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any Myostatin or SARM updates?

I was referring to S-4. You NEED to get ahold of me Pudz ASAP. There are some issues we need to resolve. You have email & pm.

bb
 
Ok verified, S-4 in about 3-4 weeks. A friend who lives overseas in a jurisdiction where its legal to try this product said 100mg/day, going 5 on and 2 off days, felt like a TRT dose of test = 250mg/week.

The recommended dosage is 300mg/wk of the S-4 so my friend thinks it would 'feel' like roughly 750mg test/week.

bb
 
SWEET! i love this forum. though i am skeptical so i'm gonna wait for ur research bb.
how much will this stuff cost though and how is it administered?
 
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good info(although many typo's) about the current SARMS that are being researched/ entering production

the problem with the ones being researched thus far, is that they seem to still act upon the HPTA, thus eventually suppressing LH and FSH which will result in low-no testosterone output and problems with sperm count and motility. BUT they still provide the benefits of being selective to muscle and bone and act MINIMALLY if at all upon the prostate, skin etc (DHT)... so when using a SARM, one can do bloodwork to determine when LH and FSH begin to plummit, and then begin a regime of HCG and HMG(if available-seems hard to find) to replace the bodies production of LH and FSH hence preserving the "natural-ish" balance of test and sperm production. Obviously, at the doses that a bber would use SARMS and becuase of their partial androgenicity in tissues other than muscle and bone at higher soes, and their HPTA suppression capabilities, a PCT would still help.

But hey: we dont have to worry about gyno, prostate enlargement, hairloss, lipids?-havent seen much with respect to serum lipid alteration, etc. it would make like MUCH simpler when we have fewer health risks/precautions to be proactive about. (the HPTA)
 
babyblu said:
Ok verified, S-4 in about 3-4 weeks. A friend who lives overseas in a jurisdiction where its legal to try this product said 100mg/day, going 5 on and 2 off days, felt like a TRT dose of test = 250mg/week.

The recommended dosage is 300mg/wk of the S-4 so my friend thinks it would 'feel' like roughly 750mg test/week.

bb
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just confused here, 100mg/day for 5 on 2 off is 500mg/wk and he felt like test 250mg/week

you say the recommended dosage is 300mg/wk which is less than your friend's 500mg/wk is supposed to feel like 750mg/wk??? did you mean to say 300mg/day?
 
pudzian2 said:
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good info(although many typo's) about the current SARMS that are being researched/ entering production

the problem with the ones being researched thus far, is that they seem to still act upon the HPTA, thus eventually suppressing LH and FSH which will result in low-no testosterone output and problems with sperm count and motility. BUT they still provide the benefits of being selective to muscle and bone and act MINIMALLY if at all upon the prostate, skin etc (DHT)... so when using a SARM, one can do bloodwork to determine when LH and FSH begin to plummit, and then begin a regime of HCG and HMG(if available-seems hard to find) to replace the bodies production of LH and FSH hence preserving the "natural-ish" balance of test and sperm production. Obviously, at the doses that a bber would use SARMS and becuase of their partial androgenicity in tissues other than muscle and bone at higher soes, and their HPTA suppression capabilities, a PCT would still help.

But hey: we dont have to worry about gyno, prostate enlargement, hairloss, lipids?-havent seen much with respect to serum lipid alteration, etc. it would make like MUCH simpler when we have fewer health risks/precautions to be proactive about. (the HPTA)
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thats true pudzian about the sides, but i had more trouble with suppressed HPTA than anything else when cycling.

its too early to tell, but yuo know how you lose anywhere from 30 -50 % roughly from any cycles in terms of strength and size, but if this SARM causes less of loss then i might be very interested despite of its HPTA suppression.

but i have a feeling if HTPA is suppressed you might lose some no matter what (PCT or not)
 
comacho said:
just confused here, 100mg/day for 5 on 2 off is 500mg/wk and he felt like test 250mg/week

you say the recommended dosage is 300mg/wk which is less than your friend's 500mg/wk is supposed to feel like 750mg/wk??? did you mean to say 300mg/day?
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Yes Comacho, that was a typo. The recommended dosage is 300mg per day. My apologies.

