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    If women can have SERMs men can have SARMs

    An interesting study I came across which I had not seen before.

    Endocrinology. 2005 Nov;146(11):4887-97. Epub 2005 Aug 11. Related Articles, Links


    Selective androgen receptor modulator treatment improves muscle strength and body composition and prevents bone loss in orchidectomized rats.

    Gao W, Reiser PJ, Coss CC, Phelps MA, Kearbey JD, Miller DD, Dalton JT.

    Division of Pharmaceutics, College of Pharmacy and Department of Oral Biology, The Ohio State University, 500 West 12th Avenue, L. M. Parks Hall, Room 242, Columbus, Ohio 43210, USA.

    The partial agonist activity of a selective androgen receptor modulator (SARM) in the prostate was demonstrated in orchidectomized rats. In the current study, we characterized the full agonist activity of S-3-(4-acetylamino-phenoxy)-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethyl-phenyl)-propionamide (a structurally related SARM referred to in other publications and hereafter as S-4) in skeletal muscle, bone, and pituitary of castrated male rats. Twelve weeks after castration, animals were treated with S-4 (3 or 10 mg/kg), dihydrotestosterone (DHT) (3 mg/kg), or vehicle for 8 wk. S-4 (3 and 10 mg/kg) restored soleus muscle mass and strength and levator ani muscle mass to that seen in intact animals. Similar changes were also observed in DHT-treated (3 mg/kg) animals. Compared with the anabolic effects observed in muscle, DHT (3 mg/kg) stimulated prostate and seminal vesicle weights more than 2-fold greater than that observed in intact controls, whereas S-4 (3 mg/kg) returned these androgenic organs to only 16 and 17%, respectively, of the control levels. S-4 (3 and 10 mg/kg) and DHT (3 mg/kg) restored castration-induced loss in lean body mass. Furthermore, S-4 treatment caused a significantly larger increase in total body bone mineral density than DHT. S-4 (3 and 10 mg/kg) also demonstrated agonist activity in the pituitary and significantly decreased plasma LH and FSH levels in castrated animals in a dose-dependent manner. In summary, the strong anabolic effects of S-4 in skeletal muscle, bone, and pituitary were achieved with minimal pharmacologic effect in the prostate. The tissue-selective pharmacologic activity of SARMs provides obvious advantages over steroidal androgen therapy and demonstrates the promising therapeutic utility that this new class of drugs may hold.

    PMID: 16099859 [PubMed - indexed for MEDLINE]
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Very interesting. Thanks for posting this!

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    some interesting new studies
    J Med Chem. 2006 Dec 28;49(26):7596-9. Links
    Discovery of potent, orally-active, and muscle-selective androgen receptor modulators based on an N-aryl-hydroxybicyclohydantoin scaffold.
    Sun C, Robl JA, Wang TC, Huang Y, Kuhns JE, Lupisella JA, Beehler BC, Golla R, Sleph PG, Seethala R, Fura A, Krystek SR Jr, An Y, Malley MF, Sack JS, Salvati ME, Grover GJ, Ostrowski J, Hamann LG.


    A novel, N-aryl-bicyclohydantoin selective androgen receptor modulator scaffold was discovered through structure-guided modifications of androgen receptor antagonists. A prototype compound (7R,7aS)-10b from this series is a potent and highly tissue-selective agonist of the androgen receptor. After oral dosing in a rat atrophied levator ani muscle model, (7R,7aS)-10b demonstrated efficacy at restoring levator ani muscle mass to that of intact controls and exhibited >50-fold selectivity for muscle over prostate.
    1 currently in clinical trials
    Pharmacological and x-ray structural characterization of a novel selective androgen receptor modulator: potent hyperanabolic stimulation of skeletal muscle with hypostimulation of prostate in rats.
    Ostrowski J, Kuhns JE, Lupisella JA, Manfredi MC, Beehler BC, Krystek SR Jr, Bi Y, Sun C, Seethala R, Golla R, Sleph PG, Fura A, An Y, Kish KF, Sack JS, Mookhtiar KA, Grover GJ, Hamann LG.


    A novel, highly potent, orally active, nonsteroidal tissue selective androgen receptor (AR) modulator (BMS-564929) has been identified, and this compound has been advanced to clinical trials for the treatment of age-related functional decline. BMS-564929 is a subnanomolar AR agonist in vitro, is highly selective for the AR vs. other steroid hormone receptors, and exhibits no significant interactions with SHBG or aromatase. Dose response studies in castrated male rats show that BMS-564929 is substantially more potent than testosterone (T) in stimulating the growth of the levator ani muscle, and unlike T, highly selective for muscle vs. prostate. Key differences in the binding interactions of BMS-564929 with the AR relative to the native hormones were revealed through x-ray crystallography, including several unique contacts located in specific helices of the ligand binding domain important for coregulatory protein recruitment. Results from additional pharmacological studies effectively exclude alternative mechanistic contributions to the observed tissue selectivity of this unique, orally active androgen. Because concerns regarding the potential hyperstimulatory effects on prostate and an inconvenient route of administration are major drawbacks that limit the clinical use of T, the potent oral activity and tissue selectivity exhibited by BMS-564929 are expected to yield a clinical profile that provides the demonstrated beneficial effects of T in muscle and other tissues with a more favorable safety window.
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Good stuff as usual !
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    This is a real science topic. Not like the rest of the **** posted in this section.
    Ansew to the few pms I've gotten since popping back on-line...

    NO I never got full amount back from 'him', still owed for FAKE t3 and wu fee... More than a year on I can't be bothered to carry on chasing it up.. Unfortunatly word is he is on another bb community forum still selling

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    Thumbs up

    excellent thread! too bad I first need to spread some reps before I can give them to DR dave again.

    two questions:

    1. since the SARMS seem to bind well to ARs in pituitary gland, it apparently can be expected that they will shut down HPTA axis? any guesses to which degree this might happen?

    2. what is with their "androgenicity"? how will they influence beard / face hairs / acne / voice etc.?

    and two more questions:

    - any ideas on hepatic metabolism / oral bioavailability?

    - is any of the SARMS already in clinical testing for humans? and if yes, for which indication / application?

    best regards


    david

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    Anthony Roberts hooker's Avatar
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    I proposed this idea almost a year ago to a research chem company to produce SARMs (*I thought it would be legal to sell as a research chem like SERMs). then about half a year ago, I worked with another chem company on the feasibility of coming out with some SARMs....we went so far as to identify which one(s) would be the best to produce. Eventually, the product was scrapped, for various reasons.

