SARMs versus AAS: Different Side Effects?

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madman

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Considerations, Possible Contraindications, and Potential Mechanisms for Deleterious Effect in Recreational and Athletic Use of Selective Androgen Receptor Modulators (SARMs) in Lieu of Anabolic-Androgenic Steroids: A Narrative Review
Steven B. Machek, Thomas D. Cardaci, Dylan T. Wilburn, Darryn S. Willoughby




ABSTRACT

Anabolic-androgenic steroids (AAS) are testosterone and testosterone-derivative compounds sporadically employed by athletes and are increasingly used recreationally to acquire a competitive edge or improve body composition. Nevertheless, users are subject to undesired side effects majorly associated with tissue-specific androgen receptor (AR) binding-mediated actions. More recently, selective AR modulators (SARMs) have gained popularity in delivering androgen-associated anabolic actions with hopes of minimal androgenic effects. While several SARMs are in preclinical and clinical phases intended for demographics subject to hypogonadism, muscle wasting, and osteoporosis, several athletic organizations and drug testing affiliates have realized the increasingly widespread use of SARMs amongst competitors and have subsequently banned their use. Furthermore, recreational users are haphazardly acquiring these compounds from the internet and consuming doses several times greater than empirically reported. Unfortunately, online sources are rife with potential contamination, despite a prevailing public opinion suggesting SARMs are innocuous AAS alternatives. Considering each agent has a broad range of supporting evidence in both human and non-human models, it is important to comprehensively evaluate the current literature on commercially available SARMs to gain a better understanding of their efficacy and if they can truly be considered a safer AAS alternative. Therefore, the purpose of this review is to discuss the current evidence regarding AAS and SARM mechanisms of action, demonstrate the efficacy of several prominent SARMs in a variety of scientific trials, and theorize on the wide-ranging contraindications and potentially deleterious effects, as well as potential future directions regarding acute and chronic SARM use across a broad range of demographics.




INTRODUCTION

The abuse of anabolic substances for performance persists as a prominent issue in athletic demographics [1]. Individuals have historically utilized anabolic androgenic steroids (AAS) in an attempt to enhance their exercise training performance outcomes and subsequent recovery [2, 3]. Since the initial speculation of Soviet Doping in the 1952 Olympic games and the subsequent synthesis of methandrostenolone, several AAS ([which are typically classic androgens such as testosterone, dihydrotestosterone (DHT), and 19-nortestosterone [structurally identical to testosterone with the 19th carbon removed]) derivatives have been developed [4]. With varying effects, elimination of half-lives, and contraindications, all androgens have a history of abuse when used with the intent of improving strength and body composition [4, 5]. The clear competitive advantage these anabolic compounds infer led to the creation of stringent regulations enforced by entities such as the International Olympic Committee (IOC) and the World Anti-Doping Agency (WADA), ultimately becoming amended into the Controlled Substances Act in 1990 as schedule III substances [4]. Interestingly, most who use AAS are not competitors, but recreational users who desire an improved aesthetic/muscular appearance [5, 6]. The internet is the most common source for procuring AAS and ancillary drugs, whereby suppliers will typically bundle packages that include combinations of testosterone, synthetic androgens, and colloquially denoted post-cycle therapy (PCT) compounds [5]. Unfortunately, illegal and unregulated abuse of AAS can lead to several unwanted side effects in males. Testicular atrophy, fluid retention, breast pain, gynecomastia, oily skin, and alopecia are typical androgenic-related side effects, but some also experience mood disturbances including depressive symptoms, lethargy, insomnia, and decreased libido [5, 6]. Furthermore, prolonged use can result in hepatotoxicity, as well as damage to the cardiovascular, renal, immunologic, and hematological systems [7-15]. While males have been reported to abuse AAS two-to-three times greater than females, use it not precluded from either sex [6]. Females may experience masculinization with clitoral hypertrophy, hair growth (hirsutism), decreased breast size, menstrual irregularities, widening of the upper torso, and voice deepening, as well as symptoms related to hypomania and depression [4, 16, 17]. The majority of side effects (i.e. reduced sperm production, impotence, testicular atrophy, etc.) in males resolve after cessation; however, many of the adverse changes in women may be irreversible. Chronic use may further result in cardiovascular disease incidence via alterations in hematological parameters related to erythropoiesis, endothelial function, and/or serum lipid profiles, as well as an associated risk in males with prostate cancer [6, 18-20]. Supraphysiological doses of androgens are, therefore, clearly dose-limiting, whereby their positive impacts on physical function are curtailed by substantial adverse risk [21].

