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MetabolicNo human studies cited

GW0742

GW0742, selective PPAR-beta/delta agonist

Written by Reviewed Sep 2026

Also known as: GW-0742, GW610742

The sibling of GW501516, sold on the same endurance story with none of the same evidence. No human study of GW0742 of any design has ever been published, and the endurance result is mice on a treadmill.

Overview

GW0742 is a selective agonist at PPAR-beta/delta, the same nuclear receptor GW501516 targets, from the same GlaxoSmithKline chemistry. It is sold in the research chemical market as the newer, cleaner cardarine.

The evidence does not support that framing in either direction. On benefit, the difference between the two compounds is stark: GW501516 has three published human trials, all of them measuring lipids over two to twelve weeks, while GW0742 has none at all. The endurance claim for GW0742 comes from a 2016 study in Balb/c mice treadmill-trained for four weeks, in which AICAR alone potentiated endurance and the combination of AICAR and GW0742 increased running time further, by 138 to 179 percent against exercised controls and 355 percent against non-exercised controls. Those are mouse running times, in a combination, not a GW0742 monotherapy result in a person.

On harm, the honest position is that the class-level cancer concern is real but unresolved, and part of the published record actually points the other way. GW501516 development stopped over rodent carcinogenicity findings that were never published as a primary paper. Meanwhile a Pennsylvania State group reported that both GW0742 and GW501516 failed to increase growth, Akt phosphorylation, VEGF or COX2 in five human cancer cell lines with or without serum, and that GW0742 attenuated rather than promoted chemically induced colon carcinogenesis in mice. So the literature contains a suppressed industrial safety finding on one side and published academic work finding no tumour promotion on the other.

Mechanism of action

Selective agonism at PPAR-beta/delta, a nuclear receptor that upregulates fatty acid oxidation and mitochondrial genes in skeletal muscle. In the mouse combination study, GW0742-treated groups tended to higher PGC-1alpha protein, and at exhaustion Pgc1a, Pdk4, Cd36 and Lpl were upregulated in muscle, with a measurable shift from carbohydrate to fat as the fuel and glycogen sparing that delayed hypoglycaemia. Whether any of this happens at a tolerable dose in a human has never been tested.

Reading the research record

No human has been given GW0742 in a published study of any design, so there is no human evidence section on this page. That absence is the most important fact about it, because it is sold next to GW501516 as though the two shared a record.

They do not. GW501516 was taken into people three times by its manufacturer, most substantially in a 268-person twelve-week lipid trial, and then abandoned when two-year rodent studies reportedly produced tumours in multiple organs. Those carcinogenicity studies were never published, which is why the site's cardarine page reports the anti-doping attestation rather than a citation. GW0742 inherited the class suspicion without inheriting any of the human safety experience, which is the worst of both positions.

The carcinogenicity question is genuinely contested in the published literature rather than settled. The Peters laboratory at Penn State published a series of studies finding no tumour promotion by either ligand in human cancer cell lines and an attenuation of chemically induced colon cancer in mice. That work is real and should be reported. It does not override an unpublished industrial two-year bioassay, and an unpublished bioassay does not override it either. Nobody can resolve this from the outside, which is itself a reason not to take the compound.

The evidence, charted

Fig. 1 · evidence composition

0of 4 citations (0%) are in people

Counted from the citation list on this page. The Human count is the same number shown in the badge at the top. Both understate any literature larger than the sources we cite.

Fig. 2 · evidence over time

Evidence spans 4 distinct years, 2007 to 2019, counted from the citation list on this page. The newest citation on file is from 2019, more than five years ago; the published record may have gone quiet.

Fig. 3 · legal status at a glance

Not approved in any of the four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.

Key studies & citations

  • Animal2016

    Combined pharmacological activation of AMPK and PPARδ potentiates the effects of exercise in trained mice

    Balb/c mice, treadmill trained for 4 weeks with AICAR and GW0742. AICAR alone potentiated endurance; the combination increased running time by 138 to 179 percent relative to exercised groups and 355 percent relative to non-exercised groups, with a fuel shift toward fat, glycogen sparing and upregulation of Pgc1a, Pdk4, Cd36 and Lpl in muscle. Mice, in combination with AICAR, not GW0742 alone in a human.

    Physiological Reports
  • Animal2019

    Complementary Immunometabolic Effects of Exercise and PPARβ/δ Agonist in the Context of Diet-Induced Weight Loss in Obese Female Mice

    Diet-induced obese female mice. Exercise and the PPAR-beta/delta agonist had complementary immunometabolic effects during weight loss. Animal work only.

    International Journal of Molecular Sciences
  • In vitro2007

    Peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta) ligands do not potentiate growth of human cancer cell lines

    GW0742 and GW501516 tested in five human cancer cell lines with and without serum. Neither increased cell growth, Akt phosphorylation, VEGF or COX2, and liver, colon and colon polyps from treated mice showed no change in these markers either. A published argument against the tumour-promotion hypothesis for this class.

    Carcinogenesis
  • Animal2008

    Ligand activation of peroxisome proliferator-activated receptor-beta/delta (PPARbeta/delta) and inhibition of cyclooxygenase 2 (COX2) attenuate colon carcinogenesis through independent signaling mechanisms

    Azoxymethane-induced colon cancer in wild-type and PPAR-beta/delta-null mice. GW0742 had inhibitory effects on colon carcinogenesis, acting through mechanisms independent of COX2 inhibition. Mouse work, and it points opposite to the class cancer fear.

    Carcinogenesis

Frequently asked questions

Is GW0742 safer than cardarine?

There is no evidence for that claim in either direction. GW501516 has published human trials and an unpublished rodent carcinogenicity finding that ended its development. GW0742 has neither: no human study at all, and no published two-year bioassay. Less data is not the same as a better safety record.

Does GW0742 improve endurance?

In mice, in combination with AICAR, running time increased substantially. There is no human endurance study of GW0742, alone or in combination, and no human has taken it in a published trial.

Does GW0742 cause cancer?

Unresolved. The class carries a carcinogenicity concern from unpublished GW501516 rodent studies. Published academic work found that GW0742 did not promote growth in human cancer cell lines and actually reduced chemically induced colon tumours in mice. Both of those statements are true at once, and neither is a human safety dataset.

Is it banned in sport?

Yes. PPAR-delta agonists are prohibited by WADA as metabolic modulators, and GW0742 is covered by that class listing.

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