GW0742 (also coded GW610742 and GW0742X) is an experimental compound that activates PPARδ (peroxisome proliferator-activated receptor delta), a nuclear receptor that switches on genes for burning fat. GlaxoSmithKline (GSK) chemists reported it in 2003 in the same paper as its better-known sibling, GW501516 (cardarine) (Sznaidman et al., Bioorg Med Chem Lett 2003).

GW0742 is sold online alongside SARMs, but it does not act on the androgen receptor and is not a hormone. The most important fact about it: no controlled human trial of GW0742 has been published, and none is registered on ClinicalTrials.gov (ClinicalTrials.gov search). Everything known about its effects comes from cell and animal studies, plus one anti-doping excretion study in which people took a single dose.

This page summarizes what the published laboratory research and anti-doping authorities report. It is for education only and is not medical advice.

Property	Detail
Drug class	Selective PPARδ agonist (not a SARM, not a steroid)
Other names	GW610742, GW0742X; CAS 317318-84-6
Developer	GlaxoSmithKline; used as a research tool, never developed into a medicine
Potency (cell assay)	EC50 1.1 nM at human PPARδ, about 1000-fold selective over the other PPAR subtypes
Human dosing data	One excretion study: a single 15 mg oral dose
Half-life	No published human value
Detection in urine	Sulfone metabolite detectable up to 20 days after a single 15 mg dose
US status	Never approved by FDA; not named in the DEA anabolic steroid schedule
WADA status	Prohibited at all times as a PPARδ agonist (class S4.4.1, metabolic modulators)

What it is

GW0742’s chemical name is 2-[4-[[2-[3-fluoro-4-(trifluoromethyl)phenyl]-4-methyl-1,3-thiazol-5-yl]methylsulfanyl]-2-methylphenoxy]acetic acid: formula C₂₁H₁₇F₄NO₃S₂, molecular weight 471.5 g/mol (PubChem). It has no steroid structure. PubChem lists GW610742 and GW0742X as synonyms, which matters because several animal studies use those codes.

GSK built a library of fat-like carboxylic acids and optimized the best hits by structure-guided design. That work produced two lead compounds, GW501516 and GW0742, and the paper reported an EC50 (the concentration giving half the maximal effect) of 1.1 nM at human PPARδ, with about 1000-fold selectivity over PPARα and PPARγ (Sznaidman et al., 2003).

The two GSK compounds are close chemical relatives:

Feature	GW0742	GW501516 (cardarine)
Formula	C₂₁H₁₇F₄NO₃S₂	C₂₁H₁₈F₃NO₃S₂
Molecular weight	471.5 g/mol	453.5 g/mol
Structural difference	Extra fluorine on the phenyl ring	No extra fluorine
Controlled human trials	None published	Four small lipid trials, 2–12 weeks
Urine detection window (single 15 mg dose)	Up to 20 days	Up to 40 days

Sources: PubChem GW0742; PubChem GW501516; Sobolevsky et al., 2012. The human trials of GW501516 are covered on the cardarine page and should not be assumed to apply to GW0742.

Not as selective as “selective” suggests

Two lines of research show that GW0742 hits more than PPARδ:

PPARα. A GSK safety study describes GW0742 as having weak PPARα agonist activity. At high doses in mice, that PPARα activity drove most of its liver and muscle toxicity (see below) (Faiola et al., Toxicol Sci 2008).
Other nuclear receptors. In cell-based screening, GW0742 acted as a broad nuclear receptor antagonist at concentrations above 12.1 μM. Its strongest blocking activity was at the vitamin D receptor and the androgen receptor (Nandhikonda et al., Biochemistry 2013). This is an in-vitro finding at concentrations far above its PPARδ potency, and its relevance to people is unknown. It does mean the compound is the opposite of a SARM at the androgen receptor, if it acts there at all.

How it works in the body

No study has reported GW0742’s absorption, peak levels or half-life in humans, so we do not give a half-life.

