PDA

View Full Version : Another myostatin inhibitor explained.



Dr Pangloss
04-06-2009, 06:58 PM
This works by making the normally cell-surface receptor for myostatin into a truncated form that is "soluble' and just floats around, not connected to the signal-transduction system. it binds myostatin and thereby inhibits myostatin from binding the cell-surface receptor and inhibiting muscle formation.

here is a schematic of roughly how it's made:

9388

Dr Pangloss
04-06-2009, 07:00 PM
1: Exp Neurol. (javascript:AL_get(this, 'jour', 'Exp Neurol.');) 2009 Mar 11. [Epub ahead of print]http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif (http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3048&itool=AbstractPlus-def&uid=19285073&db=pubmed&url=http://linkinghub.elsevier.com/retrieve/pii/S0014-4886(09)00063-6) Links (javascript:PopUpMenu2_Set(Menu19285073);)

A soluble activin type IIB receptor improves function in a mouse model of amyotrophic lateral sclerosis.

Morrison BM (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Morrison%20BM%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Lachey JL (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Lachey%20JL%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Warsing LC (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Warsing%20LC%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Ting BL (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Ting%20BL%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Pullen AE (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Pullen%20AE%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Underwood KW (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Underwood%20KW%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Kumar R (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Kumar%20R%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Sako D (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sako%20D%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Grinberg A (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Grinberg%20A%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Wong V (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Wong%20V%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Calantuoni E (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Calantuoni%20E%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Seehra JS (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Seehra%20JS%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus), Wagner KR (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Wagner%20KR%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus).
Department of Neurology, The Johns Hopkins School of Medicine, Baltimore, MD, USA.
Amyotrophic lateral sclerosis (ALS) is a neurologic disease characterized by progressive weakness that results in death within a few years of onset by respiratory failure. Myostatin is a member of the TGF-beta superfamily that is predominantly expressed in muscle and acts as a negative regulator of muscle growth. Attenuating myostatin has previously been shown to produce increased muscle mass and strength in normal and disease animal models. In this study, a mouse model of ALS (SOD1(G93A) transgenic mice) was treated with a soluble activin receptor, type IIB (ActRIIB.mFc) which is a putative endogenous signaling receptor for myostatin in addition to other ligands of the TGF-beta superfamily. ActRIIB.mFc treatment produces a delay in the onset of weakness, an increase in body weight and grip strength, and an enlargement of muscle size whether initiated pre-symptomatically or after symptom onset. Treatment with ActRIIB.mFc did not increase survival or neuromuscular junction innervation in SOD1(G93A) transgenic mice. Pharmacologic treatment with ActRIIB.mFc was superior in all measurements to genetic deletion of myostatin in SOD1(G93A) transgenic mice. The improved function of SOD1(G93A) transgenic mice following treatment with ActRIIB.mFc is encouraging for the development of TGF-beta pathway inhibitors to increase muscle strength in patients with ALS.

Strikerrjones
04-06-2009, 09:53 PM
Does myostatin do anything beneficial?

Dr Pangloss
04-07-2009, 06:48 AM
Does myostatin do anything beneficial?


It keeps people from retaining too much muscle.:D

SilverBAK
04-08-2009, 03:39 PM
It would be interesting if we could list all the currently available and still being researched myostatin inhibitors so that we could educate ourselves on each one and how they are different

SilverBAK
04-08-2009, 06:45 PM
http://jap.physiology.org/cgi/content/full/102/6/2142

