Inside the Mind of Deserusan

This has since sparked numerous studies and resulted in at present 28 patents approved by the USPTO for future application. Even more interesting is that Abbott Laboratories owns a patent as well (Myostatin gene promoter and inhibition of activation thereof: US Patent 6,284,882). However, I don’t think EAS (a subsidiary of Abbott) will be putting this out anytime soon. Any supplement at present which claims myostatin inhibition is a complete scam. Caveat emptor!

As far as I can tell there has been at least one phase I/II clinical trial complete on humans (http://clinicaltrials.gov/show/NCT00104078). The applications of this for muscle wasting diseases, ALS, sarcopenia, etc is limitless. While finding the exact outcome of this study has been fruitless. Harnessing this power, on the surface at least seems hard to tame.

From what I have read about myostatin inhibition could possibly have negative effects on smooth muscle tissue in theory and levels of adipose tissue. Some research seems to avoid this little caveat for good reason: who wants to f*ck with their heart negatively. Also, while a decrease in adiposity seems welcome by todays standards, I don’t believe having virtually no fat is healthy either. Furthermore, enlarged hearts are nothing to overlook.

Conversley, there was a study done a on young male who had a complete deacitivation of the myostatin gene. It has been observed that he does not have any cardiomyopathy as of yet but he is still to young to determine it won’t be a factor. Also, members of his family appear to have mutations of gene leaving it active but suppressed. They report some above average strength but keep in mind this is a very isolated sample pool. Here is a picture of his lower extremity at seven months.

Researchers have actually looked into genetic mutations which cause the myostatin gene to suppressed or completely shut down. Flex Wheeler was actually part of a study conducted at the University of Pittsburgh which actually showed he had a rare mutation of this gene (exon 2 position) along with a mutation in one of the genes responsible for IGF-1. Flex also had a genetic defect in his kidneys by some accounts or was it the furosemide which lead to their failure and subsequent transplant. Who knows? He was the man by all accounts.

Obviously, this does have applications in sports performance but I haven’t heard of any mainstream “gear” which utilizes this. I don’t know how hard it would be to develop something which limits myostatin expression by causing a competition for the activin receptor IIB but it could be possible I guess. It also might be possible to increase levels of follastatin or myostatin propeptide which have also shown to inhibit myostatin by binding to it before it dimerizes to form mature myostatin and binds to the activin receptor IIB. This would cause less expression which would halt gene transcription and the signal cascade. These are the claims of some of the patents and research out therr but no actual application used in humans have been reported to the public except for the aforementioned clinical trial

So who’s going to do it first? I guess we’ll see. You will be seeing this in future bodybuilding gear arsenals in the near future. The patents are out there, the technology is available, and it’s just a matter of time when their is a synergy between some eager chemist with right equipment to pull this off. Most likely it will make an appearance in professional sports before it hits the bodybuilding scene. This will make AAS and PH’s look like cotton candy.