Forum Statistics

Threads
27,576
Posts
541,654
Members
28,555
Latest Member
Kiddorism
What's New?

GW-501516 Info on why you want it

sax

sax

Senior Member
Jan 26, 2011
121
17
I'm not cracking on any suppliers\companies but this is why i have stayed away from research \peptides myself. too much unknown on both sides of it, what you're getting and what it really does .. ''research chems'' name says it all for me

I will crack on them a little bit for cherry picking older positive studies and ignoring well published negative newer ones. Either don't cite sources leaving people to do their own research, or cite both. Don't cherry pick facts.
 
U

Usealittle

Senior Member
Feb 15, 2012
196
14
The wikipedia article on this has been updated. GlaxoSmithKline stopped investigating this in 2006 when it was found to cause cancer.They found the drug rapidly causes cancers in a multitude of organs, including the liver, bladder, stomach, skin, thyroid, tongue, testes, ovaries and womb.



You do know you anyone can change info on wic.....
 
sax

sax

Senior Member
Jan 26, 2011
121
17
Here is the what was said in 2009 by the Society of Toxicology in the link I previously provided. They have no stake in the game. I can edit Wiki, I can't edit this.

895 RAT CARCINOGENICITY STUDY WITH GW501516, A PPAR DELTA AGONIST.
L. E. Geiger1, W. S. Dunsford2, D. J. Lewis2, C. Brennan3, K. C. Liu3 and S. J. Newsholme1. 1Safety Assessment, GlaxoSmithKline, King of Prussia, PA, 2Safety Assessment, GlaxoSmithKline, Ware, United Kingdom and 3Huntingdon Life Sciences, Huntingdon, United Kingdom.
GW501516, a non-genotoxic PPARδ agonist, was assessed for carcinogenic poten- tial by daily administration (oral gavage) to Han Wistar rats for a period of 104 weeks. Males were given 0, 5, 15 or 30 mg/kg/day for the first 6 weeks of the study. For the remainder of the study males were given 0, 5, 20 or 40 mg/kg/day. Females were given 0, 3, 10 or 20 mg/kg/day for the entire study. GW501516 produced test article-related neoplastic findings in multiple tissues at all doses. Increased mortal- ity was seen with females given GW501516 at all doses and uterine endometrial adenocarcinoma contributed to death in a high proportion of these animals. Neoplasms considered test-article related occurred in the liver (hepatocellular ade- noma at ≥ 10 mg/kg/day), urinary bladder (transitional cell carcinoma in males given 20 and 40 mg/kg/day), thyroid (follicular cell adenoma at ≥ 3 mg/kg/day and carcinoma in males at ≥ 20 mg/kg/day), tongue (squamous cell papilloma in males at 5 mg/kg/day and 40 mg/kg/day), stomach (squamous cell papilloma in males at ≥ 5 mg/kg/day and a female at 20 mg/kg/day, and carcinoma in a male at 40 mg/kg/day and a female at 3 mg/kg/day), skin (inverted squamous cell papilloma in males at ≥ 5 mg/kg/day and females at 3 or 20 mg/kg/day), Harderian glands (ade- noma in males at ≥ 5 mg/kg/day and adenocarcinoma in a male at 40 mg/kg/day), testes (interstitial cell adenoma at 40 mg/kg/day), ovary (Sertoli cell adenoma at ≥ 10 mg/kg/day) and uterus (polyp and endometrial adenocarcinoma at ≥ 3 mg/kg/day). Some of the tumor types observed in this study have not been reported with either PPARα or PPARγ agonists and may reflect tumor promotion mediated through PPARδ agonism.
 
Go Away

Go Away

MuscleHead
Dec 28, 2011
4,935
1,057
wouldn't it suck to be the people in this study?! damn....
 
marx

marx

MuscleHead
Sep 29, 2010
4,671
626
Pretty eye opening, being on the leading edge of research can have it's pitfalls... The stuff looks to be poison, even if the athletic protocol is say 20mg a day for someone weighing 100 kilos it seems damn risky...

Thanks for the studies, brother sax, much appreciation.
 
