Small molecule / ERR signaling
SLU-PP-915 is an experimental small molecule that activates all three estrogen-related receptor subtypes. It is chemically distinct from SLU-PP-332, despite their shared target family. Researchers have studied its chemical design, gene-expression effects, cellular recycling pathways, and mouse exercise capacity. A later mouse study demonstrated oral activity under its experimental conditions. None of these findings establishes efficacy or safety in people.
Preclinical researchA focused reference from the Disguised Alpha research network.
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Open the exact product listing for its format and documentation. Published studies do not validate a supplier’s finished product.
01 / The science
A clear starting point for the mechanisms, experimental models and questions behind the compound.
The discovery program developed a thiophene-based series and identified SLU-PP-915 as a boronic-acid-containing pan-ERR agonist. Binding and cell assays supported activity at the receptor family. Chemical changes can affect exposure and metabolism, so similar target activity does not make two compounds interchangeable.
Read the primary source ↗Mouse experiments measured running capacity alongside expression of Ddit4 and mitochondrial genes. A 2026 report explored oral administration and interaction with exercise training. These linked measurements help researchers examine a biological hypothesis, while remaining distinct from clinical evidence of improved fitness or disease treatment.
Read the primary source ↗Cell experiments examined TFEB, a regulator of the autophagy-lysosome pathway. ERR activation increased TFEB expression and related gene programs in cardiac and muscle-cell preparations. This identifies a pathway for further study; increased expression in cells is not proof of enhanced longevity or whole-body cellular repair.
Read the primary source ↗02 / Read with context
The selected evidence comes from laboratory and animal studies. It does not establish human efficacy, an appropriate human-use protocol, or the safety and performance of a commercial formulation. SLU-PP-332 and SLU-PP-915 are distinct molecules and should not be treated as interchangeable.
03 / Selected publications
Original records, study models and the limits that matter when interpreting a result.
The study identified SLU-PP-915 and connected its receptor activity to changes in ERR target-gene expression. It also examined metabolic stability during chemical optimization.
Reading limit: This is early pharmacology and compound development. It does not establish clinical effectiveness, a human exposure target, or long-term safety.
Investigators reported increased treadmill performance with oral SLU-PP-915 and compared responses with SLU-PP-332 after accounting for systemic exposure. They also examined gene-expression changes alongside exercise training.
Reading limit: Oral activity in mice is not a demonstration of human oral effectiveness or equivalence with a particular capsule product.
The researchers identified TFEB as a direct ERR-regulated gene and found increased TFEB-related expression after ERR activation. SLU-PP-915 was used to investigate this connection in cell preparations.
Reading limit: Cellular pathway measurements do not establish clinical rejuvenation, disease prevention, or a lifespan effect.
A focused selection, not a systematic review. Studies concern the tested material and do not validate a supplier’s finished product.
Explore research & source notes →04 / Common questions
Quick answers for reading the science behind SLU-PP-915.
No. They share ERR activity but have different structures. Their experimental exposure profiles also differ. A result for one compound should be attributed to that compound and its tested conditions.
Yes, in mice in the cited 2026 study. Oral activity describes an experimental finding; it does not establish a human regimen or certify that a commercial preparation matches the research material.
No. TFEB expression and related cellular measurements are mechanistic endpoints. They should not be converted into claims about longevity, rejuvenation, or protection from disease without appropriate outcome studies.
A separate mouse pressure-overload study examined ERR agonists, including SLU-PP-915, in cardiac dysfunction. Such work broadens the experimental questions but remains animal-model evidence, not a demonstrated treatment for human heart failure.
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