If you want “diet in a pill” then the GLP1 class of drugs are it. I advise eating a good diet while using them for best results.
The same applies to these “exercise in a pill” substances like SLU-PP-332.
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I’ve been doing a research deep dive on these “exercise in a pill” endurance/energy increasing substances. I’ve got a summary of all studies on both forms of cardarine GW501516 and GW0742.
Cardarine GW501516
Study analysis overview of gw501516.pdf (38.6 KB)
“Super” Cardarine GW0742
Summarize GW0742 studies.pdf (64.2 KB)
An interesting 2007 study on Cardarine GW501516 claiming that the pro-cancerous effects of Cardarine do not affect humans:
Peroxisome proliferator-activated receptor-b/d (PPARb/d) ligands do not potentiate growth of human cancer cell lines: https://academic.oup.com/carcin/article/28/12/2641/2476288
Full study readable here: Hollingshead, H. E.; Killins, R. L.; Borland, M. G.; Girroir, E. E.; Billin, A. N.; Willson, T. M.; Sharma, A. K.; Amin, S.; Gonzalez, F. J.; Peters, J. M. - Anna’s Archive
ChatGPT-5 summary of full study:
Study reference: Hollingshead HE et al., “Peroxisome proliferator‑activated receptor‑β/δ ligands do not potentiate growth of human cancer cell lines,” Carcinogenesis, 2007.
Purpose and background
- PPAR‑β/δ ligands such as GW501516 and GW0742 enhance fatty‑acid metabolism and show anti‑inflammatory effects, but some reports suggested they might promote tumourigenesis through increased cancer cell proliferation, Akt phosphorylation and up‑regulation of cyclo‑oxygenase‑2 (COX‑2) and vascular endothelial growth factor (VEGF).
- The authors aimed to clarify these conflicting findings by testing the effects of two PPAR‑β/δ ligands on several human colon (HT‑29, HCT116, LS‑174T) and liver (HepG2, HuH7) cancer cell lines under different culture conditions and comparing in‑vitro data with in‑vivo mouse results.
Methods
- Expression and activation: The researchers quantified PPAR‑β/δ and a known target gene (adipocyte differentiation‑related protein) to confirm that the cancer cell lines expressed functional PPAR‑β/δ. Both ligands increased target‑gene expression, demonstrating receptor activation.
- Cell proliferation assays: Cell growth was measured over three days in colon and liver cancer cell lines treated with GW501516 or GW0742 at various concentrations, with or without serum.
- Protein expression analyses: Western blotting assessed Akt phosphorylation, COX‑2 and VEGF expression. mRNA levels of COX‑2 were also evaluated.
- In‑vivo confirmation: Colon polyps and liver tissue from mice treated with either ligand were analysed for the same markers to compare with in‑vitro findings.
Key findings
- All cancer cell lines expressed functional PPAR‑β/δ and responded to ligand activation.
- Neither GW501516 nor GW0742 increased cell proliferation in any of the human cancer cell lines; in fact, growth inhibition was occasionally observed at higher ligand concentrations.
- No increases in phosphorylation of Akt or expression of VEGF or COX‑2 were detected in colon or liver cancer cell lines treated with either ligand, regardless of serum presence.
- In mice, both ligands activated PPAR‑β/δ (demonstrated by increased AngPTL4) but did not increase COX‑2, VEGF or phosphorylated Akt in colon polyps, colon or liver tissues.
- The authors concluded that differences in serum conditions, ligand structure or model (in‑vitro vs. in‑vivo) do not explain previous reports of pro‑tumourigenic effects; the quantitative data did not support the hypothesis that PPAR‑β/δ ligands potentiate tumourigenesis.
Implications
This study provides evidence that PPAR‑β/δ ligands GW501516 and GW0742 do not promote growth, Akt activation or COX‑2/VEGF expression in human colon and liver cancer cell lines, and similar findings were confirmed in mouse tissues. These results challenge earlier reports suggesting these ligands might drive tumour development and highlight the need for further independent studies to resolve contradictory data.
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I remember someone citing that paper on Reddit once, but the one the concerned me was the study about the very rapid progression of pancreatic lesions to cancer. This is much more recent than the old rodent studies. 2022:
Rapid acceleration of *KRAS-*mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ
https://www.nature.com/articles/s41467-022-30392-7
GPT
A synthetic PPARδ agonist (GW501516) strongly accelerates disease
Administration of GW501516 (a potent PPARδ ligand) to KRAS/PPARδ-overexpressing mice led to rapid acinar cell loss, pancreatitis, fibrosis, and aggressive neoplastic lesions, with mice dying within ~30 days.
Short-term GW treatment (3–9 days) was sufficient to induce early PanIN changes and even PDAC in these mice.
Importantly, mice lacking PPARδ expression in the epithelium (Ppard knockout) did not respond to GW treatment with accelerated tumorigenesis
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Yea it is concerning. I’d be interested to see studies in these same mice comparing cardarine to cardarine + rapamycin and cardarine + omipalisib and other mTOR inhibtor/anti-cancer drugs.
I’ve got a lot of really interesting stuff I’m about to post here on other exercise mimetic compounds in a moment.
Here are more “exercise mimetics” that I found that are worth looking into.
AICAR study summary.pdf (36.6 KB)
BAIBA study summary.pdf (54.4 KB)
Myo-inositol ITPP studies summary.pdf (59.5 KB)
O304 study summary.pdf (41.2 KB)
Summarize CNX-013-B2 studies.pdf (35.3 KB)
Summarize LaKe studies.pdf (51.6 KB)
Summarize R419 studies.pdf (41.8 KB)
SR9009 study summaries.pdf (49.8 KB)
Summarize SR9011 studies.pdf (34.5 KB)
ZLN005 study summary.pdf (59.1 KB)
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AICAR hasn’t been very popular because it’s perceived as borderline catabolic. I’ve seen positive reports about injected SR9009 and 9011 as alternatives to cardarine. I have not tried them, but all of the above are WADA banned so we know they are worthwhile.
I inject ITPP 2-3x a week and like it.
Cardarine is amazing, but I only used if a few days at a time a couple times before I saw the pancreatic cancer study, and now I won’t touch it.
Have you tried to source by of the others? I can look around.
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I’ve tried SR9009 5mg, feels ok. Only used sporadically.
Curious to try ITPP. SubQ or IM? Not orally bioavailable?
Never tried the others. Discovered recently.
Either works. You need 5-10x more orally. Only makes sense for certain types of training. I don’t think most people would get much benefit, but if you have long, intense training sessions, say you’re doing lots of intense super sets and giant sets that would otherwise gas you out, it’s very useful. Ordinary lifting (straight sets with decent rest periods) and moderate cardiovascular training, no point.
I think it would also be good for BJJ. I don’t do that anymore so I’m not sure, but it seems like a good fit
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Nor do I. Too many recurring injuries.
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Kimera has O30/ATX-304 in stock
As does everychem
I’m just looking for overall improvement of endurance to improve overall quality of life. Sort of like a nootropic/performance enhancer.
Have you tried it or are you considering trying it?
An interesting counterpoint.
Therapeutic potential of GW501516 and the role of Peroxisome proliferator-activated receptor β/δ and B-cell lymphoma 6 in inflammatory signaling in human pancreatic cancer cells
Asummary of “Therapeutic potential of GW501516 and the role of PPARβ/δ and B-cell lymphoma 6 in inflammatory signaling in human pancreatic cancer cells (PMC5614479)”:
- The study examined how GW501516 (a PPARβ/δ agonist) influences inflammation in human pancreatic ductal carcinoma cells, focusing on the interaction between PPARβ/δ and BCL6.
- PPARβ/δ overexpression suppressed both basal and TNFα-induced NF-κB activity in luciferase reporter assays.
- When activated by GW501516, PPARβ/δ further reduced TNFα-driven NF-κB activity. Knockdown of PPARβ/δ weakened this suppression.
- BCL6 worked synergistically with PPARβ/δ: reducing BCL6 levels increased TNFα-induced NF-κB activity, showing that BCL6 mediates part of the anti-inflammatory effect.
- GW501516 triggered dose-dependent upregulation of anti-inflammatory genes in the cancer cells.
- In a BCL6-dependent manner, GW501516 also suppressed certain pro-inflammatory genes such as MCP1 and lowered their promoter activity.
- Conditioned media from GW501516-treated pancreatic cancer cells reduced pro-inflammatory responses in THP-1 macrophages and decreased the invasiveness of pancreatic cancer cells in co-culture assays.
- The authors conclude that PPARβ/δ activation via GW501516, in cooperation with BCL6, may have therapeutic potential in pancreatic cancer by dampening tumor-promoting inflammatory pathways.
I think injectable ITPP from better through biology or kimera is a great thing to try. Safe, inexpensive. And you can always add MOTS-C or SLU on top.
I had not paid any attention to atx-304, but I’m interested now that you’ve made me aware of it, especially if it’s renal protective in some contexts.
I believe this one is talking about already developed cancer cell lines and inflammation, whereas the other one showed rapid initiation and progression of cancer in an actual animal model. Given that there are a handful of studies in animal models that showed cancer develop from nearly human equivalent performance doses, there is just no way I’m ever going near this substance again. It’s more useful for lipid management than anything else, but there are other ways to deal with that.
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This might be an appropriate place to mention that Chiglitazar is an alleged pan-PPAR agonist apporoved in China. Not likely to be of interest to the PED crowd, but I assume (?) there are ways to get drugs from Chinese pharmacies.
Also keep an eye on Lanifibranor, a pan agonist in late stage clinical trials. Probably not available cheaply.
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Ozempic was not the first GLP1 in use 
Exenatide approved by the FDA in 2005 for type 2 diabetes.
So we now have 20 years of data on GLP1’s in millions of people.
I agree even that is not long enough to know “for sure” but as you have noted, these GLP1’s are changing society and the food industry.
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I think GLP1s are at the leading edge of changing the economy as well. The real costs, including the externalities, of obesity, T2D, and related metabolic disorders could easily be equivalent to 20-30% of US healthcare costs. The smartest thing the federal government could do – from economic and humanitarian perspectives – is subsidize the family of drugs and stimulate universal access through various incentives.
Anyone want to bet on that happening?
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Won’t happen because GLP1 are expensive now.
It won’t happen because politicians are too often hostages of bankrupt ideologies and too seldom guided by economic good sense. Ultimately, margins are elastic to volume. We would have to see a few numbers to project details but it is likely that pharmaceuticals could realize greater EBITA if GLP-1 prices were lowered by ~75% and made available to the retired and all wage classes through various federal incentives. This would be a clear win/win/win (pharma, government, people and families). The government wins twice in reduced Medicare and Medicaid costs plus increased payroll tax revenue, FICA, and Medicare contributions.
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Grey market. But that doesn’t work for the average person. Politics currently sucks.
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I really want a good PPAR receptor agonist that can do what cardarine does minus the cancer risk. I know there is something huge here if it is done right.
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