Ostarine (MK-2866; Enobosarm) – Results, Clinical Trials & Reviews

Ostarine is the most well known and extensively studied selective androgen receptor modulator (SARM) right now.

It is categorized as a SARM because of its unique selectivity at the androgen receptor where it exhibits a significant amount of anabolic activity in the body relative to androgenic activity.

It is being researched to determine if it is a potential treatment for the management of muscle and bone wasting diseases.

This article covers Ostarine's potential therapeutic applications, dosages, side effects, and anecdotal findings based on my own personal research.

What Is Ostarine?

Ostarine, also known as Enobosarm, GTx-024 and MK-2866, is a selective androgen receptor modulator (SARM).

SARMs, like Ostarine, stimulate androgen receptors in a selective way, whereby they induce a significantly greater amount of anabolic activity in the body relative to androgenic activity [R].

Testosterone was the first anabolic androgen to be approved for use in a clinical setting, however, its scope of versatility has always been severely limited by its androgenicity and its pharmacokinetic issues.

Most notable being its lack of selectivity for muscle tissue to other androgen affected tissues like the prostate, and not being orally bioavailable [R].

Testosterone has a 2:1 selectivity for muscle to prostate [R].

This lack of selectivity disqualifies Testosterone entirely in a clinical setting for treating women, as well as men in many scenarios, due to the significant androgenic activity that would occur at a systemic level during the attempted management of muscle or bone wasting diseases.

This is where SARMs like Ostarine display such promise as viable alternatives [R].

The ideal anabolic agent should demonstrate anabolic selectivity in muscle and bone without suppressing luteinizing hormone (LH), not negatively interact with other steroid receptors in the body, exhibit a high level of oral bioavailability without being 17 alpha-alkylated, and avoid 5-alpha reduction to DHT and aromatization into Estrogen [R].

SARMs were first discovered in 1998, following which several different compounds were developed by a variety of pharmaceutical companies in order to find a viable compound to satisfy this obvious need in degenerative disease treatment [R].

Ostarine's Mechanism Of Action

By exhibiting such a favorable selectivity for stimulating increases in muscle tissue and strength relative to androgenic activity in affected tissues, Ostarine has the potential advantage that it could be used at relatively low doses, is orally bioavailable, and could potentially circumvent some of the negative effects that stem from traditionally used anabolic Steroids converting to 5α-reduced androgens in modern medicine that may raise the risk of benign prostate hyperplasia, accelerate the development of prostate carcinoma, increase the probability of acne breakouts, and exacerbate/substantially expedite androgenic alopecia (male pattern baldness).

It could also potentially eliminate the incidence of androgenic side effects in women entirely, while still potentially inducing enough anabolic activity to offset any muscle or bone loss occurring from degenerative disease.

While this is beneficial for both men and woman, its lack of androgenicity in women makes this a very promising anabolic agent.

Even minor amounts of androgens can cause virilization, making it extremely difficult to find compounds potent enough to offset degenerative diseases with no side effects in women.

Not only does Ostarine increase muscle mass and strength, it increases tendon strength, ligament health, bone density and encourages collagen turn-over [R, R].

It also has good oral bioavailability [R].

This makes oral dosing viable as opposed to intramuscular injection with traditional anabolic steroids (an obviously less practical method of medicinal intervention), or oral dosing with 17 alpha-alkylated anabolic steroids that are liver toxic and require a methyl or ethyl group, at the C17α position to be orally bioavailable.

Ostarine was the closest SARM to making it through clinical trials and being approved.

Ostarine Clinical Trials

Ostarine was the first drug to be put on the FDA's fast track development program to become an approved drug for the prevention and treatment of muscle wasting in patients with cancer.

In mid 2013, GTx announced that Ostarine had failed its late-stage phase III trials as a lung cancer drug intended to prevent muscle wasting [R].

In these trials, 325 patients were given 3 mg of Ostarine per day, or placebo (randomized trial), to assess if Ostarine would significantly prevent muscle loss in those who received the 3 mg dosage, vs those that didn't.

Power during a stair climb test was also used as a measure to assess improvements in physical function.

Secondary endpoints included an assessment of whether patients who were treated with Ostarine had any improvement in their quality of life, or if they required less healthcare resources than the placebo group.

While the trial was a failure overall, the positive takeaway was that Enobosarm (Ostarine) demonstrated significant quantitative advantage in LBM (lean body mass) compared to placebo in both trials [R].

In layman's terms, Ostarine on average increased or maintained a significantly greater amount of muscle mass in the patients that were treated with it, relative to those who were treated with placebo.

Following that, in 2016 GTx started a phase II clinical trial to assess Ostarine's viability as a stress urinary incontinence treatment for women.