The plethora of AAS-mediated side effects has been the impetus to discover androgens that have beneficial anabolic activity with reduced or substantially limited androgenic activity [4, 21]. Pharmaceutical companies have made great strides in the development of metabolic agents that demonstrate anabolic activity in skeletal muscle and bone, whilst lacking cross-reactivity with other steroid receptors, and are not substrates for[22]either 5α-reductase nor aromatase (thereby lacking conversion to DHT and estradiol, respectively) [23, 24]. One of the prominent leading compound categories is selective androgen receptor modulators (SARMs) [21]. These agents were developed as more favorable alternatives to AAS, with comparable androgen receptor (AR) affinity and minimal androgenic impacts [25, 26]. Many SARMs exist as non-steroidal compounds (quinolones, tetrahydroquinolones, tricyclics, bridged tricyclics, aryl propionamides, aniline, diaryl aniline, bicylclic hydantoins, benzimidazole, imidazolopyrazole, indole, and pyrazoline derivatives), which in-part mediate their unique effects [4, 21]. SARMs are being clinically investigated for their roles outside of performance, positioned for treatment of hypogonadism, osteoporosis, cancer cachexia, and aging-related decrements in strength and/or muscle function (i.e. sarcopenia or pre-sarcopenia) [21, 27-29]. Furthermore, recent clinical trials have further demonstrated potential SARM-mediated tumor growth suppression, whereby select compounds in clinical and pre-clinical trials positively modulate breast cancer cells via tissue-specific AR [22, 30-32]. In brief, a multiplicity of SARM compounds have been developed for their potential role in ameliorating the aforementioned pathologies, and several investigations have demonstrated mechanistic efficacy in their ability to selectively act in an anabolic fashion (improved skeletal muscle size and function, as well as to attenuate bone decrements) via AR modulation, all whilst having minimal androgenic effects (action in the prostate, seminal vesicles, testes, and accessory tissues) [21, 25, 33-35]. These compounds potentially act via tissue-specific distribution, interactions with enzymatic conversion of testosterone, differential AR structure modulation, and/or selective coregulator protein recruitment [25, 34, 36]. Unfortunately, the attractive aspects of SARMs have also garnered attention as novel recreational performance-enhancing compounds [27]. In 2008, WADA banned SARMs in absolute due to their inherent abuse risk and the then-present detection of various SARM metabolites in athlete urine samples in 2010 [26, 33, 37]. Consequently, SARM misuse has steadily increased over the last decade, whereby nearly 40 cases were reported via WADA doping control sample analysis in 2016 [38]. Similar to AAS and other ancillary performance-enhancing substances, SARM providers are commonly found on the internet and small laboratories both within and outside the US are able to synthesize these compounds for global distribution [26, 27].

Notwithstanding the several investigations and comprehensive reviews existing to illustrate both the efficacy of SARMs as promising clinical agents, as well as the contraindications for AAS use in recreational and competitive athletes, there is a dearth of evidence reporting on chronic use of the former [24]. There is also a stark paucity of any literature evaluating the potentially very serious implications of SARM abuse in otherwise healthy recreational and competitive demographics. Therefore, the purpose of this narrative review is to 1) discuss the current evidence regarding AAS and (postulated) SARM mechanisms of action, 2) demonstrate the efficacy of several prominent SARM compounds in a variety of scientific trials, as well as 3) theorize on the wide-ranging contraindications and potentially deleterious effects, as well as potential future directions regarding acute and chronic SARM use for a full breadth of subject demographics.




