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AICAR 50mg

AICAR 50mg

AICAR, by activating AMPK, enhances metabolic health by improving insulin sensitivity and reducing fat, protects cardiovascular function by reducing lipid-induced damage, promotes skeletal muscle adaptations akin to endurance exercise, and provides neuroprotective effects (PMID: 12086950, PMID: 38643934, PMID: 24347059, PMID: 20490918).

AICAR (5-aminoimidazole-4-carboxamide ribonucleotide) offers several notable benefits due to its activation of AMP-activated protein kinase (AMPK). Here are the key benefits supported by research:

  1. Enhanced Metabolic Health: AICAR improves insulin sensitivity, enhances glucose uptake, and reduces intra-abdominal fat, which collectively helps mitigate metabolic disturbances associated with insulin resistance and obesity​ (PMID: 12086950)​.​
  2. Improved Cardiovascular Function: AICAR has cardioprotective effects, including improved recovery of the heart after ischemia and reduction of lipid-induced cardiac damage. It also helps in regulating lipid metabolism by reducing ceramide levels in skeletal muscles, which are implicated in insulin resistance​ (PMID: 38643934)​.
  3. Skeletal Muscle Adaptations: AICAR promotes mitochondrial biogenesis, fatty acid oxidation, and muscle fiber type switching, mimicking the effects of endurance exercise. This results in improved muscle endurance and metabolic function​ (PMID: 24347059)​.
  4. Neuroprotective Effects: Short-term AICAR treatment enhances spatial memory, hippocampal neurogenesis, and can offer neuroprotective effects in models of neurodegenerative diseases such as Huntington’s and Parkinson’s disease​ (PMID: 20490918)​.

Structure

Sequence: 5-aminoimidazole-4-carboxamide ribonucleoside

Molecular Formula: C9H1sN40sP

Molecular Weight: 338.213 g/mol

PubChem CID: 65110

CAS Number: 3031-94-5

Synonyms: AICA ribonucleotide, z-nucleotide

AICAR Research

AICAR and Insulin Resistance 

Research in mice shows that AICAR, even at low doses, reduces inflammation in adipose tissue. Inflammation in fat is associated with increased insulin resistance and reducing inflammation leads to improved glucose homeostasis and increased insulin sensitivity even without any changes in body weight. It appears that AICAR has several pathways through which it affects inflammation in adipose tissue, with at least one of those pathways involving SIRTl and macrophages[1].

The impact of AICAR on adipose inflammation is not unexpected. AMPK has been found to attenuate inflammatory responses in metabolic disorders in both healthy and diabetic mice. In research in mice, AMPK activation, as is caused by AICAR, was found to improve insulin sensitivity, energy homeostasis, lipid metabolism, and inflammatory markers.

Exercise increases the number of GLUT-4 insulin receptors that are present on the surface of muscle cells. It is one of the most effective means of boosting glucose uptake by muscle cells and effectively reduces both glucose levels and insulin resistance. It turns out that AICAR mimics the effects of exercise very precisely and that repeated administration of AICAR has effects similar to long-term exercise[3].

AICAR and Cancer Research 
AMPK plays a complex role in the growth and metastasis of cancer, both slowing and accelerating the growth of tumors under varying circumstances. Overall, research indicates that prolonged activation of the enzyme eventually leads to cancer cell death 

by slowing cancer cell metabolism and making cancer cells more susceptible to environmental

insults. This has been demonstrated both in cell culture and in rats[4],[5]. Scientists are investigating the ability of AICAR to work in tandem with other chemotherapeutic agents to boost effectiveness. The thought is that AICAR might

  • reduce side effects,
  • allow for lower dosing of chemotherapeutic drugs, and
  • improve outcomes in chemo-resistant tumors[6].

AICAR inhibits clonal growth of glioma (C6) and prostate cells.
Source: Journal of Biological Chemistry

Research in thyroid cancer cells indicates that AICAR may also operate by causing apoptosis (programmed cell death). It appears that this activity is mediated through the induction of p21 accumulation and the eventual activation of caspase 3. The overall effect is inhibition of cancer cell proliferation and survival[7].

AMPK activators, like AICAR, influence a number of pathways that can impact cancer growth.
Source: PubMed

AICAR Anti-inflammatory Properties

AMPK activators have been shown to play an important role in inflammation at the cellular level. Research into metformin, a common and long-used diabetes medication, indicates that at least part of the reason the drug is effective is that it reduces inflammation and boosts the function of the pancreas. AICAR has a similar effects, playing a protective role in inflammatory conditions like acute lung injury, asthma, colitis, atherosclerosis, and hepatitis[8].