    I dunno...I think it would still be interesting if a chem company wanted to come out with SARMs.

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    game over DRP7's Avatar
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    Originally Posted by hooker View Post
    I proposed this idea almost a year ago to a research chem company to produce SARMs (*I thought it would be legal to sell as a research chem like SERMs). then about half a year ago, I worked with another chem company on the feasibility of coming out with some SARMs....we went so far as to identify which one(s) would be the best to produce. Eventually, the product was scrapped, for various reasons.

    I dunno...I think it would still be interesting if a chem company wanted to come out with SARMs.
    well, I would be much happier if a pharma-company (and NOT a chem-company) would start to produce this stuff, since they would be forced to first do some basic preclinical and clinical safety testing before throwing ths thing into the market.

    this has actually been the case with the SERMs. there are tons and tons of clinical data on tamoxifene, so even when somebody wants to buy this stuff from a research chem company he will know what to expect from it (with regards to effects and risks).

    Such a drug can look great in vitro or in rodents, but - just theoretically - it could have very strange and absolutely unexpected side effects in humans. plenty of very promising drugs had to be cancelled in phase I clinical studies for of exactely such reasons. You should be grateful that the chem companies refused your offer to cooperate. It's definitely better to be on the safe side, isn't it?

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    Anthony Roberts hooker's Avatar
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    Originally Posted by Dr.P View Post
    well, I would be much happier if a pharma-company (and NOT a chem-company) would start to produce this stuff, since they would be forced to first do some basic preclinical and clinical safety testing before throwing ths thing into the market.

    this has actually been the case with the SERMs. there are tons and tons of clinical data on tamoxifene, so even when somebody wants to buy this stuff from a research chem company he will know what to expect from it (with regards to effects and risks).

    Such a drug can look great in vitro or in rodents, but - just theoretically - it could have very strange and absolutely unexpected side effects in humans. plenty of very promising drugs had to be cancelled in phase I clinical studies for of exactely such reasons. You should be grateful that the chem companies refused your offer to cooperate. It's definitely better to be on the safe side, isn't it?
    I actually wasn't going to make any money off the idea, and I wasn't asking for co-operation. I just proposed it to them as an idea they may be interested in going with. I don't make any money from the sale of research chems nor would I be interested in doing so.

    Also, I believe that the end issue wasn't that they didn't want to produce the SARMs, but rather that there was an issue sourcing it. So they didn't refuse to co-operate, per se, but just were unable to follow through with my idea.

    It doesn't concern me one way or another, because as I said, I wasn't going to make anything from it...I just proposed it as something that may have interested them (I sent them a bunch of data on it).

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    Originally Posted by hooker View Post
    I actually wasn't going to make any money off the idea, and I wasn't asking for co-operation. I just proposed it to them as an idea they may be interested in going with. I don't make any money from the sale of research chems nor would I be interested in doing so.

    Also, I believe that the end issue wasn't that they didn't want to produce the SARMs, but rather that there was an issue sourcing it. So they didn't refuse to co-operate, per se, but just were unable to follow through with my idea.

    It doesn't concern me one way or another, because as I said, I wasn't going to make anything from it...I just proposed it as something that may have interested them (I sent them a bunch of data on it).
    hooker,

    I apologize if you got the impression that I intended to offend you. that was not my intention. I only tried to express my general concerns about promising drugs / substances that could reach the end-users (as research chemicals) without being proprly tested before.

    and with regards to money: if you have a brilliant idea and invent the new "blocbuster" supplemetn and earn millions of dollars - I would be glad for you!
    my only concern is: the safety of the consumer must always be in the first place. as long this is provided, you can become more rich than bill gates if you want

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    hooker is offline
    Originally Posted by Dr.P View Post
    hooker,

    I apologize if you got the impression that I intended to offend you. that was not my intention. I only tried to express my general concerns about promising drugs / substances that could reach the end-users (as research chemicals) without being proprly tested before.

    and with regards to money: if you have a brilliant idea and invent the new "blocbuster" supplemetn and earn millions of dollars - I would be glad for you!
    my only concern is: the safety of the consumer must always be in the first place. as long this is provided, you can become more rich than bill gates if you want
    I understand.

    In a lot of cases, I actally put my own head on the chopping block with regards to testing things! For example, I had an EPO releasing Peptide given to me by a friend who owns a research chem company, who had done the research and wanted to see how it worked in people (in the real world, not just studies).

    Anyway, I loaded up on it, and got extremely lethargic (barely could function) ....so it was never released. I was also the first person to try several anabolics like the Stealth Labs line (which I liked), as well as the first incarnation of Masteron Enanthate (both at high doses).

    I don't mind being the test subject for stuff, though I agree with you, I'd want to see the clinical data, then see some real world studies, then try it myself, before it reached an end consumer, in the case of pharmaceuticals like SARMs, or the EPO releasing compound I tried. On the other hand, if something had been used by humans for a number of years, then I wouldn't be concerned with trying it myself..

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    Originally Posted by Dr.P View Post
    excellent thread! too bad I first need to spread some reps before I can give them to DR dave again.

    two questions:

    1. since the SARMS seem to bind well to ARs in pituitary gland, it apparently can be expected that they will shut down HPTA axis? any guesses to which degree this might happen?

    2. what is with their "androgenicity"? how will they influence beard / face hairs / acne / voice etc.?

    and two more questions:

    - any ideas on hepatic metabolism / oral bioavailability?

    - is any of the SARMS already in clinical testing for humans? and if yes, for which indication / application?

    best regards


    david
    Some great questions Dr.P and while I am far from an expert in endocrinology I can answer to the best of my ability based on what was said in the articles. Anyone else is more than welcome to add their two cents.

    As for affecting the HPTA - yes. All of the compounds that I read about decreased blood LH level (which would lead to a decrease in Testosterone production). In fact one of the compounds S-3 was being investigated to be used as a male contraceptive (using the feedback to decrease spermatogenesis). However, the level at which they affect the HTPA is variable. For example compound BMS-564929 had a 9 fold selectivity for muscle stimulation vs LH suppression, which can be compared to testosterones 1.2 fold selectivity (aka no selectivity) for muscle stimulation vs LH suppression. You also have to take into account that they are utlizing castrated rats . . . the effect in humans is yet to be seen.
    (7R,7aS)-10b had a >50 fold selectivity for muscle vs prostate and a 30 fold selectivity for muslce vs LH suppression. However this compound is in earlier stages of development but looks great so far

    Androgenicity: The articles did not comment on androgenicity measures as endpoints, based on what has been show thus far I would expect at least a moderate level of androgenicity . . .

