AICAR (50mg)
$130.00
Additional information
| Weight | 0.0625 lbs |
|---|
Published Scientific Research
Explore the full library of peer-reviewed studies, clinical data, mechanism breakdowns, and molecular specifications for AICAR (50mg).
All research is sourced from PubMed-indexed journals for informational and educational purposes only. For Research Use Only (RUO). Not for human use.
View Full Research Library →Storage Instructions
All products from Apex Health Performance are manufactured using a lyophilization (freeze-drying) process. This method is designed to maintain product integrity and allows vials to remain stable during shipping for approximately 3–4 months.
Once a vial is reconstituted with bacteriostatic water, it should be stored in the refrigerator to help maintain stability. Under these conditions, reconstituted material is generally considered stable for up to 30 days.
Lyophilization is a dehydration technique in which compounds are frozen and then exposed to low pressure. This causes the water in the vial to sublimate directly from solid to gas, leaving behind a stable, crystalline white structure. This powder can be kept at room temperature until reconstitution.
Upon receipt, products should be stored away from heat and light. For short-term use, refrigeration at approximately 4°C (39°F) is suitable. For long-term storage (several months to years), vials may be placed in a freezer at approximately -80°C (-112°F). Freezing is the preferred method for preserving product stability over extended periods.
⚠️ Important Notice:
These products are intended for research use only. Not for human consumption.
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Research Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating research peptides
AICAR attenuates ischemia-reperfusion-induced AKI by modulating AMPK-TXNIP-NLRP3 pathway and energy metabolism.
This study aims to elucidate the synergistic protective mechanism of the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) in ischemia-reperfusion injury -associated acute kidney injury (IRI-AKI). By establishing a hypoxia/reoxygenation (H/R) injury model using human proximal tubule cells (HK-2) and IRI-AKI rat model, and employing molecular techniques including qRT-PCR, western blotting, serum biochemical assays, renal tissue hematoxylin and eosin staining, immunofluorescence, and transmission electron microscopy (TEM), we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3, blocks Caspase-1-dependent release of IL-1β and IL-18, and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
View Full Study on PubMedCD137L promotes immune surveillance in melanoma via HLTF regulation.
In summary, our findings elucidate a mechanism controlling CD137L expression and highlight a promising combination therapy to enhance the efficacy of ICBs in melanoma.
View Full Study on PubMedResistance exercise upregulates Irisin expression and suppresses myocardial fibrosis following myocardial infarction via activating AMPK-Sirt1 and inactivating TGFβ1-Smad2/3.
RESULTS: Resistance exercise increased Fndc5 mRNA level, inhibited the activation of TGFβ1-TGFβR2-Smad2/3 pathway, activated AMPK-Sirt1 pathway, reduced the levels of oxidative stress, apoptosis, and MF in the infarcted heart, and promoted cardiac function. Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in HO-treated CFs.
View Full Study on PubMedMitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.
MOTS-c mainly acts through the Folate-AICAR-AMPK pathway, thereby influencing energy metabolism, insulin resistance, inflammatory response, exercise, aging and aging-related pathologies. This review summarizes the retrograde signaling of MOTS-c toward the nucleus, the regulation of energy metabolism, stress homeostasis, and aging-related pathological processes, as well as the underlying molecular mechanisms.
View Full Study on PubMedGDF15 in Appetite and Exercise: Essential Player or Coincidental Bystander?
When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha-like). Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment.
View Full Study on PubMedAICAR attenuates postoperative abdominal adhesion formation by inhibiting oxidative stress and promoting mesothelial cell repair.
5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) is an adenosine 5'-monophosphate activated protein kinase (AMPK) pathway agonist that inhibits inflammation, reduces cell fibrosis and cellular reactive oxygen species (ROS) injury, promotes autophagy and mitochondrial function. This study aimed to explore the mechanism of AICAR in inhibiting adhesion formation.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating research peptides
AICAR attenuates ischemia-reperfusion-induced AKI by modulating AMPK-TXNIP-NLRP3 pathway and energy metabolism.
This study aims to elucidate the synergistic protective mechanism of the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) in ischemia-reperfusion injury -associated acute kidney injury (IRI-AKI). By establishing a hypoxia/reoxygenation (H/R) injury model using human proximal tubule cells (HK-2) and IRI-AKI rat model, and employing molecular techniques including qRT-PCR, western blotting, serum biochemical assays, renal tissue hematoxylin and eosin staining, immunofluorescence, and transmission electron microscopy (TEM), we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3, blocks Caspase-1-dependent release of IL-1β and IL-18, and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
View Full Study on PubMedCD137L promotes immune surveillance in melanoma via HLTF regulation.
