Myostatin Question for PA, anybody else with knowledge

Page 1 of 6 123 ... Last
  1. Myostatin Question for PA, anybody else with knowledge


    A friend sent me a link to a radio show- super human radio and they were interviewing the CEO of Celldyne, a pharmaceutical company about a new product that they created called folstaxan. In human subjects after one dose, they are reporting a 37% reduction in serum myostatin after a single dose. PA and others, what do you think about this? Complete scam or could they possibly be onto something?

    My main question would be, ok it lowered myostatin by 37%, but was there any increase in muscle tissue?


    Here's the site for the product: EDIT: Please read rules about linking.

    Here was the interview if anybody wants to listen to it:

    Super Human Radio Show Archive


  2. Bump, anybody got any input on this product?
    •   
       


  3. Quote Originally Posted by from the Folstaxan site
    Folstaxan -- a non-lipid fecundated standardized avian ovum protein supplement
    Well this says that it's an egg-based protein supplement of some sort. Seems a bit sketchy but what the hell do I know? Could be the next big thing...or not.

  4. ive been researching quite a bit on myostatin the only drug in the works for inhibiting myostatin is Stamulumab. this stuff looks like another piece of **** supplement. in the meantime until weyth brings the drug to the market i believe that activin, particularly the form that binds to the ACVR2B receptor will offer the myostatin inhibiting benifits we all look for as its actually very similar to the Stamulumab, but the Stamulumab is an antibody.

  5. Quote Originally Posted by BMW View Post
    ive been researching quite a bit on myostatin the only drug in the works for inhibiting myostatin is Stamulumab. this stuff looks like another piece of **** supplement. in the meantime until weyth brings the drug to the market i believe that activin, particularly the form that binds to the ACVR2B receptor will offer the myostatin inhibiting benifits we all look for as its actually very similar to the Stamulumab, but the Stamulumab is an antibody.
    The main protein in Folstaxan is follistatin. Follistatin binds to activin and neutralizes it and thus an elevation in follistatin equals a reduction in myostatin. Its quite simple. Dr. Carlon Colker is behind the development of Folstaxan.

    The egg yolks that the follistatin is rendered from are from fertilized eggs which have a high degree of follistatin.

    The science behind follistatin's ability to reduce myostatin was published by Se-Jin Lee's group at john Hopkins University - the same group that discovered myostatin.
    •   
       


  6. Run it and do a log. We'd all be grateful. At least, I'd be.

  7. Quote Originally Posted by Bionic View Post
    Run it and do a log. We'd all be grateful. At least, I'd be.
    I'm thinking about it. I'm a pushover when it comes to guineapigging new supplements/drugs with a lot of hype, lol.

  8. Quote Originally Posted by Speedbacker View Post
    A friend sent me a link to a radio show- super human radio and they were interviewing the CEO of Celldyne, a pharmaceutical company about a new product that they created called folstaxan. In human subjects after one dose, they are reporting a 37% reduction in serum myostatin after a single dose. PA and others, what do you think about this? Complete scam or could they possibly be onto something?

    My main question would be, ok it lowered myostatin by 37%, but was there any increase in muscle tissue?


    Here's the site for the product: EDIT: Please read rules about linking.

    Here was the interview if anybody wants to listen to it:

    Super Human Radio Show Archive

    i looked up this celldyne company and this product on the internet. i truly wished that there was something here for real

    i was dissapointed. no big surprise. this has all the appearances of a company trying to imitate a pharmaceutical company to pass on a supplement. no discussion of science, no patent applications, no published research, and a site which sorely lacks any semblance to a real pharm company.

  9. Quote Originally Posted by BMW View Post
    ive been researching quite a bit on myostatin the only drug in the works for inhibiting myostatin is Stamulumab. this stuff looks like another piece of **** supplement. in the meantime until weyth brings the drug to the market i believe that activin, particularly the form that binds to the ACVR2B receptor will offer the myostatin inhibiting benifits we all look for as its actually very similar to the Stamulumab, but the Stamulumab is an antibody.
    there is also a myostatin peptide product which is a blocker and is in development

  10. Quote Originally Posted by triceptor View Post
    The main protein in Folstaxan is follistatin. Follistatin binds to activin and neutralizes it and thus an elevation in follistatin equals a reduction in myostatin. Its quite simple. Dr. Carlon Colker is behind the development of Folstaxan.

