doi:10.3389/fnagi.2019.00257.
Lloret A, Beal MF. PGC-1α, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All. Neurochem Res. 2019;44(10):2423-2434. doi:10.1007/s11064-019-02809-1.
Ying W. NAD+ and NADH in brain functions, brain diseases and brain aging. Front Biosci. 2007;12:1863-1888. Published 2007 Jan 1. doi:10.2741/2194.
Liu D, Gharavi R, Pitta M, Gleichmann M, Mattson MP. Nicotinamide prevents NAD+ depletion and protects neurons against excitotoxicity and cerebral ischemia: NAD+ consumption by SIRT1 may endanger energetically compromised neurons. Neuromolecular Med. 2009;11(1):28-42. doi:10.1007/s12017-009-8058-1.
Liu J, Yang B, Zhou P, et al. Nicotinamide adenine dinucleotide suppresses epileptogenesis at an early stage. Sci Rep. 2017;7(1):7321. Published 2017 Aug 4. doi:10.1038/s41598-017-07343-0.
Alano CC, Garnier P, Ying W, Higashi Y, Kauppinen TM, Swanson RA. NAD+ depletion is necessary and sufficient for poly(ADP-ribose) polymerase-1-mediated neuronal death. J Neurosci. 2010;30(8):2967-2978. doi:10.1523/JNEUROSCI.5552-09.2010.
Hou Y, Lautrup S, Cordonnier S, et al. NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. ProcNatlAcadSci U S A. 2018;115(8):E1876-E1885. doi:10.1073/pnas.1718819115.
Xing S, Hu Y, Huang X, Shen D, Chen C. Nicotinamidephosphoribosyltransferase‑related signaling pathway in early Alzheimer’s disease mouse models. Mol Med Rep. 2019;20(6):5163-5171. doi:10.3892/mmr.2019.10782.
Braidy N, Grant R, Sachdev PS. Nicotinamide adenine dinucleotide and its related precursors for the treatment of Alzheimer’s disease. CurrOpin Psychiatry. 2018;31(2):160-166. doi:10.1097/YCO.0000000000000394.
Demarin V, Podobnik SS, Storga-Tomic D, Kay G. Treatment of Alzheimer’s disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study. Drugs ExpClin Res. 2004;30(1):27-33.
Fang EF, Hou Y, Lautrup S, et al. NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome. Nat Commun. 2019;10(1):5284. Published 2019 Nov 21. doi:10.1038/s41467-019-13172-8.
Dong, Y., Sameni, S., Digman, M.A. et al. Reversibility of Age-related Oxidized Free NADH Redox States in Alzheimer’s Disease Neurons by Imposed External Cys/CySS Redox Shifts. Sci Rep 9, 11274 (2019). https://doi.org/10.1038/s41598-019-47582-x.
Sorrentino, V., Romani, M., Mouchiroud, L., Beck, J. S., Zhang, H., D’Amico, D., Moullan, N., Potenza, F., Schmid, A. W., Rietsch, S., Counts, S. E., & Auwerx, J. (2017). Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity. Nature, 552(7684), 187–193. https://doi.org/10.1038/nature25143.
Wu, L. E., Gomes, A. P., & Sinclair, D. A. (2014). Geroncogenesis: metabolic changes during aging as a driver of tumorigenesis. Cancer cell, 25(1), 12–19. https://doi.org/10.1016/j.ccr.2013.12.005.
Firestein, R., Blander, G., Michan, S., Oberdoerffer, P., Ogino, S., Campbell, J., Bhimavarapu, A., Luikenhuis, S., de Cabo, R., Fuchs, C., Hahn, W. C., Guarente, L. P., & Sinclair, D. A. (2008). The SIRT1 deacetylase suppresses intestinal tumorigenesis and colon cancer growth. PloS one, 3(4), e2020. https://doi.org/10.1371/journal.pone.0002020.
Sebastián, C., Zwaans, B. M., Silberman, D. M., Gymrek, M., Goren, A., Zhong, L., Ram, O., Truelove, J., Guimaraes, A. R., Toiber, D., Cosentino, C., Greenson, J. K., MacDonald, A. I., McGlynn, L., Maxwell, F., Edwards, J., Giacosa, S., Guccione, E., Weissleder, R., Bernstein, B. E., … Mostoslavsky, R. (2012). The histone deacetylase SIRT6 is a tumor suppressor that controls cancer metabolism. Cell, 151(6), 1185–1199. https://doi.org/10.1016/j.cell.2012.10.047.
Lee MK, Cheong HS, Koh Y, Ahn KS, Yoon SS, Shin HD. Genetic Association of PARP15 Polymorphisms with Clinical Outcome of Acute Myeloid Leukemia in a Korean Population. Genet Test Mol Biomarkers. 2016;20:696–701.
Dollerup O.L., Christensen B., Svart M., Schmidt M.S., Sulek K., Ringgaard S., Stødkilde-Jørgensen H., Møller N., Brenner C., Treebak J.T., Jessen N. A randomized placebo-controlled clinical trial of nicotinamideriboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. Am. J. Clin. Nutr. 2018;108:343–353.
Martens C.R., Denman B.A., Mazzo M.R., Armstrong M.L., Reisdorph N., McQueen M.B., Chonchol M., Seals D.R. Chronic nicotinamideriboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat. Commun. 2018;9:1286.
Yaku K, Okabe K, Hikosaka K, Nakagawa T. NAD Metabolism in Cancer Therapeutics. Front Oncol. 2018;8:622. Published 2018 Dec 12. doi:10.3389/fonc.2018.00622.
Available from https://www.biorxiv.org/content/10.1101/2020.03.21.001123v1.
Sundaresan, N. R., Gupta, M., Kim, G., Rajamohan, S. B., Isbatan, A., & Gupta, M. P. (2009). Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. The Journal of clinical investigation, 119(9), 2758–2771. https://doi.org/10.1172/JCI39162.
Hafner, A. V., Dai, J., Gomes, A. P., Xiao, C. Y., Palmeira, C. M., Rosenzweig, A., & Sinclair, D. A. (2010). Regulation of the mPTP by SIRT3-mediated deacetylation of CypD at lysine 166 suppresses age-related cardiac hypertrophy. Aging, 2(12), 914–923. https://doi.org/10.18632/aging.100252.
Sundaresan, N. R., Gupta, M., Kim, G., Rajamohan, S. B., Isbatan, A., & Gupta, M. P. (2009). Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. The Journal of clinical investigation, 119(9), 2758–2771. https://doi.org/10.1172/JCI39162.
Nacarelli, T., Lau, L., Fukumoto, T., Zundell, J., Fatkhutdinov, N., Wu, S., Aird, K. M., Iwasaki, O., Kossenkov, A. V., Schultz, D., Noma, K. I., Baur, J. A., Schug, Z., Tang, H. Y., Speicher, D. W., David, G., & Zhang, R. (2019). NAD+ metabolism governs the proinflammatory senescence-associated secretome. Nature cell biology, 21(3), 397–407. https://doi.org/10.1038/s41556-019-0287-4.
Gong B, Pan Y, Vempati P, et al. Nicotinamideriboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models. Neurobiol Aging. 2013;34(6):1581-1588. doi:10.1016/j.neurobiolaging.2012.12.005.
Matasic DS, Brenner C, London B. Emerging potential benefits of modulating NAD+ metabolism in cardiovascular disease. Am J Physiol Heart Circ Physiol. 2018;314(4):H839-H852. doi:10.1152/ajpheart.00409.2017.
Alano CC, Tran A, Tao R, Ying W, Karliner JS, Swanson RA. Differences among cell types in NAD+ compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes. J Neurosci Res 85: 3378–3385, 2007. doi:10.1002/jnr.21479.
de Picciotto NE, Gano LB, Johnson LC, Martens CR, Sindler AL, Mills KF, Imai S, Seals DR. Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice. Aging Cell 15: 522–530, 2016. doi:10.1111/acel.12461.
Alano CC, Tran A, Tao R, Ying W, Karliner JS, Swanson RA. Differences among cell types in NAD+ compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes. J Neurosci Res 85: 3378–3385, 2007. doi:10.1002/jnr.21479.
Liu L, Wang P, Liu X, He D, Liang C, Yu Y. Exogenous NAD(+) supplementation protects H9c2 cardiac myoblasts against hypoxia/reoxygenation injury via Sirt1-p53 pathway. FundamClinPharmacol. 2014;28(2):180-189. doi:10.1111/fcp.12016.
Ryu D, Zhang H, Ropelle ER, Sorrentino V, Mazala DA, Mouchiroud L, Marshall PL, Campbell MD, Ali AS, Knowels GM, et al. NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation. SciTransl Med. 2016;8:361ra139.
Xu W, Barrientos T, Mao L, Rockman HA, Sauve AA, Andrews NC. Lethal Cardiomyopathy in Mice Lacking Transferrin Receptor in the Heart. Cell Rep. 2015;13:533–545.
Chan PK, Torres R, Yandim C, Law PP, Khadayate S, Mauri M, Grosan C, Chapman-Rothe N, Giunti P, Pook M, et al. Heterochromatinization induced by GAA-repeat hyperexpansion in Friedreich’s ataxia can be reduced upon HDAC inhibition by vitamin B3. Hum Mol Genet. 2013;22:2662–2675.
Martin AS, Abraham DM, Hershberger KA, Bhatt DP, Mao L, Cui H, Liu J, Liu X, Muehlbauer MJ, Grimsrud PA, et al. Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model. JCI Insight. 2017;2.
Katsyuba, E., Romani, M., Hofer, D. et al. NAD+ homeostasis in health and disease. Nat Metab 2, 9–31 (2020). https://doi.org/10.1038/s42255-019-0161-5.
Walker MA, Tian R. Raising NAD in Heart Failure: Time to Translate?. Circulation. 2018;137(21):2274-2277. doi:10.1161/CIRCULATIONAHA.117.032626.
Airhart SE, Shireman LM, Risler LJ, et al. An open-label, non-randomized study of the pharmacokinetics of the nutritional supplement nicotinamideriboside (NR) and its effects on blood NAD+ levels in healthy volunteers. PLoS One. 2017;12(12):e0186459. Published 2017 Dec 6. doi:10.1371/journal.pone.0186459.
Lee CF, Caudal A, Abell L, NaganaGowda GA, Tian R. Targeting NAD+ Metabolism as Interventions for Mitochondrial Disease. Sci Rep. 2019;9(1):3073. Published 2019 Feb 28. doi:10.1038/s41598-019-39419-4.
Zhou, B., Wang, D. D., Qiu, Y., Airhart, S., Liu, Y., Stempien-Otero, A., O’Brien, K. D., & Tian, R. (2020). Boosting NAD level suppresses inflammatory activation of PBMCs in heart failure. The Journal of clinical investigation, 130(11), 6054–6063. https://doi.org/10.1172/JCI138538.
Hsu, C. P., Oka, S., Shao, D., Hariharan, N., & Sadoshima, J. (2009). Nicotinamide phosphoribosyltransferase regulates cell survival through NAD+ synthesis in cardiac myocytes. Circulation research, 105(5), 481–491. https://doi.org/10.1161/CIRCRESAHA.109.203703.
Karamanlidis, G., Lee, C. F., Garcia-Menendez, L., Kolwicz, S. C., Jr, Suthammarak, W., Gong, G., Sedensky, M. M., Morgan, P. G., Wang, W., & Tian, R. (2013). Mitochondrial complex I deficiency increases protein acetylation and accelerates heart failure. Cell metabolism, 18(2), 239–250. https://doi.org/10.1016/j.cmet.2013.07.002.
Pillai, J. B., Isbatan, A., Imai, S., & Gupta, M. P. (2005). Poly(ADP-ribose) polymerase-1-dependent cardiac myocyte cell death during heart failure is mediated by NAD+ depletion and reduced Sir2alpha deacetylase activity. The Journal of biological chemistry, 280(52), 43121–43130. https://doi.org/10.1074/jbc.M506162200.
