SLU-PP-332 (50mg x 60 tabs = 3,000,000mcg)

SLU-PP-332

Each Bottle Contains 60 x 50mg tablets

Cost per milligram	$0.075

• Peptide Partners Manufacturer ID: NC53
• Batch Id: SLU202601

Research Studies

(for educational purposes only)

A Synthetic ERR Agonist Alleviates Metabolic Syndrome

Authors: Billon C, et al.

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC10801787/

Scientific Summary

This study introduces SLU-PP-332 as a novel pan-agonist for the estrogen-related receptors (ERRα, β, and γ), a class of nuclear receptors that are key regulators of energy metabolism. Through a series of in vitro and in vivo experiments, the authors demonstrate that SLU-PP-332 effectively mimics the physiological benefits of aerobic exercise. In cell-based assays, the compound was shown to activate all three ERR isoforms, with a slight preference for ERRα. This activation leads to an increase in the expression of genes involved in fatty acid oxidation and mitochondrial biogenesis. When administered to mouse models of obesity and metabolic syndrome, SLU-PP-332 increased energy expenditure, promoted the burning of fat, reduced overall fat mass, and improved insulin sensitivity. These findings suggest that pharmacological activation of ERRs with compounds like SLU-PP-332 could be a promising therapeutic strategy for treating metabolic diseases.

Plain English Summary

Scientists have developed a new drug called SLU-PP-332 that can trick the body into thinking it has exercised. It works by activating special sensors in our cells that are normally turned on during physical activity. In lab experiments, this drug was shown to boost the body’s ability to burn fat and increase energy use, just like a good workout. When given to obese mice, the drug helped them lose weight and become more sensitive to insulin, which is important for preventing diabetes. This research opens up the possibility of using a pill to get some of the health benefits of exercise, which could be a game-changer for people who are unable to exercise due to health reasons.

Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity

Authors: Cyrielle Billon, Sadichha Sitaula, Subhashis Banerjee, et al.

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC11584170/

Scientific Summary

This paper provides a detailed characterization of SLU-PP-332, a synthetic pan-agonist of the estrogen-related receptors (ERRs) with a notable potency for ERRα (EC50 = 98 nM). The development of SLU-PP-332 was achieved through a rational drug design approach, which involved modifying an existing ERRβ/γ agonist to enhance its activity at ERRα. In vitro experiments using the C2C12 skeletal muscle cell line demonstrated that SLU-PP-332 significantly increases the expression of ERR target genes, such as Pdk4, enhances mitochondrial respiration, and promotes mitochondrial biogenesis. These cellular effects translate to improved physical performance in vivo, as mice treated with SLU-PP-332 showed an increase in oxidative muscle fibers and enhanced exercise endurance. The study also established that the beneficial effects of SLU-PP-332 on exercise capacity are primarily mediated through the activation of ERRα.

Plain English Summary

This research delves into how the exercise-mimicking drug, SLU-PP-332, works at a cellular level. Scientists found that this drug is particularly good at activating a specific sensor in our cells called ERRα. In lab experiments on muscle cells, they observed that SLU-PP-332 revs up the cells’ energy-producing machinery, the mitochondria, making them work more efficiently. This is similar to what happens when we exercise. When they gave the drug to mice, they found that the mice could run for longer and had more of the muscle fibers that are associated with endurance. This study confirms that SLU-PP-332 can indeed mimic the effects of exercise and that it does so mainly by targeting the ERRα sensor.

Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function

Authors: Weiyi Xu, Angelica Hamilton, Aijun Bhagat, et al.

URL: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.123.066542

Scientific Summary

This study investigates the therapeutic potential of two pan-ERR agonists, SLU-PP-332 and SLU-PP-915, in a preclinical model of heart failure. The researchers found that both compounds significantly improved cardiac function, reduced fibrosis, and increased survival in mice with pressure overload-induced heart failure. The beneficial effects were attributed to the ability of the ERR agonists to enhance cardiac fatty acid metabolism and mitochondrial function. In vitro experiments using neonatal rat ventricular myocytes (NRVMs) and isolated adult mouse cardiomyocytes confirmed that these compounds increase mitochondrial oxidative capacity and fatty acid utilization. Through a series of genetic knockdown experiments, the study identified ERRγ as the primary mediator of the cardioprotective effects of these agonists. The findings provide strong evidence that pharmacological activation of ERRs could be a novel therapeutic strategy for heart failure.

Plain English Summary

This study explored whether the exercise-mimicking drugs, SLU-PP-332 and a similar compound, could be used to treat heart failure. In experiments with mice that had heart failure, both drugs were found to improve the heart’s pumping ability, reduce scarring, and help the mice live longer. The drugs worked by boosting the heart’s energy production and its ability to use fat for fuel. The scientists also tested the drugs on isolated heart cells in the lab and confirmed that they improve the function of the cells’ powerhouses, the mitochondria. They also discovered that a specific sensor in the heart cells, called ERRγ, is the main target for these drugs’ beneficial effects. This research suggests that drugs like SLU-PP-332 could one day be used to treat heart failure in humans.