    The egg yolks that the follistatin is rendered from are from fertilized eggs which have a high degree of follistatin.

    The science behind follistatin's ability to reduce myostatin was published by Se-Jin Lee's group at john Hopkins University - the same group that discovered myostatin.

    follistatin is indeed a myostatin blocker

    lets see some of this research. lets see how this stuff gets absorbed considering it is a long polypeptide. lets see how much is in the product

    lets see a patent application, they say there is one, where is it?

  11. Quote Originally Posted by Bionic View Post
    Run it and do a log. We'd all be grateful. At least, I'd be.
    F- that

    nobody buy it and nobody do a log

    its about time people said NO to this stuff

    say no until they show you some verifiable research. if they do this, then give it a shot

    companies pander to your curiousity. they know that everyone cannot resist to run their own trial. can't resist to see whether it works or not. althought your rational mind may say it has to be BS, your compulsive side will always win over

    until people learn to resist this urge, companies will keep pumping crap to you guys cuz they will make money

  12. I want to be fair so i emailed the company to give them the opportunity to substantiate their product. if they can then they will get a nice plug in MD.



    Hello,

    I write for muscular development magazine. I am doing some stuff on myostatin inhibitors and would like to see what research you have on your new product folstaxan

    Any published research, patent applications, or any other verification of the products claims would be very appreciated. I hope to give a fair and unbiased assessment

    thank you

    Patrick Arnold

  13. Quote Originally Posted by Patrick Arnold View Post
    F- that

    nobody buy it and nobody do a log

    its about time people said NO to this stuff

    say no until they show you some verifiable research. if they do this, then give it a shot

    companies pander to your curiousity. they know that everyone cannot resist to run their own trial. can't resist to see whether it works or not. althought your rational mind may say it has to be BS, your compulsive side will always win over

    until people learn to resist this urge, companies will keep pumping crap to you guys cuz they will make money
    Lol, you're right. Good points. Guess we'll wait and see some research first.

  14. Quote Originally Posted by Patrick Arnold View Post
    I want to be fair so i emailed the company to give them the opportunity to substantiate their product. if they can then they will get a nice plug in MD.



    Hello,

    I write for muscular development magazine. I am doing some stuff on myostatin inhibitors and would like to see what research you have on your new product folstaxan

    Any published research, patent applications, or any other verification of the products claims would be very appreciated. I hope to give a fair and unbiased assessment

    thank you

    Patrick Arnold
    Let us know what you find, I am curious. I emailed the celldyne ceo a few days ago and asked him some basic questions, here's what he said:

    1. How come there is no scientific published study on this compound?

    There are two publications, from the October 2006 Journal of the American
    College of Nutrition. See abstracts 65 and 66. Nine more publications are
    underway. See abstract 66 below.

    >
    >You've said that you've tested this in healthy young men, i'm
    >wondering where is the study and why you didn't tell us more
    >details about the results?

    See the above publications.
    >
    > 2. From the test subjects, did any muscle tissue hypertrophy result
    >from this 37% reduction in serum myostatin?

    Tissue hypertrophy was not a variable or endpoint in the study.
    >
    >3. Also, why is it that no patent entry can be found? Wouldn't you
    >want to protect this product with a patent?

    Several patents have been filed. It takes two to three years for a patent
    to become official and publicly registered.
    >
    >4. Many people have also been wondering about the unprofessional web
    >presence that looks like it was whipped up in an hour?

    The website was literally whipped up over night because we knew that the
    Super Human Radio interview would drive many inquiries . We will be
    updating the site regularly. If you have any feedback or suggestions about
    that site, please send them.


