GW-0742 (GW610742)

What GW-0742 is

GW-0742 is a small synthetic molecule from the thiazole phenoxyacetic acid group. It was described in the early 2000s in the same paper as GW501516: from a library of lipophilic carboxylic acids, structure-guided optimization produced two highly selective agonists of human PPAR-delta, with an effective concentration of 1.1 nanomoles per litre for the optimized compound and roughly thousand-fold selectivity over the other PPAR forms.

Unlike Cardarine, GW-0742 never became a drug candidate with a clinical program. Its career took place in the laboratory: anyone who wants to look up what happens when PPAR-delta is switched on will find hundreds of papers in which exactly this molecule serves as the tool, from models of heart attack and lung disease through liver and gut to neuroimmunology. In the training scene, on the other hand, it appears as a supposedly stronger version of Cardarine, occasionally under the name Fitorine. That role has little to do with its research history.

How it is supposed to work

PPAR-delta is a sensor in the cell nucleus that switches genes of fatty acid metabolism on and off. When it is activated, muscle burns more fatty acids in animal experiments and spares glucose, and the liver increases the oxidative use of fats. That is exactly what GW610742 showed in rat muscle: after six days of administration the key protein PDK4 had doubled, an enzyme of fatty acid burning was more active and the fuel had shifted from carbohydrate to fat, without the mitochondria working any worse.

That the receptor responds to such signals in humans too has been shown in cell experiments on human material: in primary human T cells, PPAR-delta activation increased the capacity for fatty acid oxidation. A cell experiment is not a human being, however, and between the two lies everything a substance goes through in the body: uptake, distribution, breakdown, and effects over weeks.

One further observation belongs to the mechanism, and it is missing from the marketing. Above about 12 micromoles per litre, GW-0742 no longer behaves as a pure PPAR-delta agonist but inhibits several nuclear receptors in cell experiments, most strongly the vitamin D receptor and the androgen receptor; at the PPAR itself it activates transcription at lower concentrations and inhibits it at higher ones. So the molecule is very selective in the range in which it is meant to serve as a tool, and less selective above it.

What the studies show

Sobolevsky et al. 2012 – the only administration to humans

A Russian doping laboratory investigated how PPAR-delta agonists can be detected in urine. To that end it first reproduced the breakdown in vitro and then ran a controlled excretion study in which volunteers took GW-0742 and, for comparison, GW501516 once each. The result: both substances are best found through their sulfone metabolites, GW501516 for up to 40 days and GW-0742 for up to 20 days after intake. The unchanged substances are measurable only briefly and at low levels, and the amounts in urine were about ten times lower for GW-0742 than for GW501516. This is the complete human literature on this substance, and it says nothing about effect or tolerability, because neither was measured.

Manio et al. 2016 – the endurance experiment, read closely

Mice trained on a treadmill for four weeks and received the AMPK activator AICAR, GW-0742 or both. AICAR alone improved endurance; the combination of AICAR and GW-0742 improved it considerably more: 138 to 179 percent more running time than in trained control animals and 355 percent more than in untrained ones. This went together with a shift towards fat as the energy source shortly before exhaustion, more muscle glycogen and a strong upregulation of PGC-1alpha. For GW-0742 on its own the authors mainly report the increase in PGC-1alpha; in this paper the performance gain belongs to the combination, not to the single substance.

Constantin et al. 2007 – the inconvenient finding

Twenty-four rats received GW610742 at two strengths or a vehicle for six days. Metabolism shifted towards fat as expected, and the mitochondria remained intact. At the same time, at the higher dose the breakdown markers MuRF1 and MAFbx rose both as transcripts and as protein, while Akt1 fell, which is the signature of a muscle atrophy programme. The authors read this as a shared signalling route for fuel selection and muscle breakdown via Akt1 and FOXO. For a substance traded in forums as an agent for shape and performance, this is a finding that does not fit the advertising picture.

Wagner et al. 2009 – the heart reacts quickly

Mice received a single dose of GW-0742 or GW501516. Five hours later new blood vessel formation in the heart was increased, and after 24 hours the heart was larger relative to body weight because the heart muscle cells had grown. The authors found no signs of pathological hypertrophy, that is no cell death, fibrosis or loss of function; the route ran through the enzyme calcineurin. The paper is an example of how quickly and how broadly this receptor acts. What sustained activation would do to the human heart, for better or worse, is open.

