TL;DR
GlaxoSmithKline's cleaner Cardarine. 1000-fold PPARδ selectivity. Zero human trials. The class flunked 2-year rodent carcinogenicity.
What: Small molecule PPARδ agonist disclosed by Sznaidman in 2003 (PMID 12699745). 489 Da. Structurally related to GW501516 (Cardarine) but with fluorine and higher selectivity. Has not advanced to an IND.
Does: Binds PPARδ, heterodimerizes with RXR, activates PPREs. Upregulates fatty-acid oxidation, PGC-1α-driven mitochondrial biogenesis, and type I oxidative fiber programs. Suppresses NF-κB in macrophages.
Evidence: Entirely preclinical. Wang 2004 (PMID 15328533) "marathon mouse" phenotype (transgene, not GW-0742). Narkar 2008 (PMID 18674809) exercise-mimetic story using GW501516. GW501516's 2-year rodent carcinogenicity killed the PPARδ clinical program.
Used by: PPARδ biology research labs. Endurance communities adopt it as a "cleaner" Cardarine without matching safety testing.
Bottom line: Real receptor. Real rodent endurance. The class flunked long-term safety. Not a peptide.
What It Is
GW-0742 (also referenced as GW610742 or GW0742X) is a synthetic high-selectivity PPARδ 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 S4.5 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. 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 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 prudent assumption until proven otherwise is that the same carcinogenicity risk applies. 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. The compound has never been administered to humans in a controlled study registered on ClinicalTrials.gov or documented in a peer-reviewed clinical pharmacology report.
- 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 18285555) 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 entirely outside published human controlled evidence. The compound's pharmacokinetic profile in humans, optimal dose, duration tolerance, and long-term safety are unknown.
Dosing from the Literature
No FDA-approved dose exists for GW-0742. Preclinical rodent studies and uncontrolled community reports inform the dose-ranges below — neither is equivalent to human clinical dosing guidance.
| 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. |
| Community (endurance / fat loss) | 5–15 mg (oral) | Once daily | Extrapolated from Cardarine dosing conventions and allometric scaling. No human PK data. |
| Community (conservative start) | 2.5–5 mg | Once daily | Lower starting dose given the uncharacterized human safety profile. |
| Cycle pattern (community) | — | 6–8 weeks on / 4–6 weeks off | Speculative cycling; not based on clinical evidence. Rationale is hedging against chronic PPARδ stimulation given the class carcinogenicity concern. |
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. WADA-banned — not viable for tested athletes.
Reconstitution & Storage
GW-0742 is a small-molecule compound, not a peptide. It does not require reconstitution in the peptide sense (no BAC water, no lyophilized powder). Research-grade GW-0742 is supplied either as a crystalline powder or as a DMSO stock solution from life-sciences suppliers. Oral dosage forms used in uncontrolled community channels are typically compounded oral capsules or oral suspensions.
| Supply Form | Typical Vehicle | Handling | Storage |
|---|
| Crystalline powder (research) | DMSO stock 10–100 mM | Weigh, dissolve in DMSO, dilute into aqueous vehicle | Powder: −20°C desiccated; DMSO stock: −20°C protected from light |
| Oral capsule (community) | Lactose / MCC filler | Oral ingestion; taken with food to mitigate GI upset | Room temperature, away from light and moisture |
| Oral liquid (community) | Ethanol / propylene glycol / flavored carrier | Oral drop dosing; dose accuracy depends on calibration | Room temperature, tightly sealed |
- Stability — GW-0742 is chemically stable as a dry powder for extended periods when stored desiccated and protected from light. Solutions are less stable; DMSO stocks should be single-use-aliquoted.
- Purity — Research-grade supply typically >98% purity by HPLC. Community-channel purity varies substantially; independent COA (HPLC + mass spec) is the practical floor.
- Oral bioavailability — Rodent oral bioavailability is substantial; human data do not exist. Taken with dietary fat is mechanistically sensible given the lipophilic profile.
- Not a peptide — Does not degrade in gastric acid or gut proteases. Oral route is viable without parenteral administration.
→ Use the Kalios Dosing Calculator for oral-dose conversions
Side Effects & Risks
Important
Class-level 2-year rodent carcinogenicity terminated GW501516's clinical program. GW-0742 has no matched long-term safety testing. WADA-banned. Talk to someone licensed before touching it.
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. Monitor ALT/AST periodically if used.
- Gastrointestinal discomfort — Mild nausea, loose stools, and abdominal discomfort are reported in community channels, typically mild and resolving with food co-administration.
- Headache — Occasionally reported in community use; mechanism unclear.
- 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. Avoid in pregnancy, lactation, and reproductive-age females without contraception.
- Drug interactions — PPARδ transcriptional effects may alter CYP450 expression in liver; clinically meaningful interactions not characterized. Caution with 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 (S4.5) — Banned at all times under "metabolic modulators." Detection methods established.
- Sourcing risk — Gray-market GW-0742 quality varies. Compound identity, purity, and dose-per-capsule accuracy are frequent failure modes in non-research-grade channels. Independent COAs are the practical floor.