    Oral bioavailability: all compunds that I saw were orally available and not expected to cause hepatotoxicity based on structure, clinical trials should help with that one

    clinical trials:
    BMS-564929 is reportedly in clinical trials for age related decline in muscle mass.
    One of the other ones I think it was S-3 (although I could be wrong on that one) was supposed to be in clinical trials as a male contraceptive
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Thumbs up

    Originally Posted by Dr.Dave1 View Post
    Some great questions Dr.P and while I am far from an expert in endocrinology I can answer to the best of my ability based on what was said in the articles. Anyone else is more than welcome to add their two cents.

    As for affecting the HPTA - yes. All of the compounds that I read about decreased blood LH level (which would lead to a decrease in Testosterone production). In fact one of the compounds S-3 was being investigated to be used as a male contraceptive (using the feedback to decrease spermatogenesis). However, the level at which they affect the HTPA is variable. For example compound BMS-564929 had a 9 fold selectivity for muscle stimulation vs LH suppression, which can be compared to testosterones 1.2 fold selectivity (aka no selectivity) for muscle stimulation vs LH suppression. You also have to take into account that they are utlizing castrated rats . . . the effect in humans is yet to be seen.
    (7R,7aS)-10b had a >50 fold selectivity for muscle vs prostate and a 30 fold selectivity for muslce vs LH suppression. However this compound is in earlier stages of development but looks great so far

    Androgenicity: The articles did not comment on androgenicity measures as endpoints, based on what has been show thus far I would expect at least a moderate level of androgenicity . . .

    Oral bioavailability: all compunds that I saw were orally available and not expected to cause hepatotoxicity based on structure, clinical trials should help with that one

    clinical trials:
    BMS-564929 is reportedly in clinical trials for age related decline in muscle mass.
    One of the other ones I think it was S-3 (although I could be wrong on that one) was supposed to be in clinical trials as a male contraceptive

    awesome information, DrDave!!!

    I literally can see thousands o bodybuilders running to their doc and asking for "the new contraceptive"

    haha, substances that easily surpass testosterone - and we don't even need to mention alkylated orals - with regards to effectivity and adverse effects as a prescription for every male! great times are coming!

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    icariin

    Applied Nutriceuticals's RPM brought my attention to icariin, which they refer to as a phytochemical SARM (It has other properties as well but not necessarily pertinent to SARMs) . . . sounded interesting and seems to have some potential . . .

    Asian J Androl. 2006 Sep;8(5):601-5. Epub 2006 Jun 5.
    The testosterone mimetic properties of icariin.
    Zhang ZB, Yang QT.

    AIM: To evaluate the testosterone mimetic properties of icariin. METHODS: Forty-eight healthy male Sprague-Dawley rats at the age of 15 months were randomly divided into four groups with 12 rats each: the control group (C), the model group (M), the icariin group (ICA) and the testosterone group (T). The reproductive system was damaged by cyclophosphamide (intraperitoneal injection, 20 mg/kg x day) for 5 consecutive days for groups M, ICA and T, at the sixth day, ICA (gastric gavage, 200 mg/kg x day) for the ICA group and sterandryl (subcutaneous injection, 5 mg/rat . day) for the T group for 7 consecutive days, respectively. The levels of serum testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), serum bone Gla-protein (BGP) and tartrate-resistant acid phosphatase activity in serum (StrACP) were determined. The histological changes of the testis and the penis were observed by microscope with hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase biotin-dUTP-X nick end labeling (TUNEL), respectively. RESULTS: (1) Icariin improved the condition of reproductive organs and increased the circulating levels of testosterone. (2) Icariin treatment also improved the steady-state serum BGP and might have promoted bone formation. At the same time, it decreased the serum levels of StrACP and might have reduced the bone resorption. (3) Icarrin suppressed the extent of apoptosis of penile cavernosal smooth muscle cells. CONCLUSION: Icariin has testosterone mimetic properties and has therapeutic potential in the management of hypoandrogenism.

    PMID: 16751992 [PubMed - indexed for MEDLINE]
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    A study on a differrent class of SARMs. Interesting although not quite as promising as some of the other compounds previously mentioned based on the limited info.

    J Med Chem. 2007 Apr 17; [Epub ahead of print] Links
    Novel Series of Potent, Nonsteroidal, Selective Androgen Receptor Modulators Based on 7H-[1,4]Oxazino[3,2-g]quinolin-7-ones.
    Higuchi RI, Arienti KL, Lopez FJ, Mani NS, Mais DE, Caferro TR, Long YO, Jones TK, Edwards JP, Zhi L, Schrader WT, Negro-Vilar A, Marschke KB.


    Recent interest in orally available androgens has fueled the search for new androgens for use in hormone replacement therapy and as anabolic agents. In pursuit of this, we have discovered a series of novel androgen receptor modulators derived from 7H-[1,4]oxazino[3,2-g]quinolin-7-ones. These compounds were synthesized and evaluated in competitive binding assays and an androgen receptor transcriptional activation assay. A number of compounds from the series demonstrated single-digit nanomolar agonist activity in vitro. In addition, lead compound (R)-16e was orally active in established rodent models that measure androgenic and anabolic properties of these agents. In this assay, (R)-16e demonstrated full efficacy in muscle and only partially stimulated the prostate at 100 mg/kg. These data suggest that these compounds may be utilized as selective androgen receptor modulators or SARMs. This series represents a novel class of compounds for use in androgen replacement therapy.

    PMID: 17439112 [PubMed - as supplied by publisher]
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    MHP Sarm-X . . . supp based SARM

    Their claims
    More Selective And Powerful Than Testosterone!
    Prohormones are a thing of the past - SARM-X is the Future! SARM-X represents the start of a new era in hormone induced hypertrophic muscle growth. SARM-X is the first of a new class of designer androgenic/anabolic steroid memetic compounds called SARMs (Selective Androgen Receptor Modulators). SARMs are bio-technically engineered to exert powerful androgenic/testosterone effects. With the advent of SARM technology, the scientific community boasts this new class of compounds is capable of superceding the effectiveness of testosterone in producing massive muscle building effects, due to the potent and selective actions specifically engineered for targeting androgenic receptors in muscle tissue and stimulating more rapid muscle growth.