The results of that did not achieve statistical significance [R].

Looking at the results of Ostarine in totality across all of its clinical trials, we can make a more educated assessment on its viability for the purposes of selective increases in muscle mass relative to androgenic activity.

Ostarine has been evaluated in 27 completed or ongoing clinical trials.

About 1500 subjects in total have been treated with Ostarine in some capacity, with dosages ranging from as low as 0.1 mg all the way up to 100 mg.

Ostarine was observed to be generally safe and well tolerated in all of those trials.

One notable Phase 2 clinical trial that evaluated Ostarine as a form of hormonal therapy for women with estrogen receptor positive (ER+) and androgen receptor positive (AR+) breast cancer was broken down into two dose cohorts (9 mg and 18 mg daily).

The Phase 2 trial pre-specified threshold for success, clinical benefit response (CBR), was attained meeting the trial’s primary efficacy endpoint.

The trial enrolled the predefined number of evaluable patients in both dosage arms with at least 44 patients in each of two cohorts receiving 9 mg or 18 mg daily doses of Ostarine (Enobosarm) respectively [R, R].

This study in particular presented the first opportunity for us to gather clinical data representing what results would occur from what would generally be considered “high dosages” of Ostarine.

Is Ostarine As Strong As Steroids?

While Ostarine did help me reach my goal I set for myself, I absolutely do not think that it is as strong as most steroids are (in certain contexts).

However, I think it does have the ability to match the same level of anabolic activity that moderate doses of certain “milder” steroids provide.

Anavar and Primobolan come to mind when I think of good steroids to compare the results to.

With Ostarine displaying a blatant dose dependent increase in muscle mass, it would be desirable to investigate where the point of diminishing returns is in humans with regards to increases in lean muscle mass, as dosages as low as 10-25 mg of Ostarine are commonly compared to 50-100 mg dosages of traditional anabolic androgenic steroids, which is obviously a ridiculous way to assess overall potency relative to one another.

10 mg of Ostarine will outperform 10 mg of Anavar, Turinabol, Primobolan, Equipoise, and many other traditional anabolic steroids, with a favorable selectivity for anabolic:androgenic activity, and less endocrine suppression.

Ostarine Vs Nandrolone

Milligram:Milligram, Ostarine is multiple times more effective at increasing lean muscle mass than Nandrolone, a very commonly used anabolic androgenic steroid.

More commonly known as “Deca” (Nandrolone with the Decanoate ester) or “NPP” (Nandrolone with the phenylpropionate ester).

Ostarine Vs Anavar

I truly believe that Ostarine is stronger than Anavar now.

When I first started experimenting with SARMs, I was hesitant to imply that it could be as strong as any anabolic steroid that has a notable androgenic effect in the body, as I simply did not think it would be possible to stack up against any of them.

Throughout countless anecdotal experiences now, I have personally seen Ostarine mg:mg outperform Anavar in terms of sheer muscle and strength increases, as well as in terms of side effects.

Ostarine is less suppressive than Anavar, outperforms it in an anabolic capacity, and displays a significantly lower incidence of side effects and androgenic activity in the body.

For women especially, after seeing multiple women try Anavar and Ostarine on separate occasions, Ostarine always outperformed the Anavar and appears to clearly be the candidate of choice when it comes to performance enhancement.

How Ostarine Stacks Up Against Other SARMs

Ostarine has the most clinical data available, so one would generally jump to the conclusion that it is the best overall SARM, however, I feel that is not necessarily the case and should be explored further.

Ostarine Vs LGD-4033

While Ostarine exhibits a blatantly favorable selectivity for muscle tissue to prostate (and other androgen affected tissues), in comparison to LGD-4033 it is outperformed in almost all aspects.

Milligram:Milligram LGD-4033 (VK5211) outperforms Ostarine (Enobosarm) with greater increases in lean muscle mass and strength.

Despite LGD-4033 being more potent, Ostarine is less suppressive, which would make recovering natural testosterone levels a smoother and quicker process after discontinuation.

Ostarine Vs S4 (Andarine)

Ostarine's effect on muscle tissue and overall body composition is most similar to Andarine (also called GTx-007, S-4).

Milligram:Milligram, Ostarine is stronger than S4 for building lean muscle mass, however, it does not seem to have the same cosmetic drying out effect of the physique that S4 provides.

Ostarine also has the obvious advantage of not binding to the ocular receptors in the eyes, which is the biggest detriment to S4's potential applications, whereby it causes notable vision impairment in dark settings.

S4 however has less of a detriment to HDL cholesterol levels than Ostarine.

