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slu-pp-915

the orally active successor to SLU-PP-332. same pan-ERR exercise-mimetic mechanism, re-engineered to survive the gut. still mouse-only, still no human data, and its best-known fat-loss claims actually belong to 332.

tier C · weight loss · oral ERR agonist · preclinical

verdict

a small molecule, not a peptide. the Burris lab's orally bioavailable follow-up to SLU-PP-332: the same pan-ERR exercise-mimetic mechanism, redesigned so it works by mouth. preclinical only, no human data.

if you're asking how it differs from SLU-PP-332 — one real advance: oral bioavailability. 332 had to be injected; 915 was chemically redesigned (a boronic-acid thiophene instead of the acylhydrazone) to resist metabolism and work orally. in mice the exercise-capacity effect was comparable to 332, and it held up when given by mouth, adjusted for systemic exposure. on the underlying biology it is the same pan-ERR story.

if you're asking about fat loss and metabolic benefits — watch the attribution. the well-known fat-mass, energy-expenditure and glucose results belong to SLU-PP-332, not 915. 915's own published efficacy is mainly exercise capacity and a heart-failure model. the obesity case for 915 is inferred from its parent, not demonstrated for the molecule itself.

if you're asking what is known in humans — nothing in vivo. zero trials, zero human pharmacokinetics, zero human safety. the only human-derived work is test-tube liver-enzyme metabolite profiling, run so anti-doping labs can detect it. that is the opposite of a human efficacy or safety study.

based on published preclinical evidence. not medical advice. an unapproved research compound with no human data.

why C-tier

C-tier, and marginally below SLU-PP-332 within the tier. Same target class, same maturity wall: preclinical only, no human in-vivo data, no toxicology, limited independent replication. Its one real advance, oral bioavailability, is a genuine drug-development step but does not change evidence maturity, because the data is still entirely mouse and cell. Its standalone record is thinner than 332's (the headline metabolic and fat-loss results belong to 332, not 915), which is why it sits just below its parent. Not D-tier, because nothing has failed and there is no published safety signal. Not B-tier, because there is no human data and key claims attached to it are borrowed from the parent compound.

the core tension

SLU-PP-915 is the sequel to SLU-PP-332, and it inherits both the promise and the problem. The promise: it solves the one concrete liability of its parent by being orally bioavailable, which is the difference between an injectable probe and a plausible drug candidate. The problem: it is still entirely preclinical, still mouse-and-cell only, still from one lab, and its own published efficacy is narrower than the reputation it carries. The fat-loss and metabolic-syndrome results that get attached to '915' were actually generated with 332. The exact ERR potency numbers on vendor pages are paper-attributed, not cleanly established. And the only human-derived data that exists is test-tube metabolite work, done to help anti-doping labs catch it. Where the research supports a claim for 915 specifically, the report says so; where the claim is borrowed from 332, it says that too.

what it is

SLU-PP-915 is a small-molecule pan-agonist of the estrogen-related receptors (ERRα/β/γ), developed in the Burris lab as the orally bioavailable successor to SLU-PP-332. It is not a peptide: it is a boronic-acid-bearing thiophene carboxamide, formula C17H13BFNO3S, about 341 Da. The boronic acid was added specifically to slow metabolism (it raised stability in both mouse and human liver microsomes), which is what gives 915 the oral activity its parent lacks. Like 332 it does not activate the classical estrogen receptors; it is a more balanced pan-agonist, with lower ERRα activity than the parent acylhydrazide scaffold.

what it does

Mechanistically it is the same as 332: activate ERRs, drive the PGC-1α mitochondrial program (oxidative phosphorylation, fatty-acid oxidation, mitochondrial biogenesis), and reproduce an acute-exercise gene signature in muscle. In mice a single injected dose raised exercise-response genes (Ddit4, Pdk4, PGC-1α) in muscle within an hour, a multi-day course increased treadmill endurance, and in the dedicated 2025 study the effect held when the compound was given orally. It also improved outcomes in a mouse heart-failure model alongside 332. Its anti-obesity effect has not been demonstrated for 915 directly; that data belongs to 332.

origin

developed in the Thomas Burris laboratory as part of a new chemical series (the discovery paper, Eur J Med Chem 2023, calls it 'compound 10s'), explicitly to solve SLU-PP-332's lack of oral bioavailability. The dedicated characterization paper is Billon et al., J Pharmacol Exp Ther (2025). Intellectual property is held by Saint Louis University. No registered human trial exists as of 2026.

why researchers are interested

it is the version that could plausibly become a drug. oral activity is the difference between a probe you inject into mice and a molecule you could imagine testing in people, and 915 is the first ERR agonist to clear that bar. the exercise-mimetic story carries over from 332, and the heart-failure model adds a second disease setting. the appeal is real; the human evidence still is not there.

does it work

in mice, yes, for exercise capacity, and the oral-dosing result is the genuinely novel part. but the standalone dataset is thinner than 332's, the metabolic and fat-loss claims attached to it are actually 332's, the exact ERR potencies quoted on vendor pages are paper-attributed rather than cleanly tabulated, and there is no human data of any kind. 915 is at once the more promising molecule to develop and the one riding more on its parent's reputation.

key facts

  • molecular formula: C17H13BFNO3S
  • molecular weight: about 341.2 Da (PubChem CID 142532359)
  • amino acids: not a peptide; a boronic-acid thiophene-2-carboxamide
  • half-life: human half-life not reported; engineered for metabolic stability (microsomal half-life at least about 60 min in mouse and human liver microsomes). oral bioavailability is real but not quantified in the open literature
  • type: small-molecule orally-bioavailable pan-ERR (ERRα/β/γ) agonist; not a peptide despite being sold alongside them
  • CAS: 2285432-92-8 (synonyms DA-57928, HY-150244)
  • 0 registered human clinical trials
  • oral first orally active ERR agonist (vs injected 332)
  • 332 source of the fat-loss data often credited to 915
  • mouse only; no human efficacy or safety data

frequently asked questions

What is SLU-PP-915?

SLU-PP-915 is a small-molecule pan-agonist of the estrogen-related receptors (ERRα/β/γ), 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.

related peptides

  • slu-pp-332 — the parent compound; deeper evidence base, but not orally bioavailable
  • 5-amino-1mq — another metabolic small molecule sold as a 'peptide', mouse data only
  • retatrutide — the metabolic compound with real human trials, for the contrast

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.