There is ongoing research into the use of AICAR to mediate the effects of auto-immune diseases and other inflammatory conditions. For instance, studies in mice indicate that ACIAR may be effective in reducing inflammation in colitis. It appears that AICAR acts as a central inhibitor of immune responses in this setting by reducing NF-kappaB activation in macrophages as well as TH1- and TH17-type cytokines[9].

AICAR Research and the Heart

Much of heart disease is related to inflammation. The ability to control inflammation could reduce the progression of vascular disease, including atherosclerosis. Research in rabbit models of atherosclerosis indicated that AICAR suppression vascular smooth muscle proliferation. This is not only an important component of cardiovascular disease, but is also one of the reasons that cardiac stents fail over time. Controlling vascular inflammation could reduce both short-term and long-term complications of stent placement without the need for drugs that increase the risk of bleeding[10].

Research also suggests that AMPK activation can suppression certain immune responses that lead to atherosclerosis. The buildup of LDL, often referred to as “bad cholesterol,” leads to macrophage proliferation. This process is integral to the formation of plaques that can eventually lead to heart attack[11]. Anything that can mitigate this proliferation has the potential to reduce heart disease and even heart attack prevalence.

AICAR Research and Fertility

A great deal of AICAR research has revolved around the ability of the peptide to improve sperm motility, energy metabolism, and fertilizing ability. Research in both cats, goats, and chickens indicates that AMPK activators like AICAR can improve sperm motility by improving energy metabolism[12]. It appears that AICAR regulates the activity of energetic enzymes in spermatozoa and therefore impacts overall fertilizing ability[13].

AICAR exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. AICAR for sale at Life Link Research is limited to educational and scientific research only, not for human consumption. Only buy AICAR if you are a licensed researcher.

Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Scientific Journal Author

SRencer Gaskin, M.D., Ph.D. is an American Board of Internal Medicine certified cardiologist and medical practitioner. His expertise of Internal medicine and cardiology sources from UT Southwestern Cardiology, Washington University lnterventional Cardiology, and the Mid America Heart Institute. Dr. Gaskin led a study that examined the prevention of Postischemic Leukocyte Rolling and Adhesion via preconditioning with AICAR.

Spencer Gaskin, M.D., Ph.D. is being referenced as one of the leading scientists involved in the research and development of AICAR. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Life Link Research and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Gaskin is listed in [14] under the referenced citations.

Referenced Citations

1. Z. Yang et al., “The full capacity of AICAR to reduce obesity-induced inflammation and insulin resistance requires myeloid SIRTl,” PloS One, vol. 7, no. 11, p. e49935, 2012.

2. K. Pan et al., “AMPK activation attenuates inflammatory response to reduce ambient PM2.5-induced metabolic disorders in healthy. and diabetic mice,” Ecotoxicol. Environ. Saf., vol. 179, pp. 290-300, Sep. 2019.

3. N. Jessen, R. Paid, E. S. Buhl, L. S. Jensen, 0. Schmitz, and S. Lund, “Effects of AICAR and exercise on insulin-stimulated glucose uptake, signaling, and GLUT-4 content in rat muscles,” J. Appl. Physiol. Bethesda Md 1985,vol.94, no.4, pp. 1373-1379,Apr. 2003.

4. J. Zhuge, “Overexpression of CYP2El induces HeRG2 cells death by the AMP kinase activator 5′-aminoimidazole-4- carboxamide-1-beta-D-ribofuranoside.{AICAR).,” Cell Biol. Toxicol., vol. 25, no. 3, pp. 253-263, Jun.2009.

5. R. Rattan, S. Giri, A. K. Singh, and I. Singh, “5-Aminoimidazole-4-carboxamide-1-beta-D­ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP-activated protein kinase/ J. Biol. Chem., vol. 280, no. 47, pp. 39582-39593, Nov. 2005.

6. M. M. H. Yung, H. Y. S. Ngan, and D. W. Chan, ‘Targeting AMPK signaling in combating ovarian cancers: opportunities and challenges,” Acta Biochim. Biophys.  Sin, vol. 48, no. 4, pp. 301-317, Apr. 2016.

7. W. G. Kim, H.-J. Choi, T. Y. Kim, Y. K. Shong, and W. B. Kim, “The effect of 5-aminoimidazole-4-carboxamide­ribonucleoside was mediated by_p38 mitogen activated protein kinase signaling pathway in FRO thyroid cancer cells,” Korean J. Intern. Med., vol. 29, no. 4, pp. 474-481, Jul. 2014.