Ostarine and S4 are reported to have great synergy with one another when used concurrently, with several users accomplishing very impressive body composition transformations with the combination.

Ostarine Vs S-1

Ostarine is commonly mistaken as S-1, but it should be noted that (S)-3-(4-chloro-3-fluorophenoxy)-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethylphenyl)propionamide (C-6), also called S-1 was one of the earliest SARMs developed, and is far weaker than Ostarine [R].

Ostarine Dosage

Predictably, Ostarine caught the attention of the bodybuilding industry with its impressive pre-clinical profile and blatant potential advantages in a performance enhancement context.

While Ostarine was initially trialed at 0.1 mg, 0.3 mg, 1 mg, and 3 mg per day, it is not well known that dosages of 9 mg and 18 mg per day were generally well tolerated by women in a less commonly known phase II clinical trial [R, R, R].

Lean gains upwards of 5 – 10 pounds are typical among recreational users, with average dosages ranging from 10 – 25 mg per day.

These dosages were determined by recreational users based upon anecdotal logs and personal experimentation, and are not concrete guidelines that dictate correct or incorrect use.

Ostarine Side Effects

Decreased Good Cholesterol (HDL)

The clinical data on this is inconsistent as there are some studies that show reductions in serum lipids (namely HDL and LDL) occurring in a dose dependent manner with Ostarine usage, as well as data showing only reductions in HDL levels (otherwise known as “good cholesterol”) [R, R].

We at least know for sure that Ostarine has a negative effect on HDL levels, which is notable as this is a common side effect of all traditional anabolic steroids, and other SARMs.

Despite SARMs ability to avoid significant androgenic activity in the body, they evidently do not differ much from anabolic steroids in their effects on lipid profiles.

Testosterone Suppression

SARMs have shown to suppress luteinizing hormone (LH) and follicle stimulating hormone (FSH) through the hypothalamus-pituitary-testis axis, thus decreasing testosterone in a dose-dependent manner [R].

Ostarine has also shown to significantly lower Sex Hormone-Binding Globulin (SHBG) and serum total testosterone levels in clinical trials in subjects treated with 1 mg of Ostarine or higher [R].

While SHBG was always significantly impacted at notable dosages, suppression of LH and FSH wasn't consistently proven throughout Ostarine's clinical trials.

However, after referencing anecdotal logs of baseline pre-Ostarine blood work compared to mid-Ostarine blood work with dosages several times higher than the 0.1 mg, 0.3 mg, 1 mg, 3 mg dosages used in trials (users commonly use Ostarine at upwards of 25 mg per day for several months), I believe it's safe to say that Ostarine does also show blatant reductions in all of these hormones markers in a dose dependent manner, the dosages in the studies just weren't high enough to yield this data.

The degree to which even high dosages of Ostarine suppress LH and FSH is far less than that of traditional anabolic steroids though, which should be noted.

The process of recovering to baseline healthy endocrine function would be hindered to a far greater extent in steroid users.

Elevated Estrogen Or Decreased Estrogen

Ostarine does not aromatize into Estrogen directly, however, via the suppression of natural Testosterone levels, it can create an unfavorable balance between Testosterone and Estrogen in the body.

In addition, by occupying the androgen receptor with such a high affinity, Ostarine can actually divert a significant amount of Testosterone to aromatize into Estrogen that wouldn't have otherwise.

This in turn, can create an elevation of Estrogen levels in the body, which is commonly mistaken as the compound being laced with prohormones, or being an anabolic steroid.

Common symptoms of high estrogen include:

• Acne, oily skin
• Erectile dysfunction
• Low libido
• Lethargy
• Gynecomastia (man boobs)
• Irritability
• Depression
• Water retention
• High blood pressure
• Enlarged prostate
• Shrunken testicles
• Sugar cravings

While Ostarine can cause an elevation in Estrogen via the increased aromatization of circulating Testosterone, long-term use, or high dosages of Ostarine can cause an opposite effect, where the body has such a low level of circulating Testosterone via endocrine suppression that you no longer have enough aromatization occurring in the body, leading to an array of health problems derived from the lack of Estrogen needed to fulfill certain physiological functions.

Common symptoms of low estrogen include:

• Dull weak orgasms
• Dry skin and lips
• Dehydration
• Erectile dysfunction
• Low libido
• Irritability
• Mood swings
• Loss of appetite
• Fatigue
• Lethargy

Applications In Alternative Hormone Replacement Therapy In Men

As Ostarine does not aromatize into Estrogen, it disqualifies it as a viable form of standalone hormone replacement therapy in men.

A variety of basic physiological functions in men rely on the aromatization of Testosterone into Estrogen, as low Estrogen side effects can be just as harmful to one's health as high Estrogen side effects.