    Abstract:

    ABSORPTION PROFILE AND HORMONAL INFLUENCES OF Fertilized EGG YOLK INGESTION
    IN THE HUMAN
    Colker. C. Peak Wellness, Inc. Greenwich, CT

    Fertile egg yolks contain significant concentrations of follistatin. In an
    effort to identify whether this orally ingested source of naturally
    occurring follistatin is actually absorbed and pharmacokinetically active in
    the human model, this study was undertaken. A male subject was chosen
    because the nornma1basline male physiology does not regularly contain any
    measurable concentration of follistatin. Follistatin-rich fertile egg yolk
    powder properly processed to preserve active follistatin (FolstaxanTM) was
    obtained (Celldyne Biopharma, San Antonio, TX). After initial blood draw and
    subsequential oral Folstaxan dosing, serum follistatin levels were
    qualitatively and quantitatively) measured as an indicator of absorption. In
    addition, since we know follistatin is a negative modulator of myostatin,
    serum myostatin levels were qualitatively and quantitatively measured as an
    indication of hormonal influence and thus true pharmacokinetic activity.
    Testing utilized purchased follistatin and myostatin standardized for
    verification. Confirmations were run by ELISA and quantitations by Liquid
    Chromatography Tandem Mass Spectrometer with third degree fragmentation
    (Expertox, Deer Park, TX). Results showed as predicted, a zero level of
    follistatin at baseline with a myostatin level of 46 pg/ml, 12 hours after
    FolstaxanTM dosing. Serum follistatin measured 57.1 pg/ml with a decline of
    myostatin to 34 pg/m1, 24 hours after the initial dosing, follistatin levels
    began to predictably drop from the time of initial dosing to 11.4 pg/ml. Yet
    myostatin continued to decline slightly with a 24-hour level of 31 pg/ml.
    These results clearly indicate that a fertile egg yolk powder properly
    processed to preserve active follistatin, when orally ingested, results in
    detectable serum follistatin. Furthermore, this resultant follistatin
    presence has significant pharmacokinetic activity is shown by the hormonal
    down regulation of serum follistatin.

  15. The wierd thing is that when I looked at the October 2006 Journal of the American College of Nutrition, I didn't see a single thing about this. I looked in abstracts 65 and 66 and throught the whole thing, but didn't find a thing. Neither did friends of mine, in case I was missing something. Here's a link to the October issue, let me know if I was just being stupid and missed it, I don't think I was though: Journal of the American College of Nutrition -- Table of Contents (25 [5])

  16. Here's another response from the celldyne ceo:

    I asked Mr. Green- I know you said hypertrophy was not an endpoint or a variable in the study, but are there any early indications that you noticed
    that show this will increase hypertrophy? Or is it all theory
    going on the fact that a reduction in myostatin means an increase
    in muscle hypertrophy? Thank you for your time.


    He said: Thanks again for your interest. We don't consider the reduction of myostatin leading to muscle fiber proliferation to be theoretical at this time. When we designed the study, the endpoint of myostatin reduction more than 20% was the goal. The literature and studies are well supported that such a reduction will lead to muscle fiber and cell proliferation. This endpoint is more about muscle density and size increase.

    An analogy would be that X units of insulin R will lead to Y reduction in glucose. We are that confident in the results of myostatin reduction.

    On a technical point, we are talking about a proliferation of muscle fibers and cells. Technically, this could be termed hyperplasia vs. hypertrophy. Perhaps we need new terminology.

    We are undertaking mice pair studies so that we can biopsy the subjects in order to quantify the increase in muscle fibers. Lean body mass composition is an important, but secondary endpoint. The open label human study will look extensively at LBM increase.

    Unfortunately, we are limited in the information we can discuss about a study before is published. If we discuss results, it won't be published.

    I hope you can draw your own inference from that statement.


    What do you think?

  17. Quote Originally Posted by Speedbacker View Post
    The wierd thing is that when I looked at the October 2006 Journal of the American College of Nutrition, I didn't see a single thing about this. I looked in abstracts 65 and 66 and throught the whole thing, but didn't find a thing. Neither did friends of mine, in case I was missing something. Here's a link to the October issue, let me know if I was just being stupid and missed it, I don't think I was though: Journal of the American College of Nutrition -- Table of Contents (25 [5])

    the abstract looked viable. Without peer review there is no way to verify its aunthenticity. if someone can find this published somewhere that would be nice

    It is important to note that fertilized egg yolk supplements are not new to the supplement market. I dunno the level of follistatin in them however

  18. Quote Originally Posted by Speedbacker View Post
    Here's another response from the celldyne ceo:

    I asked Mr. Green- I know you said hypertrophy was not an endpoint or a variable in the study, but are there any early indications that you noticed
    that show this will increase hypertrophy? Or is it all theory
    going on the fact that a reduction in myostatin means an increase
    in muscle hypertrophy? Thank you for your time.


