DOSEGUY

GW-0742

guinea pig

Also seen as: GW0742, GW 0742, GW610742, GW

The Dose Guy’s verdict
Sep 1, 2026
4 sources

Skip it unless you already understand what you’re signing up for. GW-0742 is cardarine’s lesser-known sibling, the same PPAR-delta mechanism, the same fat-oxidation and endurance story, and a fraction of the already-thin evidence. The community that runs it is betting the different structure dodges the cancer signal that killed cardarine’s development, but that’s a hope, not a finding. If you want fat loss with actual human outcomes, tirzepatide and retatrutide are where the data is.

Would I take it?No, even less data than cardarine.

What it is

A synthetic agonist of PPAR-delta, the nuclear receptor that regulates fatty-acid oxidation and energy expenditure. GW-0742 binds it about as potently as cardarine does, with high selectivity over the other PPAR subtypes. The intended effect is the same: push the body to burn more fat for fuel, improve endurance, and shift the metabolic profile toward oxidation. Both compounds came out of the same GlaxoSmithKline research program in the early 2000s, and both were abandoned after long-term rodent studies on cardarine grew tumors across multiple organ systems. GW-0742 was never taken through that same long carcinogenicity screen, which is simultaneously the reason some people prefer it and the reason you shouldn’t be comforted by the absence of bad news.

What the research shows

No human trials. Zero. Everything below is animal or in-vitro work. Read it as “interesting,” not “evidence it works in you.”

No human efficacy or safety trial exists. The published work is cells, mice, rats, and one human excretion study run for anti-doping detection:

GW-0742 activated human PPAR-delta with an EC50 of 1.1 nM and showed 1000-fold selectivity over the other human PPAR subtypes.Bioorg Med Chem Lett 2003 · in vitro
In diet-induced obese mice, GW-0742 produced a slight decrease in fat mass.PPAR Res 2007 · mouse
Toxicological GW-0742 dosing for 10 days caused skeletal myopathy in wild-type mice, predominantly mediated by cross-activation of PPAR-alpha.Tox Sci 2008 · mouse · 10-day
GW-0742 acted as a pan-nuclear-receptor antagonist above 12.1 micromolar, with its highest antagonist activity at the vitamin D receptor and the androgen receptor.Biochemistry 2013 · in vitro
No randomized human efficacy trial or human safety study of GW-0742 has been published.as of Aug 2026

Realistic protocols

I’m not writing a protocol around an untested analog of a compound shelved for growing tumors. For the record, forum lore runs 10 to 20 mg per day orally, sometimes cycled 8 weeks on and 4 off, mirroring old cardarine protocols. That’s lore, not evidence. The one published human data point is an anti-doping excretion study that gave a single 15 mg oral dose and tracked metabolites in urine for 20 days, which tells you detection windows, not what GW-0742 does to your body. If you run it anyway, keep the dose low, keep the cycle short, log any unusual muscle soreness, and get creatine kinase checked. Don’t kid yourself that the absence of a carcinogenicity study is the same as a clean bill.

Side effects

No human safety data exists. The animal signals that do exist are worth knowing:

monitorSkeletal muscle damage at toxicological doses in mice, driven by off-target activation of PPAR-alpha. Whether this occurs at the doses the community runs is unknown.
unknownGW-0742 was never run through a long-term carcinogenicity screen. The compound it’s modeled on was, and didn’t survive it. The absence of bad data isn’t the same as the absence of risk.
monitorIn cell assays above 12.1 micromolar, GW-0742 antagonized the vitamin D receptor and the androgen receptor. Whether oral dosing reaches those concentrations in a person is unmeasured.

Where to buy

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