In hypothetical long-term HRT applications, Ostarine would likely need to be used in conjunction with exogenous Estrogen to maintain in range blood serum concentrations to fulfill basic physiological functions that otherwise would be dependent on the body's endogenous aromatization of Testosterone to Estrogen.

Androgenic Activity

Ostarine has a dose dependent increase in androgen activity in the body.

While it is extremely selective for muscle and bone relative to androgen affected tissues, all SARMs (Ostarine included) display a systemic increase in androgen activity, hence there is still potential for androgen related side effects, just to a far lesser extent.

The ratio of anabolic:androgenic activity is favorable enough whereby the therapeutic dose necessary to yield the desired level of muscle retention and bone mass would ideally not be high enough where any notable androgenic activity could take place, and that the drug would still be generally well tolerated with a great safety profile.

Establishing the balance between all of these factors is the reason why no SARM has yet been approved for human use, as it is very difficult to develop a compound with a substantial amount of anabolic activity, with a near complete absence of androgenic activity.

Hair Loss

All androgens can cause hair follicle miniaturization, the extent to which they do this is dependent on their individual selectivity, binding affinity, and the dosage used.

In general, Ostarine (at the dosages commonly used) would not cause any notable androgenic alopecia.

However, this does not exclude temporary shedding caused by a hormonal fluctuation.

Anything that causes a hormonal fluctuation in the body, can potentially cause a temporary shed.

This is not to be confused with androgenic alopecia, but it is hair loss nonetheless, albeit temporary.

Liver Toxicity

Short-lived increases in ALT to above the upper limit of normal were observed in eight subjects in one of Ostarine's clinical trials.

The ALT observations in seven of eight subjects had resolved while still continuing their daily dosage, and no subject had clinically significant abnormal levels of ALT or AST at the end of study.

One subject was discontinued due to an elevation in ALT 4.2 times the upper limit of normal.

The ALT level in that subject returned to normal levels after discontinuation of the Ostarine [R].

This was with dosages of no higher than 3 mg per day, so it is only logical to assume that common recreational dosages of Osatarine (upwards of 25 mg) may exhibit some level of liver enzyme elevation.

This is contradictory to common broscience theories that assert that there is zero chance of liver toxicity from SARMs at any dosage amount, or that an increase in ALT in their blood work must mean that they received methylated prohormones instead of SARMs.

At therapeutic dosages, there appears to be a low risk profile, but it should be noted that there may be some notable degree of liver toxicity at dosages commonly used for performance enhancement, which would likely resolve itself after cycling off.

Lack Of Aromatization And 5-Alpha Reduction

Ostarine does not aromatize or create a layer of subcutaneous water retention.

Increases in lean muscle mass are absent of artificially inflated water weight, not only making the SARM favorable from a cosmetic standpoint in a clinical setting, but also from a health standpoint, as water retention induced from previously approved anabolic androgenic steroids like Anadrol can often lead to increased cardiovascular stress, increased heart rate and blood pressure, electrolyte imbalances, among a myriad of other issues.

More importantly, the lack of aromatization limits potential side effects that could occur from aromatization from traditional anabolic steroids like Testosterone.

Ostarine does not undergo 5-alpha reduction, which is speculated to contribute to its sparing effect on the prostate and other androgen related tissue.

This is not the case though, as there are several androgens that do not undergo conversion to a more androgenic compound when they hit 5α-Reductase.

One of the most notable being MENT (Trestolone).

In fact, some androgens are more androgenic prior to 5-alpha reduction, and present an increase in androgenic side effects when they are inhibited with 5-alpha reductase inhibitors like Finasteride or Dutasteride.

An example of this is Nandrolone.

Ostarine is inherently selective for the androgen receptor, and its selectivity for muscle tissue and bone relative to androgen affected tissues like prostate is not a result of its inability to be altered by 5-alpha reductase.

Half-Life

Ostarine has a half-life of 23.8 hours, making once per day dosing a viable option for maintaining stable blood serum concentrations [R].

Ostarine PCT (Post Cycle Therapy)

Ostarine will suppress natural Testosterone levels (and overall endocrine function) in a dose dependent manner.

It is wise to complete a PCT phase (post-cycle therapy) after an Ostarine cycle.

Due to Ostarine's half-life, PCT should be started the day after the last Ostarine dosage was taken.

Forgoing PCT will put one at risk of muscle loss, fat gain, among all of the other standard side effects associated with Testosterone suppression.

If you are dead set on using performance enhancing drugs shortly after Ostarine, I would not advise following the broscience derived “time on = time off” equation.

Time off should be dictated by a variety of more individual specific factors, and blood work.

Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice.