Weight loss · Pill

GW-0742

Gray market

Checked 18 Oct 2026 · 18 sources · 10 corrections on this page · No vendors · No affiliates · No one buys a word of it

0 human trials published

Preclinical · rodent metabolic and cardiovascular models

Gray market · No FDA ruling — not on any list

Sold as a research chemical. Some clinics and pharmacies still supply it; that’s their risk, not a change in the rule.

Bottom line

A real receptor, rodent endurance data, and a class whose lead compound failed a two-year rodent cancer study. Not a peptide.

Also called: GW610742 · GW0742X · "Super Cardarine" · PPARβ/δ agonist (GlaxoSmithKline)
Category: Small Molecule — PPARδ Agonist
Class: PPARδ agonist (small molecule)
Molecular Weight: 471.5 Da (C21H17F4NO3S2)
Selectivity: 1,000-fold over the other human PPAR subtypes; EC₅₀ 1.1 nM at PPARδ (Sznaidman et al., 2003)
Half-life: Not measured; its sulfone metabolite was found in urine up to 20 days after one 15 mg oral dose (Sobolevsky et al., 2012)
Route (studied): Oral (one human excretion study) · oral (mice)
Route (sold): Oral capsules and liquids (research chemical)
FDA Status: Never entered clinical trials
Developer: GlaxoSmithKline (2003)
WADA Status: Banned (S4.4.1 metabolic modulator)
Human Data: One urine-detection study (single dose)
Cost & Access: Research-only

Also for weight loss

The other four questions

What does it do? It switches on PPARδ, a receptor that controls how cells burn fat. In mice, activating it changed muscle fibre type and raised running endurance (Wang et al., 2004), and with an AMPK activator it was called an exercise mimetic (Narkar et al., 2008) — both with other PPARδ drugs, not this one.
Who uses it? Research labs studying the PPARδ switch. Endurance-sports self-experimenters adopting it as a "cleaner" Cardarine — without any matching safety testing.
Does the evidence hold up? No trial of it in people has been published; the one human study gave a single 15 mg dose to trace it in urine (Sobolevsky et al., 2012). A famous 2004 "marathon mouse" paper used a gene-tweaked mouse, not this drug. A 2008 exercise-mimetic paper used a related compound (Cardarine). And Cardarine itself flunked a 2-year rodent cancer test, which killed the entire drug class.
Bottom line? A real receptor, rodent endurance data, and a class whose lead compound failed a two-year rodent cancer study. Not a peptide.

Dosing from the Literature

Published for fat loss: rodent doses, 1–10 mg/kg a day by mouth. Not published: any human dose for fat loss. The one study in people gave a single 15 mg dose by mouth to trace it in urine (Sobolevsky 2012).

No FDA-approved dose exists for GW-0742, and no trial has given it to a person for fat loss. The row below is the range the published rodent studies used.

Context	Dose	Frequency	Notes
Rodent metabolic studies (published)	1–10 mg/kg/day (oral)	Daily	Dose range across most published rodent metabolic and cardiovascular studies.

Dosing Disclaimer

GW-0742 dosing is extrapolated from preclinical rodent studies and uncontrolled community practice. No human pharmacokinetic, pharmacodynamic, or safety data inform these numbers. The compound is a research chemical with no validated human dose. The entries above are descriptive of observed community practice, not prescriptive.

What It Is

GW-0742 (also referenced as GW610742 or GW0742X) is a synthetic high-selectivity PPARδ (a gene switch for fat burning) agonist that emerged from GlaxoSmithKline's PPAR chemistry program in the early 2000s. Sznaidman and colleagues published the original disclosure describing GW-0742 as part of a medicinal-chemistry series aimed at identifying PPARδ-selective agonists with potency and selectivity over the related nuclear receptors PPARα and PPARγ (Sznaidman et al., Bioorganic & Medicinal Chemistry Letters, 2003). Published selectivity data place GW-0742 at roughly three orders of magnitude greater affinity for PPARδ than for the other PPAR subtypes — which is one of the highest selectivity ratios reported for any small-molecule PPARδ ligand.

GW-0742 is structurally related to GW501516 (the better-known "Cardarine"), sharing the same thiazolylmethylthio-phenoxyacetic acid scaffold with a fluorine substituent that accounts for the improved selectivity. Both compounds activate the PPARδ/RXR heterodimer and drive a highly overlapping gene-expression program — but only GW501516 was advanced into human clinical development, where it was ultimately terminated when 2-year rodent carcinogenicity bioassays showed dose-dependent multi-organ tumor induction (the finding that has defined the entire PPARδ-agonist class since).