Yamamoto, T., Byun, J., Zhai, P., Ikeda, Y., Oka, S., & Sadoshima, J. (2014). Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and reperfusion. PloS one, 9(6), e98972. https://doi.org/10.1371/journal.pone.0098972.
Mattagajasingh, I., Kim, C. S., Naqvi, A., Yamamori, T., Hoffman, T. A., Jung, S. B., DeRicco, J., Kasuno, K., & Irani, K. (2007). SIRT1 promotes endothelium-dependent vascular relaxation by activating endothelial nitric oxide synthase. Proceedings of the National Academy of Sciences of the United States of America, 104(37), 14855–14860. https://doi.org/10.1073/pnas.0704329104.
Uddin, G. M., Youngson, N. A., Doyle, B. M., Sinclair, D. A., and Morris, M. J. (2017). Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise. Sci. Rep. 7:15063. doi: 10.1038/s41598-017-14866-z.
Porter LC, Franczyk MP, Pietka T, et al. NAD+-dependent deacetylase SIRT3 in adipocytes is dispensable for maintaining normal adipose tissue mitochondrial function and whole body metabolism. Am J PhysiolEndocrinolMetab. 2018;315(4):E520-E530. doi:10.1152/ajpendo.00057.2018.
Martens CR, Denman BA, Mazzo MR, et al. Chronic nicotinamideriboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nat Commun. 2018;9(1):1286. Published 2018 Mar 29. doi:10.1038/s41467-018-03421-7.
Yoshino, M., Yoshino, J., Kayser, B. D., Patti, G. J., Franczyk, M. P., Mills, K. F., Sindelar, M., Pietka, T., Patterson, B. W., Imai, S. I., & Klein, S. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science (New York, N.Y.), 372(6547), 1224–1229. https://doi.org/10.1126/science.abe9985.
Camacho-Pereira, J., Tarragó, M. G., Chini, C., Nin, V., Escande, C., Warner, G. M., Puranik, A. S., Schoon, R. A., Reid, J. M., Galina, A., & Chini, E. N. (2016). CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell metabolism, 23(6), 1127–1139. https://doi.org/10.1016/j.cmet.2016.05.006.
Escande, C., Nin, V., Price, N. L., Capellini, V., Gomes, A. P., Barbosa, M. T., O’Neil, L., White, T. A., Sinclair, D. A., & Chini, E. N. (2013). Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes, 62(4), 1084–1093. https://doi.org/10.2337/db12-1139.
Koetz, K., Bryl, E., Spickschen, K., O’Fallon, W. M., Goronzy, J. J., & Weyand, C. M. (2000). T cell homeostasis in patients with rheumatoid arthritis. Proceedings of the National Academy of Sciences of the United States of America, 97(16), 9203–9208. https://doi.org/10.1073/pnas.97.16.9203.
Fyhrquist, F., Tiitu, A., Saijonmaa, O., Forsblom, C., Groop, P. H., & FinnDiane Study Group (2010). Telomere length and progression of diabetic nephropathy in patients with type 1 diabetes. Journal of internal medicine, 267(3), 278–286. https://doi.org/10.1111/j.1365-2796.2009.02139.x.
Testa, R., Olivieri, F., Sirolla, C., Spazzafumo, L., Rippo, M. R., Marra, M., Bonfigli, A. R., Ceriello, A., Antonicelli, R., Franceschi, C., Castellucci, C., Testa, I., & Procopio, A. D. (2011). Leukocyte telomere length is associated with complications of type 2 diabetes mellitus. Diabetic medicine : a journal of the British Diabetic Association, 28(11), 1388–1394. https://doi.org/10.1111/j.1464-5491.2011.03370.x.
Niren N. M. (2006). Pharmacologic doses of nicotinamide in the treatment of inflammatory skin conditions: a review. Cutis, 77(1 Suppl), 11–16.
Kaneko, S., Wang, J., Kaneko, M., Yiu, G., Hurrell, J. M., Chitnis, T., Khoury, S. J., & He, Z. (2006). Protecting axonal degeneration by increasing nicotinamide adenine dinucleotide levels in experimental autoimmune encephalomyelitis models. The Journal of neuroscience : the official journal of the Society for Neuroscience, 26(38), 9794–9804. https://doi.org/10.1523/JNEUROSCI.2116-06.2006.
Damian, D. L., Patterson, C. R., Stapelberg, M., Park, J., Barnetson, R. S., & Halliday, G. M. (2008). UV radiation-induced immunosuppression is greater in men and prevented by topical nicotinamide. The Journal of investigative dermatology, 128(2), 447–454. https://doi.org/10.1038/sj.jid.5701058.
Gensler H. L. (1997). Prevention of photoimmunosuppression and photocarcinogenesis by topical nicotinamide. Nutrition and cancer, 29(2), 157–162. https://doi.org/10.1080/01635589709514618.
Yiasemides, E., Sivapirabu, G., Halliday, G. M., Park, J., & Damian, D. L. (2009). Oral nicotinamide protects against ultraviolet radiation-induced immunosuppression in humans. Carcinogenesis, 30(1), 101–105. https://doi.org/10.1093/carcin/bgn248.
Omran, H. M., & Almaliki, M. S. (2020). Influence of NAD+ as an ageing-related immunomodulator on COVID 19 infection: A hypothesis. Journal of infection and public health, 13(9), 1196–1201. https://doi.org/10.1016/j.jiph.2020.06.004.
Hiromatsu, Y., Yang, D., Miyake, I., Koga, M., Kameo, J., Sato, M., Inoue, Y., & Nonaka, K. (1998). Nicotinamide decreases cytokine-induced activation of orbital fibroblasts from patients with thyroid-associated ophthalmopathy. The Journal of clinical endocrinology and metabolism, 83(1), 121–124. https://doi.org/10.1210/jcem.83.1.4478.
Hiromatsu, Y., Sato, M., Tanaka, K., Ishisaka, N., Kamachi, J., & Nonaka, K. (1993). Inhibitory effects of nicotinamide on intercellular adhesion molecule-1 expression on cultured human thyroid cells. Immunology, 80(2), 330–332.
Silwal P., Shin K., Choi S., Namgung U., Lee C.Y., Heo J.-Y.-Y. Tryptophan negatively regulates IgE-mediated mast cell activation. Korean J Phys Anthropol. 2017;30:53. doi: 10.11637/kjpa.2017.30.2.53.
Picard, F., Kurtev, M., Chung, N., Topark-Ngarm, A., Senawong, T., Machado De Oliveira, R., Leid, M., McBurney, M. W., & Guarente, L. (2004). Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-gamma. Nature, 429(6993), 771–776. https://doi.org/10.1038/nature02583.
Rodgers, J. T., Lerin, C., Haas, W., Gygi, S. P., Spiegelman, B. M., & Puigserver, P. (2005). Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature, 434(7029), 113–118. https://doi.org/10.1038/nature03354.
Yang, F., Vought, B. W., Satterlee, J. S., Walker, A. K., Jim Sun, Z. Y., Watts, J. L., DeBeaumont, R., Saito, R. M., Hyberts, S. G., Yang, S., Macol, C., Iyer, L., Tjian, R., van den Heuvel, S., Hart, A. C., Wagner, G., & Näär, A. M. (2006). An ARC/Mediator subunit required for SREBP control of cholesterol and lipid homeostasis. Nature, 442(7103), 700–704. https://doi.org/10.1038/nature04942.
Remie CME, Roumans KHM, Moonen MPB, et al. Nicotinamideriboside supplementation alters body composition and skeletal muscle acetylcarnitine concentrations in healthy obese humans [published online ahead of print, 2020 Apr 22]. Am J ClinNutr. 2020;nqaa072. doi:10.1093/ajcn/nqaa072.
deGuia RM, Agerholm M, Nielsen TS, et al. Aerobic and resistance exercise training reverses age-dependent decline in NAD+ salvage capacity in human skeletal muscle. Physiol Rep. 2019;7(12):e14139. doi:10.14814/phy2.14139.
Ryu D, Zhang H, Ropelle ER, et al. NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation. SciTransl Med. 2016;8(361):361ra139. doi:10.1126/scitranslmed.aaf5504.
Zhou CC, Yang X, Hua X, et al. Hepatic NAD(+) deficiency as a therapeutic target for non-alcoholic fatty liver disease in ageing. Br J Pharmacol. 2016;173(15):2352-2368. doi:10.1111/bph.13513.
Guarino M, Dufour JF. Nicotinamide and NAFLD: Is There Nothing New Under the Sun?. Metabolites. 2019;9(9):180. Published 2019 Sep 10. doi:10.3390/metabo9090180.
Wang S, Wan T, Ye M, et al. Nicotinamideriboside attenuates alcohol induced liver injuries via activation of SirT1/PGC-1α/mitochondrial biosynthesis pathway. Redox Biol. 2018;17:89-98. doi:10.1016/j.redox.2018.04.006.
Pham TX, Bae M, Kim MB, et al. Nicotinamideriboside, an NAD+ precursor, attenuates the development of liver fibrosis in a diet-induced mouse model of liver fibrosis. BiochimBiophysActaMol Basis Dis. 2019;1865(9):2451-2463. doi:10.1016/j.bbadis.2019.06.009.
Han X, Bao X, Lou Q, et al. Nicotinamideriboside exerts protective effect against aging-induced NAFLD-like hepatic dysfunction in mice. PeerJ. 2019;7:e7568. Published 2019 Aug 28. doi:10.7717/peerj.7568.
Ralto KM, Rhee EP, Parikh SM. NAD+ homeostasis in renal health and disease. Nat Rev Nephrol. 2020;16(2):99-111. doi:10.1038/s41581-019-0216-6.
Hershberger KA, Martin AS, Hirschey MD. Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases. Nat Rev Nephrol. 2017;13(4):213-225. doi:10.1038/nrneph.2017.5.
PoyanMehr A, Parikh SM. PPARγ-Coactivator-1α, Nicotinamide Adenine Dinucleotide and Renal Stress Resistance. Nephron. 2017;137(4):253-255. doi:10.1159/000471895.
PoyanMehr A, Tran MT, Ralto KM, et al. De novo NAD+ biosynthetic impairment in acute kidney injury in humans. Nat Med. 2018;24(9):1351-1359. doi:10.1038/s41591-018-0138-z.
Zhuo, L., Fu, B., Bai, X., Zhang, B., Wu, L., Cui, J., Cui, S., Wei, R., Chen, X., & Cai, G. (2011). NAD blocks high glucose induced mesangial hypertrophy via activation of the sirtuins-AMPK-mTOR pathway. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 27(6), 681–690. https://doi.org/10.1159/000330077
Guan, Y., Wang, S. R., Huang, X. Z., Xie, Q. H., Xu, Y. Y., Shang, D., & Hao, C. M. (2017). Nicotinamide Mononucleotide, an NAD+ Precursor, Rescues Age-Associated Susceptibility to AKI in a Sirtuin 1-Dependent Manner. Journal of the American Society of Nephrology : JASN, 28(8), 2337–2352. https://doi.org/10.1681/ASN.2016040385
Morigi, M., Perico, L., Rota, C., Longaretti, L., Conti, S., Rottoli, D., Novelli, R., Remuzzi, G., & Benigni, A. (2015). Sirtuin 3-dependent mitochondrial dynamic improvements protect against acute kidney injury. The Journal of clinical investigation, 125(2), 715–726. https://doi.org/10.1172/JCI77632.
Tran, M. T., Zsengeller, Z. K., Berg, A. H., Khankin, E. V., Bhasin, M. K., Kim, W., Clish, C. B., Stillman, I. E., Karumanchi, S. A., Rhee, E. P., & Parikh, S. M. (2016). PGC1α drives NAD biosynthesis linking oxidative metabolism to renal protection. Nature, 531(7595), 528–532. https://doi.org/10.1038/nature17184.