bb
 
I guess this would be comparable to a reallllly good oral steroid whose only side is the effect on hpta; and if that is the case then IMO its pretty damn good deal b/c I go into a cycle understanding I will be surpressed. Therefore the supression is NOT the problem (for me) its the high BP, the effect on the liver, the effect on my cholesterol, etc. Those sides make oral cycles VERY uncomfortable for me even when Im using Cycle Support + Red Yeast Rice + extra Hawthorne + garlic + about every vitamin you can think of.

bb
 
babyblu said:
I guess this would be comparable to a reallllly good oral steroid whose only side is the effect on hpta; and if that is the case then IMO its pretty damn good deal b/c I go into a cycle understanding I will be surpressed. Therefore the supression is NOT the problem (for me) its the high BP, the effect on the liver, the effect on my cholesterol, etc. Those sides make oral cycles VERY uncomfortable for me even when Im using Cycle Support + Red Yeast Rice + extra Hawthorne + garlic + about every vitamin you can think of.

bb
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not only do they make it uncomfortable but they can add up to long term permanent damage if not careful. I stay away from orals. Even injectables (depending on the compound and the individual) can put ya at risk for heart disease from messed up lipids, really messed up HPTA, INFERTILITY, prematurely enlarged prostate etc.

hell, If all we have to worry about is HPTA to SOME degree then its ALMOST perfect. even if 5 on 2 off eventually leads to hpta suppression, it would probably take ALOT longer than the equivalent dose of test.....and we could do pre cycle bloodwork and then periodic bloodwork to determine when suppression sets in and/or if any of the minimalistic androgenicity on the prostate etc is happening. then we cease use, do a small/proper PCT which SHOULD be a breeze with this stuff and back on it is! this can really minimize the gain and look/feel great, come off to be healthy and feel/look ****ty up and down BS with reg AAS.
 
If you use hcg then the shutdown should be minimal. Thats what I will do is run hcg with it to prevent shutdown. Maybe use Primordial Performance's Dermacrine too. Also a good friend of mine is developing a natural test booster supplement so I will probably use that too.


bb
 
babyblu said:
If you use hcg then the shutdown should be minimal. Thats what I will do is run hcg with it to prevent shutdown. Maybe use Primordial Performance's Dermacrine too. Also a good friend of mine is developing a natural test booster supplement so I will probably use that too.


bb
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well the shut down of the TESTES will be minimal/ non existent, BUT your LH will be fully suppressed with HCG as it replaces it. Also this does nothing for FSH....in the end it could prevent testicular atrophy and keep the testes producing test, but why do this if they the HPTA is maintaining a good balance with the S-4 WITHOUT the HCG. IT would seem premature use of HCG would only further suppress the system. That is probably why 5 on 2 off is used....that way the NET time it takes to become suppressed if at all is longer than 7 days on straight. So It is trial and error to see how long it takes on average to be suppressed, but at this point it would seem likely to just come off, restore HPTA (which shouldnt take long becuase suppression should be minimal) and continue use.

Bloodwork is the best way to determine the time it takes to be suppressed. Once known, we can then take a more intelligent approach to using this stuff for bbing
 
I also wonder what kind of comparison can be made between aspects of female birth control (the "pill') and S-4 amongst other SARMs as male contraceptives. Some are thought to have a plausible application in male contraception (one would assume longer term plans). Females take a hormone which suppresses their normal hormone balance (from my limited understanding of female contraception), but appon cessation they are EXPECTED to return to normal. who's ever heard of PCT after a birth control cycle>>>???