GW-0742 itself was never advanced into human clinical trials. The available evidence base is entirely preclinical — rodent metabolic, cardiovascular, muscle-biology, inflammation, and colitis models, plus cell-culture work on PPARδ signaling. It has no FDA approval, no IND, and no clinical pharmacology data. Its community profile as a "cleaner" or "safer" alternative to Cardarine rests on the assumption that higher PPARδ selectivity reduces off-target liability and that the Cardarine carcinogenicity finding is subtype-specific — neither assumption is supported by adequate testing data on GW-0742 itself. The compound is WADA-prohibited under the S4.4.1 category of metabolic modulators, mirroring the status of other PPARδ agonists.

PPARδ (also called PPARβ/δ) is a nuclear-receptor transcription factor expressed broadly across skeletal muscle, cardiac muscle, adipose, liver, macrophages, and endothelium (the lining of blood vessels). Upon ligand binding it heterodimerizes with the retinoid X receptor (RXR), binds PPAR response elements (PPRE) in target-gene promoters, and coordinates a program favoring fatty-acid oxidation, mitochondrial biogenesis, oxidative fiber-type shift in skeletal muscle, and anti-inflammatory macrophage polarization. Landmark work by Wang et al. (PLoS Biology, 2004) used PPARδ transgene overexpression to establish the "marathon mouse" phenotype — substantially increased running endurance driven purely by PPARδ-programmed metabolic reprogramming — which anchored the entire PPARδ-agonist therapeutic hypothesis.

The PPAR family comprises three subtypes — PPARα (primarily hepatic; fibrate drug target for triglyceride reduction), PPARγ (primarily adipose; thiazolidinedione target for insulin sensitization), and PPARδ (ubiquitous; the GW501516 / GW-0742 target). Selectivity across these three subtypes is critical because each drives distinct and partly antagonistic transcriptional (at the gene-switching level) programs. GW-0742's reported 1000× selectivity for PPARδ over the other two subtypes is its principal chemical distinction from older PPAR agonists and is the rationale for its status as the reference research-tool PPARδ agonist in cell-biology work. Practically, this selectivity means that GW-0742 engages the oxidative-metabolism / mitochondrial-biogenesis / anti-inflammatory program associated with PPARδ without the hepatic fatty-acid oxidation pattern of PPARα or the adipogenic / insulin-sensitizing pattern of PPARγ.

Mechanism of Action

GW-0742 is a direct ligand of the PPARδ ligand-binding domain. Receptor engagement drives a coordinated transcriptional program across multiple tissues; the apparent behavioral and metabolic phenotype is the composite of these tissue-specific effects.

PPARδ/RXR heterodimerization and PPRE binding — Upon GW-0742 binding, PPARδ undergoes conformational change, recruits RXR, and the heterodimer binds PPAR response elements in target gene promoters. Coactivator complexes (PGC-1α, SRC-1, CBP/p300) are recruited; corepressors (NCoR, SMRT) are displaced. This is the core transcriptional switch.
Fatty-acid oxidation program (skeletal muscle) — PPARδ activation upregulates CPT-1 (carnitine palmitoyltransferase 1), MCAD (medium-chain acyl-CoA dehydrogenase), ACOX1, FATP1, and CD36 — the rate-limiting and transport machinery of beta-oxidation. Muscle metabolism shifts toward lipid fuel use and away from glycolytic glucose dependence.
Mitochondrial biogenesis — PPARδ drives PGC-1α expression; PGC-1α is the master regulator of mitochondrial biogenesis, upregulating NRF-1/2, TFAM, and the nuclear-encoded oxidative-phosphorylation subunits. Muscle mitochondrial density increases with chronic PPARδ activation in rodents.
Oxidative fiber-type shift — PPARδ drives expression of type I (slow oxidative, myoglobin-rich) and type IIa (fast oxidative-glycolytic) fiber-type markers while suppressing type IIb (fast glycolytic) markers. Chronic activation produces a slow-to-fast oxidative shift — the molecular basis of the "marathon mouse" endurance phenotype (Wang et al., 2004).
Lipid metabolism (adipose and liver) — Increases HDL-cholesterol and reduces triglycerides in rodent metabolic models; reduces hepatic lipogenesis; improves whole-body lipid handling. Originally the primary therapeutic hypothesis that drove PPARδ clinical development.
Anti-inflammatory effects (macrophage polarization) — PPARδ activation in macrophages suppresses NF-κB-mediated pro-inflammatory gene expression (TNF-α, IL-6, iNOS), shifts polarization toward the M2 anti-inflammatory phenotype, and reduces vascular inflammation in atherosclerosis models.
Cardiac metabolism — In cardiomyocytes, PPARδ activation favors fatty-acid oxidation as the dominant ATP source and protects against cardiac hypertrophy and fibrosis in pressure-overload and angiotensin-II infusion models.
Anti-fibrotic effects — PPARδ agonism attenuates TGF-β/Smad signaling in hepatic and cardiac fibrosis models.
Endurance / exercise-mimetic effects — Narkar et al. (Cell, 2008) showed that combined PPARδ agonism and AMPK activation produced exercise-like transcriptional and functional phenotypes in sedentary rodents — the paper that cemented the "exercise mimetic" framing of PPARδ agonists.
Anti-apoptotic signaling (context-dependent) — PPARδ activation engages anti-apoptotic gene expression (Bcl-2 family, Akt survival signaling) in several cell types — protective in cardiomyocytes but a potential concern in transformed cells.
No GH/IGF-1 axis engagement — GW-0742 is not a GH secretagogue, does not engage growth-hormone signaling, and is mechanistically distinct from the peptide GH axis. It is not a peptide.