THE ANDROGEN RECEPTOR

*Androgen Receptor Structure, Androgens, and Ligand Binding Mechanisms

*Impact of Selective Androgen Receptor Modulator Mechanisms





EXISTING EVIDENCE ON SARM COMPOUNDS

*GTx-024/ Enobosarm/ MK-2866/ Ostarine

*LGD-4033/ Ligandrol

*RAD140/ Testalone

*S-4/ Andarine

*YK11


*SARM-2f, S-101479, & GSK2881078




SARM CONTRAINDICATIONS & POTENTIAL MECHANISMS FOR DELETERIOUS EFFECT


*Physiologic Concerns of SARM Administration




FUTURE DIRECTIONS AND CONCLUDING STATEMENTS

This review illustrates the enigmatic nature of SARMs. While the previous sections have provided information on AR function, androgen action, and the available literature on compounds commonly marketed as SARMs, there is much to still be elucidated. Future research is foremost tasked with extending investigations on the aforementioned compounds, demonstrating further efficacy in clinically-approved human trials amongst healthy populations, including longitudinal research, whilst also providing novel human investigations amongst the compounds that remain in preliminary stages [24]. It appears enobosarm, GSK2881078, and RAD140 are the most empirically viable SARMs amidst clinical therapies, while the remaining are either under-researched (either lacking human trials or sufficient evidence) or have otherwise ceased production [30, 74, 75, 84, 86, 121-123]. Clearly, few have reached clinical trial stages and those existing have both mixed outcome variables and often inconsistent findings. It is not then unreasonable to surmise that potential SARM candidates are being pharmacologically produced at a speed surpassing the rate at which they can be sufficiently vetted. Furthermore, the ultimate consequences of SARMs in black market-supplied doses may only become known as current and future abusers report potential side effects. Given the popularity of recreational use, doping research is pushed to elucidate short-and long-term metabolites to detect the multiplicity of SARMs available. As previously stated, several of the aforementioned compounds have varied primary outcomes (pharmacokinetic, strength, body composition, etc.), disabling more conclusive statements to be made on individual SARM efficacy and/or their individual effects. The necessity to substantiate SARM mechanisms of action also persists; it is not well understood how each compound uniquely functions, nor is the general operation of SARMs well described. Considering SARMs are not subject to aromatization, they are often perceived as having no effect on the HPG axis [24]. The formerly described investigations, however, clearly demonstrate a wide range of impacts on gonadotropins. Oddly, LGD-4033 administration results in dose-dependent reductions in FSH without concomitant attenuations in LH [75]. This is in direct contrast to enobosarm which experienced no changes in gonadotropins, as well as S-4 and S-23 which either solely inhibited LH or dually (using higher doses) suppressed both gonadotropins [23, 81, 83]. Perhaps LGD4033 contains some dual receptor cross-reactivity with S-4 and S-23; whereby LGD-4033 antagonizes LH receptors at the Leydig cells to inhibit testosterone whilst maintaining GnRH and simultaneously facilitating normal inhibin-mediated negative feedback at the Sertoli cells (see Figure 2) [42]. Conversely, it can only be speculated based on limited evidence in S-4 and S-23 that these compounds act more robustly on the opposite arm of the HPG axis, inhibiting LH at every dose whilst only affecting FSH at higher dosages. Although we are unaware of any literature investigating the role of either S-4 or S-23 on testosterone suppression, it stands to reason that substantial reductions in LH would lead to decreased androgen concentrations. Since androgens are known to impart negative feedback on FSH via inhibin, perhaps potentially robust decreases in testosterone following non-steroidal-S-4 and -S-23-mediated LH reductions continue FSH secretion [124]. Conversely, higher doses may act concentration-dependently in a manner similar to the putative LGD-4033 mechanism to antagonize LH receptors and/or suppress upstream GnRH akin to traditional AAS. Therein remains the possibility that several SARMs modulate activin and/or inhibin to impart negative feedback on gonadotropins. As structurally-related members of the TGF-ß superfamily, it is known that gonadotropins are regulated by the opposite effects of activin and inhibin [125]. Considering inhibin can interact with the activin receptor, perhaps SARMs with differential effects on either gonadotropin may also impact their concentrations. This may represent a promising avenue for LGD-4033 mechanisms specifically, which demonstrated a preferential suppression in FSH with equivocal LH changes at any dose [75]. Nevertheless, these speculations require an extensive examination to confirm the potential varying impacts amongst the multiplicity of SARM compounds. It is worth noting that relatively high enobosarm dosages provided via internet distributors (>20mg per serving) relative to the highest clinically evaluated trials (3mg/day) had no detrimental effects on upstream gonadotropins [23, 27]. This may indicate that enobosarm, with the most modestly suppressive effects and efficacy in human trials, is the most accurate representation of a compound that may elicit the benefits of AAS with the fewest HPG axis impacts.