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Sodium Carboxymethyl Beta Glucan (CM-Glucan), natural antioxidant and moisturizer

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CM-Glucan - The Repair and Defense Molecule

Sodium Carboxymethyl Beta Glucan (CM-Glucan) is a water-soluble derivative of natural beta-glucan, derived from oats or yeast, designed to deliver advanced skin hydration, soothing effects, and antioxidant protection. It is a multifunctional cosmetic ingredient used in moisturizers, serums, creams, and more.

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Ideal for use in moisturizers, eye creams, serums, after-sun care, masks, and makeup primers.
Forms a clear gel in water with a smooth, luxurious texture.
Enhances formulation viscosity while delivering a light, non-greasy feel.

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Chemical Information

INCI Name: Sodium Carboxymethyl Beta-Glucan
Synonyms: CM-Glucan™, GluCare™, Sodium Carboxymethyl β-Glucan
Molecular Formula: C18H32O16
Molecular Weight: 35,600~650,000 Dalton
CAS #: 9050-93-5
Form: White to off-white powder
Solubility: Water-soluble, forms a gel-like solution
Recommended Use Level: 0.02%~0.1%

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OxyGen® Oxytocin Nasal Spray (20 IU per spray)

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Oxytocin nasal spray is a scientifically formulated peptide-based wellness product designed to support social bonding, emotional regulation, stress reduction, and mood enhancement. Known as the "love hormone," oxytocin plays a critical role in a wide range of physiological and psychological functions—making it a valuable tool in both therapeutic and wellness settings.

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Product Specifications

Dosage: 20 IU per spray
Peptide Sequence: Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH₂
Molecular Formula: C₄₃H₆₆N₁₂O₁₂S₂
Molecular Weight: 1007.2 g/mol
CAS #: 50-56-6

How It Works

Oxytocin binds to oxytocin receptors (OXTRs), activating pathways that:

Trigger positive social behaviors and reduce stress
Influence neurotransmitters like dopamine, serotonin, and GABA
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Potential Side Effects

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Nausea
Dizziness
Gastrointestinal discomfort
Rare allergic reactions

Further research is ongoing to assess long-term use for neuropsychiatric support.

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N-Acetyl-Semax

$59.00

N-Acetyl Semax is a synthetic polypeptide analogous to the naturally occurring adrenocorticotropic hormone (ACTH). The peptide is similar to a fragment from the adrenocorticotropic hormone ACTH (4-7), specifically Met-Glu-His-Phe, combined with a Pro-Gly-Pro extension at the C-terminus.⁽¹⁾ The addition of Pro-Gly-Pro (PGP) to N-Acetyl Semax might enable an enhanced permeability through the blood-brain barrier (BBB) by increasing the peptide's lipophilicity via improving passive diffusion or uptake via lipid raft-mediated endocytosis, which may potentially allow it to bypass the tight junctions of the BBB. The PGP addition at the C-terminus might also alter the peptide's interaction with specific BBB transporters or receptors, possibly promoting receptor-mediated transcytosis. Additionally, the acetylation of the peptide might increase its resistance to enzymatic degradation, prolonging its half-life in experimental models.

Overview

N-Acetyl Semax appears to exhibit potential nootropic (memory enhancing) and neuroprotective characteristics, which researchers have proposed may be produced via several routes:

By potentially interacting with dopamine, serotonin, enkephalin, and brain-derived neurotrophic (BDNF) levels;⁽²⁾⁽³⁾
Or by potentially modulating gene expression and increasing the efficacy of the immune system.⁽⁴⁾

Based on studies suggesting that the peptide may inhibit serum enkephalin-degrading enzymes, it is plausible to hypothesize about the interactions between Semax and enkephalins. Researchers suggest Semax's inhibitory potential on enkephalin-degrading enzymes may lead to an increase in the levels of enkephalins by preventing their degradation. Enkephalins are endogenous opioids that are considered to play roles in nociception and stress response. Further, an increase in enkephalin levels might also influence other neurotransmitter systems due to the complex interplay between the opioid system and neurotransmitters like dopamine and serotonin.⁽²⁾

According to studies, Semax may potentially increase the striatal levels of 5-hydroxyindoleacetic acid (5-HIAA), a serotonin metabolite, suggesting a possible enhancement of serotonergic activity. This potential action on serotonin metabolism might amplify serotonin-mediated pathways, possibly influencing central nervous system functioning. On the other hand, Semax does not appear to directly alter dopamine levels or its metabolites. Still, it may modulate the dopaminergic system's responsiveness, enhancing the dopaminergic agonists' action.⁽⁵⁾

Chemical Info⁽⁶⁾

Molecular Formula: C₃₇H₅₁N₉O₁₀S
Molecular Weight: 858.97 g/mol
Synonyms: ACTH (4-7)PGP, HY-P1146

Research and Clinical Studies

N-Acetyl Semax and Nootropic Potential

A study⁽⁵⁾ was conducted on experimental rodents to determine the nootropic potential of ACTH hormone and its analogs, such as Semax. After exposure to Semax, all tested rodents were examined for 5-hyrodxyindoleacetic acid (5-HIAA) levels. Based on the results, it was noted that the 5-HIAA levels increased by 25% after just 2 hours following exposure; they increased progressively up to a maximum of 180% after 4 hours. As per Kirill O Eremin et al., “Our results reveal the positive modulatory [action] of Semax on the striatal serotonergic system and the ability of Semax to enhance both the striatal release of dopamine and locomotor behavior elicited by D-amphetamine.”

In another research study,⁽⁷⁾experimental models under excessive stress conditions were exposed to Semax. Upon analyzing behavior 24 hours after peptide exposure, it was noted that they appeared to show signs of enhanced memory and attention. As per the reports, "In the majority of cases, the peptide exhibited positive [actions], and in no case did it produce negative side actions or complications connected with its administration. There is good reason to believe that … potentialities of Semax have not been exhausted and in the future new possibilities … will be revealed." The study is shared here for educational and research purposes, and studies on the Semax peptide are still being conducted.

N-Acetyl Semax and SSRI Interaction

Selective Serotonin reuptake inhibitors (SSRIs) are a class of antidepressants. In pregnant research models, the compounds may risk passing through the placenta and impacting fetal brain development. In a preclinical research study,⁽⁸⁾ experimental rats aged between 1 and 14 days were presented first with an SSRI compound, followed by the Semax peptide. After 4 weeks, it was observed that the rats exposed to SSRIs showcased anxious behavior, especially when exposed to new stimuli. When they were given the Semax peptide, these same rats later reportedly exhibited a reduction in their anxiety levels and potential enhancement in their learning abilities.

N-Acetyl Semax and Separation Anxiety

Young offspring face separation anxiety when they are away from their mothers. Separating for a prolonged period may lead to impaired emotional reactivity. A research study⁽⁹⁾ examined young rats facing maternal deprivation. After four weeks of separation from their mothers, these rats reportedly exhibited increased anxiety and excessive physical activity. When the rats were presented with Semax, their reactions improved, indicating reduced anxiety. As per M. A. Volodina et al., these results suggest that “Semax [weakens] the impact of deprivation on animal body weight and [normalizes] the levels of anxiety in rats.”

N-Acetyl Semax and the Cardiovascular System

For this study,⁽¹⁰⁾ rodents were induced with myocardial infarction (MI), which may lead to vascular damage. These rodents were then divided into two groups – one was given Semax peptide for six days, and the second was given a placebo. Following 28 days after the occurrence of myocardial infarction, it was reported by the researchers that the control rodents appeared to exhibit reduced arterial blood pressure and cardiac hypertrophy, both of which may signal impending heart failure. In contrast, the peptide-exposed rodents reportedly exhibited signs of prevention of diastolic blood pressure, which may indicate possible remodeling of the heart ventricle and inhibition of heart failure.

N-Acetyl Semax and Neuroprotection

In a clinical study,⁽¹¹⁾ research models of ischemic strokes were evaluated for 10 days. Of these, 30% were presented with conventional compounds and the Semax peptide, while the remaining 70% were presented with conventional compounds only. After 10 days, all models were examined via electroencephalogram (EEG). Based on the EEG mapping, the researchers reported that the experimental group exposed to both the peptide and compound exhibited apparently notable improvement in restoring damaged brain activity.

N-Acetyl Semax peptide is available for research and laboratory purposes only. Please review and adhere to our Terms and Conditions before ordering.