    Through the implementation of breakthrough SARM technology, SARM-X offers all bodybuilders, regardless of their genetic predisposition, the potential to experience the single-most intense muscular development ever seen in bodybuilding science. Potent super anabolic stimulation of skeletal muscle is now possible with SARM-X.

    The Power & Selectivity of SARMs

    SARM-X possesse more powerful muscle building effects than other androgens such as testosterone and other steroid derivatives. SARM-X has the unique ability to selectively target androgen receptors specifically in muscle tissue and not bind to the androgen receptors in other tissues and organs. This greatly increases its anabolic activity in muscle tissue.

    While testosterone and other steroid derivatives possess powerful anabolic actions, these actions do not take place exclusively on the androgen receptors found in muscle mass. Therefore, a significant portion ends up being utilized on other androgen receptors found throughout the body. This non-selectivity limits the delivered dose to muscle tissue and minimized its anabolic effects. SARM-X selectively targets muscle and delivers a full mega dose directly to muscle tissue. This superior selectivity triggers the greatest possible anabolic muscle building reaction and makes SARM-X the most advanced legal over-the-counter compound available anywhere.
    I did a search on the active ingredient Trans-4-Hydroxy-3-Methoxycinnamic Acid . . . aka ferulic acid




    Experientia. 1979 May 15;35(5):696-9. Links
    Trans-4-hydroxy-3-methoxycinnamic acid (ferulic acid) inhibits the effect of androgens on the rat prostate.
    Saito T, Nohno T, Yoshida H, Yokoya H.
    Trans-4-hydroxy-3-methoxycinnamic acid (ferulic acid, FA) antagonized the effect of exogenous androgens on the ventral prostate (VP) in castrated rats as well as the effect of endogenous androgens in intact rats. FA, however, had no effect on the seminal vesicles (SV) and levator ani muscle (LAM), nor oestrogenic effect in female rats and mice. FA did not antagonize the receptor binding of testosterone nor inhibit the conversion of testosterone into 5 alpha-dihydrotestosterone (DHT).

    PMID: 446686 [PubMed - indexed for MEDLINE]
    Based on that info it looks like it specifically blocks androgens @ the prostrate but I see no results to support any anabolic effects . . . it said levator ani muscles were unaffected. Maybe MHP has more info . . ?

    As a side not I found some articles supporting it's use as an antioxidant
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    Sci bump
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    new SARMs in development

    1: J Med Chem. 2007 Jun 28;50(13):3015-3025. Epub 2007 Jun 7. Links
    Discovery of Potent and Muscle Selective Androgen Receptor Modulators through Scaffold Modifications.
    Li JJ, Sutton JC, Nirschl A, Zou Y, Wang H, Sun C, Pi Z, Johnson R, Krystek SR, Seethala R, Golla R, Sleph PG, Beehler BC, Grover GJ, Fura A, Vyas VP, Li CY, Gougoutas JZ, Galella MA, Zahler R, Ostrowski J, Hamann LG.

    A novel series of imidazolin-2-ones were designed and synthesized as highly potent, orally active and muscle selective androgen receptor modulators (SARMs), with most of the compounds exhibiting low nM in vitro potency in androgen receptor (AR) binding and functional assays. Once daily oral treatment with the lead compound 11a (AR Ki = 0.9 nM, EC50 = 1.8 nM) for 14 days induced muscle growth with an ED50 of 0.09 mg/kg, providing approximately 50-fold selectivity over prostate growth in an orchidectomized rat model. Pharmacokinetic studies in rats demonstrated that the lead compound 11a had oral bioavailability of 65% and a plasma half-life of 5.5 h. On the basis of their preclinical profiles, the SARMs in this series are expected to provide beneficial anabolic effects on muscle with minimal androgenic effects on prostate tissue.
    50 fold selectivity for muscle over prostate and 65% oral bioavailability is not bad
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    info on another potential SARM with interesting info on it's affect on female rats sexual behavior . . .

    1: Endocrine. 2007 Aug;32(1):41-51. Epub 2007 Oct 2.Links
    A selective androgen receptor modulator with minimal prostate hypertrophic activity enhances lean body mass in male rats and stimulates sexual behavior in female rats.
    Allan GF, Tannenbaum P, Sbriscia T, Linton O, Lai MT, Haynes-Johnson D, Bhattacharjee S, Zhang X, Sui Z, Lundeen SG.


    Androgen receptor (AR) ligands with tissue selectivity (selective androgen receptor modulators, or SARMs) have potential for treating muscle wasting, hypogonadism of aging, osteoporosis, female sexual dysfunction, and other indications. JNJ-28330835 is a nonsteroidal AR ligand with mixed agonist and antagonist activity in androgen-responsive cell-based assays. It is an orally active SARM with muscle selectivity in orchidectomized rat models. It stimulated growth of the levator ani muscle, stimulating maximal growth at a dose of 10 mg/kg. At the same time, JNJ-28330835 reduced prostate weight in intact rats by a mean of 30% at 10 mg/kg, while having no inhibitory effect on muscle. Using magnetic resonance imaging (MRI) to monitor body composition, it prevented half of the loss of lean body mass associated with orchidectomy, and restored about 30% of lost lean mass to aged orchidectomized rats. It had agonist effects on markers of both osteoclast and osteoblast activity, suggesting that it reduces bone turnover. In a model of sexual behavior, JNJ-28330835 enhanced the preference of ovariectomized female rats for sexually intact male rats over nonsexual orchidectomized males. JNJ-28330835 is a prostate-sparing SARM with the potential for clinically beneficial effects in muscle-wasting diseases and sexual function disorders.

    PMID: 17992601 [PubMed - in process]
    SARMs may have a role in a larger number of applications . . . osteoporosis for eample. This is good for those of us interested in SARMs as the more applications a drug has the more likely it is to receive research support
    1: Curr Opin Investig Drugs. 2007 Oct;8(10):821-9.Links
    Selective androgen receptor modulators for frailty and osteoporosis.
    Kilbourne EJ, Moore WJ, Freedman LP, Nagpal S.