8. X.-W. Peng, H.-H. Zhou, J. Dai, and L. Zhang, “[Advances on the anti-inflammatory and protective effect of AMPK activators],” Sheng Li Xue Bao, vol. 71, no. 2, pp. 319-326, Apr. 2019.

9. A. Bai et al., “Novel anti-inflammatory action of 5-aminoimidazole-4-carboxamide ribonucleoside with protective effect in dextran sulfate sodium-induced acute and chronic colitis,” J. Pharmacol. Exp. Ther., vol. 333, no.3, pp. 717-725,Jun. 2010.

10. M. lgata et al., “Adenosine monophosphate­ activated protein kinase suppresses vascular smooth muscle cell proliferation through the inhibition of cell cycle progression,” Circ. Res., vol. 97, no. 8, pp. 837-844, Oct. 2005.

11. M. Sakai, S. Kobori, A. Miyazaki, and S. Horiuchi, “Macrophage proliferation in atherosclerosis,” Curr. Opin. Lipidol., vol. 11, no. 5, pp. 503-509, Oct. 2000.

12. P. Thuwanut, P. Comizzoli, K. Pruksananonda, K. Chatdarong, and N. Songsasen, “Activation of adenosine monophosphate-activated protein kinase (AMPK) enhances energy metabolism, motility, and fertilizing ability of cryopreserved spermatozoa in domestic cat model,” J. Assist. Reprod. Genet., May 2019.

13. Z. Zhu et al., “5′-AMP-Activated Protein Kinase Regulates Goat Sperm Functions via Energy Metabolism In Vitro,” Cell. Physiol. Biochem. Int. J. Exp. Cell. Physiol. Biochem. Pharmacol., vol. 47, no. 6, pp. 2420-2431, 2018.

14. F. Spencer Gaskin, Kazuhiro Kamada, Mozow Yusof, William Durante, Garrett Gross & Ronald J. Korthuis (2009) AICAR Preconditioning Prevents Postischemic Leukocyte Rolling and Adhesion: Role of KATP Channels and Heme  Oxygenase, Microcirculation, 16:2, 167- 176, DOI: 10.1080/10739680802355897 

$58.00

Description

AICAR, by activating AMPK, enhances metabolic health by improving insulin sensitivity and reducing fat, protects cardiovascular function by reducing lipid-induced damage, promotes skeletal muscle adaptations akin to endurance exercise, and provides neuroprotective effects (PMID: 12086950, PMID: 38643934, PMID: 24347059, PMID: 20490918).

AICAR (5-aminoimidazole-4-carboxamide ribonucleotide) offers several notable benefits due to its activation of AMP-activated protein kinase (AMPK). Here are the key benefits supported by research:

  1. Enhanced Metabolic Health: AICAR improves insulin sensitivity, enhances glucose uptake, and reduces intra-abdominal fat, which collectively helps mitigate metabolic disturbances associated with insulin resistance and obesity​ (PMID: 12086950)​.​
  2. Improved Cardiovascular Function: AICAR has cardioprotective effects, including improved recovery of the heart after ischemia and reduction of lipid-induced cardiac damage. It also helps in regulating lipid metabolism by reducing ceramide levels in skeletal muscles, which are implicated in insulin resistance​ (PMID: 38643934)​.
  3. Skeletal Muscle Adaptations: AICAR promotes mitochondrial biogenesis, fatty acid oxidation, and muscle fiber type switching, mimicking the effects of endurance exercise. This results in improved muscle endurance and metabolic function​ (PMID: 24347059)​.
  4. Neuroprotective Effects: Short-term AICAR treatment enhances spatial memory, hippocampal neurogenesis, and can offer neuroprotective effects in models of neurodegenerative diseases such as Huntington’s and Parkinson’s disease​ (PMID: 20490918)​.

Structure

Sequence: 5-aminoimidazole-4-carboxamide ribonucleoside

Molecular Formula: C9H1sN40sP

Molecular Weight: 338.213 g/mol

PubChem CID: 65110

CAS Number: 3031-94-5

Synonyms: AICA ribonucleotide, z-nucleotide

AICAR Research

AICAR and Insulin Resistance 

Research in mice shows that AICAR, even at low doses, reduces inflammation in adipose tissue. Inflammation in fat is associated with increased insulin resistance and reducing inflammation leads to improved glucose homeostasis and increased insulin sensitivity even without any changes in body weight. It appears that AICAR has several pathways through which it affects inflammation in adipose tissue, with at least one of those pathways involving SIRTl and macrophages[1].