"The present study is one of the first to explore haplotype structure of candidate genes and their associations with skeletal muscle phenotypes and shows for the first time that the ACVR2B and follistatin loci may contribute to interindividual variation in muscle mass and strength. The results show that follistatin haplotype 3 is associated with lower skeletal muscle mass in men and that ACVR2B Hap Group 1 is associated with lower skeletal muscle strength in women. Although these associations cannot be verified as causal from the present data, the use of haplotype structure in the present study accounts for a greater fraction of genetic variation than single-polymorphism studies. The results of the present study can be used to generate specific hypotheses regarding the genetic influence of the target genes on muscle phenotypes, and subsequent studies can be aimed at identifying the causal variant(s) associated with each haplotype as well as its mechanism of action (31 (http://jap.physiology.org/cgi/content/full/102/6/2142#R31)). The strong role of myostatin in both muscle development and the maintenance of muscle mass in adults (22 (http://jap.physiology.org/cgi/content/full/102/6/2142#R22)) provides a rationale to address whether genetic variation in members of its pathway (e.g., ACVR2B and follistatin) influence muscle phenotypes. The molecular basis for the haplotype associations observed for the ACVR2B and follistatin genes with skeletal muscle phenotypes is uncertain and cannot be addressed by the present study; however, we speculate that these associations may be the result of altered ACVR2B (myostatin receptor) activity, either directly through genetic influence on ACVR2B itself or indirectly through the influence of follistatin. Follistatin has been shown to have a strong affinity for myostatin and can completely prevent myostatin receptor activation and downstream phosphorylation of Smad3 (1 (http://jap.physiology.org/cgi/content/full/102/6/2142#R1)). Phosphorylation of Smad3, a key step in the myostatin cascade in negatively regulating skeletal muscle, induces binding of Smad3 to MyoD and represses the activity of the MyoD family of transcription factors, resulting in inhibition of myoblast differentiation (16 (http://jap.physiology.org/cgi/content/full/102/6/2142#R16), 19 (http://jap.physiology.org/cgi/content/full/102/6/2142#R19)). On the basis of these relationships, it can be hypothesized that a causal mutation, yet to be identified within the target genes, leads to either increased activity of myostatin (via lower follistatin inhibition) or greater ACVR2B activation, which would result in greater phosphorylation of Smad3. Such influences could be envisioned to affect either total muscle mass or fiber-type composition, the latter of which would have relevance to muscle strength or muscle quality. The soleus muscle of myostatin null mice displays a larger proportion of fast-twitch type II fibers and a reduced proportion of slow-twitch type I fibers compared with wild-type animals (9 (http://jap.physiology.org/cgi/content/full/102/6/2142#R9)). Thus higher receptor activation (e.g., due to genetic variation in follistatin haplotype 3, or ACVR2B Hap Group 1) would be envisioned to result in lower muscle mass and/or lower type II fiber proportions. Obviously, further studies will be required to test these hypotheses, but the present results do provide support for the generation of such hypotheses."

I wonder if any guys are experimenting with exogenous follistatin administration?

Dr Pangloss
04-08-2009, 07:22 PM
Follistatin and follistatin related protein bind to and inhibit myostatin, but there is no direct evidence that follistatin or FRP work to enhance muscle mass. Follistatin and FRP also bind activin and prehaps other members of the tgf-beta superfamily (activin and myostatin belong to this large family). follistatin knockout animals don't get big muscles...

myostatin proprotein, an immature form of myostatin, apparently enhances muscle mass in animal models.

myo-29, a monoclonal antibody to mysotatin, works in animal models and has a more modest effect in human trials.

Fragments of ActivinIIB receptor that are free floating and soluble (ie, the above) also work.

SilverBAK
04-11-2009, 12:01 AM
follistatin and follistatin related protein bind to and inhibit myostatin, but there is no direct evidence that follistatin or frp work to enhance muscle mass. Follistatin and frp also bind activin and prehaps other members of the tgf-beta superfamily (activin and myostatin belong to this large family). Follistatin knockout animals don't get big muscles...

myostatin proprotein, an immature form of myostatin, apparently enhances muscle mass in animal models.

myo-29, a monoclonal antibody to mysotatin, works in animal models and has a more modest effect in human trials.

fragments of activiniib receptor that are free floating and soluble (ie, the above) also work.

acvr2b?

Dr Pangloss
04-11-2009, 09:17 AM
acvr2b?

that's activin receptor BII. IT's actually fragments of it, which i have included above. using the whole thing doesn't work. It's a membrane protein.