so with that in mind and becuase I have read somewhere that SARMs COULD be used more effectively than testosterone at long term male contraception (more effectively because less sides and the selectivity of the AR binding affinity). so I feel it is fair to assume that ALTHOUGH they may eventually suppress FSH (sperm production), and possibly LH as well, the effect is minimal and takes a WHILE longer than steroids to happen. It is also fair to assume that since it is a better form of male contraception, that even if one is to be suppressed, the rebound should be EASY and QUICK. This is assuming a SARM like this CAN be compared to female birth control pills (which may be a long shot.)
 
interesting interesting...

cant wait to see some results from the first round users.

pudzian, is that your strategy? 5 on 2 off then wait to recover (2wks?) then come back on?

not sure if thats better or 2month on straight then come off with SERM in terms of gains made / HPTA suppression

too early to tell i suppose, this is pretty cutting edge in bodybuilding LOL.
 
I should be running it soon and I will be running 5 on 2 off to help minimize shutdown. Dont know if Pudz will have the opportunity or not.

bb
 
I am just speaking to this compound for discussion sake. If I were presented with the opportunity, I would gladly take it, But I foresee SARMs being introduced into the bbing community very soon. The technology is there, now it must be applied.

to recap: 5 on 2 off was referring to days correct? or is it weeks....

my strategy was not to come off of it at all (well eventually yea) but no REASON to unless shutdown is occurring. If I were to run it it would be similar to the 5 on 2 off, or maybe 4 on 3 off ( so in a pulsatile fashion)-really depends on the half life of the compound. I would run it this way and wait to see when/if my HPTA is being suppressed. once this issue is addressed we can have a better understanding of how SARM's specifically S-4 react when applied to bbing specific hypertrophy.
 
"Other studies in our laboratory have shown that S-4 does not affect LH or FSH levels (data not shown), highlighting an important difference between steroidal AR agonists and nonsteroidal SARMs."

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yes it was performed in female rats I think but still...
 
The current report by Gao et al. (9) describes the tissue selectivity in intact male rats of two SARMs, designated S1 and S4, that behave as partial agonists in androgen-responsive tissues, such as prostate and seminal vesicles, but full agonists in anabolic tissues such as the levator ani muscle (12). Both S1 and S4 bind with high affinity to AR, with dissociation constant of the ligand inhibitor-receptor complex (Ki) values of 6.1 and 4.0 nM, respectively; which is similar to T, much higher than hydroxyflutamide (Ki = 25 nM), but lower than DHT (Ki = 0.2 nM). In immature castrated rats, S1 and S4 exhibited full AR agonist activity in levator ani muscle but only partial agonist activity in prostate and seminal vesicles. The relative rates of efficacy of S1 and S4 in prostate were 12 and 29%, respectively, compared with T propionate. As reported by Gao et al. (9) for intact male rats, S1 selectively decreased prostate weight with efficacy similar to that of the 5{alpha}-reductase inhibitor finasteride without affecting the levator ani muscle or altering the plasma levels of T, LH, or FSH. By contrast, hydroxyflutamide decreased both the prostate and levator ani muscle weights without selectivity and increased plasma hormone levels in a dose-dependent fashion. Neither S1 nor S4 affected 5{alpha}-reductase type I or II isozyme activities. These results show that S1 and S4 act as partial AR agonists with tissue-selective activity that suppresses androgen-dependent prostate growth without influencing the anabolic effects of T on weight of the levator ani muscle. Moreover, the maintenance of normal serum T levels and lack of effect of S1 and S4 on pituitary gonadotropin secretion further exemplify the tissue selectivity of their action.


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Might be cheaper now, this was about a year ago and there are a lot of SARM's out there but it was the best one we could find. I mean the dosages are definitely low because you don't have to worry about them being wasted in tissues that you don't want androgen expression in anyways, but still no one wants to fork out that kind of cash. The price goes up a lot of you go below a kg. They want you to buy in bulk of course.
 