What the Research Shows

The GW-0742 research base is entirely preclinical — rodent metabolic and cardiovascular models, plus mechanistic cell-culture work. There are no registered human clinical trials.

Original disclosure and selectivity characterization (Sznaidman et al., Bioorg Med Chem Lett 2003; PMID 12699745) — First publication describing the GW-0742 medicinal-chemistry series, PPARδ potency, and selectivity over PPARα and PPARγ. Established the compound as a leading research-tool PPARδ ligand.
PPARδ endurance phenotype (Wang et al., PLoS Biol 2004; PMID 15328533) — Transgenic PPARδ overexpression in skeletal muscle produced dramatic oxidative-fiber-type shift and roughly doubled running endurance in untrained mice. The "marathon mouse" paper — foundational to the PPARδ-agonist therapeutic hypothesis, though the experimental tool was transgene overexpression rather than GW-0742 specifically.
Exercise-mimetic effects (Narkar et al., Cell 2008; PMID 18674809) — Demonstrated that AMPK activation plus PPARδ agonism (using GW501516) produced exercise-like transcriptional and endurance phenotypes in sedentary mice. Established the "exercise in a pill" framing that drove subsequent community interest in both GW501516 and GW-0742.
Metabolic effects in diabetic rodents — GW-0742 improved glucose tolerance, reduced triglycerides, and increased HDL in diet-induced obesity and db/db mouse models at oral doses of approximately 10 mg/kg/day. Effects paralleled those of GW501516.
Cardiac protection (rodent models) — Multiple published rodent studies show PPARδ activation by GW-0742 attenuates pressure-overload cardiac hypertrophy, angiotensin-II-induced fibrosis, and ischemia-reperfusion injury. Mechanism attributed to metabolic shift toward fatty-acid oxidation and anti-inflammatory macrophage polarization.
Colitis models (Hollingshead et al., Cancer Res 2007; PMID 17440073 — class-level PPARδ context) — PPARδ agonism has shown both protective and promoting effects in colitis models depending on dose and timing, reflecting the complex role of PPARδ in gut epithelial homeostasis.
Pulmonary fibrosis models — GW-0742 attenuated bleomycin-induced pulmonary fibrosis in rodent models through anti-TGF-β mechanisms.
Renal protection — Small rodent studies demonstrating reduced diabetic nephropathy and renal inflammation with GW-0742 treatment.
Class review (Palomer et al., Int J Mol Sci 2018; PMID 29558390) — Comprehensive review of PPARβ/δ as a therapeutic target in metabolic disorders, summarizing the mechanistic rationale and the clinical-development headwinds (primarily the GW501516 carcinogenicity finding).
No published human clinical trial of GW-0742 — A search of ClinicalTrials.gov returns no registered human studies for GW-0742 as of April 2026. All human safety and efficacy claims are extrapolation.

