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Anti Myostatin polyclonal anti-body

But, once you stop taking the PEG-anti-GDF-8 wouldn't the effects start reversing. Who wants or can afford to take this for the rest of thier life?
 
The effects wouldn't reverse that much if hyperplasia occurs. Even if you did loose some of the LBM you would still retain the new muscle cells which would allow you to reach the LBM you once achieved much much faster. If this compound could cause extreme hyperplasia it would be very beneficial and would allow more people to achieve the Flex Wheeler type of density, which is definately a result of much more muscle cells than the norm. So I think this would be the best compound to hit the bodybuilding drug market if it caused real hyperplasia, as this part would be permanent.
 
Well, the pharmaceuticals company "Wyeth" that was doing most of the testing on this product decided to cancel it's research of MYO-029.

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velikimajmun said:
Short of gene therapy, that would be extremely difficult if not impossible. You could maybe give the recombinant protein IV but that would likely have more off target effects than would a monoclonal given IV.
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Old post, but had to say this.

HDAC inhibitors upregulate follistatin. So there.
 
TheCrownedOne said:
Old post, but had to say this.

HDAC inhibitors upregulate follistatin. So there.
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Being functionally insane, I bought some of the myostatin polyclonal antibody a couple of years ago and used it i.v. Only after I bought it and used it did I carefully research what kind of doses were being used in the mouse experiments. It turned out that to be using it at an equivalent dose, I would need something like 80mg/day. The entire amount I bought (for several hundred dollars) was just a couple of micrograms, I think. Of course it didn't do anything.

The Wyeth drug "Myo-29," which I think now has a brand name, is in Phase III clinical trials, which means it is being used on humans (children) with Duchenne's Muscular Dystrophy. There are some vague anecdotal reports of results on some muscular dystrophy websites, but I don't think Wyeth has put out any official reports on its efficacy.

Recently I've been looking at HDAC inhibitors, on the theory that if you upregulate follistation robustly enough you would suppress myostatin. The supplement HMB is an HDAC -- has anyone experimented with massive doses of that? Also, the anti-seizure medication Depakene (valproic acid, aka sodium valproate) is an HDAC. Has anyone seen any research on using Depakene for muscle growth??
 
I have been reading this thread for some time and reading what i have been able to find on the net. I am surprised to find that there are already many companies selling this stuff, including human anti myostatin inhibitors, but still dont find anybody telling about their experience?

Teamlife was one of them, they had been selling this stuff for a long time, but their website is off the market now, for a reason i have yet to know.

If so many companies are manufacturing and selling this stuff, how come we dont hear much about people's experiences?
 
ersatz said:
Can anyone post any pics of this wunderkid? The article from New England Journal of Medicine seems to imply that it's possible to build muscle mass without the associated hypertrophy of the heart as this kid is twice the size but his heart appears to be normal sized.
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Screwtape said:
Why not just take androgens? They are effective at decreasing myostatin expression.
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Because an equivalent dose in a 100kg man of 300mg in the gastrocnemius/ plantaris complex actually increased myostatin while a 600mg dose yielded just a small reduction. It took a whopping 1.2g dose to give a significant reduction.

These unimpressive results though are compared to injections in the soleus. In the soleus the results were impressive with significant myostatin reductions across all dosing schemes.

So what is the difference between the fiber make up of the soleus and the gastrocnemius?

It may be that testosterone has more of a significant reduction in myostatin across the slower twitch fiber types?
 
datBtrue said:
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Because an equivalent dose in a 100kg man of 300mg in the gastrocnemius/ plantaris complex actually increased myostatin while a 600mg dose yielded just a small reduction. It took a whopping 1.2g dose to give a significant reduction.

These unimpressive results though are compared to injections in the soleus. In the soleus the results were impressive with significant myostatin reductions across all dosing schemes.

So what is the difference between the fiber make up of the soleus and the gastrocnemius?

It may be that testosterone has more of a significant reduction in myostatin across the slower twitch fiber types?
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ouch thats going to hurt a bit, though i guess we could squeeze test suspension through a 25g.
but those results are site specific? i mean as the test goes systemic surely the soleus would benefit as much from the gastrocnemius shot? or site specific effects only?
so this would add weight to the age old argument about whether site injections of AAS cause localized growth.
 
pumbertot said:
ouch thats going to hurt a bit, though i guess we could squeeze test suspension through a 25g.
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I squeeze grapeseed oil based compounds through a 25 gauge.

pumbertot said:
but those results are site specific? i mean as the test goes systemic surely the soleus would benefit as much from the gastrocnemius shot? or site specific effects only?
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I assume that they didn't care.

Inject in the soleus cut the bastard open but don't bother looking elsewhere.

Inject in the gastrocnemius cut the bastard open but don't bother looking elsewhere.

Report findings and start writing up the next grant-based study proposal...

pumbertot said:
so this would add weight to the age old argument about whether site injections of AAS cause localized growth.
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Not really. ...it is only relevant to the extent you think the anti-myostatin effect takes place locally ...then there is a matter of degree (meaning is it even enought to notice).
 
datBtrue said:
I squeeze grapeseed oil based compounds through a 25 gauge.



I assume that they didn't care.

Inject in the soleus cut the bastard open but don't bother looking elsewhere.

Inject in the gastrocnemius cut the bastard open but don't bother looking elsewhere.

Report findings and start writing up the next grant-based study proposal...



Not really. ...it is only relevant to the extent you think the anti-myostatin effect takes place locally ...then there is a matter of degree (meaning is it even enought to notice).
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ok bro. yeah ive squeezed plenty of AAS in oil(warmed in bowl of boiled water) through a 25 gauage too.
 
I saw this thread and kinda skipped to the end. I just wanted to point out that anti-bodies are used in a lab to measure the amount of a substance in blood. There are companies that sell a whole list of every anti-body you could think of. I have no idea what would happen if you injected them, Im guessing your immune system would attack them since they are a foreign substance??????
Im also guessing that these websites selling research chemicals are just selling it because it sounds good. Again, I dont know, this is out of my league. I do know that anti-bodies are used with very expensive machines to measure things like growth hormone and stuff.
 
BEEFY said:
I saw this thread and kinda skipped to the end. I just wanted to point out that anti-bodies are used in a lab to measure the amount of a substance in blood. There are companies that sell a whole list of every anti-body you could think of. I have no idea what would happen if you injected them, Im guessing your immune system would attack them since they are a foreign substance??????
Im also guessing that these websites selling research chemicals are just selling it because it sounds good. Again, I dont know, this is out of my league. I do know that anti-bodies are used with very expensive machines to measure things like growth hormone and stuff.
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LOL!!!
 
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