LakeMountD said:
Might be cheaper now, this was about a year ago and there are a lot of SARM's out there but it was the best one we could find. I mean the dosages are definitely low because you don't have to worry about them being wasted in tissues that you don't want androgen expression in anyways, but still no one wants to fork out that kind of cash. The price goes up a lot of you go below a kg. They want you to buy in bulk of course.
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lakemount, i want whatever you're on lol
 
GTx, Inc. (Nasdaq: GTXI), the Men's Health Biotech Company, today announced that ostarine, a first-in-class selective androgen receptor modulator (SARM), met its primary endpoint in a Phase II proof ofconcept double blind, randomized, placebo controlled clinical trial in 120 subjects (60 elderly men and60 postmenopausal women). Without a prescribed diet or exercise regimen, all subjects treated with ostarine had a dose dependent increase in total lean body mass (muscle), with the 3 mg cohortachieving an increase of 1.3 kg compared to baseline and 1.4 kg compared to placebo (p<0.001) afterthree months of treatment. Treatment with ostarine also resulted in a dose dependent improvement infunctional performance measured by a stair climb test, with the 3 mg cohort achieving a clinicallysignificant improvement in both speed (p=0.006) and power (p=0.005). Ostarine continued todemonstrate a favorable safety profile, with no serious adverse events reported. Ostarine also exhibited tissue selectivity with beneficial effects on lean body mass and performance and with no apparent change in measurements for serum PSA (prostate), sebum production (skin and hair), or serum LH (pituitary) compared to placebo."These results are exciting," said William J. Evans, Ph.D., Professor of Geriatrics, Physiology, andNutrition at the Donald W. Reynolds Institute of Aging of the University of Arkansas for MedicalSciences. "Not only was there a change in lean body mass in the clinically significant range, but asignificant change in functional performance was also seen. A clear anabolic effect with little to nounwanted androgenic effect was demonstrated, which should be the hallmark of a SARM." The Phase II clinical trial evaluated four doses of ostarine (0.1 mg, 0.3 mg, 1 mg, and 3 mg) versusplacebo for three months in 60 elderly men (average age 66 years) and 60 postmenopausal women (average age 63 years). The trial was conducted in five clinical sites in the United Kingdom andGermany.A summary of the topline data is as follows:Primary endpoint: total lean body mass (LBM) measured by dual energy x-ray absorptiometry (DEXA) atbaseline compared to three months -- Among all subjects (n=114), ostarine treatment resulted in a dose dependent increase in total leanbody mass, with an increase of 1.3 kg compared to baseline and 1.4 kg compared to placebo (p<0.001) at the 3 mg dose. -- Among females (n=56), ostarine treatment resulted in a dose dependent increase in LBM with the 3 mg dose having an increase of 1.7 kg compared to baseline and an increase of 1.4 kg compared toplacebo (p=0.02).-- Among males (n=58), treatment with a 1 mg dose of ostarine resulted in a LBM increase of 0.7 kgcompared to baseline and an increase of 1.2 kg compared to placebo (p=0.03), and treatment with a 3 mg dose of ostarine resulted in an increase of 1.0 kg compared to baseline and an increase of 1.4 kgcompared to placebo (p=0.005).Secondary endpoints: performance, fat mass, bone mineral density, and bone turnover markers-- In a stair climb functional performance test that measured speed (time to completion) and powerexerted (watts), subjects treated with a 3 mg dose of ostarine demonstrated on average a 15.5% fastertime to completion (p=0.006) and exerted on average 25.5% more power (p=0.005) than subjects receiving placebo.-- Total tissue percent fat decreased compared to placebo in a dose dependent fashion and achievedstatistical significance at the 1 mg dose (p=0.02) and 3 mg dose (p=0.006) of ostarine. Total fat masswas lower in subjects receiving either the 3 mg or 1 mg ostarine dose, although not at a statisticallysignificant level (p = 0.08 for both doses). For subjects receiving the 3 mg ostarine dose, total fat onaverage declined 0.6 kg compared to placebo. The site of fat loss differed among male and femalesubjects, with males losing fat primarily from the trunk and abdomen, and females losing fat primarilyfrom the thighs and legs.-- In this short trial, ostarine had no apparent effect on bone mineral density, and bone turnover markers
