SLU-PP-915
The orally active successor to SLU-PP-332: the same pan-ERR exercise-mimetic mechanism, chemically re-engineered to survive the gut, but still mouse-only.
SLU-PP-915 is a small-molecule pan-agonist of the estrogen-related receptors (ERRalpha/beta/gamma) developed in the Thomas Burris laboratory as the orally bioavailable follow-up to SLU-PP-332. It is not a peptide but a boronic-acid thiophene carboxamide (C17H13BFNO3S, about 341 Da), redesigned so the exercise-mimetic mechanism works by mouth. Its own published efficacy is mainly exercise capacity in mice plus a heart-failure model; the well-known fat-loss and metabolic-syndrome results usually attributed to it actually belong to SLU-PP-332. There is no human efficacy, pharmacokinetic, or safety data of any kind.
Class
Small-molecule orally-bioavailable pan-ERR (ERRalpha/beta/gamma) agonist (not a peptide)
Half-life
Human half-life not reported; engineered for metabolic stability with a microsomal half-life of at least about 60 minutes in mouse and human liver microsomes.
Routes
Oral, Injectable (in early mouse studies)
Category
Weight Loss & Metabolic
Researched benefits
What it's studied for
Oral bioavailability
The one genuine advance over its parent: SLU-PP-332 had to be injected, while SLU-PP-915 was chemically redesigned (a boronic-acid thiophene replacing the acylhydrazone) to resist metabolism and work by mouth. In mice the exercise-capacity effect held up when the compound was given orally, adjusted for systemic exposure.
Increased exercise capacity
In mice a multi-day course of SLU-PP-915 increased treadmill endurance, reproducing an acute-exercise phenotype. This is the molecule's best-characterized standalone effect.
Exercise-mimetic gene signature in muscle
A single dose raised exercise-response genes (Ddit4, Pdk4, PGC-1alpha) in muscle within an hour, driving the PGC-1alpha mitochondrial program of oxidative phosphorylation, fatty-acid oxidation, and mitochondrial biogenesis.
Heart-failure model improvement
SLU-PP-915 improved outcomes in a mouse heart-failure model alongside SLU-PP-332, adding a second preclinical disease setting to the exercise-mimetic story.
Inferred metabolic / fat-loss potential
Because it shares the pan-ERR mechanism of SLU-PP-332, an anti-obesity effect is plausible, but note the caveat: the fat-mass, energy-expenditure and glucose results usually credited to 915 were actually generated with 332, not demonstrated for 915 itself.
Mechanism
How it works
SLU-PP-915 is a small-molecule pan-agonist of the estrogen-related receptors (ERRalpha, ERRbeta, and ERRgamma). It does not activate the classical estrogen receptors. Compared with the parent acylhydrazide scaffold of SLU-PP-332 it is a more balanced pan-agonist, with lower ERRalpha activity.
Mechanistically it is the same as SLU-PP-332: activating the ERRs drives the PGC-1alpha transcriptional program governing oxidative phosphorylation, fatty-acid oxidation, and mitochondrial biogenesis. The net effect is to reproduce an acute-exercise gene signature in skeletal muscle without the exercise itself, which is why the class is described as exercise-mimetic.
In mice, a single dose raised the exercise-response genes Ddit4, Pdk4 and PGC-1alpha in muscle within an hour, and a multi-day course increased treadmill endurance. In the dedicated 2025 characterization study this effect held when the compound was administered orally, which is the genuinely novel finding for 915.
The key chemical difference from its parent is a boronic acid appended to a thiophene carboxamide core. This group was added specifically to slow metabolism; it raised stability in both mouse and human liver microsomes, and that metabolic stability is what gives 915 the oral activity SLU-PP-332 lacks.
Evidence
Research & clinical studies (2)
Discovery of a new chemical series of ERR agonists (the medicinal-chemistry paper describing SLU-PP-915 as 'compound 10s')
Reported the new ERR-agonist chemical series designed to overcome SLU-PP-332's lack of oral bioavailability, with the boronic-acid modification improving stability in mouse and human liver microsomes.
Characterization of the orally bioavailable pan-ERR agonist SLU-PP-915 (Billon et al.)
Dedicated in vivo characterization showing that SLU-PP-915 induces exercise-response genes and increases exercise capacity in mice, with the effect retained when the compound is given orally.
Safety
Side effects & considerations
Contraindications & cautions
- Any human use — there is no human safety data
- Athletes subject to anti-doping testing (prohibited substance class; detectable via published metabolite profiling)
Safety is unknown. There is no published toxicology package and no human data of any kind. The short mouse efficacy studies were not designed as safety studies. Broad activation of the estrogen-related receptors and the novel boronic-acid chemistry are open safety questions that have not been characterized.
FAQ
SLU-PP-915 — common questions
What is SLU-PP-915?
SLU-PP-915 is a small-molecule pan-agonist of the estrogen-related receptors (ERRalpha/beta/gamma), developed in the Burris lab as the orally bioavailable successor to SLU-PP-332. It is not a peptide; it is a boronic-acid thiophene carboxamide (C17H13BFNO3S, about 341 Da). Its published efficacy is in mice, mainly for exercise capacity, plus a heart-failure model. There is no human data.
Is SLU-PP-915 a peptide?
No. It is a small molecule, a boronic-acid-bearing thiophene carboxamide with the formula C17H13BFNO3S and a molecular weight of about 341 Da. It has no amino-acid backbone, and is mislabeled a 'peptide' only because it is sold through research-chemical channels.
How is SLU-PP-915 different from SLU-PP-332?
The headline difference is oral bioavailability. SLU-PP-332 had to be injected; SLU-PP-915 was chemically redesigned to survive metabolism and work orally, which is its one real advance. The ERR mechanism is the same. Note that the well-known fat-loss and metabolic-syndrome results belong to 332; 915's own published efficacy is narrower.
Does SLU-PP-915 cause fat loss?
The fat-loss and metabolic-syndrome data most often attributed to '915' were actually generated with SLU-PP-332. SLU-PP-915's own published mouse efficacy is mainly exercise capacity, plus a heart-failure model. There is no human data, so any fat-loss claim for 915 is an extrapolation from its parent compound.
Is SLU-PP-915 safe?
Unknown. There is no published toxicology package and no human data of any kind. Short mouse efficacy studies were not designed as safety studies. Broad activation of ERRs, and the boronic-acid chemistry, are open safety questions that have not been characterized.
Is SLU-PP-915 FDA approved?
No. It has no approval and is not in any registered human trial. It is sold under research-chemical labeling. As with 332, it falls in a prohibited substance class in sport, and anti-doping researchers have already published metabolite profiling for it.