References

T. Kolomin et al., A New Generation of Drugs: Synthetic Peptides based on Natural Regulatory peptides. Neuroscience & Medicine, 2013, 223-252. Published Online December 2013. http://dx.doi.org/10.4236/nm.2013.44035
Kost NV, Sokolov OIu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA. Ingibiruiushchee deĭstvie semaksa i selanka na énkefalindegradiruiushchie fermenty syvorotki krovi cheloveka [Semax and selank inhibit the enkephalin-degrading enzymes from human serum]]. Bioorg Khim. 2001 May-Jun;27(3):180-3. Russian. doi: 10.1023/a:1011373002885. PMID: 11443939. https://pubmed.ncbi.nlm.nih.gov/11443939/
Shih-Jen Tsai, Semax, an analogue of adrenocorticotropin (4–10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome, Medical Hypotheses, Volume 68, Issue 5, 2007, Pages 1144-1146. https://doi.org/10.1016/j.mehy.2006.07.017
Medvedeva, E.V., Dmitrieva, V.G., Povarova, O.V. et al. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics 15, 228 (2014). https://doi.org/10.1186/1471-2164-15-228
Eremin KO, Kudrin VS, Saransaari P, Oja SS, Grivennikov IA, Myasoedov NF, Rayevsky KS. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res. 2005 Dec;30(12):1493-500. doi: 10.1007/s11064-005-8826-8. PMID: 16362768. https://pubmed.ncbi.nlm.nih.gov/16362768/
National Center for Biotechnology Information (2023). PubChem Compound Summary for CID 9811102, Semax.
Asmarin IP, Nezavibat'ko VN, Miasoedov NF, Kamenskiĭ AA, Grivennikov IA, Ponomareva-Stepnaia MA, Andreeva LA, Kaplan AIa, Koshelev VB, Riasina TV. Nootropnyĭ analog adrenokortikotropina 4-10-semaks (15-letniĭ opyt razrabotki i izucheniia) [A nootropic adrenocorticotropin analog 4-10-semax (l5 years experience in its design and study)]. Zh Vyssh Nerv Deiat Im I P Pavlova. 1997 Mar-Apr;47(2):420-30. Russian. PMID: 9173745. https://pubmed.ncbi.nlm.nih.gov/9173745/
Nataliya Yu. Glazova, Daria M. Manchenko, Maria A. Volodina, Svetlana A. Merchieva, Ludmila A. Andreeva, Vladimir S. Kudrin, Nikolai F. Myasoedov, Natalia G. Levitskaya, Semax, synthetic ACTH(4–10) analog, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats, Neuropeptides, Volume 86, 2021, 102114, ISSN 0143-4179. https://doi.org/10.1016/j.npep.2020.102114
Volodina MA, Sebentsova EA, Glazova NY, Levitskaya NG, Andreeva LA, Manchenko DM, Kamensky AA, Myasoedov NF. Semax attenuates the influence of neonatal maternal deprivation on the behavior of adolescent white rats. Bull Exp Biol Med. 2012 Mar;152(5):560-3. English, Russian. doi: 10.1007/s10517-012-1574-2. PMID: 22803132. https://pubmed.ncbi.nlm.nih.gov/22803132/
Gavrilova SA, Golubeva AV, Lipina TV, Fominykh ES, Shornikova MV, Postnikov AB, Andrejeva LA, Chentsov IuS, Koshelev VB. [Protective effect of peptide semax (ACTH(4-7)Pro-Gly-Pro) on the rat heart rate after myocardial infarction]. Ross Fiziol Zh Im I M Sechenova. 2006 Nov;92(11):1305-21. Russian. PMID: 17385423. https://pubmed.ncbi.nlm.nih.gov/17385423/
Gusev EI, Skvortsova VI, Miasoedov NF, Nezavibat'ko VN, Zhuravleva EIu, Vanichkin AV. Effektivnost' semaksa v ostrom periode polusharnogo ishemicheskogo insul'ta (klinicheskoe i élektrofiziologicheskoe issledovanie) [Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Zh Nevrol Psikhiatr Im S S Korsakova. 1997;97(6):26-34. Russian. PMID: 11517472. https://pubmed.ncbi.nlm.nih.gov/11517472/

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Selank (Tuftsin) Peptide

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Selank Peptide

Selank is a synthetic analog of the peptide tuftsin, an endogenous peptide that regulates the immune system [1]. Informally, it falls under the category of nootropic agents, which are substances known for their ability to improve learning, memory, and other cognitive processes.

Originally created by the Russian Academy of Sciences, Selank has primarily been studied for its anti-anxiety effects. The mechanism of action of Selank is believed to involve the modulation of various neurotransmitters in the brain, including serotonin, dopamine, and GABA [2]. By influencing these neurotransmitters, Selank can effectively reduce anxiety and induce a state of calmness without causing any sort of impairment.

Selank is also antinociceptive, anti-inflammatory, and immune-enhancing [3]. Preclinical and clinical studies have displayed promising results regarding its effectiveness in treating certain psychiatric disorders, brain damage, and chronic stress.

Because of the way Selank interacts with the body’s opioid receptors and enkephalin-degrading enzymes, it has the ability to induce all the desirable effects of benzodiazepines without the risk of side effects or addiction [4].

Because Selank interacts with different bodily systems, the route by which it is administered can partially determine its effects. Selank injections, for example, increase GABA receptor binding sites without affecting NMDA receptors. By contrast, Selank nasal spray does not appear to affect GABA receptors while primarily increasing NMDA binding sites [5].

Overview

Selank is a peptide chain composed of two fragments – one is Tuftsin at the N-terminus, and the other is a tripeptide Pro-Gly-Pro (PGP) at the C-terminal end of the molecule. The inclusion of a Pro-Gly-Pro (PGP) sequence in the peptide Selank might enhance its potential to penetrate various biological barriers, including the blood-brain barrier (BBB). The BBB is a highly selective and semi-permeable membrane that delineates the circulating blood from brain tissues and extracellular fluid within the central nervous system. It is deemed to play a pivotal role in controlling the entry of molecules. Integrating the PGP sequence might modify the peptide's hydrophilicity or lipophilicity, which might increase its compatibility with the lipid-rich milieu of the BBB. Moreover, the PGP motif might interact with certain transport systems or receptors on the BBB membrane, potentially facilitating receptor-mediated endocytosis or active transport. These mechanisms may permit Selank to circumvent the tight junctions that typically impede the transit of larger molecules through the BBB. Additionally, the presence of the PGP sequence might alter the tertiary structure of Selank, potentially rendering it more amenable to traversing the BBB. This alteration might arise from changes in the peptide's spatial configuration, which may influence its interaction with the cellular components of the BBB.⁽⁶⁾

Chemical Makeup

Molecular Formula: C₃₃H₅₇N₁₁O₉
Molecular Weight: 751.88 g/mol
Other Known Titles: TP-7, Selan

Research and Clinical Studies

Selank Peptide and BDNF Levels

There is a possibility that Selank may influence the expression of brain-derived neurotrophic factor (BDNF), deemed a crucial protein in the brain that supports neuronal survival and growth.⁽¹⁾Research indicates that Selank may markedly increase the levels of BDNF mRNA in the hippocampus, an integral region of the brain involved in memory and emotional responses. The potential of Selank to boost BDNF expression, particularly under conditions where stress and glucocorticoids suppress BDNF levels, suggests its relevance in research studies within the context of neuroplasticity decline. This protein's perceived role in synaptic function and neuronal adaptation underscores the significance of such investigations.

Selank Peptide and Serotonin Signaling

Selank may potentially influence serotonin signaling mechanisms. Serotonin signaling is theorized to play a crucial role in the management of mood and anxiety within the brain. Research utilizing murine models where serotonin synthesis was inhibited has indicated that Selank might be able to alter serotonin levels in cases where the serotonergic system is impaired. It has been proposed by researchers that Selank may potentially boost serotonin metabolism in the brainstem, indicating its potential action on the serotonin system. More specifically, the peptide is thought to facilitate an increase in the metabolic processing of serotonin in brain regions considered essential for mood and anxiety regulation. Additionally, the hypothesis that Selank may enhance serotonin metabolism suggests a potential pathway by which Selank might ameliorate issues stemming from diminished serotonin activity.

Selank Peptide and GABA Signaling

Studies have suggested that Selank may act on the gamma aminobutyric acid (GABA) receptors. GABA is considered an inhibitory neurotransmitter within this context, playing a role in diminishing neuronal excitability, fostering relaxation, and mitigating anxiety observations, as observed in animal research models. In one study,⁽⁷⁾ the expression of 84 genes involved in neurotransmission was studied in murine models. The experimental murine models were exposed to either Selank or GABA, and gene expression was studied after one and three hours via a PCR method. All the gene expressions studied for Selank and GABA appeared positively correlated. The results suggested that Selank had the potential to induce several alterations in the neurotransmission process, suggesting by proxy that Selank may exert possible action via modulating the GABAergic system. Moreover, the literature indicates that the influence of Selank might not be confined to mere direct actions on the transcriptional activity of genes associated with GABA receptors. It might also involve allosteric modulation of the GABAergic system. This is inferred from observed variations in gene expression following exposure to Selank compared to GABA, where Selank has been speculated to distinctly affect the expression of specific genes. Such differential gene expression alludes to a more complex interaction of Selank with the GABAergic system, possibly diverging from the direct receptor activation typically seen with GABA. Selank has also been proposed to instigate enduring modifications within neurotransmitter systems, a characteristic that might account for its extended anxiolytic actions observed in experimental frameworks. These alterations suggest a broader and potentially long-term impact on neurotransmitter dynamics beyond potential receptor interaction, emphasizing the complex potential of Selank on neural regulation.

Selank Peptide and Genome Expression

Studies have been conducted to understand the potential of Selank peptide on genome expression and its involvement in the inflammatory process. These studies⁽⁸⁾ were conducted on male murine models weighing 250 grams. These murine models were separated into three groups – a control group, an experimental group with a single exposure to Selank, and an experimental group under routine exposure to Selank. After the study, the RNA was isolated from the rat spleen and hippocampus and studied via PCR method. Based on the results, it was suggested by the researchers that Selank might have the potential to impact gene expression, exhibited more definitively in the spleen and the hippocampus. One of the gene expressions reported during the study was the change in CX3CR1, which was involved in the inflammatory process. This suggested that Selank might regulate the inflammatory process through the mechanism of gene expression, mainly the CX3CR1 alteration.

Selank Peptide and Enkephalin Signaling

In a clinical study,⁽⁹⁾ 62 research models of Generalized Anxiety Disorder (GAD) were examined. These models were divided into two groups – 48% were exposed to Selank, whereas 52% were exposed to a generic benzodiazepine compound. Following the study, the psychometric levels of all models were analyzed. Results suggested that the impact of Selank appeared to be similar to those of the generic compound. Researchers also reported that enkephalin levels of tau leu-enkephalin were apparently reduced in the Selank-exposed group before the experiment, and the addition of Selank may have reversed this observation. Selank is hypothesized to exert suppressive actions on enzymes that break down enkephalins. Enkephalins, which are endogenous ligands for opioid receptors, have been implicated in the regulation of pain, mood, and stress responses. Therefore, the potential inhibition of these degrading enzymes by Selank might result in increased levels of enkephalins, potentially augmenting their physiological actions. This could lead to a noticeable elevation in tau(1/2) leu-enkephalin concentrations during experiments involving anxiety models where Selank is evaluated.

