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Sr93.0
SR9009 (Stenabolic) – Forschung
Überwiegend Mechanismus / Beobachtung
5 begutachtete Studien
Was die Evidenz sagt
Überwiegend Mechanismus / Beobachtung
Die meisten Studien zu SR9009 (Stenabolic) sind mechanistisch oder beobachtend statt RCTs, die einen klinischen Effekt messen — betrachte die Ergebnisse als vorläufig.
Die meiste Evidenz stammt aus gemischt-qualitativen Studien, veröffentlicht 2012–2024.
Basierend auf 5 Studien
Konfidenz
Geringe Konfidenz
Nach Outcome
Metabolism & fat loss (preclinical)
Überwiegend Mechanismus / Beobachtung4 Studien
Exercise capacity (preclinical)Erhöhte Laufleistung nur bei Mäusen; Off-Target-Effekte und keine Humanevidenz. · Nicht etabliert (keine Humandaten)
Zu wenige bewertete Studien2 Studien
Weight managementReduzierte Fettmasse und verbesserte Blutfettwerte bei Mäusen als REV-ERB-Agonist; keine Humandaten, schlechte orale Bioverfügbarkeit und von der WADA verboten. · Nicht etabliert (keine Humandaten)
Zu wenige bewertete Studien2 Studien
Safety profile
Zu wenige bewertete Studien2 Studien
Aktives Forschungsgebiet
2 Studien in den letzten 5 Jahren
201220182024
1Tierstudie2012
Treatment of diet-induced obese mice with a REV-ERB agonist decreased obesity by reducing fat mass and markedly improving dyslipidaemia and hyperglycaemia.
Solt LA, Wang Y, Banerjee S, Hughes T, Kojetin DJ, Lundasen T, et al. · Nature (2012)
Foundational paper introducing potent synthetic REV-ERB agonists (the SR9009/SR9011 series) with in-vivo activity in mice
REV-ERB agonism altered circadian behaviour and clock-gene expression in the hypothalamus and shifted rhythmic metabolic-gene expression in liver, muscle and adipose tissue, increasing energy expenditure
In diet-induced-obese mice, treatment reduced fat mass and improved dyslipidaemia and hyperglycaemia
Muscle overexpression or pharmacological activation of Rev-erb-α in vivo increased exercise capacity.
Woldt E, Sebti Y, Solt LA, Duhem C, Lancel S, Eeckhoute J, et al. · Nature medicine (2013)
REV-ERB-α is highly expressed in oxidative skeletal muscle and controls mitochondrial content and oxidative function via the LKB1–AMPK–SIRT1–PGC-1α pathway
REV-ERB-α deficiency reduced mitochondrial content, increased autophagy, and compromised exercise capacity in mice
Pharmacological REV-ERB activation in vivo increased exercise capacity — the origin of the 'exercise mimetic' framing
SR9009 can decrease cell viability, rewire cellular metabolism, and alter gene transcription in hepatocytes and embryonic stem cells lacking both REV-ERBα and -β ... Thus, the effects of SR9009 cannot be used solely as surrogate for REV-ERB activity.
Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, et al. · Proceedings of the National Academy of Sciences of the United States of America (2019)
The key counter-evidence: the authors generated mice with conditional deletion of BOTH REV-ERB-α and -β
SR9009 still decreased cell viability, rewired metabolism, and altered transcription in hepatocytes and embryonic stem cells with no REV-ERB present
Demonstrates that a meaningful share of SR9009's effects are REV-ERB-independent (off-target), not the advertised mechanism
The results of multiple studies in preclinical models demonstrate that Rev-Erb is an attractive target for positively influencing dysregulated metabolism, inflammation, and fibrosis, but more specific tools and studies would be needed.
Raza GS, Sodum N, Kaya Y, Herzig KH. · International journal of molecular sciences (2022)
Review framing REV-ERB as a master regulator of metabolism, mitochondrial biogenesis, inflammation and fibrosis across liver, heart, lung, muscle and adipose tissue
Summarizes that REV-ERB activation alleviated cardiac hypertrophy and increased exercise capacity, reduced pulmonary fibrosis, and reduced fat mass in adipose tissue
Explicitly notes the evidence is from preclinical models and that more specific tools and studies are needed before therapeutic potential is established
It failed to receive the United States Food and Drug Administration (USFDA) approval and its illegal distribution has raised concerns. As a result, it has been classified as a prohibited substance by the World Anti-Doping Agency.
Kwak YB, Yoon J, Yoo HH · Journal of pharmaceutical and biomedical analysis (2024)
In-vitro liver-microsome study mapping SR9009 phase-I metabolites for anti-doping forensic detection
States plainly that SR9009 failed to receive FDA approval, that its illegal distribution is a concern, and that it is prohibited by the World Anti-Doping Agency and horse-racing authorities
Anchors the regulatory/grey-market reality and the rapid hepatic metabolism that underlies SR9009's poor bioavailability