SLU-PP-332 vs Cardarine
Research Comparison

Research Overview

SLU-PP-332 vs Cardarine compares two receptor families, not two versions of one compound. SLU-PP-332 activates all three estrogen-related receptors (ERRs) and is most potent at ERR alpha (Billon et al., 2023). Cardarine is the common name for GW501516, a selective agonist of peroxisome proliferator-activated receptor delta (PPARδ) first reported by GlaxoSmithKline scientists (Oliver et al., 2001), so SLU PP 332 vs GW501516 is the same comparison under another name. Neither compound is a peptide.

The two meet in skeletal muscle: in mouse and muscle cell studies, each raised oxidative metabolism genes and mitochondrial markers, through a different receptor and with a different fiber-type outcome. No human trial of SLU-PP-332 is indexed in PubMed, while GW501516 reached short human studies before rodent tumor findings ended its development.

Structure and Class

Both are synthetic small molecules. SLU-PP-332 is an acylhydrazone built from 4-hydroxybenzohydrazide and naphthalene-2-carbaldehyde: C₁₈H₁₄N₂O₂, 290.3 g/mol. GW501516 is a phenoxyacetic acid joined through a thioether to a trifluoromethylphenyl thiazole: C₂₁H₁₈F₃NO₃S₂, 453.5 g/mol. The figures are from the SLU-PP-332 capsules page and the Cardarine product page; PubChem CID 5338394 and CID 9803963 agree.

The ERRs are orphan nuclear receptors related to the estrogen receptors, but they do not bind estrogen-receptor ligands and are active without one. In reporter assays SLU-PP-332 reached half maximal activity at 98 nM for ERR alpha, 230 nM for ERR beta and 430 nM for ERR gamma (Billon et al., 2023). PPARδ, also written PPARβ/δ, is one of three PPAR subtypes, dietary lipid sensors that regulate fatty acid and carbohydrate metabolism; GW501516 was designed to be potent and selective for it (Oliver et al., 2001).

Genetic work links the families in muscle. Mice expressing an activated PPARδ in skeletal muscle formed more type I fibers, and wild-type mice given GW501516 for 10 days raised genes for slow fiber proteins, mitochondrial biogenesis and beta-oxidation (Wang et al., 2004). Mouse gain- and loss-of-function work found that PPARβ/δ acts on the type I fiber program through a muscle microRNA network that depends on ERR gamma, which raised miR-499 and miR-208b (Gan et al., 2013).

Side by Side

Research Context: SLU-PP-332

In the founding paper, 24 hours of exposure raised the ERR target gene Pdk4 and maximal mitochondrial respiration in C2C12 mouse myoblasts (Billon et al., 2023). Mice that received 50 mg/kg twice daily for 15 days had more oxidative type IIa fibers in the quadriceps, more mitochondria and more mitochondrial DNA. One 50 mg/kg amount raised Ddit4, a gene of the acute aerobic exercise program, about threefold, against about sixfold after a 40 minute treadmill run. The Ddit4 response was lost in myocytes and mice lacking ERR alpha.

The SLU-PP-332 research guide covers later heart, kidney and metabolic mouse work. PubMed lists 10 records naming SLU-PP-332 as of 9 October 2026, none a trial in people, and a 2026 systematic review of animal and cell studies concludes that clinical trials are still needed (de Souza-Lima et al., 2026).

Research Context: Cardarine (GW501516)

The first report measured cholesterol efflux in cultured cells and blood lipids in obese, insulin-resistant rhesus monkeys: HDL cholesterol rose, while small dense LDL, fasting triglycerides and fasting insulin fell (Oliver et al., 2001). In rat L6 myotubes and mouse skeletal muscle, GW501516 switched on genes for fatty acid transport, beta-oxidation and mitochondrial respiration (Tanaka et al., 2003).

A 2008 Salk Institute study tested the compound with and without training. In sedentary mice, four weeks of GW501516 (GW1516 in the paper) raised Ucp3, Cpt1b and Pdk4 in muscle without changing the proportion of type I fibers; trained mice given the agonist had about 38 percent more type I fibers than sedentary mice given vehicle (Narkar et al., 2008).

In Apc(min) mice, which are prone to intestinal polyps, GW501516 increased the number and size of polyps, with a fivefold increase in polyps larger than 2 mm (Gupta et al., 2004).