The only published human dosing is an anti-doping study from the Moscow anti-doping laboratory (Sobolevsky et al., Drug Test Anal 2012):

Finding	Detail
Main metabolic route	Oxidation of the sulfur atom to a sulfoxide and then a sulfone (shown in vitro)
Unchanged drug in urine	Measurable only for a short time and at low ng/mL levels
Best urine marker	Sulfone metabolite, detectable up to 20 days after a single 15 mg oral dose
Amount in urine vs GW501516	About ten times lower for GW0742 and its metabolites

Regulatory status

Never approved. GW0742 has no FDA or other regulatory approval, and ClinicalTrials.gov lists no studies under GW0742 or GW610742 (ClinicalTrials.gov search).
Not a scheduled steroid. GW0742 is not named in the US Schedule III list of anabolic steroids (21 CFR 1308.13).
Banned in sport. The 2026 WADA Prohibited List bans “peroxisome proliferator-activated receptor delta (PPARδ) agonists” under S4.4.1, metabolic modulators. It names GW1516 as an example, and the class wording covers other PPARδ agonists such as GW0742. Class S4 is prohibited in and out of competition, and S4.4 substances are non-specified (WADA 2026 Prohibited List). Anti-doping researchers have flagged GW0742 by name as a PPARδ agonist relevant to sports drug testing (Thevis and Schänzer, Rapid Commun Mass Spectrom 2016).

What the research shows

All efficacy data below come from mice or rats. None of it has been tested in people, and doses in mg/kg in rodents do not translate directly to human doses.

Muscle fiber type and endurance (animal studies)

Fast muscle remodeling in mice. GW0742 at 1 mg/kg/day by injection increased the number of oxidative (fatigue-resistant) fibers 1.63-fold and capillaries 1.55-fold in a mouse leg muscle, with the change completed within 2 days (Gaudel et al., Am J Physiol Endocrinol Metab 2008). Running performance was not measured.
No endurance gain on its own in trained mice. In treadmill-trained mice given GW0742 (5 mg/kg by injection), AICAR, both, or vehicle for 4 weeks, only the AICAR plus GW0742 group ran significantly longer than trained mice on vehicle. GW0742 alone did not. Liver weight was higher in the GW0742 group than in sedentary controls (Manio et al., Physiol Rep 2016).
Worse muscle performance at high doses in rats. GW610742 at 100 mg/kg/day for 6 days raised markers of a muscle-breakdown (atrophy) program, MuRF1 and MAFbx, in rat muscle (Constantin et al., J Physiol 2007). In a follow-up, the same dose cut muscle carbohydrate burning during prolonged contraction and lowered muscle tension by 25% compared with control (Constantin-Teodosiu et al., J Physiol 2009). Both findings were at the 100 mg/kg dose.

About “endurance in a pill.” GW0742 is often sold as a stronger or “safer” cardarine. No study has tested either claim in people. In the one trained-mouse endurance study we found, GW0742 alone did not improve running time, and at high doses in rats it reduced muscle force during sustained work.

Body fat and metabolism (animal studies)

Study	Animals and dose	Main finding
Harrington et al., PPAR Res 2007	Diet-induced obese mice	Only a slight decrease in fat mass with GW0742 alone
Toral et al., J Hypertens 2015	Mice on a high-fat diet; 3 mg/kg/day by mouth for 11–13 weeks	Prevented weight gain and fat accumulation, high blood pressure, raised fasting glucose and insulin resistance; HDL rose
Le Garf et al., Int J Mol Sci 2019	Obese female mice switched to a normal diet; 3 mg/kg/day for 8 weeks, with or without exercise	Lower visceral fat, less muscle inflammation and better insulin sensitivity with the agonist and/or training

Blood vessels and atherosclerosis (animal studies)

In LDL-receptor-deficient mice, a standard model of atherosclerosis, GW0742X reduced plaque area by up to 50%. It did not change total, HDL or LDL cholesterol; the effect was linked to lower inflammatory signals in the artery wall (Graham et al., Atherosclerosis 2005).

