A new class of exciting body-transformation pharmaceuticals are currently in development – myostatin inhibitors. YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM). Compared to other SARMS, YK-11 is in a class of its own. It’s a gene-selective partial agonist of the androgen receptor and myostatin inhibitor, essentially reducing muscle degradation and increasing muscle formation. Studies have shown that YK-11 has high anabolic potency, with a higher ratio of anabolic to androgen activity than Dihydrotestosterone (DHT).
What Is YK-11
YK-11 is a synthetic steroidal selective androgen receptor modulator (SARM). Unlike other non-steroidal SARMS which have a high affinity for muscle and bone, YK-11 is only a partial agonist of the androgen receptor (AR). The real power of YK-11 is through it’s unique mechanisms of myostatin inhibition.
How Does YK-11 Work, What Does YK-11 Do
To fully grasp how YK-11 works and the fascinating etiology, you must unravel how SARMS work and what myostatin and why myostatin inhibition is important for performance body-transformation science.
How Do SARMS Work
Selective androgen receptor modulators (SARMS) are non-steroidal compounds that promote anabolic and androgenic effects, that bind to selective androgen receptors. While steroidal SARMS have been around since the 1940s, (compounds like Winstrol, Anavar, and Turinabol) a number of nonsteroidal SARMs that do not serve as substrates for CYP19 aromatase or 5α-reductase, that act as full agonists in muscle and bone and as partial agonists in prostate have been in development since the 1990s and early 2000s, in an attempt to overcome the pharmacologic and pharmacokinetic limitations of steroidal androgen receptor agonists (i.e., testosterone and DHT), which have known associations with liver and heart disease [R].
SARMS have been investigated for several indications muscle wasting (cachexia), osteoporosis, stress urinary incontinence, erectile dysfunction, symptomatic benign prostatic hyperplasia, Alzheimer’s disease, muscular dystrophy, breast cancer [R].
SARMS are not anabolic steroids; rather, they are synthetic ligands that bind to androgen receptors. Depending on their molecular structure, they act as agonists, partial agonists, and antagonists. It is thus in a selective manner, that SARMS modulate or mediate coregulators and transcription factors or signaling cascade proteins to promote anabolic activity.
Unlike anabolic steroids which bind to androgen receptors in many tissues all over the body, individual SARMs selectively bind to androgen receptors in certain tissues, but not in others.
Nonetheless, they are still exhibit androgenic and anabolic effects.
Androgen receptors are ubiquitous in muscle tissue and bone, thus making them highly receptive to activate or be inhibited my anabolic agents, creating undesirable systemic effects. SARMS have a high binding affinity for muscle tissue and bone, in a dose dependent selective manner, thus limiting growth in undesirable tissue, such as the prostate.
SARMS serve as alternative to anabolic-androgenic steroids, with fewer limitations, also exhibiting high-bioavailability.
All that being said, YK-11 is uniquely classified as both a SARM and steroid, due to its molecular and chemical structure.
YK-11 is similar to DHT with a steroidal backbone and a partial agonist effect. Yet from the limited data, has selectivity like a SARM. It’s also important to note, that the term SARM can be applied to any compound that selectively activates the androgen receptor.
What Are Myostatin Inhibitors
Now, onto myostatin and the important of myostatin inhibition. Myostatin also known as growth differentiation factor 8 (GDF-8) is the greatest anabolic inhibiting factor. Myostatin is catabolic, and limits muscle growth as well as bone formation.
The gene encoding myostatin was discovered in 1997. Researchers produced a knockout strain of mice and found that the mice that lacked this gene, had twice as much muscle mass.
Essentially, myostatin is an antagonist of SARMS, with a direct opposite effect, catabolizing muscle, and bone; it’s a negative regulator of muscle mass. It can inhibit bone formation and produces bone degradation directly associated with the aging process, resulting in higher accumulations of body fat, degradation of muscle mass, and bone density.
Clinically, myostatin inhibitors can provide therapeutic benefit as an efficacious treatment in muscle wasting disorders, as well as a potential treatment in the aging process. They are also used to build more muscle mass for those seeking off-label performance benefit.
Myostatin can naturally be suppressed through physical exercise, and nutrition.
Physical exercise and nutrition protocols, including high protein, are essential to inhibit myostatin and potent anabolic stimuli, increasing muscle mass through muscle protein synthesis and protein turnover [R].
Actively working out and eating healthy can therefore help induce greater changes in muscle mass, through the inhibition of myostatin and increase of muscle protein synthesis. Myostatin inhibitors, like YK-11, can further suppress myostatin activity, while also promoting anabolism by from high tissue selectivity of muscle and bone.
YK-11 is unique, due to the fact that it inhibits myostatin inducing higher expression of follistatin, with high selectivity and affinity for androgen receptors, making it an ideal anabolic androgenic agent to promote performance, muscle mass, and strength.
Lean Muscle Mass
Unfortunately, research is very limited on the potential therapeutic benefits and efficacy of YK-11. No human clinical trials exists, however theory suggests, YK-11 could be used in performance enhanced due to its underlying mechanisms.
Pre-clinical animal studies have shown that YK-11 can revert inflammation associated with muscle wasting [R]. It’s pharmacokinetic profile, is promising, that it may help increase lean muscle mass and bone mineral density, while also suppressing muscle wasting and degradation. Together, preventing muscle mass breakdown and increasing muscle protein synthesis, could make for a powerful anabolic agent.
However, several studies have reported that although myostatin inhibition increases muscle hypertrophy, muscle quality decreases, (force, power, and strength). Potential mechanisms may include suppression of mitochondrial biogenesis and/or protein turnover as a (in)direct result of myostatin inhibition [R, R].
YK-11 Side Effects
It’s hard to determine the potential side effects of YK-11, considering that there are no human safety, efficacy or pharmacokinetic studies to determine dosage, or safety profile.
However, YK-11 is a steroidal SARM, meaning that it will effect and suppress natural testosterone levels, do it’s high binding affinity for the androgen receptor.
The use of anabolic androgenic steroids (AAS) suppresses the secretion of the pituitary luteinizing hormone (LH), sexual binding hormone binding globulin (SHBG), and follicle stimulating hormone (FSH). This effect results from negative feedback of androgens on the hypothalamic-pituitary–gonadal (HPG) axis.
Anecdotal side effects have reported joint pain while using YK-11. Myostatin is expressed in joints and ligaments. Studies have shown that myostatin deficient mice, have weak and brittle tendons, which suggests that myostatin is important for tendon maintenance [R].
Studies have shown that myostatin inhibition, can affect other tissues, particularly testicle size and fertility [R].
Theoretically, YK-11 seems that it has a promising etiology and anabolic profile. More research is needed to determine the long-term side effects, safety, and efficacy of YK-11 through human clinical trials. Unfortunately, the status of YK-11 is currently unknown, as there is very little research or data available.
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