The impact of AICAR on adipose inflammation is not unexpected. AMPK has been found to attenuate inflammatory responses in metabolic disorders in both healthy and diabetic mice. In research in mice, AMPK activation, as is caused by AICAR, was found to improve insulin sensitivity, energy homeostasis, lipid metabolism, and inflammatory markers.

Exercise increases the number of GLUT-4 insulin receptors that are present on the surface of muscle cells. It is one of the most effective means of boosting glucose uptake by muscle cells and effectively reduces both glucose levels and insulin resistance. It turns out that AICAR mimics the effects of exercise very precisely and that repeated administration of AICAR has effects similar to long-term exercise[3].

AICAR and Cancer Research 
AMPK plays a complex role in the growth and metastasis of cancer, both slowing and accelerating the growth of tumors under varying circumstances. Overall, research indicates that prolonged activation of the enzyme eventually leads to cancer cell death 

by slowing cancer cell metabolism and making cancer cells more susceptible to environmental

insults. This has been demonstrated both in cell culture and in rats[4],[5]. Scientists are investigating the ability of AICAR to work in tandem with other chemotherapeutic agents to boost effectiveness. The thought is that AICAR might

  • reduce side effects,
  • allow for lower dosing of chemotherapeutic drugs, and
  • improve outcomes in chemo-resistant tumors[6].

AICAR inhibits clonal growth of glioma (C6) and prostate cells.
Source: Journal of Biological Chemistry

Research in thyroid cancer cells indicates that AICAR may also operate by causing apoptosis (programmed cell death). It appears that this activity is mediated through the induction of p21 accumulation and the eventual activation of caspase 3. The overall effect is inhibition of cancer cell proliferation and survival[7].

AMPK activators, like AICAR, influence a number of pathways that can impact cancer growth.
Source: PubMed

AICAR Anti-inflammatory Properties

AMPK activators have been shown to play an important role in inflammation at the cellular level. Research into metformin, a common and long-used diabetes medication, indicates that at least part of the reason the drug is effective is that it reduces inflammation and boosts the function of the pancreas. AICAR has a similar effects, playing a protective role in inflammatory conditions like acute lung injury, asthma, colitis, atherosclerosis, and hepatitis[8].

There is ongoing research into the use of AICAR to mediate the effects of auto-immune diseases and other inflammatory conditions. For instance, studies in mice indicate that ACIAR may be effective in reducing inflammation in colitis. It appears that AICAR acts as a central inhibitor of immune responses in this setting by reducing NF-kappaB activation in macrophages as well as TH1- and TH17-type cytokines[9].

AICAR Research and the Heart

Much of heart disease is related to inflammation. The ability to control inflammation could reduce the progression of vascular disease, including atherosclerosis. Research in rabbit models of atherosclerosis indicated that AICAR suppression vascular smooth muscle proliferation. This is not only an important component of cardiovascular disease, but is also one of the reasons that cardiac stents fail over time. Controlling vascular inflammation could reduce both short-term and long-term complications of stent placement without the need for drugs that increase the risk of bleeding[10].

Research also suggests that AMPK activation can suppression certain immune responses that lead to atherosclerosis. The buildup of LDL, often referred to as “bad cholesterol,” leads to macrophage proliferation. This process is integral to the formation of plaques that can eventually lead to heart attack[11]. Anything that can mitigate this proliferation has the potential to reduce heart disease and even heart attack prevalence.

AICAR Research and Fertility

A great deal of AICAR research has revolved around the ability of the peptide to improve sperm motility, energy metabolism, and fertilizing ability. Research in both cats, goats, and chickens indicates that AMPK activators like AICAR can improve sperm motility by improving energy metabolism[12]. It appears that AICAR regulates the activity of energetic enzymes in spermatozoa and therefore impacts overall fertilizing ability[13].

AICAR exhibits minimal side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. AICAR for sale at Life Link Research is limited to educational and scientific research only, not for human consumption. Only buy AICAR if you are a licensed researcher.

Article Author

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Scientific Journal Author

SRencer Gaskin, M.D., Ph.D. is an American Board of Internal Medicine certified cardiologist and medical practitioner. His expertise of Internal medicine and cardiology sources from UT Southwestern Cardiology, Washington University lnterventional Cardiology, and the Mid America Heart Institute. Dr. Gaskin led a study that examined the prevention of Postischemic Leukocyte Rolling and Adhesion via preconditioning with AICAR.

