Myostatin Question for PA, anybody else with knowledge
- 05-03-2007, 09:27 AM
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
- 05-03-2007, 07:48 PM
05-03-2007, 08:44 PM
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.Originally Posted by from the Folstaxan site
05-03-2007, 08:55 PM
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.
05-04-2007, 01:45 PM
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.
05-06-2007, 02:38 PM
05-06-2007, 03:11 PM
05-06-2007, 08:39 PM
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.
05-06-2007, 08:41 PM
05-06-2007, 08:43 PM
05-06-2007, 08:45 PM
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
05-06-2007, 08:52 PM
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.
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
05-06-2007, 09:22 PM
05-06-2007, 09:34 PM
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.
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.
05-06-2007, 09:37 PM
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 )
05-06-2007, 09:39 PM
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?
05-06-2007, 10:15 PM
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
05-06-2007, 10:16 PM
05-06-2007, 10:20 PM
Journal of the American College of Nutrition -- Search
despite using author, volume, title key words, everything i could think of i saw nothing
05-06-2007, 10:39 PM
05-06-2007, 10:39 PM
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.
05-06-2007, 10:40 PM
05-06-2007, 10:47 PM
05-07-2007, 12:20 AM
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?
05-07-2007, 05:43 AM
Similar Forum Threads
- By MachineMan in forum SupplementsReplies: 7Last Post: 05-03-2008, 01:45 PM
- By awmcdon in forum SupplementsReplies: 0Last Post: 06-29-2007, 03:38 PM
- By nmarco37 in forum AnabolicsReplies: 3Last Post: 09-21-2005, 02:03 PM
- By str8flexed in forum SupplementsReplies: 9Last Post: 02-25-2005, 10:25 PM