Luka Treska
04-12-2009, 12:43 AM
That's pretty cool, but I'm guessing this would act in a competitive manner with the body's own receptors? If so, then would one be able to get the same result with every injection? And also does it work locally or systemically (I'm guessing the latter)?

Dr Pangloss
04-12-2009, 07:57 AM
That's pretty cool, but I'm guessing this would act in a competitive manner with the body's own receptors? If so, then would one be able to get the same result with every injection? And also does it work locally or systemically (I'm guessing the latter)?


In the paper its systemic injection. Since it antagonizes by simply binding myostatin it should be dose-dependent, so you should be able to get similar results with repeated administratin.

This is the kind of thing that could be made in a lab easily, but i would not expect anyone to jump in and make it available underground until clinicals have been (at least stage II) concluded successfully.

Luka Treska
04-12-2009, 09:11 AM
Thank you for the clerification. In your honest opinion (I don't know much about myostatin inhibitors) could this compound be comparable to AAS (or the usual pro drug protocols today) as far as muscle gains go...could it be even better?

I know this PLUS all the goods already available will be much better, but a lot of people say once myostatin inhibitors are in production, AAS will become a thing of the past (I doubt it, but as I said, I don't know much about myostatin inhibitors).

Dr Pangloss
04-12-2009, 07:29 PM
Thank you for the clerification. In your honest opinion (I don't know much about myostatin inhibitors) could this compound be comparable to AAS (or the usual pro drug protocols today) as far as muscle gains go...could it be even better?

I know this PLUS all the goods already available will be much better, but a lot of people say once myostatin inhibitors are in production, AAS will become a thing of the past (I doubt it, but as I said, I don't know much about myostatin inhibitors).


Judging by the results of total mysostatin inhibition (ie, the myo knockout dog and cow), strong myostatin inhibitors will be better than anything so far. Dogs and Cows have been admininistered steroids and growth hormone for various reasons for years but nothing ever looked like the myo knockout dogs or bulls.

If the other stuff is additive and not occlusive (you know, they work independently so you get gains from both), myostatin inhibitors will not render the other drugs obsolete.

Luka Treska
04-12-2009, 08:37 PM
Judging by the results of total mysostatin inhibition (ie, the myo knockout dog and cow), strong myostatin inhibitors will be better than anything so far. Dogs and Cows have been admininistered steroids and growth hormone for various reasons for years but nothing ever looked like the myo knockout dogs or bulls.

If the other stuff is additive and not occlusive (you know, they work independently so you get gains from both), myostatin inhibitors will not render the other drugs obsolete.

That's a good point, I never saw it that way. Geez if the human results look anything like the dog and cows plus all the gear bodybuilders already take, it will be something I can't even imagine at this point.

Yolo
04-17-2009, 02:08 PM
Myostating inhibition is, indeed, a fascinating prospect. I am curious about the side-effects myostatin inhibition might have on the heart though...:confused:

Strikerrjones
04-17-2009, 07:43 PM
Myostating inhibition is, indeed, a fascinating prospect. I am curious about the side-effects myostatin inhibition might have on the heart though...:confused:

Yeah, I guess heart enlargement could be a problem. From the studies, it seems like cancer growth could be another.

Dr Pangloss
04-17-2009, 08:03 PM
do the knockout animals exhibit heart problems and cancer? No. Question answered.

Strikerrjones
04-17-2009, 08:41 PM
do the knockout animals exhibit heart problems and cancer? No. Question answered.

Yeah, good point. It just seems so weird that something would evolve that does nothing but make animals weaker. How would a weaker animal survive over a stronger animal? It has to do something beneficial.

Dr Pangloss
04-17-2009, 08:47 PM
Yeah, good point. It just seems so weird that something would evolve that does nothing but make animals weaker. How would a weaker animal survive over a stronger animal? It has to do something beneficial.

that is a fantastic question. bodies that are better adapted to the last 50,000 years of strife are selected for. You have to conclude that there is, in most cases, a limit to the value of muscle and little limit to the value of fat under the prevailing conditions of the last ten to hundreds of thousands of years.