Spencer Gaskin, M.D., Ph.D. is being referenced as one of the leading scientists involved in the research and development of AICAR. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between Life Link Research and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Gaskin is listed in [14] under the referenced citations.

Referenced Citations

1. Z. Yang et al., “The full capacity of AICAR to reduce obesity-induced inflammation and insulin resistance requires myeloid SIRTl,” PloS One, vol. 7, no. 11, p. e49935, 2012.

2. K. Pan et al., “AMPK activation attenuates inflammatory response to reduce ambient PM2.5-induced metabolic disorders in healthy. and diabetic mice,” Ecotoxicol. Environ. Saf., vol. 179, pp. 290-300, Sep. 2019.

3. N. Jessen, R. Paid, E. S. Buhl, L. S. Jensen, 0. Schmitz, and S. Lund, “Effects of AICAR and exercise on insulin-stimulated glucose uptake, signaling, and GLUT-4 content in rat muscles,” J. Appl. Physiol. Bethesda Md 1985,vol.94, no.4, pp. 1373-1379,Apr. 2003.

4. J. Zhuge, “Overexpression of CYP2El induces HeRG2 cells death by the AMP kinase activator 5′-aminoimidazole-4- carboxamide-1-beta-D-ribofuranoside.{AICAR).,” Cell Biol. Toxicol., vol. 25, no. 3, pp. 253-263, Jun.2009.

5. R. Rattan, S. Giri, A. K. Singh, and I. Singh, “5-Aminoimidazole-4-carboxamide-1-beta-D­ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP-activated protein kinase/ J. Biol. Chem., vol. 280, no. 47, pp. 39582-39593, Nov. 2005.

6. M. M. H. Yung, H. Y. S. Ngan, and D. W. Chan, ‘Targeting AMPK signaling in combating ovarian cancers: opportunities and challenges,” Acta Biochim. Biophys.  Sin, vol. 48, no. 4, pp. 301-317, Apr. 2016.

7. W. G. Kim, H.-J. Choi, T. Y. Kim, Y. K. Shong, and W. B. Kim, “The effect of 5-aminoimidazole-4-carboxamide­ribonucleoside was mediated by_p38 mitogen activated protein kinase signaling pathway in FRO thyroid cancer cells,” Korean J. Intern. Med., vol. 29, no. 4, pp. 474-481, Jul. 2014.

8. X.-W. Peng, H.-H. Zhou, J. Dai, and L. Zhang, “[Advances on the anti-inflammatory and protective effect of AMPK activators],” Sheng Li Xue Bao, vol. 71, no. 2, pp. 319-326, Apr. 2019.

9. A. Bai et al., “Novel anti-inflammatory action of 5-aminoimidazole-4-carboxamide ribonucleoside with protective effect in dextran sulfate sodium-induced acute and chronic colitis,” J. Pharmacol. Exp. Ther., vol. 333, no.3, pp. 717-725,Jun. 2010.

10. M. lgata et al., “Adenosine monophosphate­ activated protein kinase suppresses vascular smooth muscle cell proliferation through the inhibition of cell cycle progression,” Circ. Res., vol. 97, no. 8, pp. 837-844, Oct. 2005.

11. M. Sakai, S. Kobori, A. Miyazaki, and S. Horiuchi, “Macrophage proliferation in atherosclerosis,” Curr. Opin. Lipidol., vol. 11, no. 5, pp. 503-509, Oct. 2000.

12. P. Thuwanut, P. Comizzoli, K. Pruksananonda, K. Chatdarong, and N. Songsasen, “Activation of adenosine monophosphate-activated protein kinase (AMPK) enhances energy metabolism, motility, and fertilizing ability of cryopreserved spermatozoa in domestic cat model,” J. Assist. Reprod. Genet., May 2019.

13. Z. Zhu et al., “5′-AMP-Activated Protein Kinase Regulates Goat Sperm Functions via Energy Metabolism In Vitro,” Cell. Physiol. Biochem. Int. J. Exp. Cell. Physiol. Biochem. Pharmacol., vol. 47, no. 6, pp. 2420-2431, 2018.

14. F. Spencer Gaskin, Kazuhiro Kamada, Mozow Yusof, William Durante, Garrett Gross & Ronald J. Korthuis (2009) AICAR Preconditioning Prevents Postischemic Leukocyte Rolling and Adhesion: Role of KATP Channels and Heme  Oxygenase, Microcirculation, 16:2, 167- 176, DOI: 10.1080/10739680802355897 

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