    Androgens play an important role not only in male sexual differentiation, puberty, sexual behavior and spermatogenesis, but also in the maintenance of bone architecture and muscle mass and strength. For decades, steroidal androgens have been used by hypogonadal and aging men as hormone replacement therapy, and abused by prominent athletes as anabolic agents for enhancing physical performance. The use of steroidal androgens is associated with hepatotoxicity, potential for prostate stimulation, virilizing actions and other side effects resulting from their cross-reactivity to related steroid receptors. Therefore, to utilize the therapeutic potential of the androgen receptor for the treatment of indications such as osteoporosis and frailty, several pharmaceutical and biotechnology companies are developing non-steroidal tissue-selective androgen receptor modulators (SARMs) that retain the beneficial properties of natural androgens and exhibit better therapeutic indices. This article reviews the mechanism of androgen action, novel non-steroidal ligands under development and future directions of SARM research for the discovery of novel modulators for frailty and osteoporosis.

    PMID: 17907058 [PubMed - in process]
    Semi-intersting study not specific to SARMs but SARMs were utilized to explore the mechanism of action of anabolic agents, providing additional targets for future research
    1: Endocrinology. 2007 Dec 6 [Epub ahead of print] Links
    Cell-specific activation of the human skeletal {alpha}-actin by androgens.
    Hong MH, Sun H, Jin CH, Chapman M, Hu J, Chang W, Burnett K, Rosen J, Negro-Vilar A, Miner JN.


    Although it is evident that androgens increase muscle mass and strength, little is known about the critical molecular targets of androgens in skeletal muscle. In rodents, the skeletal alpha-actin gene is a tissue-specific gene only expressed in the levator ani, and other skeletal muscles, but not in the prostate or preputial gland, the well-known androgen target tissue. We have identified tissue-specific androgen-regulated genes in the skeletal muscle in rats following oral administration of androgens and focused on androgen-dependent up-regulation of the skeletal alpha-actin gene. To investigate the mechanism of action, an in vitro system with various cell lines and a series of deletion mutants of the alpha-actin promoter were utilized. The human skeletal alpha-actin promoter was activated by androgens in the muscle cell line C2C12, but not in the liver, prostate or breast cancer cell lines where exogenous human androgen receptor expressed. The sequence of the promoter is sufficient for cell-specific androgen response, providing a model for the tissue specificity demonstrated in vivo. Using a series of deletion mutants, the androgen response can be maintained using just the proximal promoter region. The importance of androgen regulation of this small portion of the human skeletal alpha-actin promoter was demonstrated by the correlation between muscle and the alpha-actin promoter activity for an array of selective androgen receptor modulators (SARMs), including an orally active SARM LGD2226. Taken together, the results suggest that the regulation of skeletal alpha-actin by androgens/SARMs may represent an important model system for understanding androgen anabolic action in the muscle.

    PMID: 18063690 [PubMed - as supplied by publisher]
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Interesting read.

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    here's one which i found pretty... interesting:

    http://www.ncbi.nlm.nih.gov/pubmed/1...ractPlusDrugs1
    Summarizing these data it is obvious that DMT is a powerful anabolic steroid with selective androgen receptor modulators (SARM) like properties
    accoring to this, wouldn't any compound with a high Q (i.e. effective on levator ani, but not prostate) be considered a SARM?

    THE INTERLOCUTOR
    this account has been closed. for any further inquiries or questions kindly refer to the expert advice of LakunaKoil aka. Joel.

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    Originally Posted by Interlocutor View Post
    here's one which i found pretty... interesting:

    http://www.ncbi.nlm.nih.gov/pubmed/1...ractPlusDrugs1


    accoring to this, wouldn't any compound with a high Q (i.e. effective on levator ani, but not prostate) be considered a SARM?

    THE INTERLOCUTOR
    It seems that way. It looks as though any steroid with a decent seperation between their anabolic actions and androgenic actions are now being called SARMs. lol.
    Here is a recent study which calls the old prohormone Norandrodiol a steroidal SARM:

    Endocrinology. 2007 Dec 20

    Tissue Selectivity of the Anabolic Steroid, 19-Nor-4-Androstenediol-3{beta},17{beta}-diol in Male Sprague Dawley Rats: Selective Stimulation of Muscle Mass and Bone Mineral Density Relative to Prostate Mass.

    Page ST, Marck BT, Tolliver JM, Matsumoto AM.

    Department of Medicine, University of Washington School of Medicine, Seattle, WA, United States, 98195; Geriatric Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, WA, United States, 98108 and Office of Diversion Control, Drug Enforcement Administration, Department of Justice, Arlington, VA, United States, 22202.

    Stimulation of prostate growth is a major concern with testosterone therapy in older hypogonadal men. As a result, non-steroidal selective androgen receptor modulators (SARMs) with anabolic activity but less prostate stimulation are being developed. Anabolic steroids might exhibit similar tissue selectivity. We hypothesized the anabolic steroid 19-nor-4-androstenediol-3beta,17beta-diol (3beta,19-NA)) would increase muscle, lean body mass (LBM), and bone mineral density (BMD) with little stimulation of prostate growth. Male Sprague Dawley rats were implanted with silastic capsules containing 3beta,19-NA (4,8 or 16 cm), dihydrotestosterone (DHT) (8cm), 19-nortestosterone (19-NT) (16cm) or four empty capsules after undergoing either a sham-operation (Intact) or orchidectomy (ORX). Serum gonadotropins, measured after 4, 8 or 24 weeks of treatment, were significantly lower in 3beta,19-NA-treated versus untreated, intact and ORX rats (P<0.05), and testosterone was lowered by 3beta,19-NA-treatment of intact animals. LBM and BMD were assessed after 20 weeks, and 4 weeks later rats were sacrificed for levator ani muscle (LA) and prostate weights. Compared to ORX rats, 3beta,19-NA-treated rats had dose-dependent higher LA weights, LBM and BMD, which were similar to intact and DHT-treated rats at the highest 3beta,19-NA dose. In contrast, prostate weights in all 3beta,19-NA-treated groups were similar to ORX rats and lower than intact, DHT- and 19-NT-treated rats even at the highest 3beta,19-NA dose. In summary, 3beta,19-NA increases muscle and bone mass without significant stimulation of prostate growth, suggesting it may have some properties of a steroidal SARM. Anabolic steroids such as 3beta,19-NA should be studied further to determine their mechanisms of tissue selectivity and effects in men.
    http://www.ncbi.nlm.nih.gov/pubmed/18096666

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    looks like they are starting to look into ways to screen for SARMs . . .