More efforts are also required to determine specific coregulator recruitment following SARMAR binding and how exercise modulates the effects of individual compounds. A trial in S-101479 demonstrated that several cofactors, including ß-catenin, were not recruited via SARM ligand binding [34]. Moreover, Spillane et al. [50] discovered that full-body resistance training resulted in both higher upregulations of AR and ß-catenin proteins at 3 and 24 hours post-exercise. Mechanical tension can mediate ß-catenin signaling and may therefore compensate for potentially reduced recruitment via SARM administration [126].
It is also unknown if SARMs can interact with the more recently discovered membrane-bound GPCR/AR that facilitates mTOR activation (and upstream PI3K/Akt) [115]. Possibly, activation of this putative receptor may increase cytosolic ß-catenin for AR-coactivation via glycogen synthase kinase 3ß (GSK3ß) phosphorylation downstream of PI3K/Akt. GSK3ß is part of the destruction complex for ß-catenin that tags it for degradation, and thus phosphorylation facilitates complex dissociation and subsequent increased cytosolic ß-catenin [126]. ß-catenin’s role in cell-cell adhesion via actin cytoskeleton-adherens junction linking (formed by cadherin and α-catenin) and its release from the complex further frees supervillin protein. Supervillin not only functions to transduce signals from cellular adhesion sites but can function similarly to ß-catenin as a coactivator to modulate gene transcription [36]. Potential attenuations in SARM-induced ß-catenin coregulatory protein recruitment might also be compensated for by exercise-mediated stimulation of kinase cascades via phosphorylation of AR. Focal adhesion kinase (FAK) is commonly phosphorylated in response to mechanotransduction, displaying significant crosstalk with MAPK to increase AR transcriptional activity [36]. Nevertheless, specific cellular pathways modulated via SARM administration are almost entirely unknown and require elucidation.

Sex-specific SARM effects on humans also remain considerably nebulous. SARMs may represent a more tempting option for female recreational use given potential previous tendencies towards less androgenic AAS (i.e. oxandrolone) [103]. Regardless, as the latter still imposes a risk for permanent masculinization and hepatotoxicity, SARMs are largely uncharacterized for female-specific impacts. Despite the previously mentioned female-directed clinical treatments regarding breast cancer and urinary incontinence, potential HPO axis impacts require further investigation [22, 30-32, 64]. Enobosarm displayed sex-specific differential effects on gonadotropins, with females experiencing decrements in LH and FSH [23]. However, the lowered hormones did not impact estradiol or any other physical/biochemical index. As previously stated, Clark et al. [92] and Neil et al. [93] represent a limited number of trials aimed at determining sex-specific pharmacokinetic differences via GSK2881078 administration. Both employed sex-specific dosing with typically larger male doses, but these investigations collectively found consistently longer female-oriented measurable concentrations following their last dose, as well as a female-favored sensitivity resulting in greater relative lean mass gained. Overall, select trials have investigated the effects of SARMs in female animals, but few beyond those already highlighted have aimed to determine sex-specific differences [64, 81, 90].

No research exists evaluating the impacts of combining SARM compounds, which is especially relevant given the common occurrence of AAS compounds either concerted with one another or with ancillary substances [42]. The combination of compounds that selectively target specific tissues may provide an avenue to avoid the deleterious influence of potentially suppressed systemic peripheral testosterone.
Furthermore, given the possibility of chronic SARM-mediated decrements in circulating estradiol, it might be pragmatic to concurrently administer a selective estrogen receptor modulator (SERM). While previous data on tamoxifen has displayed negative impacts on pancreatic beta cells, including concomitant insulin resistance, increased hypertriglyceridemia, and subsequent weight gain, a more novel SERM such as bazedoxifene (BZA) might represent a promising candidate [127-131]. BZA demonstrates ER agonist activity in bone, as well as antagonistic activity in the breast and uterus. Furthermore, it facilitates increases in estradiol and bioavailable testosterone, whilst promoting favorable effects on lipid and glucose metabolism [128, 129, 132]. BZA has also displayed further efficacy by restoring the skeletal muscle satellite cell pool in estradiol-deficient mice [117]. Furthermore, the combination of SARMs and SERMs demonstrated credence in an investigation previously referenced by Furuya et al. [87]. Co-administration of S-101479 and raloxifene (1mg/kg each) significantly increased BMD relative to a single treatment of either compound alone. Therefore, perhaps co-administration of these or similar SERMs may facilitate estradiol-mediated systemic benefits during a SARM cycle.