Selank Peptide and Memory

This study⁽¹¹⁾ was conducted on murine models that were enrolled in a "training" session of four days for learning conditioned avoidance response (CAR). CAR is a learned response in delaying or preventing avoidance behavior. Selank exposure was begun 15 minutes before the training session on all four days. Upon monitoring the behavior of the murine models, researchers suggested that the learning abilities of the murine models appeared to improve with each exposure of the peptide, as the number of errors reduced and the number of correct solutions increased. This potential impact might be mediated through multiple interconnected pathways, including the modulation of neuropeptide systems within the brain. These neuropeptides are deemed critical as they are believed to play significant roles in various cognitive functions, potentially boosting processes related to learning and memory. Additionally, the peptide Selank might alter neural circuits involved in memory consolidation. This alteration may enhance synaptic stability and efficiency in learning processes. Moreover, Selank might indirectly boost cognitive performance by mitigating anxiety-related factors that frequently impede learning efficiency. This suggests that Selank may influence the emotional aspects of cognition, enhancing the overall cognitive process. Furthermore, Selank may promote neural plasticity or the capacity of neurons to adapt, particularly in cognitive circuits that are not performing optimally, thus potentially elevating their function. This enhancement of neural adaptability may be vital for the maintenance and improvement of cognitive abilities, suggesting that Selank might be a valuable compound for further research in neurocognitive fields.

Selank Peptide and Immunomodulation

This clinical study⁽¹²⁾ was conducted on research models of GAD with neurasthenia, with a control group and experimental group exposed Selank peptide for 14 days. After the study, the peripheral blood samples were collected and analyzed. The analytical results suggested peak elevation in the levels of IL-6 cytokine and changes in the Th1 and Th2 cytokine ratio, all of which are believed to regulate the immune system.

Selank Peptide and Withdrawal

In this study,⁽¹³⁾ murine models were infused with 10% ethanol as their sole fluid source for 24 weeks. Consequently, these murine models were experimentally induced with alcohol withdrawal symptoms once the ethanol drip was removed. The murine models were then exposed to Selank, to study its potential impact on the withdrawal symptoms. After 48 hours, researchers reported that the alcohol withdrawal symptoms appeared to have reduced, based on the results of their social interaction and maze tests.

Selank Peptide and Cardiovascular Activity

In this study,⁽¹⁴⁾ Selank was presented to feline models. The main goal of this study was to examine the cardiovascular and respiratory potential of the peptide in this specific model. Upon exposure to the peptide, it was reported by the researchers that there appeared to be a 32% decrease in arterial blood pressure within 3 minutes of peptide presence. Moreover, the peptide possibly induced a 24% increase in cerebral blood flow within the first 10 minutes, slowly decreasing to optimal levels. Selank was not reported to have induced any action on the respiratory system or the heart rate.

Selank Peptide and Weight, Cholesterol

In this study,⁽¹⁵⁾ murine models were first exposed to a high-fat diet for 6 consecutive weeks until the weights of murine models were measured between 280g to 300g. Later, these murine models were divided into two groups, a control group given sodium chloride, and an experimental group exposed to Selank peptide. Additionally, a group of control murine models were used for this study, which were not presented with either of the agents but were simply monitored for the purpose of the study. Upon analysis, it was suggested by the researchers that the Selank group exhibited apparently decreased levels of cholesterol and fat anywhere between 25% and 58%. Based on the findings, Selank may also reduce specific forms such as low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL) cholesterol, and triglycerides. This indicates that Selank might play either a direct or an indirect role in influencing the mechanisms of lipid metabolism and could potentially display actions that lower cholesterol (hypocholesterolemic) and lipid levels (hypolipidemic). Moreover, the investigation noted discernible enhancements in parameters related to hemostasis, including elevated total fibrinolytic activity and decreased platelet aggregation, which may suggest improvements in conditions that favor clot formation. Additionally, the study points to a possible modulatory action of Selank on glucose homeostasis, which involves maintaining stable blood glucose levels. The fat metabolism rate of the Selank group also was reportedly improved and was eventually measured at the same rate as those in control models. Upon weight determination of the murine models, it was noted that the control group exhibited an average weight gain of 40g throughout the study, whereas the experiment group maintained the same weight throughout the study, with gradual weight reduction upon peptide presentation.

Selank peptide is available for research and laboratory purposes only. Please review and adhere to our Terms and Conditions before ordering.

References:

Inozemtseva, L. S., Karpenko, E. A., Dolotov, O. V., Levitskaya, N. G., Kamensky, A. A., Andreeva, L. A., & Grivennikov, I. A. (2008). Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections, 421, 241–243. https://doi.org/10.1134/s0012496608040066
Najjar VA. Tuftsin, a natural activator of phagocyte cells: an overview. Ann N Y Acad Sci. 1983;419:1-11. doi: 10.1111/j.1749-6632.1983.tb37086.x. https://pubmed.ncbi.nlm.nih.gov/6370072/
Semenova, T. P., kozlovskiĭ, I. I., Zakharova, N. M., & Kozlovskaia, M. M. (2009). Eksperimental'naia i klinicheskaia farmakologiia, 72(4), 6–8.
Fridkin M, Stabinsky Y, Zakuth V, Spirer Z. Tuftsin and some analogs: synthesis and interaction with human polymorphonuclear leukocytes. Biochim Biophys Acta. 1977 Jan 24;496(1):203-11. https://pubmed.ncbi.nlm.nih.gov/576412/
Kozlovskaya MM, Kozlovskii II, Val'dman EA, Seredenin SB. Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress. Neurosci Behav Physiol. 2003 Nov;33(9):853-60. https://pubmed.ncbi.nlm.nih.gov/14969422/
Elena Filatova et al., GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. https://doi.org/10.3389/fphar.2017.00089
Volkova, A., Shadrina, M., Kolomin, T., Andreeva, L., Limborska, S., Myasoedov, N., & Slominsky, P. (2016). Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in pharmacology, 7, 31. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757669/
T.A Kolomin et al., Transcriptomic Response of Rat Hippocampus and Spleen Cells to Single and Chronic Administration of the Peptide Selank. June 2, 2009. DOI: 10.1134/S1607672910010023
Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, Serebriakova EV, Siranchieva OA, Andriushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Miasoedov NF, Seredenin SB. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. Russian. https://pubmed.ncbi.nlm.nih.gov/18454096/
Medvedev VE, Tereshchenko ON, Israelian AIu, Chobanu IK, Kost NV, Sokolov OIu, Miasoedov NF. A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2014;114(7):17-22. Russian. https://pubmed.ncbi.nlm.nih.gov/25176261/
Kozlovskii II, Danchev ND. The optimizing action of the synthetic peptide Selank on a conditioned active avoidance reflex in rats. Neurosci Behav Physiol. 2003 Sep;33(7):639-43. https://pubmed.ncbi.nlm.nih.gov/14552529/
Uchakina ON, Uchakin PN, Miasoedov NF, Andreeva LA, Shcherbenko VE, Mezentseva MV, Gabaeva MV, Sokolov OIu, Zozulia AA, Ershov FI. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(5):71-5. Russian. https://pubmed.ncbi.nlm.nih.gov/18577961/
Kolik LG, Nadorova AV, Kozlovskaya MM. Efficacy of peptide anxiolytic selank during modeling of withdrawal syndrome in rats with stable alcoholic motivation. Bull Exp Biol Med. 2014 May;157(1):52-5. https://pubmed.ncbi.nlm.nih.gov/24913576/
Gan'shina TS, Kozlovskiĭ II. [Effects of the new peptide anxiolytic drug selank on the cardiovascular system functioning and respiration in cats]. Eksp Klin Farmakol. 2005 Jul-Aug;68(4):33-5. Russian. https://pubmed.ncbi.nlm.nih.gov/16193654/
N.F. Mjasoedov et al, The Influence of Selank on the Parameters of the Hemostasis System, Lipid Profile, and Blood Sugar Level in the Course of Experimental Metabolic Syndrome. April 14, 2014.

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Cerebrolysin, nootropic for brain function, protection and recovery

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Cerebrolysin, nootropic for brain function, protection and recovery

From $119.00

Cerebrolysin is a nootropic drug, which means that it has the capacity to enhance a number of cognitive functions such as memory, concentration, and thinking skills. It is used in the treatment of memory disorders, concentration disorders, and degenerative dementia, including Alzheimer’s disease. Cerebrolysin is also used in the treatment of acute neurological disorders, such as cerebral stroke and craniocerebral trauma. The brain-boosting effects of cerebrolysin may be attributed to the neuropeptides it contains. These neuropeptides are active brain peptides (chains of amino acids) that are used by nerve cells (neurons) to enhance their communication with each other.

Cerebrolysin is a natural compound derived from the brains of pigs using a safe and standardized enzymatic process. In order to achieve its therapeutic effect, cerebrolysin needs to be administered in the form of injections.

How Cerebrolysin Works

Cerebrolysin works by increasing the levels of neurotrophic factors (NFT) and brain-derived neurotrophic factors (BDNF). This in turn stimulates the formation and repair of neurons (nerve cells) in the brain.