Yolo
04-18-2009, 02:37 PM
do the knockout animals exhibit heart problems and cancer? No. Question answered.

Indeed they do not...I guess my biggest issue with this (and indeed with every other medical breakthrough) is a constant doubt in the back of my mind "what if they got this wrong?" meaning what if, 10 years for now, some reasearch shows up stating that myostatin is actually essential for <insert vital function>. I am being a bit paranoid here though..

MRT
04-18-2009, 02:47 PM
It keeps people from retaining too much muscle.:D

God's cruel joke!

Northman
04-20-2009, 07:23 PM
Myostating inhibition is, indeed, a fascinating prospect. I am curious about the side-effects myostatin inhibition might have on the heart though...:confused:

People die early.

Dr Pangloss
04-20-2009, 08:01 PM
People die early.


post a paper to support your assertion. otherwise, i take it as wrong and meaningless.:)

snu183
04-22-2009, 06:20 PM
do the knockout animals exhibit heart problems and cancer? No. Question answered.

thats animal studies yes? i thought with individuals who show the genetic mutation where their body isnt producing any myostatin all had heart problems till this recent case study of the little boy.

-d

Dr Pangloss
04-22-2009, 06:49 PM
thats animal studies yes? i thought with individuals who show the genetic mutation where their body isnt producing any myostatin all had heart problems till this recent case study of the little boy.

-d


i'm not aware of that. if you could post support, that would be great.

Almaz
05-04-2009, 02:54 PM
God i really want to be the first human they try it on..even if it would not and i would get a 3rd eye or something ..

Dr Pangloss
05-04-2009, 04:50 PM
thats animal studies yes? i thought with individuals who show the genetic mutation where their body isnt producing any myostatin all had heart problems till this recent case study of the little boy.

-d


i have been unable to find any support for your assertion in pubmed.

fury-
05-22-2009, 09:18 PM
Yeah, good point. It just seems so weird that something would evolve that does nothing but make animals weaker. How would a weaker animal survive over a stronger animal? It has to do something beneficial.
I wouldnt say its there to make u 'weaker', just to inhibit u from becoming a beast... honestly it is energy taxing to carry around a ton of muscle, you will die quicker without food to try and support a ton of mass... and about the heart thing, i would hope it wouldnt show up but these animals were born with the mutation... if we just start injecting stuff idk but sides could occur

Dr Pangloss
05-22-2009, 09:23 PM
I wouldnt say its there to make u 'weaker', just to inhibit u from becoming a beast... honestly it is energy taxing to carry around a ton of muscle, you will die quicker without food to try and support a ton of mass... and about the heart thing, i would hope it wouldnt show up but these animals were born with the mutation... if we just start injecting stuff idk but sides could occur

the above are certainly my previously tacit arguments for why muscle is not adaptive....

fury-
05-30-2009, 03:50 PM
I thought i would add to this thread because i just listened to superhuman radio and 51:00 mins in ep.309 he brings up a study that he says vindicates his thoughts that myostatin inhibition alone would not provide muscle gains, but there must also be an up regulation in mgf and igf

Monitor of the myostatin autocrine action during differentiation of embryonic chicken myoblasts into myotubes: effect of IGF-I.

Kurokawa M (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Kurokawa%20M%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Sato F (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Sato%20F%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Aramaki S (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Aramaki%20S%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Soh T (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Soh%20T%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Yamauchi N (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Yamauchi%20N%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract), Hattori MA (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term=%22Hattori%20MA%22%5BAuthor%5D&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstract).

Laboratory of Reproductive Physiology and Biotechnology, Department of Animal and Marine Bioresource Sciences, Graduate School of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan.