Bloodwork & Monitoring
Monitoring for any PPARδ-agonist use should include baseline and periodic labs plus age-appropriate cancer screening given the class carcinogenicity concern.
- Lipid panel — Baseline and at 6–8 weeks. Expected direction: HDL rise, triglyceride reduction, modest LDL change. Lipid normalization is the most consistent PPARδ-agonist biomarker.
- Fasting glucose and HbA1c — Baseline and periodic. PPARδ activation may improve glucose handling; monitor for unexpected hypoglycemia if combining with other agents.
- Liver enzymes (ALT, AST, alkaline phosphatase, total bilirubin) — Baseline and at 6–8 weeks. Hepatic PPARδ expression and lipid-handling effects warrant hepatic surveillance.
- hsCRP — Baseline and periodic. Anti-inflammatory effects of PPARδ activation should reduce hsCRP.
- CBC and CMP — Standard baseline screen.
- TSH — Baseline. GW501516 produced thyroid tumors in rodent bioassays; baseline thyroid function is reasonable prior to any PPARδ-agonist use.
- Age-appropriate cancer screening — Colonoscopy, skin exam, mammography / prostate screening per age and family history guidelines. Given the class carcinogenicity concern, cancer screening prior to initiation is reasonable.
- Cardiac assessment — Baseline EKG and lipid-focused CV risk assessment in users with cardiovascular history.
- Reproductive counseling — For reproductive-age users, discuss the reproductive-toxicology class uncertainty.
- Baseline cardiac imaging in chronic use — Echocardiography may be reasonable for users contemplating multi-month dosing given the combined PPARδ/AMPK cardiac effects; not required for short courses but a reasonable floor for any chronic protocol.
- Urine PPARδ-agonist screen (sports context) — For any user subject to WADA or equivalent anti-doping oversight, understand that GW-0742 is detectable in routine LC-MS/MS urinary screening for at least days to weeks after cessation. The detection-window consideration is germane to competition planning.
- Body composition (DEXA) — Baseline and periodic for objective tracking of fat mass and lean mass across cycles; the lipolytic and oxidative-metabolism shifts of PPARδ activation are most visible in body-composition metrics rather than scale weight.
Commonly Stacked With
GW-0742 community stacking generally mirrors GW501516 stacking patterns. Emphasis should be on the carcinogenicity risk compounding with any chronic use.
SLU-PP-332 is an estrogen-related-receptor (ERR) pan-agonist with overlapping exercise-mimetic transcriptional effects via a parallel nuclear-receptor pathway. Combined PPARδ + ERR activation is explored in preclinical exercise-mimetic studies but has no human evidence. Stacking compounds oxidative-metabolism adaptations and compounds safety uncertainty.
5-Amino-1MQ inhibits nicotinamide N-methyltransferase, preserving NAD+ and SAM pools; combining with PPARδ agonism pushes metabolic flux toward oxidative phosphorylation. Preclinical-only combination.
TRT + PPARδ agonism is the classical "cutting cycle" bodybuilding combination — androgenic anabolic signaling paired with oxidative-metabolism reprogramming for simultaneous lean-mass preservation and fat loss. Requires clinician oversight; compounds PPARδ safety concerns.
AMPK activators (metformin, AICAR)
Narkar et al. (2008) established that combined AMPK + PPARδ activation produces additive exercise-mimetic effects. Metformin is the practical AMPK activator; AICAR is banned by WADA and not used clinically. Combination has preclinical rationale but no human evidence.
→ Check compound compatibility in the Stack Builder
Regulatory 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 a peptide and is not on the FDA Category 2 bulk drug substances list (which addresses peptides specifically). 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.
The January / February 2026 HHS peptide reclassification announcements do not apply to GW-0742 — it is not a peptide. GW-0742's regulatory status in the United States is unchanged by those announcements.
GW-0742 is banned by WADA under the S4.5 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.
Cost & Access
GW-0742 is not approved for human use in any jurisdiction. It is sold by life-sciences suppliers (Tocris, Cayman Chemical, Sigma-Aldrich, MedChemExpress) 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; independent laboratory verification is the practical floor for any user choosing that route. 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 is not under review in the HHS Secretary Robert F. Kennedy Jr. February 2026 Category 2 peptide reclassification announcement; as a small-molecule non-peptide research compound, it is outside that framework. 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.
Related Compounds
People researching GW-0742 often also look at these:
AMPK activator (AICA ribonucleotide). Exercise-mimetic small molecule with WADA ban history.
16-amino-acid mitochondrial-encoded peptide. AMPK-activating longevity peptide.
SS-31 + MOTS-c + NAD+ — mitochondrial longevity stack targeting cellular energetics.
Triple monoamine reuptake inhibitor (5-HT, DA, NE). Non-GLP-1 weight-loss alternative.
Key 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: 18285555. (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: 17693662. (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: 15721862. (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: 20026354.
- WADA. 2026 World Anti-Doping Code Prohibited List. Section S4.5 — 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.
Last updated: April 2026 | Profile authored by Kalios Peptides research team