    He said: Thanks again for your interest. We don't consider the reduction of myostatin leading to muscle fiber proliferation to be theoretical at this time. When we designed the study, the endpoint of myostatin reduction more than 20% was the goal. The literature and studies are well supported that such a reduction will lead to muscle fiber and cell proliferation. This endpoint is more about muscle density and size increase.

    An analogy would be that X units of insulin R will lead to Y reduction in glucose. We are that confident in the results of myostatin reduction.

    On a technical point, we are talking about a proliferation of muscle fibers and cells. Technically, this could be termed hyperplasia vs. hypertrophy. Perhaps we need new terminology.

    We are undertaking mice pair studies so that we can biopsy the subjects in order to quantify the increase in muscle fibers. Lean body mass composition is an important, but secondary endpoint. The open label human study will look extensively at LBM increase.

    Unfortunately, we are limited in the information we can discuss about a study before is published. If we discuss results, it won't be published.

    I hope you can draw your own inference from that statement.


    What do you think?
    the last statement is understandable

  19. Quote Originally Posted by Speedbacker View Post
    The wierd thing is that when I looked at the October 2006 Journal of the American College of Nutrition, I didn't see a single thing about this. I looked in abstracts 65 and 66 and throught the whole thing, but didn't find a thing. Neither did friends of mine, in case I was missing something. Here's a link to the October issue, let me know if I was just being stupid and missed it, I don't think I was though: Journal of the American College of Nutrition -- Table of Contents (25 [5])
    this is the search engine for that journal

    Journal of the American College of Nutrition -- Search

    despite using author, volume, title key words, everything i could think of i saw nothing

  20. Quote Originally Posted by Patrick Arnold View Post
    the abstract looked viable. Without peer review there is no way to verify its aunthenticity. if someone can find this published somewhere that would be nice
    He said he would fax it to me. Hopefully I will get it tomorrow. Once I receive it, I will post it.

  21. Quote Originally Posted by Speedbacker View Post
    Let us know what you find, I am curious. I emailed the celldyne ceo a few days ago and asked him some basic questions, here's what he said:

    1. How come there is no scientific published study on this compound?

    There are two publications, from the October 2006 Journal of the American
    College of Nutrition. See abstracts 65 and 66. Nine more publications are
    underway. See abstract 66 below.

    >
    >You've said that you've tested this in healthy young men, i'm
    >wondering where is the study and why you didn't tell us more
    >details about the results?

    See the above publications.
    >
    > 2. From the test subjects, did any muscle tissue hypertrophy result
    >from this 37% reduction in serum myostatin?

    Tissue hypertrophy was not a variable or endpoint in the study.
    >
    >3. Also, why is it that no patent entry can be found? Wouldn't you
    >want to protect this product with a patent?

    Several patents have been filed. It takes two to three years for a patent
    to become official and publicly registered.
    >
    >4. Many people have also been wondering about the unprofessional web
    >presence that looks like it was whipped up in an hour?

    The website was literally whipped up over night because we knew that the
    Super Human Radio interview would drive many inquiries . We will be
    updating the site regularly. If you have any feedback or suggestions about
    that site, please send them.


    Abstract:

    ABSORPTION PROFILE AND HORMONAL INFLUENCES OF Fertilized EGG YOLK INGESTION
    IN THE HUMAN
    Colker. C. Peak Wellness, Inc. Greenwich, CT