Side effects and risks

No human safety data

Apart from a single 15 mg dose given for drug-testing research, GW0742 has no published human exposure. There are no data on side effects, safe doses, drug interactions or long-term use in people.

Liver and muscle toxicity in mice

GSK’s own safety scientists gave mice toxicological doses of GW0742 for 10 days (Faiola et al., 2008). They found:

enlarged livers and blood markers of liver injury;
peroxisome proliferation (a growth of fat-burning cell compartments) in liver and muscle;
skeletal myopathy (muscle damage), seen on both blood tests and tissue examination.

These effects were weaker in mice lacking PPARα, showing that GW0742’s side activity at PPARα caused most of them.

Heart growth in mice

Within 24 hours of an injection of GW0742 or GW501516, mice had a higher heart-to-body-weight ratio because their heart muscle cells had enlarged. The authors saw no signs of harmful hypertrophy such as fibrosis or worse heart function (Wagner et al., Cardiovasc Res 2009). What this rapid heart growth would mean with repeated use in people is unknown.

Cancer: an unresolved question

The role of PPARδ activation in cancer is disputed, and the animal evidence points in both directions:

Against a risk (GW0742, mice). In a chemically induced colon cancer model, GW0742 reduced colon polyp numbers, and this depended on PPARδ (Marin et al., Cancer Res 2006).
For a risk (same receptor class, mice). GW501516 increased the number and size of intestinal polyps in mice prone to them (Gupta et al., Nat Med 2004). Mice engineered to overexpress PPARδ in blood vessels had faster tumor growth, more tumor blood vessels and more metastases (Wagner et al., Cells 2019).

We found no published long-term carcinogenicity study of GW0742. Development of GW501516 was abandoned after carcinogenic findings in animals (see the cardarine page), and no data show that GW0742 avoids that problem.

Athletes

GW0742 falls under WADA’s prohibited PPARδ agonist class at all times (WADA 2026 Prohibited List). Its sulfone metabolite remained detectable in urine for up to 20 days after one 15 mg dose (Sobolevsky et al., 2012).

Key takeaways

A PPARδ agonist, not a SARM. GW0742 is a GSK research compound that switches on fat-burning genes; it has no androgen activity and in cell assays even blocked the androgen receptor at high concentrations.
No human trials. The only published human dosing is a single 15 mg dose in an anti-doping excretion study, and no trials are registered.
Animal effects are mixed. It shifted mouse muscle toward oxidative fibers and limited diet-induced weight gain, but did not improve running on its own in trained mice and lowered muscle force at high doses in rats.
Toxicity signals in rodents. High doses enlarged the liver and damaged skeletal muscle in mice, largely through its side activity at PPARα.
Cancer risk is unresolved. Its sibling GW501516 was abandoned after carcinogenic findings in animals, and no long-term carcinogenicity data exist for GW0742.
Banned in sport. WADA prohibits PPARδ agonists at all times, and a GW0742 metabolite can be detected for up to 20 days after one dose.