    1: Anal Bioanal Chem. 2008 Feb 13 [Epub ahead of print] Links
    Determination of benzimidazole- and bicyclic hydantoin-derived selective androgen receptor antagonists and agonists in human urine using LC-MS/MS.Thevis M, Kohler M, Thomas A, Maurer J, Schl?rer N, Kamber M, Sch?nzer W.
    Center for Preventive Doping Research, Institute of Biochemistry, German Sport University Cologne, Carl-Diem-Weg 6, 50933, Cologne, Germany, m.thevis@biochem.dshs-koeln.de.

    Selective androgen receptor modulators (SARMs) represent a novel class of drugs with tissue-specific agonistic and antagonistic properties, which are prohibited in sports from January 2008 according to the World Anti-Doping Agency. Preventive approaches to restrict the use of SARMs include early implementation of target analytes into doping control screening assays. Five model SARMs were synthesized, four of which are analogs to prostate-specific androgen receptor antagonists with a 5,6-dichloro-benzimidazole nucleus. The fifth SARM is a muscle-tissue specific agonist with a bicyclic hydantoin structure (BMS-564929). Dissociation pathways after negative electrospray ionization were studied using an LTQ-Orbitrap mass analyzer, and diagnostic product ions and common fragmentation patterns were employed to establish a screening procedure that target the intact SARMs as well as putative metabolic products. Sample preparation based on solid-phase extraction and subsequent LC-MS/MS measurement allowed for detection limits of 1-20 ng/mL, intra- and interday precisions of between 2.4 and 13.2% and between 6.5 and 24.2%, respectively. Recoveries varied from 89 to 106%, and tests for ion suppression or enhancement effects were negative for all analytes. Figure Precursor ion scanning as a tool to screen for the common nucleus of benzimidazole-derived SARMs.
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    somewhat unexpected yet interesting results . . . note, I am not promoting the use of 19-norandrostendione

    1: Toxicol Lett. 2008 Apr 1;177(3):198-204. Epub 2008 Feb 2. Links
    The prohormone 19-norandrostenedione displays selective androgen receptor modulator (SARM) like properties after subcutaneous administration.
    Diel P, Friedel A, Geyer H, Kamber M, Laudenbach-Leschowsky U, Sch?nzer W, Schleipen B, Thevis M, Vollmer G, Zierau O.

    One of the most frequently misused steroid precursors (prohormones) is 19-norandrostenedione (4-estrene-3,17-dione, NOR), which is, after oral administration, readily metabolised to nortestosterone, also known as nandrolone (durabolin). In this study we have characterised molecular mechanisms of its action determined its tissue specific androgenic and anabolic potency after subcutaneous (s.c.) administration and investigated potential adverse effects. Receptor binding tests demonstrate that NOR binds with high selectivity to the AR. The potency of NOR to transactivate androgen receptor (AR) dependent reporter gene expression was 10 times lower as compared to dihydrotestosterone (DHT). In vivo experiments in orchiectomised rats demonstrated that s.c. treatment with NOR resulted only in a stimulation of the weight of the levator ani muscle; the prostate and seminal vesicle weights remained completely unaffected. Like testosterone, administration of NOR resulted in a stimulation of AR and myostatin mRNA expression in the gastrocnemius muscle. NOR does not affect prostate proliferation, the liver weight and the expression of the tyrosine aminotransferase gene (TAT) in the liver.

    Summarizing these data it is obvious that NOR, if administrated s.c. and in contrast to its metabolite nandrolone, highly selectively stimulates the growth of the skeletal muscle but has only weak androgenic properties. This observation may have relevance with respect to therapeutic aspects but also doping prevention.
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    GSK phase I trial of what looks to be a SARM . . . if you're a healthy male and you live near Evansville, IN you may be able to participate as it looks like they are still enrolling patients for the safety trial. Of course with a safety trial it is unlikely you would be taking it long enough to really benefit and ya know ya could get seriously ill or die, oh well :P . . . interesting to see a SARM in clinical trials none the less

    link to clinical trial page http://clinicaltrials.gov/ct2/show/NCT00540553

    Study to Test Safety, Tolerability and Blood Levels of GSK971086 After 1 Dose & 7 Days of Dosing in Healthy Adult Males

    This study is currently recruiting participants.
    Verified by GlaxoSmithKline, October 2007

    Sponsored by: GlaxoSmithKline

    Information provided by: GlaxoSmithKline
    ClinicalTrials.gov Identifier: NCT00540553

    Purpose
    This research study is the first administration of GSK971086 in humans. The purpose of this study is to assess the safety and tolerability of GSK971086, as well as, how much GSK971086 is in your blood after different doses



    Condition Intervention Phase
    Healthy Volunteer
    Drug: placebo
    Drug: GSK971086
    Phase I



    U.S. FDA Resources

    Study Type: Interventional
    Study Design: Treatment, Randomized, Double-Blind, Placebo Control, Single Group Assignment, Safety Study

    Official Title: A Randomized, Double-Blind, Placebo Controlled, Dose Escalation Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of GSK971086 After a Single Dose and 7 Days of Repeat Dosing in Healthy Adult Male Volunteers


    Further study details as provided by GlaxoSmithKline:


    Primary Outcome Measures:
    Adverse events: [ Time Frame: all visits ]

    hematology, clinical chemistry, urinalysis: [ Time Frame: Part A Days -2,2,3,14,28 & Part B Days -2,2,5,8,14,21,35 ]

    vital signs & 12-lead ECGs: [ Time Frame: Part A Days -2-3,7,28 & Part B Days -2-9,14,35 ]



    Secondary Outcome Measures:
    GSK 971086 Plasma blood level: [ Time Frame: art A Days 1,2,3,7,14,21,28 & Part B Days 1-9,14,21,28,35 ]

    PBone & muscle biomarkers: [ Time Frame: Part A Days 1,2,7,14,21,28 & Part B Days 1,3,8,14,21,28,35 ]


    Estimated Enrollment: 132
    Study Start Date: August 2007


    Eligibility
    Ages Eligible for Study: 18 Years to 50 Years
    Genders Eligible for Study: Male
    Accepts Healthy Volunteers: Yes