Chemical Structure of Cerebrolysin

Research on Cerebrolysin

A. Boosts Cognitive Function

There is increasing evidence that cerebrolysin may help improve cognitive function and counter the effects of certain medical conditions that lead to cognitive impairment:

In patients with schizophrenia dominated by negative symptoms, administration of cerebrolysin in addition to antipsychotic medication appears to improve cognitive function and memory. [1]
In healthy older adults with memory loss, the administration of a derivative of cerebrolysin, N-PEP-12, improved memory. [2]
In healthy elderly adults, a single dose of cerebrolysin improved memory performance.[3]
In patients with Alzheimer’s disease and dementia, high doses of cerebrolysin reduced psychological symptoms and slowed disease progression. [4]
In animals with Alzheimer’s disease, cerebrolysin administration reduced the build-up of brain beta-amyloid plaques, which are sticky proteins known to cause the disease. [5-7]
In patients with stroke and traumatic brain injury (TBI), cerebrolysin administration appears to improve cognitive recovery without any adverse side effects. [8-14]
In infants with communication defects due to severe brain damage during pregnancy, cerebrolysin treatment for 3 months improved communication and social interaction.[15]
In mouse and rat models of Parkinson’s disease, cerebrolysin promoted survival of brain cells, improved motor symptoms, and slowed disease progression. [16-18]
The combination of cerebrolysin with recombinant tissue-Plasminogen Activator produced a more favorable response in neurological outcome measures as compared to the placebo group. [19]
In patients with stroke who were treated with cerebrolysin (30 mL over seven days followed by 10 mL until day 30) once daily over a period of four weeks, a significant improvement in neurological and global function outcomes was observed compared to the group who received placebo treatment. [20]
In dementia models and stroke animal models, cerebrolysin decreased the accumulation of abnormal protein structures in the brain, improved the transmission of signals by the neurons (nerve cells), restored neuron structures, induced restorative processes, decreased infarct volume (dead tissue) and formation of edema (swelling), resulting in improved cognitive and behavioral performance. [21-23]
In patients with ischemic stroke (insufficient blood flow to the brain), the administration of cerebrolysin produced significant improvements in motor and cognitive recovery. [24-28]
In elderly patients with vascular dementia of mild to moderate severity, cerebrolysin administration produced beneficial effects on general cognitive function as measured by mini-mental state examination (MMSE). [29]

B. Improves Mood

The brain-boosting effect of cerebrolysin also has a beneficial effect on mood, especially in depressive symptoms. Studies show that administration of cerebrolysin produces an antidepressant effect:

In elderly patients with depression, intravenous infusions of cerebrolysin reduced symptoms of depression, anxiety, and apathy (lack of interest, enthusiasm, or concern). [30]
In patients with Alzheimer’s disease, cerebrolysin treatment improved scores on the Cornell Depression Scale. [31]
In patients with treatment-resistant depression, cerebrolysin therapy improved depressive symptoms without any adverse side effects. [32]
In rats, cerebrolysin administration produced an anti-anxiety effect. [33]

C. Improves Symptoms of Autism

Autism, or autism spectrum disorder (ASD), refers to a wide range of medical conditions that affect social interaction, behavior, speech, and nonverbal communication. Since cerebrolysin has the capacity to enhance a number of cognitive functions, this nootropic drug has also been studied for its beneficial effect on autism:

In patients with childhood autism and Asperger’s syndrome (one of the autism spectrum disorders), cerebrolysin therapy improved various areas of cognitive function (expressive and receptive speech, fine motoring, and playing). [34]
In children with autism, cerebrolysin therapy improved symptoms and scores on the Childhood Autism Rating Scale (CARS). [35]
In a rat model of autism, cerebrolysin therapy improved behavior and brain cell communication. [36]

D. Improves Symptoms of Attention Deficit Hyperactivity Disorder (ADHD)

ADHD is a mental disorder characterized by hyperactivity, impulsivity, and short attention span. This mental disorder affects children and teens and can transition into adulthood. Studies show that administration of cerebrolysin may help reduce symptoms of ADHD:

In children with ADHD, cerebrolysin administration at a dose of 1 ml per 10 kg of weight intramuscularly for 1 month improved the core symptoms of ADHD. [37]
In patients with ADHD of unknown cause, cerebrolysin treatment reduced impulsivity and hyperactivity. [38]

E. Improves Symptoms of Cerebral Palsy (CP)

CP is a developmental disability that affects muscle tone, movement, and motor skills. It is believed that CP is caused by brain damage during pregnancy or birth. Studies show that cerebrolysin administration in patients with CP improves functional outcomes:

In patients with CP, intramuscular administration of cerebrolysin as a single daily dose of 0.1 cc/kg for 10 days and then continued weekly for 4 months appears to improve gross motor function. [39]
In patients with infantile cerebral paralysis, the administration of cerebrolysin improved symptoms without any adverse side effects. [40]
In pediatric patients living with CP, the combination of standard rehabilitation therapy with cerebrolysin improved gross motor skills. [41]
In children with traumatic brain injury and cerebral palsy, cerebrolysin therapy induced the repair of nerve cells of the brain. [42]

F. Repairs Nerve Damage

With nerve damage, there can be a broad range of symptoms depending on the location and types of nerves affected. In addition, chronic nerve damage may impair the sensation or function of the affected body part. Interestingly, numerous studies support the therapeutic benefits of cerebrolysin in different medical conditions associated with nerve damage:

In patients with diabetic neuropathy (nerve damage caused by diabetes), daily cerebrolysin infusion over a period of 10 days alleviated pain and tingling sensations. [43]
In a mouse model of diabetic neuropathy, the administration of cerebrolysin improved dysfunction of the sciatic nerve (the largest single nerve located on each side of the lower spine going all the way down to the foot). [44]
In patients with different nerve injuries, cerebrolysin treatment was associated with rapid neurological recovery after various peripheral nerve lesions than conventional therapies. [45]
In aged rats, cerebrolysin treatment ameliorated performance deficits and nerve damage. [46]
In mice, low-dose cerebrolysin administration promoted regeneration of injured spinal motor neurons. [47]
In animals with nerve injury related to microsurgical suturing, cerebrolysin administration promoted regeneration of the injured peripheral nerve. [48]
In patients with various forms of nerve injury, cerebrolysin was more associated with rapid recovery of neurological functions than other therapies such as steroids and supportive therapies such as vitamins and antioxidants. [49]

G. Treats Hyperthermia-Induced Neurotoxicity

Adverse environmental circumstances such as heat stress related to hot climates can lead to disturbed mental function. This condition is known as hyperthermia-induced neurotoxicity. Researchers suggest that one of the suitable therapeutic strategies to treat heat-induced mental anomalies related to this condition is cerebrolysin administration. Studies show that cerebrolysin exerts its therapeutic effect through the following important mechanisms:

In rats exposed to whole body hyperthermia (increased temperature), cerebrolysin administration induced a marked reduction in brain toxicity, thus preventing mental dysfunction related to heat stress. [50]
In rats suffering from heat stroke, cerebrolysin exerted superior neuroprotective effects as compared to other neuroprotective agents. [51]

H. Treats Morphine Withdrawal Symptoms

Prolonged use of morphine changes the way nerve receptors in the brain work. As a result, sudden withdrawal from this drug can lead to debilitating symptoms such as sleep problems, restlessness, anxiety, digestive problems, high blood pressure, rapid heartbeat, and vision problems. Studies suggest that cerebrolysin can be considered a therapeutic option for morphine withdrawal symptoms:

A study reported that morphine withdrawal can activate heat shock protein which triggers unpleasant symptoms, suggesting that cerebrolysin can produce beneficial effects through its ability to suppress the activation of these proteins. [52]
Rat studies showed that cerebrolysin counteracted the activation of heat shock protein, thus alleviating the negative effects of morphine withdrawal. [53-54]

I. Boosts Immune Function

There is mounting evidence that cerebrolysin may help heighten the immune response and prevent a wide array of diseases. Studies show that cerebrolysin positively affects the production of different cells of the immune system:

In mice, cerebrolysin treatment increased the production of Thy-1 cells. [55]
In patients with mental developmental delay, cerebrolysin therapy at a dose of 0.1 mg/1kg of body mass for 42 days improved immune status. [56]
In patients with minimal cerebral dysfunction, intrasmuscular cerebrolysin administration at a dose of 1 ml per 10 kg of body weight for 1 month increased the blood levels of CD19(+) and CD16(+) cells with a simultaneous normalization of blood IgG, IgA, and natural killer cell levels. [57]
A laboratory study showed that cerebrolysin exerts its immune-boosting properties by increasing the production of T- and B-lymphocytes, and promoting the survival of immunocompetent cells. [58]
Studies found that cerebrolysin can help decrease the levels of free radicals, which are unstable molecules that damage cells and impair the function of immune system cells. [59-62]

J. Improves Eye Health

IMG
Cerebrolysin has the capacity to stimulate the regeneration of various nerves and cells in the body. Studies show that this regenerative ability may help maintain visual health:

In a rat model of optic nerve crush, the injection of cerebrolysin promoted the survival of retinal cells. [63]
In a patient with vision loss in both eyes, intense photophobia (light sensitivity), and eye pain, cerebrolysin administration appears to reduce eye pressure and improve visual acuity. [64]

Associated Side Effects and Adverse Events of Cerebrolysin

Cerebrolysin side effects are very uncommon, but adverse events have been reported. There is also a potential for serious adverse events with Cerebrolysin use, including an increase in non-fatal serious adverse events. There have been some side effects associated with the use of this drug wherein the patient had one of the issues listed below at some point while being on cerebrolysin. However, these side effects weren’t confirmed to be associated with the treatment and could have been a coincidence and not related to the use of cerebrolysin. Despite this, it was listed as a side effect associated with cerebrolysin even though these associated side effects are very uncommon.

Side effects associated with cerebrolysin may include the following:

Agitation
Changes in blood pressure
Confusion
Constipation
Diarrhea
Fatigue
Feeling hot
Nausea
Seizure
Vertigo
Vomiting

Cortexin ® vs Cerebrolysin ®

Cortexin® and Cerebrolysin® are both peptide-based drugs used primarily in neurology for their neuroprotective and neurotrophic effects, but they have distinct compositions and slightly different applications. Cortexin® is derived from the cerebral cortex of pigs and contains a complex of polypeptide fractions along with amino acids that influence the central nervous system. It is administered to improve brain function, protect against damage, and enhance recovery from various neurological conditions. Unlike Cerebrolysin, which is derived from pig brain proteins and contains a mixture of low-molecular-weight peptides and free amino acids, Cortexin’s active components are smaller and potentially more focused in their action.

In terms of clinical use, both Cortexin® and Cerebrolysin are utilized to treat similar conditions, including traumatic brain injuries, stroke recovery, and cognitive disorders such as Alzheimer’s disease. However, the specific indications and the perceived efficacy can vary. Cortexin is often noted for its neuroprotective properties and its ability to stabilize cell membranes and reduce oxidative stress. Cerebrolysin, on the other hand, is more explicitly recognized for its role in enhancing cognitive functions and supporting neuronal growth and repair, making it particularly useful in the treatment of dementia and similar degenerative conditions.

The choice between Cortexin® and Cerebrolysin often comes down to clinical objectives, patient response to treatment, and the preferences of the healthcare provider. Both medications are administered via injection, requiring similar protocols for use. Side effects for both drugs are generally mild but can include discomfort at the injection site, dizziness, and headaches. While both treatments are supported by a substantial amount of research, the body of evidence is more robust for Cerebrolysin, particularly in its effects on a broad range of neurodegenerative and cognitive disorders, as documented in the database of systematic reviews. Ultimately, the decision to use Cortexin or Cerebrolysin should be tailored to the individual patient’s condition and needs, often guided by the experience and observation of their healthcare team. Consulting the database of systematic reviews can provide valuable insights into the comparative efficacy and safety of these treatments. Additionally, continuous reference to the database of systematic reviews helps ensure that treatment decisions are based on the most comprehensive and up-to-date evidence available.