Where the data stop

• The human being. There is no study on endurance, fat loss, blood lipids, body composition or tolerability. A query of the ClinicalTrials.gov interface for GW0742, GW-0742 and GW610742 returns no entry on October 14, 2026.
• Long term and cancer. No long-term carcinogenicity study on GW-0742 has been published. For its close relative GW501516, development ended in 2006 according to the manufacturer after cancer findings in long-term animal studies, which can be read on the Cardarine page. For PPAR-delta itself the tumour data are inconsistent: in the colon model GW-0742 was protective, while in other models PPAR-delta ligands accelerated the growth of intestinal adenomas.
• Translating from animals. The amounts used in the animal experiments are, per kilogram, far above anything that would make sense in humans, and some were injected. No human effect can be derived from such experiments.
• The product. Offers are formally addressed to research laboratories. Identity, purity and content are not verified, and confusion with GW501516 is easy because the molecules barely differ. More on this under grey market (German).

Status, approval and legal

GW-0742 is not approved as a medicine in Germany, the EU or the USA, and it is not a food supplement. No clinical development is known, and as of October 14, 2026 there is no entry in ClinicalTrials.gov. The substance is sold as a research chemical.

In sport the situation is clear: the WADA Prohibited List 2026 lists, in section S4.4.1 under metabolic modulators, the class of peroxisome proliferator activated receptor delta agonists and names GW1516 or GW501516 as the example. It is the class that is prohibited, not just the named example, and it is prohibited at all times, in and out of competition; substances in class S4.4 count as non-specified. GW-0742 is a PPAR-delta agonist and is therefore covered.

In Germany this carries over through the Anti-Doping Act. The annex to section 2 (3) lists, among the metabolic modulators, the PPAR-delta agonists with GW501516 as the example and states expressly at the end that salts, esters, ethers, isomers, complexes and derivatives are included. Acquiring, possessing and importing more than a small quantity for doping purposes in sport is therefore prohibited, as is trading in it, supplying it or prescribing it for that purpose. We do not give dosages.

Safety

There are no safety data in humans. Nobody has systematically recorded blood values, liver, heart, blood counts or side effects under GW-0742, and there is no drug safety monitoring because the substance is not a medicine. What exists are signals from animal and cell experiments, and they point in both directions: protective effects in models of colon cancer, heart attack and inflammation, alongside a muscle atrophy programme in rat muscle, rapid heart growth after a single dose in mice, and a shift of the immune system towards regulatory T cells, which can dampen an immune response. The authors of the immune paper consider adverse effects possible that would barely show up in blood samples.

On top of this comes the open cancer question of the substance class: for GW-0742 the long-term study is missing, and for its close relative GW501516 that was precisely the reason development was stopped. For people with cancer or an increased cancer risk, in pregnancy and breastfeeding, and in heart or liver disease the substance is therefore unsuitable, and combinations with other substances have not been studied. Anyone competing in organized sport additionally risks a ban, because detection through the sulfone metabolites works reliably and reaches back weeks.

Sources

• Sznaidman et al., Bioorganic & Medicinal Chemistry Letters 2003 – first description of the series with GW501516 and GW0742
• Sobolevsky et al., Drug Testing and Analysis 2012 – controlled excretion study in humans, metabolites and detection windows
• Constantin et al., Journal of Physiology 2007 – GW610742 in rat muscle, fuel metabolism and atrophy programme
• Manio et al., Physiological Reports 2016 – AICAR plus GW0742 and training in mice
• Wagner et al., Cardiovascular Research 2009 – angiogenesis and heart growth in mice
• Marin et al., Cancer Research 2006 – GW0742 reduces chemically induced colon cancer in mice
• Nandhikonda et al., Biochemistry 2013 – GW0742 inhibits several nuclear receptors at higher concentrations
• Sibille et al., International Journal of Molecular Sciences 2021 – PPAR-beta/delta agonists in sport, fatty acid oxidation and T cells
• WADA Prohibited List 2026, informational German translation by NADA – S4.4.1 PPARδ agonists
• Annex to section 2 (3) of the German Anti-Doping Act – metabolic modulators including derivatives