    Criteria

    Inclusion Criteria:

    healthy male.
    18 to 50 years old, inclusive.
    willing and able to provide written informed consent before the start of any study-related procedures.
    able to understand and comply with protocol requirements, instructions, and protocol-stated restrictions.
    Exclusion Criteria:

    history of clinically significant endocrine, gastrointestinal, hepatic, cardiovascular, neurological, haematological, immunological, renal, respiratory, or genitourinary abnormalities or diseases.
    history at any time in the past of coronary artery disease, congestive heart failure, angina, myocardial infarction, any cardiac surgery, valvular heart disease, clinically significant arrhythmia, dyspnea, pulmonary edema, stroke, or transient ischemic attack.
    history of regular alcohol consumption greater than 14 drinks per week for males.
    positive drug or alcohol test at screening or check-in to the clinic.
    participated in another clinical trial within 30 days prior to screening in which you have received an investigational drug.
    donated a pint of blood within 56 days before the first dose of study drug.
    history of malignancy that is not in complete remission for at least 5 years, 1 year for non-melanomatous skin carcinoma
    abnormal lab test results more than 10% outside the normal range.
    History of serious psychological disorders such as schizophrenia, uncontrolled bipolar disorder, and suicidal behaviour
    positive results for hepatitis C or B, or HIV at screening.
    male subject who is unwilling to either abstain from sexual activity or unwilling to use birth control during the course of the study.
    using prescription or non-prescription drugs, vitamins, herbal or dietary supplements (including St John’s Wort) within 7 days before the first dose of study medication,
    Contacts and Locations


    Please refer to this study by its ClinicalTrials.gov identifier: NCT00540553

    Locations


    United States, Indiana
    GSK Clinical Trials Call Center Recruiting
    Evansville, Indiana, United States, 47714
    Contact: Randall Stoltz 877-379-3718


    Sponsors and Collaborators


    GlaxoSmithKline


    Investigators


    Study Director: GSK Clinical Trials, MD GlaxoSmithKline

    More Information

    Study ID Numbers: SAR109935
    First Received: October 4, 2007
    Last Updated: October 4, 2007
    ClinicalTrials.gov Identifier: NCT00540553
    Health Authority: United States: Food and Drug Administration


    Keywords provided by GlaxoSmithKline:
    SARM,
    FTIH,
    pharmacokinetics




    Study placed in the following topic categories:
    Healthy



    ClinicalTrials.gov processed this record on March 28, 2008
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Red face Call me a pessimist...

    Just as a side note, I think it's important to recognize that SERMs are found in men *and* women and from the research conducted, it appears that SARMs are inducers rather than competitive inhibitors (like traditional SERMs)-- therefore, SERMs and SARMs are not performing analogous actions in women and men, respectively.

    SERMs are typically used for breast cancer that is sensitive to estrogen. Therefore by inhibiting the receptor, the cancer's/breast tissue growth is hindered.

    SARMs (appear to be) stimulatory-- They removed the rat testes and with administration of S-4/SARM, the rats *only* increased their lean muscle mass and had slightly increased prostate mass. Interestingly, the levator ani & soleus muscles returned to normal (note: all other muscles didn't return to baseline, they just "increased" lean muscle mass. Meaning the effects of castration/lack of testosterone on the majority of the rats' muscles were still present)-- why specifically these two muscles returned to normal (and not all) perplexes me. It seems a bit random, especially the levator ani.

    So they are trying to create an anabolic-type molecule-- and the rats resulted in increased muscle mass (but not to pre-castration size except in the levator ani and soleus) and increased prostate mass-- by scientific standards, that they were "successful" in their trials. However, it has to be questioned: If the rats had their own endogenous testosterone (ie. they weren't castrated), would the SARM have had similar effects as anabolics (in terms of increased muscle mass however minimal)? Hmmm... I don't know. It's evident in the study that S-4 pales in comparison to DHT (activated testosterone)- which makes sense. Although the increased bone density is a good attribute to S-4 (After all, men can get osteoporosis too).

    Ultimately I don't think SARMs are going to go far. S-4 seems to be too weak. Maybe S-4/SARMs would be good for the old men who have had a bilateral orchidectomy secondary to prostate cancer (which I think is what they were going for)... but for bodybuilding supplement purposes? I'm kind of on the doubting side due to the fact that it appears to marginally increase muscle mass. The vast majority of bodybuilders/people who hope to build [major] muscle mass are above the baseline (AND have their testes!). That being said, S-4 is certainly a good starting point for further study development!

    Keep in mind though that it's important to read these studies with a suspicious eye because they want to showcase their findings as amazing (to get more grants/funding/etc)-- when in truth, they're likely just mediocre. I mean the people in this study were doing a continuation of a prior study where a partial SARM agonist (read: a weaker S-4 like molecule) showed positive results; S-4 was used as a *full* SARM agonist (and it only had marginal positive results). Just something to think about.

  28. #28
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    Originally Posted by EVentura84 View Post
    Just as a side note, I think it's important to recognize that SERMs are found in men *and* women and from the research conducted, it appears that SARMs are inducers rather than competitive inhibitors (like traditional SERMs)-- therefore, SERMs and SARMs are not performing analogous actions in women and men, respectively.
    yes, that is the whole point of SARMs . . . to get anabolic effects without some of the side effects like prostate hypertrophy

    SERMs are typically used for breast cancer that is sensitive to estrogen. Therefore by inhibiting the receptor, the cancer's/breast tissue growth is hindered.

    SARMs (appear to be) stimulatory-- They removed the rat testes and with administration of S-4/SARM, the rats *only* increased their lean muscle mass and had slightly increased prostate mass. Interestingly, the levator ani & soleus muscles returned to normal (note: all other muscles didn't return to baseline, they just "increased" lean muscle mass. Meaning the effects of castration/lack of testosterone on the majority of the rats' muscles were still present)-- why specifically these two muscles returned to normal (and not all) perplexes me. It seems a bit random, especially the levator ani.
    Again, SARMs are indeed stimulatory. As for the part about the levator ani and soleus . . . sometimes they pick a representative muscle or two to compare across groups, which is probably what was done here. This does not mean other muscles did not have similar results

    So they are trying to create an anabolic-type molecule-- and the rats resulted in increased muscle mass (but not to pre-castration size except in the levator ani and soleus) and increased prostate mass-- by scientific standards, that they were "successful" in their trials. However, it has to be questioned: If the rats had their own endogenous testosterone (ie. they weren't castrated), would the SARM have had similar effects as anabolics (in terms of increased muscle mass however minimal)? Hmmm... I don't know. It's evident in the study that S-4 pales in comparison to DHT (activated testosterone)- which makes sense. Although the increased bone density is a good attribute to S-4 (After all, men can get osteoporosis too).
    yes, an anabolic molecule which is selective for muscle over prostate to avoid side effects of anabolics. Which results from the study show that S4 pales in comparison to DHT?

