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The mice lacking intestinal Bmal1 gained weight normally on a chow (low-fat) diet (Fig. 1a). However, on a high-fat diet (HFD, 60% kcal from fat), Bmal1iKO mice gained less weight as compared to controls (Fig. 1a–c). After 10 weeks on HFD feeding, Bmal1iKO mice weighed 22% less than did control mice (Fig. 1a), and their fat mass was 46% lower with no significant difference in lean body weight (Fig. 1d). Supporting this, gonadal, mesenteric and inguinal white adipose tissues (gWAT, mWAT and iWAT) and brown adipose tissue (BAT) were all lighter in Bmal1iKO than in control mice (Fig. 1e). Histological analysis revealed adipocyte hypertrophy in control mice, and adipocytes from HFD-fed Bmal1iKO mice were 41% smaller than those from controls (Fig. 1f). We also observed a lower concentration of serum leptin in Bmal1iKO mice (Fig. 1g), which was expected considering a positive association of circulating leptin with adipose tissue mass23. Altogether, intestinal Bmal1 deficiency protects mice from HFD-induced obesity.

They were also protected from hepatic steatosis as illustrated by decreased hepatic lipids, lower liver mass and histological examinations (Fig. 1i–k). Meanwhile, HFD-fed Bmal1iKO mice had lower fasting blood glucose and insulin levels (Supplementary Fig. 3a). They showed better glucose tolerance and improved insulin sensitivity according to oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) (Supplementary Fig. 3b). Therefore, intestinal Bmal1 deficiency also protects mice against hyperlipidemia, hepatic steatosis and glucose intolerance.


Decreased dietary fat absorption in Bmal1 iKO mice

To investigate the mechanisms underlying the phenotype of Bmal1iKO mice, we first analyzed the energy balance. Food intake and feeding rhythm were similar between two genotypes (Supplementary Fig. 4a). Bmal1iKO mice showed no changes in locomotor activity as compared to controls (Supplementary Fig. 4b). They did not show a difference either in energy expenditure normalized by body weight (Supplementary Fig. 4c). These data suggested that reduced adiposity and alleviated comorbidities in Bmal1iKO mice were not due to an alteration in energy expenditure. We next examined intestinal absorption of dietary fat. On an HFD, Bmal1iKO mice had a decreased efficiency in converting food into body mass, and the food efficiency was ~45% of controls (Fig. 2a). The mice also had lower levels of intestinal lipids (Fig. 2b), which was illustrated by oil red O staining (Fig. 2c). Conversely, fecal fat was higher in HFD-fed Bmal1iKO mice than in control mice (Fig. 2d). Furthermore, when fasted Bmal1iKO mice were refed with HFD for 1 h, they showed lower levels of serum TAG and FFA as well as decreased intestinal lipids compared to controls (Fig. 2e/f). This was consistent with a decreased number of and reduced size of lipid droplets in the enterocytes of Bmal1iKO mice (Fig. 2g). Additionally, when fasted mice were gavaged with olive oil, Bmal1iKO mice showed lower circulating TAG and FFA with reduced serum lactescence (decreased chylomicrons), and their TAG absorption was ~50% of controls (Fig. 2h/i). In line with this, intestinal and hepatic lipids were lower in olive oil-treated Bmal1iKO mice (Fig. 2j-m). These findings indicate that intestinal Bmal1 deficiency results in reduced absorption of dietary fat, potentially accounting for protection of the animals against HFD-induced obesity and comorbidities.




Improves Stamina, Endurance & Speeds fat burning!

This is what most original studies were based, SR-9009 increases cellular reproduction via speeding the circadian clock in the body (first thought only in the muscle, bone and liver) it would increase metabolism for diabetics needing to burn off excess sugar and those that were obese.

These turned out to be side benefits getting SR9009 the nickname exercise in a bottle. As the cellular reproduction speeds in the body one can only hypothesize that the metabolism would go at a faster pace which in turn burns off excess fat and without increasing the appetite! Tests on mice confirm a spiraling energy to partake in more physical activity. This results from the stimulation of Rev-ErbA or the speeding of he internal clock of the cell to produce more energy. With all these combined SR 9009 took off as the leading fat burner in the race to produce a pharmaceutical weight loss miracle.

SR-9009 preserves lean muscle mass.

When we increase the rate at which the muscle can rebuild cellularly we also create an anabolic or muscle building environment. This makes SR 9009 a more versatile product for retaining muscle in a caloric deficit or to build lean muscle mass while converting fat storage into the energy needed to build muscle.

Improves cardiovascular health.

The most widely researched use of SR 9009 is in the number 1 killer in the USA heart disease because of its unique ability to lower LDL cholesterol and in studies over a 7 week period it reduces the size of the blood vessel lesions in mice at risk of hardening of the arteries. Furthermore it has been shown that SR 9009 can improve cardiovascular function when taken for 28 days or more.

May aid in anxiety reduction

Anxiety as a mental disorder effects over 4 million in the US alone. By providing the body with more cellular energy the body calms for not having been overloaded by excess toxins and burdensome inability to rebuild. So if there be a product that may help with the over stressed individual in the future this may just be the best yet.

Inflammation reduction

Shown in studies to reduce TNF-Alpha formation in the lungs to aid in recovery of those suffering with COPD or any of its like respiratory disorders even healing the lesions caused by smoke inhalation in rat models.


What else is SR 9009 being researched for?

SR9009 administered for one day after myocardial ischemia-reperfusion prevents heart failure in mice by targeting the cardiac inflammasome

Pharmacological activation of REV-ERBs is lethal in cancer and oncogene-induced senescence

G Sulli, A Rommel, X Wang, MJ Kolar, F Puca… – Nature, 2018 –

… agonists of REV-ERBs—SR9009 and SR9011—are specifically lethal to cancer cells and … The
regulation of autophagy and de novo lipogenesis by SR9009 and SR9011 has a … Notably, the
selective anticancer properties of these REVERB agonists impair glioblastoma growth in

REV-ERB agonism improves liver pathology in a mouse model of NASH

Time’s up for tumors

Decreasing glucose via SR 9009 

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