Cerebrolysin in Stroke and Vascular Dementia

Cerebrolysin has garnered attention in the medical community for its potential therapeutic effects in treating stroke and vascular dementia. This peptide-based treatment is believed to confer neuroprotective and neurotrophic benefits, making it a viable option for promoting neural repair and functional recovery post-stroke. The neurotrophic factors present in Cerebrolysin are thought to enhance neurogenesis, reduce inflammation, and improve synaptic connectivity, which can be critical in the acute phase following a stroke. Clinical trials and studies have shown that when administered soon after a stroke, Cerebrolysin can help improve neurological function and reduce the extent of brain damage, with a low incidence of serious adverse events.

In the context of vascular dementia, Cerebrolysin’s ability to improve cognitive functions and protect neural structures offers a promising approach to managing this condition. Vascular dementia, which results from impaired blood flow to the brain leading to cognitive decline, can benefit from Cerebrolysin’s mechanisms that enhance cerebral blood flow and neuronal resilience. Patients treated with Cerebrolysin have reported improvements in memory, attention, and executive function. Continuous research and clinical trials suggest that Cerebrolysin not only helps in stabilizing the symptoms of vascular dementia but may also slow its progression, offering a better quality of life for patients, with minimal serious adverse events.

Despite the promising outcomes, the use of Cerebrolysin in stroke recovery and vascular dementia must be carefully considered by healthcare professionals. The treatment involves a series of injections or infusions, which require monitoring and management by medical personnel. Side effects, though generally mild, can include headache, nausea, and dizziness. The risk of serious adverse events, while low, requires careful monitoring. Reviews in the Cochrane Database of Systematic Reviews highlight the importance of such vigilance in clinical practice. The cost of treatment and the variability in patient responses also pose challenges. Therefore, while Cerebrolysin offers a potentially effective treatment modality for stroke and vascular dementia, it should be part of a comprehensive therapeutic plan that includes other medical interventions and lifestyle adjustments tailored to individual patient needs. Ongoing vigilance for any serious adverse events is critical, as emphasized by findings from the Cochrane Database of Systematic Reviews. Additionally, systematic reviews and meta-analyses, such as those found in the Cochrane Database of Systematic Reviews, provide valuable insights into the efficacy and safety of Cerebrolysin, guiding healthcare professionals in making informed decisions about its use in diverse patient populations.