SARMs were developed as safer alternatives to AAS, maximizing anabolic, and minimizing androgenic effects. While their intention was originally clinical in nature, recreational and competitive users have become privy to these compounds and their potential for improving body composition and athletic performance. Several trials have managed to demonstrate efficacy in select SARMs, however, there is insufficient research demonstrating potential health risks. Relatively few SARMs have displayed efficacy in human models, and internet providers are quick to advertise doses several times greater than the empirically-based investigations. Furthermore, several of these compounds elicit unfavorable alterations in testosterone, gonadotropins, serum lipids, and other hematological parameters. Insufficient time has elapsed to evaluate the efficacy of anecdotal dosing regimens and whether post-cycle therapies are warranted and might mirror those used in AAS. Additionally, reported SARM-induced fat-free mass increases are a mere fraction of that reported in modest doses of testosterone derivatives in similar timeframes (~1.5kg versus ~7kg in SARMs and testosterone, respectively) [21]. The available literature best depicts these compounds as promising clinical agents in hypogonadal, cachectic, as well as aging scenarios, but leaves the user in recreational and/or athletic endeavors both unclear and potentially hazardous due to possible contraindications which have been discussed herein.
 

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madman

Super Moderator
Highlights

SARMs were developed to provide clinical androgen benefits without side effects


SARMs are becoming more common in recreational abuse

SARMs were recently FDA banned and lack supporting evidence

SARMs may impact hypothalamic-pituitary regulation with systemic ramifications
 

madman

Super Moderator
Figure 1. A depiction of the differences potentially defining AR-binding between androgens (testosterone & DHT) compared with non-steroidal SARMs. In brief, SARMs ideally denote beneficial anabolic actions in androgen-responsive tissues such as skeletal muscle and bone, without unwanted androgenic side effects. They do not undergo conversion to DHT or estradiol, which partially mediates a lack of SARM-induced androgenic impact. The SARM mechanism of action is far from elucidated, but potentially may be sourced in 5α-reductase or aromatase modulation, as well as a potential inability for N/C interaction between the ligand-independent NH2-terminal transactivation domain (AF-1) located in the DBD and the ligand-dependent carboxy-terminal transactivation domain (AF-2) located in the LBD. Through this incomplete interaction that is typically deemed necessary for full AR agonist activation, SARMs may also impact AR DBD topology and affect the ability of the transcriptional binding complex to recognize specific DNA sequences. Incomplete N/C interaction ostensibly alters coregulator recruitment, indicating that SARMs selectively inducing different coactivators and corepressors, as well as recruiting them in differential magnitudes relative to androgens [21, 25, 34, 36, 40, 50, 64, 65].
Screenshot (2573).png

ARE = androgen response elements; AF-1 = activation function 1; AF-2 = activation function 2; AR = androgen receptor; DBD = DNA-binding domain; ECF = extracellular fluid; ER = estrogen receptor HSP = heat shock proteins ICF = intracellular fluid; LBD = ligand-binding domain; SARM = selective estrogen receptor modulator
 

madman

Super Moderator
Figure 2. The potential impacts of varying SARMs on the male hypothalamic-pituitary-gonadal axis. Amongst those most comprehensively researched and commercially available compounds with regards to these effects (gonadotropins and testosterone outcomes) are enobosarm, LGD-4033, and S-4. Each display widely varying effects on the axis along with the entire feedback system, along with wholly underresearched downstream impacts on systemic physiology. Mechanisms of each SARM and the drug class, in general, are unclear but may be sourced in dose-dependent effects and/or the potential for specific receptor-mediated antagonism. We also posit the putatively deleterious impacts of attenuated androgen and subsequent estradiol following high-dose and/or chronic SARM use.
Screenshot (2574).png

