SR9009 is not a SARM but rather a potent non-addictive Nootropic in the REV-ERB agonist category. REV-ERB proteins regulate the body’s core clock and circadian rythm , they alter the expression of genes involved in lipid and glucose metabolism, cartilage breakdown, and may reduce the risk of heart disease via atherosclerosis.
Several studies suggest that SR9009 and other REV-ERB agonists may be useful in aiding the maintenance of wakefulness in pathological conditions affection sleep [1,2,3]. SR9009 is able to induce wakefulness at different times during the light period and maintained its efficacy even when administered throughout the day . This is attractive for those who travel frequently and must train while jet-lagged.
SR9009 has demonstrated in vitro and in vivo to increase basal oxygen consumption, decrease lipogenesis, increase mitochondrial content of muscle tissue, decrease fat storage, and increase glucose and fatty acid oxidation in skeletal muscles. These effects make it attractive for endurance athletes and for the treatment of several metabolic disorders .
REV-ERB proteins have been shown to function as transcription repressors in articular cartilage. Treatment of chondrocyles with known catabolic agents causes the induction of REV-ERB alpha as a defense mechanism, whereas stimulation with anabolic agents decreases REV-ERB activity . Overexpression of REV-ERB activity is shown to decrease matrix-degrading enzymes like matrix metalloproteinase 13 and aggrecanase .
Recent studies have also linked REV-ERB proteins to reduced risk of atherosclerosis [5, 6]. REV-ERB knockout mice have shown increased atherosclerosis, while atherosclerotic mice given SR9009 twice per day showed improvement in atherosclerosclerotic lesions as well as significant improvements in plasma lipid levels .
SR9009 Investigational Benefits Summary:
1. Induces Wakefulness
2. Increases oxidation of fatty acids and glucose and decreases fat storage
3. Increases skeletal muscle mitochondria content
4. Potentially accelerates recovery of connective tissue
5. May decrease arterial buildup/atherosclerosis
1. Geldof, Lore et al. “In Vitro Metabolic Studies of REV-ERB Agonists SR9009 and SR9011.” Ed. Chang Won Choi. International Journal of Molecular Sciences 17.10 (2016):1676.
2. Möller-Levet, Carla S. et al. “Effects of Insufficient Sleep on Circadian Rhythmicity and Expression Amplitude of the Human Blood Transcriptome.” Proceedings of the National Academy of Sciences of the United States of America 110.12 (2013): E1132–E1141.
3. Amador, Ariadna et al. “Pharmacological Targeting the REV-ERBs in Sleep/Wake Regulation.” Ed. Nicolas Cermakian. PLoS ONE 11.9 (2016):e0162452.
4. Chaturvedi P1, Pratta M, Steplewski K, Connor J, Kumar S. Functional characterization of an orphan nuclear receptor, Rev-ErbAalpha, in chondrocytes and its potential role in osteoarthritis. Arthritis Rheum. 2006 Nov;54(11):3513-22.
5. Sitaula, Sadichha et al. “Suppression of Atherosclerosis by Synthetic REV-ERB Agonist.” Biochemical and biophysical research communications 460.3 (2015):566–571.
6. Ma H, et al. “Increased atherosclerotic lesions in LDL receptor deficient mice with hematopoietic nuclear receptor Rev-erba knock- down.” J Am Heart Assoc. 2013;2:e000235.