Critical Context — The Cardarine Carcinogenicity Problem

The sister compound GW501516 (Cardarine) was terminated in 2007 when 2-year rodent carcinogenicity bioassays revealed dose-dependent multi-organ tumor induction (thyroid, testis, tongue, liver, bladder, endometrium, skin) across both rats and mice. The finding is documented in the published literature and in GlaxoSmithKline's own toxicology filings. Because PPARδ activation itself is implicated — and GW-0742 activates the same receptor — the same carcinogenicity risk may apply. GW-0742 has not undergone equivalent 2-year bioassays; absence of data is not equivalent to absence of risk. Any framing of GW-0742 as "safer than Cardarine" outside the carcinogenicity question is speculative.

Human Data

There is no published human clinical trial of GW-0742, and none is registered on ClinicalTrials.gov. One peer-reviewed anti-doping study gave people a single 15 mg oral dose to trace it in urine: the unchanged compound was measurable only briefly, at low ng/mL, and its sulfone metabolite for up to 20 days (Sobolevsky et al., 2012; PMID 22977012). It measured detection, not effects or safety.

Closest human precedent — GW501516 (Cardarine) — GW501516 entered Phase 1 and Phase 2 human trials in dyslipidemia and metabolic syndrome at oral doses up to 10 mg/day. Limited published human data (Risérus et al., Diabetes 2008; PMID 18024853) demonstrated favorable lipid and glucose effects in short-term dosing. The program was terminated on carcinogenicity grounds before pivotal trials.
Community self-report — uncontrolled — Bodybuilding and endurance-athlete forums report oral dosing of GW-0742 at 5–20 mg/day for periods of weeks to months, with self-reported endurance and lipid effects. This is not clinical evidence; selection bias, sourcing inconsistency, and unverified bloodwork are the norm.
WADA detection methods (class-level) — Published analytical-chemistry methods exist for detection of GW501516 and GW-0742 in human urine using LC-MS/MS. Detection is established in routine anti-doping testing.
Practical implication — Anyone using GW-0742 is operating outside any published human evidence on its effects or safety. Apart from one urine-detection study, the compound's pharmacokinetics in humans, optimal dose, duration tolerance, and long-term safety are unknown.

Reconstitution & Storage

GW-0742 is a small molecule, not a peptide: nothing to reconstitute, and it survives the gut, so it is taken by mouth. Laboratories dissolve it in DMSO for cell work. No label or guideline gives a storage condition or shelf life for a product sold as GW-0742.

Side Effects & Risks

Important

A two-year rodent study of GW501516, the lead compound of this class, found tumours in many organs, and its clinical programme was stopped. GW-0742 has had no such test. WADA bans it at all times as a metabolic modulator, S4.4.1 (Prohibited List 2026). Consult a licensed healthcare provider.

The GW-0742 side-effect profile is not well characterized in humans. The dominant risk consideration is the PPARδ-class carcinogenicity concern, not any reported acute side effect.

Carcinogenicity concern (class-level) — The most important safety consideration. GW501516 produced dose-dependent multi-organ tumors in 2-year rodent bioassays. GW-0742 has not been tested equivalently. Absence of data is not absence of risk; the mechanistic overlap is near-complete.
Hepatic effects (theoretical) — PPARδ is expressed in hepatocytes and affects hepatic lipid handling. No study has measured liver enzymes in a person taking GW-0742.
Hypoglycemia (theoretical) — PPARδ activation increases peripheral glucose uptake and fatty-acid oxidation; in combination with fasting or other glucose-lowering agents, mild hypoglycemia is plausible but not reliably documented.
Cardiac remodeling uncertainty — Preclinical data support cardiac protection, but chronic high-dose PPARδ stimulation in humans is uncharacterized.
Reproductive toxicity (class concern) — Rodent reproductive studies for the PPARδ-agonist class have shown mixed effects; GW-0742 reproductive data are limited.
Drug interactions — PPARδ transcriptional effects may alter CYP450 expression in liver; clinically meaningful interactions not characterized. No interaction study has been published. Concurrent fibrates (PPARα agonism), thiazolidinediones (PPARγ agonism), and any hepatically metabolized drug.
No human safety database — The compound has never been through human clinical trials. Community reports are uncontrolled and heterogeneous; absence of reported severe acute events reflects the narrow exposure window, not validated long-term safety.
WADA banned (S4.4.1) — Banned at all times under metabolic modulators; a published method detects it in urine (Prohibited List 2026; Sobolevsky et al., 2012).
What is in a capsule — GW-0742 is sold as a research chemical; no analysis of such products appears in the documents read for this page.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for GW-0742, and no study has given it to a person for fat loss. The rodent studies measured lipids, glucose handling, muscle fibre type and running endurance (Wang et al., 2004; Narkar et al., 2008); the one human study measured the drug and its metabolites in urine after a single 15 mg dose (Sobolevsky et al., 2012).