Myogenesis is regulated through the proliferation and differentiation of myoblasts expressing myostatin which functions as a negative regulator by generating Smad signals. Here, we monitored the autocrine action of myostatin in quiescent chicken myoblasts transfected with the Smad-mediated promoter reporter vector to evaluate the modulation of several growth factors. During differentiation of myoblasts into myotubes, stretched and spherical types of myoblasts were observed at 12 h after induction, at which the promoter activity began to increase. Maximal promoter activity was observed at approximately 30 h. Multinucleated myotubes were markedly formed at 72 h, but the activity was very low. IGF-I, known as a positive regulator of myogenesis, increased the promoter activity, but the increase was rather small at its high concentration (100 ng/ml). IGF-I significantly increased the level of myostatin transcript in myoblasts and newly formed myotubes at 24 h, but not at 36 h. However, the cell fusion of myoblasts was not accelerated in the presence of IGF-I. Consequently, this study indicates that the autocrine action of myostatin is partially enhanced by IGF-I through increasing its expression.

acetrenbo100
07-09-2009, 03:08 PM
i have acvr2b from abcam,how i can know if my acvr2b is whole or fragments ?
is possible that if shoot dose acvr2b produce anaphylactic shock as omalizumab (Xolair) ?
and which is the whole exact name for fragments of activiniib receptor

Dr Pangloss
07-09-2009, 07:20 PM
i have acvr2b from abcam,how i can know if my acvr2b is whole or fragments ?
is possible that if shoot dose acvr2b produce anaphylactic shock as omalizumab (Xolair) ?
and which is the whole exact name for fragments of activiniib receptor


Woooooooooooaaaaaaa bro!! dont shoot any antibody that's not humanized and designed expressly for human use.

anaphylactic shock is a real possibilty here.

saiyajinali
07-10-2009, 01:53 PM
Woooooooooooaaaaaaa bro!! dont shoot any antibody that's not humanized and designed expressly for human use.

anaphylactic shock is a real possibilty here.

Hey Doc, what's the story with these myostain inhibitors that the research chem companies sell?

All I know that they are really expensive, & there really isnt any explanation to how they work or what they will do. Have you heard of anyone using them?

Dr Pangloss
07-10-2009, 02:44 PM
Hey Doc, what's the story with these myostain inhibitors that the research chem companies sell?

All I know that they are really expensive, & there really isnt any explanation to how they work or what they will do. Have you heard of anyone using them?

follistatin should be the only one available now. Follistatin binds myostatin and other tgf-beta family members and prevents their action on target receptors. it's supposed to work, but Im not at all excited about it, because it binds all kinds of tgf-beta family proteins, and they are all growth or mitogen related.

Dr Pangloss
07-10-2009, 02:50 PM
follistatin should be the only one available now. Follistatin binds myostatin and other tgf-beta family members and prevents their action on target receptors. it's supposed to work, but Im not at all excited about it, because it binds all kinds of tgf-beta family proteins, and they are all growth or mitogen related.


there are some others but they are in pre-clinical or clinical trials.

acetrenbo100
07-21-2009, 02:10 PM
i dont understand you,follistatin shot or swallow ?
because abcam and others comps sell follistatin antibody,you talk about it ?

better is shot not swallow,i guess,yeah is better shot,because abcam assures that reacting in human,i guess does not it create antibodies in human body

Dr Pangloss
07-21-2009, 07:09 PM
i dont understand you,follistatin shot or swallow ?
because abcam and others comps sell follistatin antibody,you talk about it ?

better is shot not swallow,i guess,yeah is better shot,because abcam assures that reacting in human,i guess does not it create antibodies in human body


It must be a human antibody. Be very careful.

acetrenbo100
07-24-2009, 01:29 PM
yeah my acvr2b is goat polyclonal to human, i have the paper test,i post soon,this is mine look http://www.abcam.com/Activin-Receptor-Type-IIB-antibody-ab10596.html

mts
07-24-2009, 04:27 PM
Follistatin and follistatin related protein bind to and inhibit myostatin, but there is no direct evidence that follistatin or FRP work to enhance muscle mass. Follistatin and FRP also bind activin and prehaps other members of the tgf-beta superfamily (activin and myostatin belong to this large family). follistatin knockout animals don't get big muscles...

I thought that follistatin showed to have an effect on muscle mass even without myostatin.