Reference

Xiao S, Xue H, Li G. Therapeutic effects of cerebrolysin added to risperidone in patients with schizophrenia dominated by negative symptoms. The Australian and New Zealand journal of psychiatry. 2012; 46(2):153-60. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22311531
Crook TH, Ferris SH, Alvarez XA, Laredo M, Moessler H. Effects of N-PEP-12 on memory among older adults. International clinical psychopharmacology. 2005; 20(2):97-100. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/15729085
Alvarez XA, Lombardi VR, Corzo L. Oral Cerebrolysin enhances brain alpha activity and improves cognitive performance in elderly control subjects. Journal of neural transmission. Supplementum. 2000; 59:315-28. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/10961443
Allegri RF, Guekht A. Cerebrolysin improves symptoms and delays progression in patients with Alzheimer’s disease and vascular dementia. Drugs of today (Barcelona, Spain: 1998). 2012; 48 Suppl A:25-41. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22514793
Rockenstein E, Torrance M, Mante M. Cerebrolysin decreases amyloid-beta production by regulating amyloid protein precursor maturation in a transgenic model of Alzheimer’s disease. Journal of neuroscience research. 2006; 83(7):1252-61. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/16511867
Rockenstein E, Mallory M, Mante M. Effects of Cerebrolysin on amyloid-beta deposition in a transgenic model of Alzheimer’s disease. Journal of neural transmission. Supplementum. 2002. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12456076.
Rockenstein E, Adame A, Mante M, Moessler H, Windisch M, Masliah E. The neuroprotective effects of Cerebrolysin in a transgenic model of Alzheimer’s disease are associated with improved behavioral performance. Journal of neural transmission (Vienna, Austria : 1996). 2003; 110(11):1313-27. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14628195
Ladurner G, Kalvach P, Moessler H, .Neuroprotective treatment with cerebrolysin in patients with acute stroke: a randomised controlled trial. Journal of neural transmission (Vienna, Austria : 1996). 2005; 112(3):415-28. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/15583955
Muresanu DF, Heiss W-D, Hoemberg V, et al. Cerebrolysin and Recovery After Stroke (CARS): A Randomized, Placebo-Controlled, Double-Blind, Multicenter Trial. Stroke; a Journal of Cerebral Circulation. 2016;47(1):151-159. doi:10.1161/STROKEAHA.115.009416. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4689177/.
Guekht A, Vester J, Heiss WD. Safety and efficacy of Cerebrolysin in motor function recovery after stroke: a meta-analysis of the CARS trials. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 2017; 38(10):1761-1769. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28707130.
Chen CC, Wei ST, Tsaia SC, Chen XX, Cho DY. Cerebrolysin enhances cognitive recovery of mild traumatic brain injury patients: double-blind, placebo-controlled, randomized study. British journal of neurosurgery. 2013; 27(6):803-7. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23656173.
Bornstein N, Poon WS. Accelerated recovery from acute brain injuries: clinical efficacy of neurotrophic treatment in stroke and traumatic brain injuries. Drugs of today (Barcelona, Spain : 1998). 2012; 48 Suppl A:43-61. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22514794
Wong GK, Zhu XL, Poon WS. Beneficial effect of cerebrolysin on moderate and severe head injury patients: result of a cohort study. Actaneurochirurgica. Supplement. 2005; 95:59-60. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/16463821.
Zhang D, Dong Y, Li Y, Chen J, Wang J, Hou L. Efficacy and Safety of Cerebrolysin for Acute Ischemic Stroke: A Meta-Analysis of Randomized Controlled Trials. BioMed Research International. 2017;2017:4191670. doi:10.1155/2017/4191670. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474547/.
Hassanein SM, Deifalla SM, El-Houssinie M, Mokbel SA. Safety and Efficacy of Cerebrolysin in Infants with Communication Defects due to Severe Perinatal Brain Insult: A Randomized Controlled Clinical Trial. Journal of clinical neurology (Seoul, Korea). 2016; 12(1):79-84. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/26365023.
Ozkizilcik A, Sharma A, Muresanu DF. Timed Release of Cerebrolysin Using Drug-Loaded TitanateNanospheres Reduces Brain Pathology and Improves Behavioral Functions in Parkinson’s Disease. Molecular neurobiology. 2017. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28875428.
Ozkizilcik A, Sharma A, Muresanu DF. Timed Release of Cerebrolysin Using Drug-Loaded TitanateNanospheres Reduces Brain Pathology and Improves Behavioral Functions in Parkinson’s Disease. Molecular neurobiology. 2017. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28875428.
Requejo C, Ruiz-Ortega JA, Cepeda H. Nanodelivery of Cerebrolysin and Rearing in Enriched Environment Induce Neuroprotective Effects in a Preclinical Rat Model of Parkinson’s Disease. Molecular neurobiology. 2017. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28840482.
Noor NA, Mohammed HS, Mourad IM, Khadrawy YA, AboulEzz HS. A promising therapeutic potential of cerebrolysin in 6-OHDA rat model of Parkinson’s disease. Life sciences. 2016; 155:174-9. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/27210889
KalynIaB, Safarova TP, Sheshenin VC, Gavrilova SI. [Comparative efficacy and safety of antidepressant mono- and multimodal therapy in elderly patients with depression (a clinical experience in a psychogeriatric hospital)]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 2014; 114(6 Pt 2):20-9. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25042499.
Gharagozli, K., Harandi, A. A., Houshmand, S., Akbari, N., Muresanu, D. F., Vester, J., Winter, S., & Moessler, H. (2017). Efficacy and safety of Cerebrolysin treatment in early recovery after acute ischemic stroke: a randomized, placebo-controlled, double-blinded, multicenter clinical trial. Journal of medicine and life, 10(3), 153–160.
Masliah, E., & Díez-Tejedor, E. (2012). The pharmacology of neurotrophic treatment with Cerebrolysin: brain protection and repair to counteract pathologies of acute and chronic neurological disorders. Drugs of today (Barcelona, Spain: 1998), 48 Suppl A, 3–24. https://doi.org/10.1358/dot.2012.48(Suppl.A).1739716
Fiani, B., Covarrubias, C., Wong, A., Doan, T., Reardon, T., Nikolaidis, D., & Sarno, E. (2021). Cerebrolysin for stroke, neurodegeneration, and traumatic brain injury: review of the literature and outcomes. Neurological sciences: official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 42(4), 1345–1353. https://doi.org/10.1007/s10072-021-05089-2
Zhang, C., Chopp, M., Cui, Y., Wang, L., Zhang, R., Zhang, L., Lu, M., Szalad, A., Doppler, E., Hitzl, M., & Zhang, Z. G. (2010). Cerebrolysin enhances neurogenesis in the ischemic brain and improves functional outcome after stroke. Journal of neuroscience research, 88(15), 3275-3281. https://doi.org/10.1002/jnr.22495.
Bornstein, N. M., Guekht, A., Vester, J., Heiss, W. D., Gusev, E., Hömberg, V., Rahlfs, V. W., Bajenaru, O., Popescu, B. O., & Muresanu, D. (2018). Safety and efficacy of Cerebrolysin in early post-stroke recovery: a meta-analysis of nine randomized clinical trials. Neurological sciences: official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 39(4), 629–640. https://doi.org/10.1007/s10072-017-3214-0.
Heiss, W. D., Brainin, M., Bornstein, N. M., Tuomilehto, J., Hong, Z., & Cerebrolysin Acute Stroke Treatment in Asia (CASTA) Investigators (2012). Cerebrolysin in patients with acute ischemic stroke in Asia: results of a double-blind, placebo-controlled randomized trial. Stroke, 43(3), 630–636. https://doi.org/10.1161/STROKEAHA.111.628537.
Chang, W. H., Lee, J., Shin, Y. I., Ko, M. H., Kim, D. Y., Sohn, M. K., Kim, J., & Kim, Y. H. (2021). Cerebrolysin Combined with Rehabilitation Enhances Motor Recovery and Prevents Neural Network Degeneration in Ischemic Stroke Patients with Severe Motor Deficits. Journal of personalized medicine, 11(6), 545. https://doi.org/10.3390/jpm11060545
Tran, L., Alvarez, X. A., Le, H. A., Nguyen, D. A., Le, T., Nguyen, N., Nguyen, T., Nguyen, T., Vo, T., Tran, T., Duong, C., Nguyen, H., Nguyen, S., Nguyen, H., Le, T., Nguyen, M., & Nguyen, T. (2022). Clinical Efficacy of Cerebrolysin and Cerebrolysin plus Nootropics in the Treatment of Patients with Acute Ischemic Stroke in Vietnam. CNS & neurological disorders drug targets, 21(7), 621–630. https://doi.org/10.2174/1871527320666210820091655
Stan, A., Birle, C., Blesneag, A., & Iancu, M. (2017). Cerebrolysin and early neurorehabilitation in patients with acute ischemic stroke: a prospective, randomized, placebo-controlled clinical study. Journal of medicine and life, 10(4), 216–222.
Chen, N., Yang, M., Guo, J., Zhou, M., Zhu, C., & He, L. (2013). Cerebrolysin for vascular dementia. The Cochrane database of systematic reviews, (1), CD008900. https://doi.org/10.1002/14651858.CD008900.pub2.
Lang, W., Stadler, C. H., Poljakovic, Z., Fleet, D., & Lyse Study Group (2013). A prospective, randomized, placebo-controlled, double-blind trial about safety and efficacy of combined treatment with alteplase (rt-PA) and Cerebrolysin in acute ischaemic hemispheric stroke. International journal of stroke: official journal of the International Stroke Society, 8(2), 95–104. https://doi.org/10.1111/j.1747-4949.2012.00901.x.
Panisset M, Gauthier S, Moessler H, Windisch M, .Cerebrolysin in Alzheimer’s disease: a randomized, double-blind, placebo-controlled trial with a neurotrophic agent. Journal of neural transmission (Vienna, Austria: 1996). 2002; 109(7-8):1089-104. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12111446.
Retrieved from http://www.wfsbp.org/doi/wfsbp2011-abstractscd/en/abstracts/10025.html.
Shabanov PD, Lebedev AA, Pavlenko VP, Ganapol’skiĭ VP. [Comparative study of behavioral effects of cortexin and cerebrolysine upon intraventricular and intraperitoneal administration in rats]. Eksperimental’naia i klinicheskaiafarmakologiia. ; 70(3):13-9. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17650626
Krasnoperova MG, Bashina VM, Skvortsov IA, Simashkova NV. [The effect of cerebrolysin on cognitive functions in childhood autism and in Asperger syndrome]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 2003; 103(6):15-8. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12872620.
Chutko LS, Yakovenko EA, Surushkina SY, Kryukova EM, Palaieva SV. [The efficacy of cerebrolysin in the treatment of autism spectrum disorders]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 2017; 117(9):71-75. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/29053124.
Cuevas-Olguin R, Roychowdhury S, Banerjee A. Cerebrolysin prevents deficits in social behavior, repetitive conduct, and synaptic inhibition in a rat model of autism. Journal of neuroscience research. 2017; 95(12):2456-2468. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28609577.
Sotnikova NY, Gromova OA, Novicova EA. Dual effect of cerebrolysin in children with attention deficit syndrome with hyperactivity: neuroprotection and immunomodulation. Russian journal of immunology: RJI : official journal of Russian Society of Immunology. 2002; 7(4):357-64. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12687248
Chutko LS, Yakovenko EA, Surushkina SY, Anisimova TI, Kropotov YD. [Clinical and neurophysiological heterogeneity of attention deficit hyperactivity disorder]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova.; 116(10):117-121. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/27845323.
Nasiri J, Safavifar F. Effect of cerebrolysin on gross motor function of children with cerebral palsy: a clinical trial. ActaneurologicaBelgica. 2017; 117(2):501-505. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28074392.
Gershman RN, Vasilenko MA. [Use of cerebrolysin and ATP in treating infantile cerebral paralysis]. Pediatriiaakusherstvo i ginekologiia.. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/1228606.
Retrieved from https://cerebralpalsynewstoday.com/2017/06/07/cerebrolysin-can-help-improve-motor-skills-in-cerebral-palsy-patients/.
Retrieved from https://clinicaltrials.gov/ct2/show/NCT02116348
Biesenbach G, Grafinger P, Eichbauer-Sturm G, Zazgornik J. [Cerebrolysin in treatment of painful diabetic neuropathy]. Wiener medizinischeWochenschrift (1946). 1997; 147(3):63-6. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9173675.
Dong H, Jiang X, Niu C, Du L, Feng J, Jia F. Cerebrolysin improves sciatic nerve dysfunction in a mouse model of diabetic peripheral neuropathy. Neural Regeneration Research. 2016;11(1):156-162. doi:10.4103/1673-5374.175063. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4774211/
Retrieved from https://www.researchgate.net/publication/286293430_Cerebrolysin_as_a_nerve_growth_factor_for_treatment_of_acquired_peripheral_nervous_system_diseases.
Masliah E, Armasolo F, Veinbergs I, Mallory M, Samuel W. Cerebrolysin ameliorates performance deficits, and neuronal damage in apolipoprotein E-deficient mice. Pharmacology, biochemistry, and behavior. 1999; 62(2):239-45. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9972690.
Keilhoff G, Lucas B, Pinkernelle J, Steiner M, Fansa H. Effects of cerebrolysin on motor-neuron-like NSC-34 cells. Experimental cell research. 2014; 327(2):234-55. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24997385.
Shchudlo NA, Shchudlo MM, Borisova IV. [The effect of cerebrolysin on the regeneration of the peripheral nerve depending on the scheme of paraneural administration]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 2013; 113(12):76-80. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24430040.
Available from https://journals.lww.com/nrronline/Abstract/2011/06180/Cerebrolysin_as_a_nerve_growth_factor_for.10.aspx.
Sharma HS, Sharma A, Mössler H, Muresanu DF. Neuroprotective effects of cerebrolysin, a combination of different active fragments of neurotrophic factors and peptides on the whole body hyperthermia-induced neurotoxicity: modulatory roles of co-morbidity factors and nanoparticle intoxication. International review of neurobiology. 2012; 102:249-76. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22748833.
Sharma A, Muresanu DF, Mössler H, Sharma HS. Superior neuroprotective effects of cerebrolysin in nanoparticle-induced exacerbation of hyperthermia-induced brain pathology. CNS & neurological disorders drug targets. 2012; 11(1):7-25. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22229316.
Martínez-Laorden E, Hurle MA, Milanés MV, Laorden ML, Almela P. Morphine withdrawal activates hypothalamic-pituitary-adrenal axis and heat shock protein 27 in the left ventricle: the role of extracellular signal-regulated kinase. The Journal of pharmacology and experimental therapeutics. 2012; 342(3):665-75. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22647273.
Sharma HS, Ali SF, Patnaik R, Zimmermann-Meinzingen S, Sharma A, Muresanu DF. Cerebrolysin Attenuates Heat Shock Protein (HSP 72 KD) Expression in the Rat Spinal Cord Following Morphine Dependence and Withdrawal: Possible New Therapy for Pain Management. Current neuropharmacology. 2011; 9(1):223-35. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21886595.
Belokrylov GA, Malchanova IV. [Levamin and cerebrolysin as immunostimulants]. Biulleten’ eksperimental’noibiologii i meditsiny. 1992; 113(2):165-6. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/1611065.
Govorin NV, Zlova TP, Akhmetova VV, Tarasova OA. [The pathophysiological analysis of cerebrolysin therapy of children with mental developmental delay caused by ecological factors]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 2008; 108(5):51-5. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/18577958.
Sotnikova NY, Gromova OA, Novikova EA, Burtsev EM. Immunoactive Properties of Cerebrolysin. Russian journal of immunology: RJI : official journal of Russian Society of Immunology. 2000; 5(1):63-70. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/12687163.
Garmanchuk LV, Perepelitsyna EM, SidorenkoMv, Makarenko AN, Kul’chikov AE. [Cytoprotective effect of neuropeptides on immunocompetent cells (in vitro study)]. Eksperimental’naia i klinicheskaiafarmakologiia.; 72(4):28-32. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19803367
González ME, Francis L, Castellano O. Antioxidant systemic effect of short-term Cerebrolysin administration. Journal of neural transmission. Supplementum. 1998; 53:333-41. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9700669.
Gromova OA, Avdeenko TV, Burtsev EM, Skal’nyĭ AV, Solov’ev OI. [Effects of cerebrolysin on the oxidant homeostasis, the content of microelements and electrolytes in children with minimal brain dysfunction]. Zhurnalnevrologii i psikhiatriiimeni S.S. Korsakova. 1998; 98(1):27-30. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9505400.
Retrieved from https://www.researchgate.net/publication/270571093_Antioxidant_properties_of_cerebrolysin_-_an_old_drug_with_a_newly_discovered_capabilities
González ME, Francis L, Castellano O. Antioxidant systemic effect of short-term Cerebrolysin administration. Journal of neural transmission. Supplementum. 1998; 53:333-41. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9700669.
Retrieved from http://europepmc.org/abstract/med/9505400.
Huang TL, Huang SP, Chang CH, Lin KH, Sheu MM, Tsai RK. Protective effects of cerebrolysin in a rat model of optic nerve crush. The Kaohsiung journal of medical sciences. 2014; 30(7):331-6. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24924838.
Retrieved from http://www.roneurosurgery.eu/atdoc/16CostinDCombined.pdf.

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OxyGen® Selank Nasal Spray - 20mg/10mL

$109.00

Selank is a synthetic peptide (a small chain of amino acids) that was originally developed in Russia. It belongs to a class of compounds known as nootropics, which are substances believed to enhance cognitive function and mental performance.

Why is Selank important?

Anxiety Reduction: Selank has anxiolytic (anti-anxiety) effects. It may help reduce feelings of stress, fear, and anxiety without causing sedation or impairing cognitive function.

Mood Enhancement: Selank may improve mood and emotional well-being. It has been reported to have antidepressant-like effects, potentially by modulating neurotransmitter activity in the brain.

Cognitive Enhancement: Some users of Selank report improvements in cognitive function, including enhanced focus, concentration, and memory retention.

Neuroprotective Properties: Selank may have neuroprotective effects, meaning it could help protect brain cells from damage and degeneration. This could have implications for preventing age-related cognitive decline and neurodegenerative diseases.

How does Selank nasal spray work?

Selank nasal spray delivers the peptide directly into the bloodstream through the nasal mucosa, bypassing the digestive system. This allows for rapid absorption and may result in more consistent blood levels compared to oral administration.

Potential Benefits of Selank Nasal Spray:

Fast-Acting Anxiety Relief: Selank nasal spray may offer quick relief from symptoms of anxiety and stress, making it useful for managing acute episodes of anxiety or situational stress.

Improved Mood: Regular use of Selank nasal spray may promote a more positive mood and emotional stability, potentially reducing feelings of sadness or depression.

Enhanced Cognitive Function: Selank may support cognitive performance by improving focus, attention, and memory. This could be beneficial for individuals seeking to optimize mental performance in academic, professional, or creative endeavors.

Safe and Well-Tolerated: Selank is generally considered safe and well-tolerated when used as directed. It does not typically cause significant side effects or dependency, making it an attractive option for those seeking natural anxiety relief.

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