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SR9009 Stenabolic

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SR9009 Stenabolic

SR9009 is a synthetic compound, often called a REV-ERB agonist, meaning it activates the nuclear receptor proteins REV-ERBα and REV-ERBβ. These are involved in regulating circadian rhythms (your internal clock), metabolism, fat storage, and inflammation, among other functions.

It has been studied mostly in cell culture and animal (mostly rodent) models, not established in humans.

Positive Findings from Research

Here are some of the beneficial effects observed in studies. Note: many are preclinical (animals, cells), so aren’t proven in people.

Metabolic Effects / Insulin Sensitivity

In mice exposed to conditions that disrupt circadian rhythms (constant light exposure), SR9009 helped reduce weight gain, insulin resistance, and the amount of white fat tissue.

It seems to suppress adipogenesis (formation of new fat cells) in certain fat tissues.

In fish (goldfish), activation of REV-ERBα by SR9009 reduced feeding, lowered body weight gain, decreased glucose levels, reduced triglycerides, and changed liver metabolism toward less lipogenesis (making fat).

Endurance / Muscle / Exercise Capacity

One study showed that activation of REV-ERB with SR9009 increases skeletal muscle metabolic activity and improves running capacity in mice. The mice with SR9009 were able to run longer before exhaustion.

There’s evidence SR9009 increases mitochondrial function in muscle (in certain models) which is relevant to endurance.

Cardioprotective Effects

In a model of pressure overload (a way to simulate stress on the heart, e.g. from high blood pressure), SR9009 helped preserve heart function, reduce dilation of heart chambers, and improve measures like ejection fraction in mice—even in mice genetically engineered to lack REV-ERB in heart tissue. That suggests some REV-ERB-independent benefit as well.

Anti-senescence / Anti-inflammation

SR9009 has been shown to suppress the senescence-associated secretory phenotype (SASP), which are inflammatory factors secreted by old or damaged cells. It does this via activation of the NRF2 pathway, which is a major antioxidant / cellular maintenance pathway.
 
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