FSH = follicle-stimulating hormone; GnRH = gonadotropin releasing hormone, LH = luteinizing hormone
 

madman

Super Moderator
Table 1. List of compounds typically sold commercially as “Selective Androgen Receptor Modulators” and their general effects in various subject populations [23, 24, 26, 27, 34, 37, 40, 64, 67, 75-78, 81, 82, 84, 90, 92-94]
Screenshot (2577).png

Screenshot (2578).png

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T

tareload

Guest
Interesting and educational thread on many levels related to above.


a couple of anecdotes at the bottom to Nelson's point.
 

BigTex

Well-Known Member
I will give you my more anecdotal view of SARMS. I have a very close friend in China that is a biochemist so I was/am able to get some very good quality SARMS of all kinds since the early 2000's. I have read all of the supporting research on this stuff over the years and tried ALL of them. In all, I would have to say it would be a LONG SHOT to say any of them are worth trying. Compared to even low doses of anabolic steroids, SARMS are very weak to say the least. My wife seem to get a little bit out of Ostarine but only for a very short period of time, not even close to Anavar as they advertise. I seem to feel a little aggression using RAD 140 but that only lasted 1-2 workouts. I did not blood work using these but was definitely not impressed at all. Throw in the fact that they are WAY over priced here in the USA and I feel they are a complete waste of money. The only product that I feel has any value is the MK 677. That can be combined with GHRH's and GHRP's or even hGH to get some pretty good results. But again, it is way over priced.

(either lacking human trials or sufficient evidence) ....seems quite a few of these products fall under this category. IMHO the cost of doing these + side effects far outweigh the benefits.
 
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BigTex

Well-Known Member
SARMS shut down HPTA, decrease HDL, increase liver enzymes and produce smaller gains relative to anabolic steroids.
GREAT point Nelson. These products seem to be heavily marketed to teenagers who are considering using anabolic steroids but just don't know how to get them. These are easily acquired by the internet.
 

sammmy

Well-Known Member
My experience with a low dose Ostarine, clearly shows suppression of HPTA at 17 days, possibly even earlier if I measured it earlier. Most of the claims written on sites that sell SARMS are just not true.
 

Anonymon

Active Member
Well said and summarizes what we know about SARMs to date. No reason why anyone should even consider taking them.
I don’t know about that. I don’t recommend them in general but I’ve done Ostarine several times off and on TRT and know a bunch of guys that did all the SARMs. I own a bunch of them all but only did Ostarine. If you’re a guy on TRT already and your SHBG is higher, Ostarine does seem to reliably lower SHBG. In general it’s also pretty anabolic and can give you a boost at low doses like 6mg, which is closer to the studies. Makes most guys walk around looking pumped up still at those doses on TRT too. Also speeds up healing. Had something with my shoulder that went away in a week on it. Maybe even sooner.

It’s not a steroid cycle or anything, especially at low doses, but I can see at least Ostarine having its place when used with purpose.

I want to say Ostarine suppressed or shut down my test when I did it off TRT, but blood tests showed I was about the same before and after using it each time, with all my other bloodwork values being the same. Those were at 20-30mg a day doses.

On TRT, I tried 20mg a day for a spell, and it was like a super version of what I’d experienced before. They’re not AAS by any measure, but as a weak TRT boost or to help recover from something at a low dose, I think they can have their place.

I’ll agree that almost all claims online about SARMs are made up nonsense, like RAD being 100x as powerful as test and things like that. A lot of the info out there on them’s dangerous too because they tell people to stack them.
 

Wilson7

Active Member
I don’t know about that. I don’t recommend them in general but I’ve done Ostarine several times off and on TRT and know a bunch of guys that did all the SARMs. I own a bunch of them all but only did Ostarine. If you’re a guy on TRT already and your SHBG is higher, Ostarine does seem to reliably lower SHBG. In general it’s also pretty anabolic and can give you a boost at low doses like 6mg, which is closer to the studies. Makes most guys walk around looking pumped up still at those doses on TRT too. Also speeds up healing. Had something with my shoulder that went away in a week on it. Maybe even sooner.