B

Bilter

VIP Member
Jun 7, 2011
241
317
Reason for edit: study already posted on page 2
 
Last edited:
Hanzo

Hanzo

Member
May 26, 2012
36
8
The wikipedia article on this has been updated. GlaxoSmithKline stopped investigating this in 2006 when it was found to cause cancer.They found the drug rapidly causes cancers in a multitude of organs, including the liver, bladder, stomach, skin, thyroid, tongue, testes, ovaries and womb.

The clinical research was flawed, FD 50 and less. GW HAS to be ran with AICAR or you might as well not run it. I've ran 2x with great results. These were evolved to be ran together from the very beginning. The doses given to rodents were as much as 1850gm's for crying out loud!!

And yes, there is clinical research performed with human subjects. And yes, it did work with minimal sides. It's now being refered to as "cardio in a bottle".

http://atvb.ahajournals.org/content/27/2/359.short
Same study just condensed for some.
http://atvb.ahajournals.org/content/32/9/2289.full

Studies on animal subjects:

http://www.ncbi.nlm.nih.gov/pubmed/21245211

http://www.ncbi.nlm.nih.gov/pubmed/22908954

http://www.ncbi.nlm.nih.gov/pubmed/18674809

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880836/table/T2/

Here's a study with both rodent and human subjects. Seems we may have a resistance to the carcinogenesis displayed in rodents."As with any drug anticipated for chronic use in the treatment of metabolic disease, safety issues about PPARδ-targeted compounds have been raised. Particular attention has focused on a potential connection to carcinogenesis, since PPARδ was reported as a downstream target of the oncogenic Wnt/adenomatous polyposis coli (APC)/β-catenin pathway (78). A recent study disputes this connection, and further studies to decipher a role for PPARδ in cancer have been inconsistent (21, 7982). Experiments using PPARδ-null mice demonstrated that PPARδ is genetically dispensable for colon polyp formation in both the Apc[SUP]min[/SUP] genetic mutant and chemically induced colon cancer mouse models, and colon polyp formation was exacerbated in the genetic absence of PPARδ (21, 79, 80). Alternatively, xenografts of human colon cancer cells showed decreased tumorigenesis in cells somatically deleted of PPARδ, and treatment of Apc[SUP]min[/SUP] mice with high doses of the PPARδ ligand GW501516 yielded increases in the number and size of intestinal polyps (81, 82). Whether these ligand effects are truly dependent on PPARδ has not been established, and study using a PPARδ-null background is warranted. It is notable that synthetic PPARγ agonists, which have been extensively used in human subjects, enhance colon polyp formation in the Apc[SUP]min[/SUP] model yet have not been demonstrated to cause cancer in humans (83, 84). Similarly, PPARα activators cause hepatocarcinomas in rodents but fail to have such deleterious effects in humans. These findings cast doubt on the predictive power of mouse models to determine the human carcinogenicity of PPAR-targeted drugs". The 'evidence' that GW might play a role in lung cancer proliferation is being reversed now. In the study from pubmed says that even if GW puts off a cancer causing agent it's so small the body has it's own way of combatting and reducing any perceived threat.
 
Last edited:
jhotsauce7

jhotsauce7

TID Board Of Directors
Jan 18, 2011
2,805
684
There's quite a bit of evidence purporting that PPAR agonists reduce cell proliferation in many different cell lines. In the essence GW may discourage carcinogenisis and regulate cellular production for many kinds of tissue.

I think one study said that it did however cause cox-2 gene expression which can be a precursor to cancers, and thus it was suggested to take the drug with a cox-2 inhibitor.

Other points of importance are the length of administration of the PPAR agonist in not just dose to mass relation but also in relation to lifespan, whereas the most commonly cited mouse and rat studies were for a period of 2 years (average rat or mouse lifespan is probably 3 years, so administration of this for 66% lifespan) and also it is important to point out that humans have a far greater cell differentiation and much more diverse cell lines than rodent subjects so this has also cast doubt that humans would see the same carcinogenic and cellular proliferating outcomes.

Lastly I read in the most commonly sited study that GW501516 was administered in the study subsequent to administering a known carcinogen known as DBMA (7,12-Dimethylbenz[a]anthracene), which only when combined outside the control group with Carderide resulted in carcinogenisis in numerous tissue types for rodents.


Here is some interesting reading material...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171861/
 
Who is viewing this thread?

There are currently 0 members watching this topic

Top