    Ultimately I don't think SARMs are going to go far. S-4 seems to be too weak. Maybe S-4/SARMs would be good for the old men who have had a bilateral orchidectomy secondary to prostate cancer (which I think is what they were going for)... but for bodybuilding supplement purposes? I'm kind of on the doubting side due to the fact that it appears to marginally increase muscle mass. The vast majority of bodybuilders/people who hope to build [major] muscle mass are above the baseline (AND have their testes!). That being said, S-4 is certainly a good starting point for further study development!
    SARMs are in their infancy and as you mentioned are being developed for medical use not bodybuilding, but I think you are selling them short. Not to say that I think we will see many supplements based on SARMs for obvious reasons but I still see potential there

    Keep in mind though that it's important to read these studies with a suspicious eye because they want to showcase their findings as amazing (to get more grants/funding/etc)-- when in truth, they're likely just mediocre. I mean the people in this study were doing a continuation of a prior study where a partial SARM agonist (read: a weaker S-4 like molecule) showed positive results; S-4 was used as a *full* SARM agonist (and it only had marginal positive results). Just something to think about.
    I disagree with that statement. One of the major benefit to peer reviewed journals such as the ones cited above is that experts review the claims made by the researchers to make sure that outlandish claims are not made and that the claims which are made are supported by data.
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


    www.pubmed.gov . . . gotta love it

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    Red face Hmm

    Dave, I was merely making sure that those reading the thread knew that there was a differentiation between SERMs and SARMs-- and that both are present in both genders (as I'm sure you can understand might be less than clear with the title of the thread to those that aren't educated in endocrinology).

    "Which results from the study show that S4 pales in comparison to DHT?" I'm glad that you asked this because that was the impression I got when I read the abstract (and knowing what I do about DHT, I assumed some things about what was written about DHT). In truth, they don't fully disclose the results of DHT in the study. They say that DHT restores lean muscle mass "similar to S-4" (they don't give a quantifier)-- similar to S-4 as in MORE or similar as in LESS? We don't know. Unlike S-4, DHT largely increases prostate/sem. vesicle size but S-4 also increases prostate/sem. vesicle size too, just not as much. Then at the end of the abstract, the effect of DHT on the HPG axis is not included-- why not?

    I suppose for me, I always try to pick apart why these studies do not include the most that they can. Hence the pessimism. I tried to find the full article, but I couldn't get a copy via PubMed. Also, who funded the study? (I'm not trying to pick on this article, but rather just saying in general-) You never know what ulterior motives are behind such findings (and yes, peer reviewed articles are more reputable... but still, look at the recent CT scan/lung cancer debacle. That was a WIDELY praised study through Cornell U. and they just found out that it had been sponsored in part by a cigarette company, the millions in funding which was hidden by filtering it through a fictitious charity fund.)

    [http://www.nytimes.com/2008/03/26/he...h/26lung.html]

    In response to how they made their study seem more sparkly/exciting [when it's not necessarily as such], the grandiose wording, "In summary, the strong anabolic effects of S-4 in skeletal muscle, bone, and pituitary were achieved with minimal pharmacologic effect in the prostate." OK, yes S-4 did had a decreased effect on the prostate (compared to DHT, but it still caused hypertrophy), however was S-4 really "strong" on all fronts? Well we don't even really know about pituitary or muscle effects because they didn't tell us the DHT values to be able to compare. So, in that regard, they are kind of showcasing the bone and prostate effects which is sort of only giving us half the story (in my opinion).

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    Originally Posted by EVentura84 View Post
    Dave, I was merely making sure that those reading the thread knew that there was a differentiation between SERMs and SARMs-- and that both are present in both genders (as I'm sure you can understand might be less than clear with the title of the thread to those that aren't educated in endocrinology).

    "Which results from the study show that S4 pales in comparison to DHT?" I'm glad that you asked this because that was the impression I got when I read the abstract (and knowing what I do about DHT, I assumed some things about what was written about DHT). In truth, they don't fully disclose the results of DHT in the study. They say that DHT restores lean muscle mass "similar to S-4" (they don't give a quantifier)-- similar to S-4 as in MORE or similar as in LESS? We don't know. Unlike S-4, DHT largely increases prostate/sem. vesicle size but S-4 also increases prostate/sem. vesicle size too, just not as much. Then at the end of the abstract, the effect of DHT on the HPG axis is not included-- why not?

    I suppose for me, I always try to pick apart why these studies do not include the most that they can. Hence the pessimism. I tried to find the full article, but I couldn't get a copy via PubMed. Also, who funded the study? (I'm not trying to pick on this article, but rather just saying in general-) You never know what ulterior motives are behind such findings (and yes, peer reviewed articles are more reputable... but still, look at the recent CT scan/lung cancer debacle. That was a WIDELY praised study through Cornell U. and they just found out that it had been sponsored in part by a cigarette company, the millions in funding which was hidden by filtering it through a fictitious charity fund.)

    [http://www.nytimes.com/2008/03/26/he...h/26lung.html]

    In response to how they made their study seem more sparkly/exciting [when it's not necessarily as such], the grandiose wording, "In summary, the strong anabolic effects of S-4 in skeletal muscle, bone, and pituitary were achieved with minimal pharmacologic effect in the prostate." OK, yes S-4 did had a decreased effect on the prostate (compared to DHT, but it still caused hypertrophy), however was S-4 really "strong" on all fronts? Well we don't even really know about pituitary or muscle effects because they didn't tell us the DHT values to be able to compare. So, in that regard, they are kind of showcasing the bone and prostate effects which is sort of only giving us half the story (in my opinion).
    Indeed it can be beneficial to clarify the difference b/n SERMs and SARMs . . . I assumed people would realize there was a different relation but that's not always a safe bet.

    Fortunately, the study is available free @ pubmed.gov so I attached the PDF to this post for those interested in looking it over. Results seem inline with their abstract.

    LOL gotta love those cigarette companies, they're crafty. Good point on the funding as sometimes studies are funded by drug companies, which can raise questions. Based on the info from the article it looks like the study was funded by a National Institute of Diabetes and Digestiveand Kidney Diseases Grant.

    Valid points on the wording . . . I guess that's why it can be beneficial to read the full text when it's available
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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