    Fertile egg yolks contain significant concentrations of follistatin. In an
    effort to identify whether this orally ingested source of naturally
    occurring follistatin is actually absorbed and pharmacokinetically active in
    the human model, this study was undertaken. A male subject was chosen
    because the nornma1basline male physiology does not regularly contain any
    measurable concentration of follistatin. Follistatin-rich fertile egg yolk
    powder properly processed to preserve active follistatin (FolstaxanTM) was
    obtained (Celldyne Biopharma, San Antonio, TX). After initial blood draw and
    subsequential oral Folstaxan dosing, serum follistatin levels were
    qualitatively and quantitatively) measured as an indicator of absorption. In
    addition, since we know follistatin is a negative modulator of myostatin,
    serum myostatin levels were qualitatively and quantitatively measured as an
    indication of hormonal influence and thus true pharmacokinetic activity.
    Testing utilized purchased follistatin and myostatin standardized for
    verification. Confirmations were run by ELISA and quantitations by Liquid
    Chromatography Tandem Mass Spectrometer with third degree fragmentation
    (Expertox, Deer Park, TX). Results showed as predicted, a zero level of
    follistatin at baseline with a myostatin level of 46 pg/ml, 12 hours after
    FolstaxanTM dosing. Serum follistatin measured 57.1 pg/ml with a decline of
    myostatin to 34 pg/m1, 24 hours after the initial dosing, follistatin levels
    began to predictably drop from the time of initial dosing to 11.4 pg/ml. Yet
    myostatin continued to decline slightly with a 24-hour level of 31 pg/ml.
    These results clearly indicate that a fertile egg yolk powder properly
    processed to preserve active follistatin, when orally ingested, results in
    detectable serum follistatin. Furthermore, this resultant follistatin
    presence has significant pharmacokinetic activity is shown by the hormonal
    down regulation of serum follistatin.

    some very key points

    1) myostatin is expressed in muscles. it acts in muscles. its concentration in serum may or may not reflect concentration in muscles.

    2) without a placebo control done on this guy at a different time we have no way to know if his serum myostatin naturally fluctuates this way anyway

    3) he says that the male human does not normally have follistatin in his serum. that is in direct contrast to what they say below. furthermore, the levels below that are found in normal male serum normal male serum (approximately 0.45 ng/ml) seem to be on the level of 10 times greater than seen in the study above at the highest point. This bid inconsistency needs to be explained


    J Endocrinol. 1998 Feb;156(2):275-82. Links
    Development, validation and application of an ultra-sensitive two-site enzyme immunoassay for human follistatin.Evans LW, Muttukrishna S, Groome NP.
    School of Biological and Molecular Sciences, Oxford Brookes University, Headington, UK.

    Recent studies have found follistatin to be an important regulator of activin bioactivity. Whilst a number of assay formats have been described, all are of limited sensitivity and require the use of isotopes. Many use polyclonal antibodies. Furthermore, a wide range of follistatin preparations have been used as standards, complicating inter-laboratory comparison. We now describe an ultra-sensitive two-site enzyme immunoassay using a pair of mouse monoclonal antibodies raised against follistatin 288. The presence of sodium deoxycholate and Tween 20 in the diluent gave results for total (free and activin-dissociated) follistatin. The assay had a detection limit of <19 pg/ml and recovery of spiked follistatin 288 from amniotic fluid, serum seminal plasma, human follicular fluid and granulosa cell conditioned medium averaged 100.7 +/- 7.5%, 89.1 +/- 5.5%, 98 +/- 4.9%, 96 +/- 7.2% and 123.9 +/- 11% respectively. The intra- and interplate coefficients of variation were < 5%. An excess of activin-A (50 ng/ml) prior to assay did not affect follistatin recovery. Inhibin-A, inhibin-B, activin-A, activin-B and activin-AB had minimal cross-reactivity (<0.3%). However, follistatin 315 had a significant cross-reaction (9.9%). Serially diluted human samples gave dose-response curves parallel to the standard. Pooled human follicular fluid contained high concentrations of follistatin (approximately 242 ng/ml). Follistatin was also found in maternal serum during pregnancy (first trimester approximately 0.8 ng/ml, third trimester approximately 2.8 ng/ml), normal male serum (approximately 0.45 ng/ml), amniotic fluid (sixteen week approximately 3.63 ng/ml, term approximately 0.89 ng/ml), seminal plasma (2.4-30 ng/ml) and human granulosa cell conditioned media (approximately 0.44 ng/ml). Serial serum samples taken throughout the menstrual cycle of ten women showed fluctuating follistatin concentrations (approximately 0.62 ng/ml) with no apparent relationship to the stage of the cycle. Interestingly, pooled serum from postmenopausal women appeared to have higher follistatin levels than any of the normal women (approximately 1.4 ng/ml). The possible presence in certain samples of mixtures of follistatin isoforms with different immunoreactivities poses major problems of interpretation in this and all other current follistatin immunoassays. Further work is needed to identify the major immunoreactive forms in different tissues and fluids. Nevertheless, the new assay has a number of advantages over previous assays and should prove a useful tool for various clinical and physiological studies.