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results were mixed. In preclinical in vitro and in vivo models, ostarine demonstrated both anabolic and antiresorptive activity on bone. A longer clinical study is necessary to demonstrate the actual effects ofostarine on bone.Safety-- Ostarine continued to demonstrate a favorable safety profile, with no serious adverse events reported.-- At the end of three months, no subject had clinically meaningful levels in liver enzyme tests. However, one female discontinued the study per protocol due to elevated liver enzymes which returned tobaseline. -- Ostarine treatment resulted in a dose dependent decrease in both LDL and HDL cholesterol levels,with the average LDL/HDL ratio for all doses tested remaining in the low cardiovascular risk category. Selectivity-- Ostarine treatment resulted in no apparent effect on serum PSA (prostate), sebum production (skin and hair), or serum LH (pituitary)."The use of anabolic agents has previously been limited because of concerns over unwantedandrogenic and steroidal side effects and oral bioavailability," said Mitchell S. Steiner, MD, CEO of GTx."Ostarine's safety, tissue selectivity profile, and efficacy results demonstrated in our Phase II clinicaltrial, combined with oral dosing, distinguish this drug candidate from existing anabolic steroids and testosterone analogues. This opens the door for its potential use in both males and females in amultitude of diseases, including cancer cachexia, end stage renal disease muscle wasting, frailty and osteoporosis." GTx recently conducted discussions with various divisions of the United States Food & DrugAdministration to investigate the required regulatory pathways for several indications under consideration for ostarine's ongoing clinical development. With more clarity regarding the requiredregulatory pathway and with proof of concept Phase II clinical data, GTx has selected cancer cachexiaas the initial acute indication for ostarine development. GTx plans to initiate a Phase IIb ostarine clinicaltrial for cancer cachexia by the summer of 2007.Cachexia, or muscle wasting, is a serious result of many cancers, causing selective muscle loss,fatigue, and deteriorating quality of life which adversely impacts response to treatment and overall survival. Cancer cachexia has been identified as one of the two most frequent and devastating problemsaffecting individuals with advanced malignancies. It has been estimated that a third of the approximately1.3 million patients diagnosed with cancer in the United States each year will suffer from cancercachexia. A drug with the ability to increase lean body mass and improve functional performance wouldaddress significant unmet needs for the millions of patients living with cancer. GTx also intends to evaluate the ability of ostarine to treat chronic disease indications including end stage renal disease muscle wasting, frailty and osteoporosis.Collaboration with Ortho Biotech for andarineGTx has reacquired full rights to develop and commercialize andarine and all backup compoundspreviously licensed to Ortho Biotech Products, L.P., a subsidiary of Johnson & Johnson (Ortho Biotech),through a Joint Collaboration and License Agreement executed between GTx and Ortho Biotech inMarch 2004, which has been terminated by mutual agreement of the parties. GTx now has fullownership and control of its SARM portfolio."With GTx's reacquisition of all rights to andarine, we are now free to pursue any indication for ostarine,including cancer cachexia, without a concern that andarine could become a potential competitor," saidDr. Steiner. "Having positive ostarine proof of concept data and the full rights to all of our SARMs, weare now in position to maximize the value of our SARM program through clinical development and potential partnerships."In the fourth quarter 2006, GTx expects to recognize collaboration revenue of approximately $3.3 million, which represents the unamortized balance of the upfront licensing fee paid by Ortho Biotech toGTx in April 2004.Conference CallGTx will host a conference call and webcast this morning at 9:00 a.m. EST. To listen to the
 