"Results of Se-Jin Lee’s new study, appearing on August 29 in the online, open-access journal PLoS ONE, show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal, mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice."

http://www.eurekalert.org/multimedia/pub/rel/4956_rel.jpg

Dr Pangloss
07-24-2009, 06:27 PM
yeah i made that post a long time ago based on one paper i read. You are right. follistatin has since proved to be effective for muscle. I corrected myself in this thread or another related thread.

my only problem with it now is that it binds to and inhibits a lot of other tgf-beta family proteins, which means it could also inhibit growth or mitogenesis of something else besides muscle.

mts
07-24-2009, 06:33 PM
makes sense, thanks Dr P

xtremist
07-25-2009, 06:53 AM
DrP i cant seem to find any studies whatsoever on human antiGDF8 peptide, have you seen or heard any studies relating to the peptide?

Tatyana
07-25-2009, 07:36 AM
yeah my acvr2b is goat polyclonal to human, i have the paper test,i post soon,this is mine look http://www.abcam.com/Activin-Receptor-Type-IIB-antibody-ab10596.html

There is a huge possibility you are going to form heterophile antibodies because you are injecting a foreign antigen (the goat antibodies).

This can even happen to people who are in close contact with animals, and it can precipitate a pathology, for example with pigeon fancier lung.

It may seem that nothing will come of it, however, if you get any weird lab results, especially for some of your hormones that the doctors can't explain, you may want to mention heterophile antibodies to them before they start to send you for a battery of invasive examinations.

To mimic the words of Dr. P, just be careful, while we are getting quite advanced with all sorts of biomedical techniques, there are aspects of the immune system, and the huge variability of the immune system that can give rise to completely unexpected results, for example clinical trials with antibodies giving rise to cytokine storms.

Dr Pangloss
07-25-2009, 11:46 AM
dude. it's a goat antibody. Dont fucking inject it. There is a good chance of anaphylactic shock from this kind of nonesense.


dont do it.


period.

Dr Pangloss
07-25-2009, 12:50 PM
Look. there is a low but real risk of an allergic response. However, even if you dont get an allergic reaction, your body will have still mounted an immune response to that foreign protein. What does that mean practically? Your body will find it, bind it, and chew it up, rendering it useless for your purposes. Repeated rejections will only make it better at eliminating it.

Dr Pangloss
07-25-2009, 01:05 PM
DrP i cant seem to find any studies whatsoever on human antiGDF8 peptide, have you seen or heard any studies relating to the peptide?

I'm not sure if you're talking about an antibody here, or the variable domain of an antibody, or just a peptide.

Where did you find out about this?

xtremist
07-27-2009, 03:41 AM
I'm not sure if you're talking about an antibody here, or the variable domain of an antibody, or just a peptide.

Where did you find out about this?

gro-pep actually have an anti-gdf8 peptide, not the antibody. I actually heard it through an aquaintance who researches wasting diseases. I cant elaborate much but this seems like the way to go regarding myostatin inhibition and muscle growth. The only problem is that there is absolutely no studies that i can find on it, nonetheless it has some interesting prospects. All i know is that so far there has been no adverse reactions from it.

acetrenbo100
11-07-2009, 02:19 PM
i put myself(acvr2b),and only water gain not muscle;
for me god not exist, i never listen anybody ok

acetrenbo100
11-07-2009, 02:43 PM
Abcam acvr2b(poly-goat),immunogen is human recombinant fragment,therefore,maybe is 50% human and 50% goat or 60-man 'nd 40-goat, but geneticists try to make it more "clean",understood pangloos and tatyana.

i go to try anti-gdf8,maybe "strike" muscles,looking good, nice xtremist

Dr Pangloss
11-07-2009, 03:39 PM
Please be careful. Abcam antibodies are not meant for human injection. Those are for research only as far as i've ever seen. i have used many, but only in experiments.

shooting a protein of a different species is dangerous business. Just because you havent had an allergic reaction yet does not mean you won't.

acetrenbo100
11-19-2009, 02:07 PM
homie, i used that ok,
final point ! ok
you try this ok