    PMID: 9518873 [PubMed - indexed for MEDLINE]

    J Clin Endocrinol Metab. 1998 Mar;83(3):851-8. Links
    A two-site chemiluminescent assay for activin-free follistatin reveals that most follistatin circulating in men and normal cycling women is in an activin-bound state.McConnell DS, Wang Q, Sluss PM, Bolf N, Khoury RH, Schneyer AL, Midgley AR Jr, Reame NE, Crowley WF Jr, Padmanabhan V.
    Department of Pediatrics and Pathology and Nursing, University of Michigan, Ann Arbor 48109-0404, USA.

    Follistatin (FS) is a monomeric protein that binds and regulates the bioavailability of activin. Previously, we found circulating levels of total FS to be similar in men and cycling women. Because relative amounts of activin-bound and free FS are important considerations in determining activin bioavailability, we asked here whether the relative proportions of these two changed during different physiologic states. For this, we developed a two-site, solid-phase, immunochemiluminescent assay for free FS. The assay recognizes the 288 or 315 amino acid variants of human FS and has a detectable limit of 1 ng/mL. Inhibin, transforming growth factor-beta, or alpha-2-macroglobulin do not cross-react or interfere in this assay. Preincubation of FS with activin results in dose-dependent loss of immunoreactivity, confirming specificity of the assay for free FS. Human follicular fluid, pituitary extract, and serum with added FS dilute parallel with the recombinant human FS-288 standard. Recovery of recombinant human FS-288 from serum is quantitative. Using this assay, we found circulating concentrations of free FS to be at or below the detection limit of the assay throughout the menstrual cycle. Comparison of circulating total and free FS levels in postmenopausal or cycling women and normal men suggested that at least 90% is activin-bound. In contrast, measurable quantities of free FS were found in follicular fluid and pituitary extracts. The results of this study, showing that most circulating FS is normally activin-bound, argue against an endocrine role for FS and suggest that a major role of circulating FS is to bind and neutralize the bioactivity of circulating activin. The roles of FS as a local autocrine or paracrine regulator of activin in target tissues, where FS exists in free form, or as an endocrine regulator in human pathophysiology, warrants further investigation.

  22. Quote Originally Posted by Patrick Arnold View Post
    there is also a myostatin peptide product which is a blocker and is in development
    Do you know who's developing it?

  23. Quote Originally Posted by Speedbacker View Post
    He said he would fax it to me. Hopefully I will get it tomorrow. Once I receive it, I will post it.
    I also asked him for clarification on why it couldn't be found.

  24. Patrick,

    Why are people going this very indirect route when there is already a patent for a product that is developed by a reliable pharma company and shown to inhibit myostatin? "Research" companies copy and release all sorts of patented products as "research chemicals" (example; the viagra and cialis that one can buy as liquid suspensions from research sites). Why not the same treatment for the myostatin blocker that is patented and known to work? The details of its molecular structure should be in the patent documents, no?

    Sub

  25. Quote Originally Posted by Speedbacker View Post
    Do you know who's developing it?
    no, but do a google on myostatin propeptide

    i think they may be developing it to be delivered by viral based gene therapy
  •   

      
     

Similar Forum Threads

  1. Replies: 7
    Last Post: 05-03-2008, 01:45 PM
  2. Question for PA on 11-oxo
    By awmcdon in forum Supplements
    Replies: 0
    Last Post: 06-29-2007, 03:38 PM
  3. Replies: 3
    Last Post: 09-21-2005, 02:03 PM
  4. For those of you with questions about NO supplements
    By str8flexed in forum Supplements
    Replies: 9
    Last Post: 02-25-2005, 10:25 PM
Log in
Log in