Peg-anti-gdf-8 (Myostatin Inhibitor)?

FYI-

One of our members BLACK747 is currently running a custom pegylated anti gdf-8 (myostatin) antibody his friend at a biotech co. created for him. Taking 200 mcg/week and has been on it for a week.
Hopefully he will log it and was asked to start a thread.
Here is the link to another thread here where he mentions running it.

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His posts related to peg-anti-gdf-8 start at #13

I'm definitely interested in what you all think.
 
Seems awfully dangerous to mess around with myostatin. If the man is predisposed to cancer this could fast tracking him to the morgue.
 
if you do a search of myostatin blockers you should see an imageof a whippet(dog) with freaky muscle definition and muscular size...youtube had a video of a cow that had all myostatin blocked...the huge cow had muscle seemingly growing on top of muscle! The only scare I see with this is if products can inhibit without total degredation or genetic splicing of the protein. Unless you want to be bigger than markus ruhl!
 
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Se-Jin Lee at Johns Hopkins University in Baltimore and colleagues from several academic institutions and biotechnology companies, say the new compound blocks myostatin using a different mechanism from a previously developed agent, which is now being tested in clinical trials in patients with certain adult forms of muscular dystrophy...

The new compound, ACVR2B, is not an antibody. Instead, it blocks myostatin by providing it with a portion of a molecule that it normally sticks to but not the entire molecule. This partial molecule keeps myostatin from interacting with its normal molecular binding partner; and, without this interaction, myostatin can’t send its usual growth-inhibiting signals to muscle cells...

He cautions, however, that the effects of ACVR2B can be attributed to its ability to block more than just myostatin signaling, and that this is both a benefit and a risk...

This was just a recent article in the use of the blocker for muscular dystrophy. Shows that of course any product now isn't the real deal, unfortunately. hope it helps anyone!
 
SciVa627 said:
Se-Jin Lee at Johns Hopkins University in Baltimore and colleagues from several academic institutions and biotechnology companies, say the new compound blocks myostatin using a different mechanism from a previously developed agent, which is now being tested in clinical trials in patients with certain adult forms of muscular dystrophy...

The new compound, ACVR2B, is not an antibody. Instead, it blocks myostatin by providing it with a portion of a molecule that it normally sticks to but not the entire molecule. This partial molecule keeps myostatin from interacting with its normal molecular binding partner; and, without this interaction, myostatin can’t send its usual growth-inhibiting signals to muscle cells...

He cautions, however, that the effects of ACVR2B can be attributed to its ability to block more than just myostatin signaling, and that this is both a benefit and a risk...

This was just a recent article in the use of the blocker for muscular dystrophy. Shows that of course any product now isn't the real deal, unfortunately. hope it helps anyone!
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by saying it blocks more than just myostatin you are referring to....?
 
I too was wondering that...I've been looking for more detail and this so far is what i came across “The finding that myostatin is not the sole regulator of muscle mass in mice raises the question as to whether targeting myostatin alone will be the most effective strategy for manipulating this signaling pathway in humans.” I'm going to keep looking
 
SciVa627 said:
I too was wondering that...I've been looking for more detail and this so far is what i came across “The finding that myostatin is not the sole regulator of muscle mass in mice raises the question as to whether targeting myostatin alone will be the most effective strategy for manipulating this signaling pathway in humans.” I'm going to keep looking
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one would think its not that simple. I would assume that like anything else, inhibiting myostatin alone may result in some immediate changes that eventually plateau out. Now, im not very educated on these specific mechanisms so who knows. maybe the body has an immediate defense to a change in JUST myostatin to maintain a homeostatic amount of LBM
 
thats why compounds like follistatin and myostatin propeptide
is so powerfull they block alot more than myostatin ,for instance follistatin also blocks activins and myostatin propetide also blocks gdf-11
 
BLACK747 said:
thats why compounds like follistatin and myostatin propeptide
is so powerfull they block alot more than myostatin ,for instance follistatin also blocks activins and myostatin propetide also blocks gdf-11
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exactly... are those compounds being produced?
 
Pudzian wrote:
the problem with the ones being researched thus far, is that they seem to still act upon the HPTA.
Question to Pudzian:
Do you kno if this includes Osterine?
 
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