Other work disagreed: in five human cancer cell lines, GW501516 and a second PPARδ agonist did not increase growth, Akt phosphorylation, VEGF or COX2 expression, and liver, colon and polyp tissue from mice given the agonists showed no change in those markers (Hollingshead et al., 2007). GlaxoSmithKline discontinued further research after preclinical studies in rodents linked the compound to widespread tumor development (Mackenzie and Lione, 2013).

In the development program, healthy volunteers received placebo or one of two daily amounts for 2 weeks while hospitalized; HDL cholesterol rose against placebo and triglyceride clearance after a fat meal increased (Sprecher et al., 2007). The World Anti-Doping Agency has prohibited GW501516 since January 2009 (Thevis et al., 2010), and the current WADA Prohibited List names it in class S4.4.1, metabolic modulators, prohibited at all times.

Choosing Between Them for a Research Question

For Cardarine vs SLU-PP-332, the receptor question comes first. ERR signaling, ERR alpha dependence and the acute exercise gene program (Ddit4, Slc25a25) point to SLU-PP-332, with ERR alpha knockout controls as in the founding paper. PPARδ signaling, lipid handling and cholesterol efflux, or a ligand studied since 2001, point to GW501516.

Used together, the pair can separate two branches of one program. Both raised Pdk4, SLU-PP-332 in C2C12 myoblasts (Billon et al., 2023) and GW501516 in mouse muscle (Narkar et al., 2008), a shared readout, while fiber outcomes differ: type IIa with SLU-PP-332 alone, type I with GW501516 only alongside training. Since PPARβ/δ acts on fiber type through ERR gamma (Gan et al., 2013), record ERR gamma status when using both.

Exposure differs too: mouse studies gave SLU-PP-332 intraperitoneally (Billon et al., 2023) and GW501516 by oral gavage (Wang et al., 2004). The SLU-PP-915 research guide covers a later ERR agonist built for oral activity.

Handling and Storage

Amino SLU-PP-332 (Non DMSO Formulation 7.5MG/ML) is a liquid: 7.5MG/ML in a 20ML glass bottle, 150MG total, in a non-DMSO Miglyol 842 carrier. Its product page lists 15 to 25°C unopened, then 2 to 8°C once the seal is broken, kept closed, out of light and never frozen. Crystals can form in the carrier; the page states that gentle warming can return a uniform appearance, so confirm a consistent solution before any workflow. SLU-PP-332 is also listed as 100MG capsules.

Cardarine (GW-501516) comes as capsules labeled 10MG each, in a sealed bottle or resealable pouch depending on the batch, stored sealed at 15 to 25°C away from moisture and direct light.

Record the lot number and keep its certificate from the COA portal; the latest certificate for each reports measured content that differs from the label, so use the measured value. GW501516 forms a sulfoxide and a sulfone in human liver microsome assays (Thevis et al., 2010), so peaks 16 or 32 mass units above its 453.5 g/mol parent point to oxidation.

Questions Researchers Ask

SLU-PP-332 vs Cardarine: what is the main difference?

The receptor: the estrogen-related receptors for SLU-PP-332, most potently ERR alpha (Billon et al., 2023), and PPARδ for Cardarine, GW501516 (Oliver et al., 2001). Both reach oxidative gene programs in mouse muscle, with different fiber-type outcomes.

ERR agonist vs PPAR delta agonist: how do they differ?

ERRs are active without a ligand, so an ERR agonist enhances activity already present (Billon et al., 2023). PPARδ is a dietary lipid sensor, with GW501516 as a selective synthetic ligand (Oliver et al., 2001). In mouse muscle, PPARβ/δ acts on type I fibers through an ERR gamma-dependent network (Gan et al., 2013).

Has either compound been studied in people?

SLU-PP-332 has not: PubMed indexes no human trial, and a 2026 systematic review says clinical trials are still needed (de Souza-Lima et al., 2026). GW501516 reached trials of up to 12 weeks, among them a phase 2 trial in 268 people with low HDL cholesterol (Olson et al., 2012), and 2-week studies in healthy volunteers (Sprecher et al., 2007) before GlaxoSmithKline discontinued further research after preclinical studies in rodents linked the compound to widespread tumor development (Mackenzie and Lione, 2013).

Are SLU-PP-332 and Cardarine on the WADA Prohibited List?

Cardarine is. The current WADA Prohibited List names GW501516 among PPARδ agonists in class S4.4.1, metabolic modulators, prohibited at all times. SLU-PP-332 is not named on the 2026 list, whose S0 class covers substances without regulatory approval.