It’s not a steroid cycle or anything, especially at low doses, but I can see at least Ostarine having its place when used with purpose.

I want to say Ostarine suppressed or shut down my test when I did it off TRT, but blood tests showed I was about the same before and after using it each time, with all my other bloodwork values being the same. Those were at 20-30mg a day doses.

On TRT, I tried 20mg a day for a spell, and it was like a super version of what I’d experienced before. They’re not AAS by any measure, but as a weak TRT boost or to help recover from something at a low dose, I think they can have their place.

I’ll agree that almost all claims online about SARMs are made up nonsense, like RAD being 100x as powerful as test and things like that. A lot of the info out there on them’s dangerous too because they tell people to stack them.
Oxandrolone will do the same and more, been used in humans for decades, FDA approved, has an excellent safety profile, and available compounded for less than $100 for 90 x 15 mg caps. IMO, there are reasons why they are not FDA approved.
 

Anonymon

Active Member
Oxandrolone will do the same and more, been used in humans for decades, FDA approved, has an excellent safety profile, and available compounded for less than $100 for 90 x 15 mg caps. IMO, there are reasons why they are not FDA approved.
To be fair to SARMs, some are only recently even being patented and all that takes time. That’s why you can’t buy them from your TRT clinic, not because they’re bad.
 
T

tareload

Guest
Oxandrolone will do the same and more, been used in humans for decades, FDA approved, has an excellent safety profile, and available compounded for less than $100 for 90 x 15 mg caps. IMO, there are reasons why they are not FDA approved.
Wow, somebody must have dropped the price.



Sounds way low.

1652823893386.png



1652823909448.png
 

BigTex

Well-Known Member
To be fair to SARMs, some are only recently even being patented and all that takes time. That’s why you can’t buy them from your TRT clinic, not because they’re bad.


I know a few of them tried to get a patent but dropped it. At this point IMHO it would be a waste of money because every biochemical lab in China is already producing huge amounts. For instance Ostarine is also know as Enobosarm which was developed by GTx, Inc. who developed it with Merck. This SARM was involved in a few Phase II clinical trials, but failed and two Phase III trials which also failed. Millions have already been invested only to have Chinese labs market it all over the world. Not much incentive to keep spending money. It became pretty successful with people who were drug tested in sport until WADA caught on. Quite a few have been caught since then.

I think the biggest success is it being market on line as an alternative to anabolic steroids. It is usually compared to Oxandrolone (which it is not). Its very easy to buy on the internet and the FDA rarely does anything to try to stop it. This is the case with all of the SARMS, China has already developed the formulas and produced them in huge amounts meanwhile those who developed them are stuck in Clinical trials. Check this out for instance, just one of many sites that sell this direct from the Chinese labs.

Readalot.....speaking of dropping the prices, check this out (this is for real too)
Oxandrolone 25mg 100-ct $85
Oxandrolone 10mg 100-ct $55
 
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Anonymon

Active Member
I know a few of them tried to get a patent but dropped it. At this point IMHO it would be a waste of money because every biochemical lab in China is already producing huge amounts. For instance Ostarine is also know as Enobosarm which was developed by GTx, Inc. who developed it with Merck. This SARM was involved in a few Phase II clinical trials, but failed and two Phase III trials which also failed. Millions have already been invested only to have Chinese labs market it all over the world. Not much incentive to keep spending money. It became pretty successful with people who were drug tested in sport until WADA caught on. Quite a few have been caught since then.

I think the biggest success is it being market on line as an alternative to anabolic steroids. It is usually compared to Oxandrolone (which it is not). Its very easy to buy on the internet and the FDA rarely does anything to try to stop it. This is the case with all of the SARMS, China has already developed the formulas and produced them in huge amounts meanwhile those who developed them are stuck in Clinical trials. Check this out for instance, just one of many sites that sell this direct from the Chinese labs.

Readalot.....speaking of dropping the prices, check this out (this is for real too)
Oxandrolone 25mg 100-ct $85
Oxandrolone 10mg 100-ct $55
It wouldn’t be a waste of money because them patenting it is part of what would encourage people to crack down on the SARMs grey market, as the reason they’re sold online is because it’s for supposed research purposes.

At least from a pharmacy, my Oxandrolone is far more expensive.
 
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