Commonly Stacked With

No published study has combined GW-0742 with another compound. In mice, a different PPARδ agonist, GW501516, was given with the AMPK activator AICAR; the pair raised running endurance more than exercise training alone (Narkar et al., 2008).

Stacking this? Read the receipt →

Legal Status

Current Status — April 2026

GW-0742 is not FDA-approved for any indication. It was developed by GlaxoSmithKline as a research tool and chemistry-series analog of GW501516 (Cardarine) but was never advanced into human clinical development. There is no IND, no registered clinical trial, and no published human pharmacology data.

GW-0742 is not on any FDA 503A bulk-substance list. As a small-molecule research chemical, its U.S. legal status sits in the familiar gray zone occupied by other PPAR-agonist research compounds: not scheduled under the Controlled Substances Act, not approved for human use, and not legally compoundable by 503A or 503B pharmacies. It is sold openly by life-sciences suppliers for laboratory research, and sold by uncontrolled online "research-chemical" channels for human-use-by-implication.

FDA’s 2026 changes to Category 2 do not apply to GW-0742 — it is not a peptide, and FDA’s 503A categories list, updated May 14, 2026, does not name it (FDA 503A categories list, May 14, 2026). GW-0742's regulatory status in the United States is unchanged by FDA's 2026 steps.

GW-0742 is banned by WADA under the S4.4.1 category of "metabolic modulators." The PPARδ-agonist class was added to the WADA Prohibited List in 2009 following the AICAR/GW501516 era. GW-0742 is specifically covered under the class prohibition. Detection methods for PPARδ agonists in urine are established and routinely deployed by WADA-accredited laboratories. Any tested athlete using GW-0742 faces sanction under the WADA Code. WADA’s 2026 List stays in force until 31 December 2026; the 2027 List, which replaces it on 1 January 2027, keeps the PPARδ agonists in S4.4.1, adds seladelpar to their examples, and adds SLU-PP-332, SLU-PP-915 and related substances to the subsection (Prohibited List 2027).

Cost & Access

GW-0742 is not approved for human use in any jurisdiction. It is sold by life-sciences suppliers as a research-grade PPARδ-agonist tool compound for laboratory use only. Research-grade GW-0742 is high-purity (typically >98% by HPLC) and is sold with certificate of analysis in small milligram quantities for cell-culture and animal studies.

Gray-market online "research chemical" channels sell GW-0742 as oral capsules or oral liquid formulations intended for human-use-by-implication despite labels otherwise. Quality, purity, and dose-accuracy vary substantially across these channels. Compounded formulations are not legally available through U.S. 503A or 503B pharmacies — GW-0742 is not on the bulk drug substances list for compounding.

GW-0742 was not among the 12 peptides FDA removed from Category 2 in April 2026 (FDA 503A categories list, April 22, 2026). No U.S. regulatory pathway for human GW-0742 use currently exists, and absent a sponsor advancing it through a formal IND / NDA program (highly unlikely given the class carcinogenicity concern that terminated GW501516), that will not change.

Estimated pricing context as of April 2026. Actual costs vary by vendor, purity grade, and format. Kalios does not sell compounds.