In summary, our findings elucidate a mechanism controlling CD137L expression and highlight a promising combination therapy to enhance the efficacy of ICBs in melanoma.
View Full Study on PubMedResistance exercise upregulates Irisin expression and suppresses myocardial fibrosis following myocardial infarction via activating AMPK-Sirt1 and inactivating TGFβ1-Smad2/3.
RESULTS: Resistance exercise increased Fndc5 mRNA level, inhibited the activation of TGFβ1-TGFβR2-Smad2/3 pathway, activated AMPK-Sirt1 pathway, reduced the levels of oxidative stress, apoptosis, and MF in the infarcted heart, and promoted cardiac function. Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in HO-treated CFs.
View Full Study on PubMedMitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.
MOTS-c mainly acts through the Folate-AICAR-AMPK pathway, thereby influencing energy metabolism, insulin resistance, inflammatory response, exercise, aging and aging-related pathologies. This review summarizes the retrograde signaling of MOTS-c toward the nucleus, the regulation of energy metabolism, stress homeostasis, and aging-related pathological processes, as well as the underlying molecular mechanisms.
View Full Study on PubMedGDF15 in Appetite and Exercise: Essential Player or Coincidental Bystander?
When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha-like). Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment.
View Full Study on PubMedAICAR attenuates postoperative abdominal adhesion formation by inhibiting oxidative stress and promoting mesothelial cell repair.
5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) is an adenosine 5'-monophosphate activated protein kinase (AMPK) pathway agonist that inhibits inflammation, reduces cell fibrosis and cellular reactive oxygen species (ROS) injury, promotes autophagy and mitochondrial function. This study aimed to explore the mechanism of AICAR in inhibiting adhesion formation.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating research peptides
AICAR attenuates ischemia-reperfusion-induced AKI by modulating AMPK-TXNIP-NLRP3 pathway and energy metabolism.
This study aims to elucidate the synergistic protective mechanism of the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) in ischemia-reperfusion injury -associated acute kidney injury (IRI-AKI). By establishing a hypoxia/reoxygenation (H/R) injury model using human proximal tubule cells (HK-2) and IRI-AKI rat model, and employing molecular techniques including qRT-PCR, western blotting, serum biochemical assays, renal tissue hematoxylin and eosin staining, immunofluorescence, and transmission electron microscopy (TEM), we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3, blocks Caspase-1-dependent release of IL-1β and IL-18, and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
View Full Study on PubMed →CD137L promotes immune surveillance in melanoma via HLTF regulation.
In summary, our findings elucidate a mechanism controlling CD137L expression and highlight a promising combination therapy to enhance the efficacy of ICBs in melanoma.
View Full Study on PubMed →Resistance exercise upregulates Irisin expression and suppresses myocardial fibrosis following myocardial infarction via activating AMPK-Sirt1 and inactivating TGFβ1-Smad2/3.
RESULTS: Resistance exercise increased Fndc5 mRNA level, inhibited the activation of TGFβ1-TGFβR2-Smad2/3 pathway, activated AMPK-Sirt1 pathway, reduced the levels of oxidative stress, apoptosis, and MF in the infarcted heart, and promoted cardiac function. Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in HO-treated CFs.
View Full Study on PubMed →Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging.
MOTS-c mainly acts through the Folate-AICAR-AMPK pathway, thereby influencing energy metabolism, insulin resistance, inflammatory response, exercise, aging and aging-related pathologies. This review summarizes the retrograde signaling of MOTS-c toward the nucleus, the regulation of energy metabolism, stress homeostasis, and aging-related pathological processes, as well as the underlying molecular mechanisms.
View Full Study on PubMed →GDF15 in Appetite and Exercise: Essential Player or Coincidental Bystander?
When administered pharmacologically, GDF15 reduces food intake and lowers body weight via the hindbrain-situated receptor GFRAL (glial cell-derived neurotrophic factor family receptor alpha-like). Prolonged endurance exercise increases circulating GDF15 to levels otherwise associated with certain pathological states and in response to metformin treatment.
View Full Study on PubMed →AICAR attenuates postoperative abdominal adhesion formation by inhibiting oxidative stress and promoting mesothelial cell repair.
5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) is an adenosine 5'-monophosphate activated protein kinase (AMPK) pathway agonist that inhibits inflammation, reduces cell fibrosis and cellular reactive oxygen species (ROS) injury, promotes autophagy and mitochondrial function. This study aimed to explore the mechanism of AICAR in inhibiting adhesion formation.
View Full Study on PubMed →Important Research Notice: These products are research chemicals intended exclusively for in vitro laboratory research by qualified professionals. Not for human or animal consumption. Not approved by the FDA for any therapeutic purpose. Sold strictly for scientific research applications only.