Sources

Sznaidman ML, Haffner CD, Maloney PR, et al. Novel selective small molecule agonists for peroxisome proliferator-activated receptor delta (PPARdelta)–synthesis and biological activity. Bioorg Med Chem Lett. 2003;13(9):1517–1521. PubMed.
National Center for Biotechnology Information. PubChem Compound Summary for CID 9934458, GW0742. PubChem.
National Center for Biotechnology Information. PubChem Compound Summary for CID 9803963, GW501516. PubChem.
Sobolevsky T, Dikunets M, Sukhanova I, et al. Detection of PPARδ agonists GW1516 and GW0742 and their metabolites in human urine. Drug Test Anal. 2012;4(10):754–760. PubMed.
Faiola B, Falls JG, Peterson RA, et al. PPAR alpha, more than PPAR delta, mediates the hepatic and skeletal muscle alterations induced by the PPAR agonist GW0742. Toxicol Sci. 2008;105(2):384–394. PubMed.
Nandhikonda P, Yasgar A, Baranowski AM, et al. Peroxisome proliferation-activated receptor δ agonist GW0742 interacts weakly with multiple nuclear receptors, including the vitamin D receptor. Biochemistry. 2013;52(24):4193–4203. PubMed.
Gaudel C, Schwartz C, Giordano C, et al. Pharmacological activation of PPARbeta promotes rapid and calcineurin-dependent fiber remodeling and angiogenesis in mouse skeletal muscle. Am J Physiol Endocrinol Metab. 2008;295(2):E297–E304. PubMed.
Manio MC, Inoue K, Fujitani M, et al. Combined pharmacological activation of AMPK and PPARδ potentiates the effects of exercise in trained mice. Physiol Rep. 2016;4(5):e12625. PubMed; PMC.
Constantin D, Constantin-Teodosiu D, Layfield R, et al. PPARdelta agonism induces a change in fuel metabolism and activation of an atrophy programme, but does not impair mitochondrial function in rat skeletal muscle. J Physiol. 2007;583(Pt 1):381–390. PubMed.
Constantin-Teodosiu D, Baker DJ, Constantin D, et al. PPARdelta agonism inhibits skeletal muscle PDC activity, mitochondrial ATP production and force generation during prolonged contraction. J Physiol. 2009;587(1):231–239. PubMed.
Harrington WW, Britt CS, Wilson JG, et al. The effect of PPARalpha, PPARdelta, PPARgamma, and PPARpan agonists on body weight, body mass, and serum lipid profiles in diet-induced obese AKR/J mice. PPAR Res. 2007;2007:97125. PubMed.
Toral M, Gómez-Guzmán M, Jiménez R, et al. Chronic peroxisome proliferator-activated receptorβ/δ agonist GW0742 prevents hypertension, vascular inflammatory and oxidative status, and endothelial dysfunction in diet-induced obesity. J Hypertens. 2015;33(9):1831–1844. PubMed.
Le Garf S, Murdaca J, Mothe-Satney I, et al. Complementary immunometabolic effects of exercise and PPARβ/δ agonist in the context of diet-induced weight loss in obese female mice. Int J Mol Sci. 2019;20(20):5182. PubMed.
Graham TL, Mookherjee C, Suckling KE, et al. The PPARdelta agonist GW0742X reduces atherosclerosis in LDLR(-/-) mice. Atherosclerosis. 2005;181(1):29–37. PubMed.
Wagner N, Jehl-Piétri C, Lopez P, et al. Peroxisome proliferator-activated receptor beta stimulation induces rapid cardiac growth and angiogenesis via direct activation of calcineurin. Cardiovasc Res. 2009;83(1):61–71. PubMed.
Marin HE, Peraza MA, Billin AN, et al. Ligand activation of peroxisome proliferator-activated receptor beta inhibits colon carcinogenesis. Cancer Res. 2006;66(8):4394–4401. PubMed.
Gupta RA, Wang D, Katkuri S, et al. Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth. Nat Med. 2004;10(3):245–247. PubMed.
Wagner KD, Du S, Martin L, et al. Vascular PPARβ/δ promotes tumor angiogenesis and progression. Cells. 2019;8(12):1623. PubMed.
Thevis M, Schänzer W. Emerging drugs affecting skeletal muscle function and mitochondrial biogenesis - potential implications for sports drug testing programs. Rapid Commun Mass Spectrom. 2016;30(5):635–651. PubMed.
World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA 2026 Prohibited List.
US Code of Federal Regulations. 21 CFR 1308.13, Schedule III. 21 CFR 1308.13.
ClinicalTrials.gov. Search results for GW0742. ClinicalTrials.gov.

GW0742