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.
Related products
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
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 PubMedAMPK phosphorylation of K2.3 alleviates angiotensin II-induced endothelial dysfunction.
We recently demonstrated in diet-induced obese mice that adenosine monophosphate-activated protein kinase (AMPK) upregulates endothelial K2.3 expression and improves endothelial function. However, the molecular mechanism of regulation of K2.3 by AMPK remains less explored.
View Full Study on PubMedTargeting negative phosphorylation to activate AMPK.
Activation of AMPK stimulates the catabolic pathway (glucose utilization and β-oxidation) and inhibits the anabolic pathway (gluconeogenesis, protein synthesis, and lipogenesis), leading to improvement of cellular energy status. However, the mechanisms of maintaining low cellular AMPK activity are not fully understood.
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 PubMedDysregulation of Angiopoietin-like-4 Associated with Hyperlipidemia-induced Renal Injury by AMPK/ACC Pathway.
This study aimed to investigate the Angptl4 expression in renal tissue and podocyte under hyperlipidemia conditions and explore the potential molecular mechanisms. OBJECTIVE: The role of Angptl4 in hyperlipidemia-induced glomerular disease and the detailed underlying mechanisms are unclear.
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
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 PubMedAMPK phosphorylation of K2.3 alleviates angiotensin II-induced endothelial dysfunction.
We recently demonstrated in diet-induced obese mice that adenosine monophosphate-activated protein kinase (AMPK) upregulates endothelial K2.3 expression and improves endothelial function. However, the molecular mechanism of regulation of K2.3 by AMPK remains less explored.
View Full Study on PubMedTargeting negative phosphorylation to activate AMPK.
Activation of AMPK stimulates the catabolic pathway (glucose utilization and β-oxidation) and inhibits the anabolic pathway (gluconeogenesis, protein synthesis, and lipogenesis), leading to improvement of cellular energy status. However, the mechanisms of maintaining low cellular AMPK activity are not fully understood.
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 PubMedDysregulation of Angiopoietin-like-4 Associated with Hyperlipidemia-induced Renal Injury by AMPK/ACC Pathway.
This study aimed to investigate the Angptl4 expression in renal tissue and podocyte under hyperlipidemia conditions and explore the potential molecular mechanisms. OBJECTIVE: The role of Angptl4 in hyperlipidemia-induced glomerular disease and the detailed underlying mechanisms are unclear.
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
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 →AMPK phosphorylation of K2.3 alleviates angiotensin II-induced endothelial dysfunction.
We recently demonstrated in diet-induced obese mice that adenosine monophosphate-activated protein kinase (AMPK) upregulates endothelial K2.3 expression and improves endothelial function. However, the molecular mechanism of regulation of K2.3 by AMPK remains less explored.
View Full Study on PubMed →Targeting negative phosphorylation to activate AMPK.
Activation of AMPK stimulates the catabolic pathway (glucose utilization and β-oxidation) and inhibits the anabolic pathway (gluconeogenesis, protein synthesis, and lipogenesis), leading to improvement of cellular energy status. However, the mechanisms of maintaining low cellular AMPK activity are not fully understood.
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 →Dysregulation of Angiopoietin-like-4 Associated with Hyperlipidemia-induced Renal Injury by AMPK/ACC Pathway.
This study aimed to investigate the Angptl4 expression in renal tissue and podocyte under hyperlipidemia conditions and explore the potential molecular mechanisms. OBJECTIVE: The role of Angptl4 in hyperlipidemia-induced glomerular disease and the detailed underlying mechanisms are unclear.
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.