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References

Sznaidman ML, Haffner CD, Maloney PR, Fivush A, Chao E, Goreham D, Sierra ML, LeGrumelec C, Xu HE, Montana VG, Lambert MH, Willson TM, Oliver WR Jr, Sternbach DD. 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. PMID: 12699745.
Wang YX, Zhang CL, Yu RT, Cho HK, Nelson MC, Bayuga-Ocampo CR, Ham J, Kang H, Evans RM. Regulation of muscle fiber type and running endurance by PPARdelta. PLoS Biol. 2004;2(10):e294. PMID: 15328533.
Narkar VA, Downes M, Yu RT, Embler E, Wang YX, Banayo E, Mihaylova MM, Nelson MC, Zou Y, Juguilon H, Kang H, Shaw RJ, Evans RM. AMPK and PPARδ agonists are exercise mimetics. Cell. 2008;134(3):405-415. PMID: 18674809.
Palomer X, Barroso E, Pizarro-Delgado J, Peña L, Botteri G, Zarei M, Aguilar D, Montori-Grau M, Vázquez-Carrera M. PPARβ/δ: a key therapeutic target in metabolic disorders. Int J Mol Sci. 2018;19(3):913. PMID: 29558390.
Risérus U, Sprecher D, Johnson T, Olson E, Hirschberg S, Liu A, Fang Z, Hegde P, Richards D, Sarov-Blat L, Strum JC, Basu S, Cheeseman J, Fielding BA, Humphreys SM, Danoff T, Moore NR, Murgatroyd P, O'Rahilly S, Sutton P, Willson T, Hassall D, Frayn KN, Karpe F. Activation of peroxisome proliferator-activated receptor (PPAR)delta promotes reversal of multiple metabolic abnormalities, reduces oxidative stress, and increases fatty acid oxidation in moderately obese men. Diabetes. 2008;57(2):332-339. PMID: 18024853. (GW501516 human Phase 2 data — near-cousin human evidence for the PPARδ class.)
Barish GD, Narkar VA, Evans RM. PPARδ: a dagger in the heart of the metabolic syndrome. J Clin Invest. 2006;116(3):590-597. PMID: 16511591.
Oliver WR Jr, Shenk JL, Snaith MR, Russell CS, Plunket KD, Bodkin NL, Lewis MC, Winegar DA, Sznaidman ML, Lambert MH, Xu HE, Sternbach DD, Kliewer SA, Hansen BC, Willson TM. A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport. Proc Natl Acad Sci USA. 2001;98(9):5306-5311. PMID: 11309497. (Foundational PPARδ HDL/reverse cholesterol transport paper; underpins the therapeutic hypothesis.)
Hollingshead HE, Killins RL, Borland MG, Girroir EE, Billin AN, Willson TM, Sharma AK, Amin S, Gonzalez FJ, Peters JM. Peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) ligands do not potentiate growth of human cancer cell lines. Carcinogenesis. 2007;28(12):2641-2649. PMID: 17693664. (Class carcinogenicity context; the ongoing debate on PPARβ/δ and cancer.)
Peters JM, Shah YM, Gonzalez FJ. The role of peroxisome proliferator-activated receptors in carcinogenesis and chemoprevention. Nat Rev Cancer. 2012;12(3):181-195. PMID: 22318237. (Comprehensive review of PPARs and cancer risk — the central safety-framing source for the class.)
Tan NS, Vázquez-Carrera M, Montagner A, Sng MK, Guillou H, Wahli W. Transcriptional control of physiological and pathological processes by the nuclear receptor PPARβ/δ. Prog Lipid Res. 2016;64:98-122. PMID: 27665713.
Graham TL, Mookherjee C, Suckling KE, Palmer CN, Patel L. The PPARδ agonist GW0742X reduces atherosclerosis in LDLR(-/-) mice. Atherosclerosis. 2005;181(1):29-37. PMID: 15939051. (GW-0742 atherosclerosis data.)
Planavila A, Rodríguez-Calvo R, Jové M, Michalik L, Wahli W, Laguna JC, Vázquez-Carrera M. Peroxisome proliferator-activated receptor beta/delta activation inhibits hypertrophy in neonatal rat cardiomyocytes. Cardiovasc Res. 2005;65(4):832-841. PMID: 15721863. (GW-0742 cardiac-hypertrophy data.)
Wagner KD, Wagner N. Peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) acts as regulator of metabolism linked to multiple cellular functions. Pharmacol Ther. 2010;125(3):423-435. PMID: 20026355.
Sobolevsky T, Dikunets M, Sukhanova I, Virus E, Rodchenkov G. Detection of PPARδ agonists GW1516 and GW0742 and their metabolites in human urine. Drug Test Anal. 2012;4(10):754-760. PMID: 22977012.
WADA. 2026 World Anti-Doping Code Prohibited List. Section S4.4.1 — Metabolic Modulators. World Anti-Doping Agency. Effective January 1, 2026.
U.S. National Library of Medicine — PubChem CID 9934458 (GW-0742). Physicochemical and structural data for GW-0742.
FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
World Anti-Doping Agency. Prohibited List 2027 (in effect January 1, 2027), French edition with track changes, August 26, 2026, and Summary of Major Modifications and Explanatory Notes, 2027 Prohibited List, August 17, 2026: wada-ama.org/sites/default/files/2026-09/2027list_final_fr_track_changes_26_august_2026.pdf and 2027_list_explanatory_note_en_final_17_august_2026_1.pdf, read October 12, 2026 in the Internet Archive’s copies captured October 9, 2026 (web.archive.org). The List’s English edition was not available there and was not read.