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Unlocking the Mystery: What is YK-11 and Why is Everyone Talking About It?

Table of Contents
Defining YK 11 and its mechanism of action
  • Defining YK-11 and its mechanism of action (MOA) as well as pharmacokinetics 
  • Discussing the differentiation of YK-11 and other diverse SARMs 

What Is YK-11 

YK11 is a selective androgen receptor modulator (SARM) with a captivating twist. It possesses the capacity to initiate AR action, sidestepping the well-trodden path of N/C interaction, a process typically inherent to the activation of the androgen receptor (AR).

This unique mechanism of action (MOA) is only one example of how YK11 differentiates from other SARMs. YK-11’s mechanism of action is comparable to that of GW501516 and SR9009, or at least in terms of its strange behavior in comparison to other SARMs. 

YK-11 emerges as a fascinating thread. Acting as a myostatin inhibitor, it has been documented to instigate myogenic differentiation which induces rapid muscle growth and selective gene regulation.

It also plays a key role in stimulating bone formation. Evidence points towards its mimicry of specific hormones in studied subjects. This captivating symphony of effects beckons further inquiry, inviting us to delve deeper into the enigma that is YK-11

What Makes YK-11 So Unique

YK11 is veiled in a shroud of scientific wonder. It activates AR without the traditional N/C interaction, which sets it apart from its peers. What secrets does YK11 hold for the future of SARMs and their research? Read on as we unravel the mystery of its diverse mechanism of action. 


A partial AR agonist 

YK11 is a selective androgen receptor modulator (SARM) that has been identified as a partial agonist of AR. This means that YK11, unlike full agonists, does not fully activate the AR but instead induces a response in the receptor that is less than the maximum response achievable.

The identification of YK11 as a partial agonist was determined using an androgen-responsive element-luciferase reporter assay.

This type of assay is a common experimental technique used in molecular biology to measure the activity of certain biological pathways. In this case, it was used to measure the activation of the AR by YK11.

The AR is linked to a luciferase reporter gene in the assay. When an agonist like YK11 binds to the AR, it activates the receptor, which activates the reporter gene, causing it to produce luciferase.

The amount of luciferase produced is then measured, providing a quantitative measure of the androgen receptors’ activation level by the agonist.

In the case of YK11, the amount of luciferase produced was less than that produced by a full agonist, indicating that YK11 is a partial agonist of the AR.

This unique characteristic of YK11 may offer potential benefits such as a more targeted action and fewer side effects compared to full agonists.

N/C Terminal 

Unlike the majority of its counterparts, YK11 has the unique ability to activate androgen receptors (AR) without engaging in the N/C interaction.

The N/C interaction, or the interaction between the N-terminal and C-terminal parts of the AR, is a crucial step in the conventional process for the activation of the AR. This interaction is vital for many proteins to function correctly, including ARs.

In the context of androgen receptors, the N/C interaction is an interdomain interaction that occurs upon hormone binding and is necessary for normal AR function.

It involves interactions between the carboxy-terminal ligand-binding domain and the highly conserved N-terminal domain.

However, YK11 breaks away from this usual path. It triggers AR action without the necessity for this N/C interaction. This unique mode of action potentially allows for more selective targeting of tissues, which could lead to fewer adverse effects compared to traditional SARMs. 


Regarding pharmacodynamics, information on YK-11 is limited, nonetheless, this study suggests YK11 may promote muscle mass and mitigate inflammation during sepsis, highlighting its potential preventative capabilities. This could be constituted as an indication of a tolerable status

Terminal Half life

In order to definitively identify urinary metabolites of YK11, a study was performed using YK11 that had been labeled with six deuterium atoms.

The specimens collected after administering this deuterated YK11 were examined using a combination of hydrogen isotope ratio mass spectrometry and single quadrupole mass spectrometry. This approach was used to pinpoint the metabolites, using basic mass spectrometric data for reference. 

When YK11 is metabolized or broken down, it forms various byproducts known as metabolites. These metabolites can be in two forms: unconjugated and conjugated (which includes glucuronidated and sulfated metabolites).

In the elimination study mentioned, no original, unaltered YK11 was found in the urine samples, which was expected. This is because the subjects processed compounds like YK11 by breaking them down into metabolites, which are then expelled. 

The unconjugated metabolites, which are the initial byproducts of YK11, were no longer detectable in the subject within 24 hours after the administration of YK11. This means that these metabolites were quickly processed, broken down, and eliminated. 

On the other hand, the glucuronidated and sulfated metabolites, which are further transformations of the original metabolites, remained in the body for a longer time.

These metabolites have undergone additional chemical changes (glucuronidation and sulfation) which make them more water-soluble and hence, easier for the body to eliminate.

However, they were still traceable in the body for more than 48 hours after YK11 was administered.

YK-11 In a “Clinical” Setting

The use of quotations for the word clinical in this heading is hardly sarcastic as the evidence surrounding the clinical significance is limited for YK-11 in a laboratory setting. However there are still some important factors to be dissected regarding the effects of YK-11 in test subjects. 

Myogenic Differentiation  

In this study, YK-11 triggered the myogenic differentiation of C2C12 myoblast cells and increased follistatin, generating effects on the subject’s muscle growth.

C2C12 myoblast cells are a type of cell line that is often used in biological and medical research. These cells were initially derived from the thigh muscle of a two-month-old female C3H mouse, specifically from the satellite cells which are a type of stem cell responsible for muscle regeneration.

The term “myoblast” refers to an immature muscle cell. Myoblasts play a crucial role in muscle development as they can differentiate into mature muscle cells through a process known as myogenesis.

During this process, myoblasts fuse together to form multinucleated myotubes, which eventually mature into muscle fibers, in turn promoting muscle mass.

In the study, the stimulation of crucial myogenic regulatory factors (MRFs) – including the myogenic differentiation factor (MyoD), myogenic factor 5 (Myf5), and myogenin – were pronounced when YK11 was present.

When C2C12 cells were administered YK11, it led to an increase in the production of a protein called follistatin (Fst). This protein is known to be involved in muscle growth and development.

However, this muscle differentiation process, which was facilitated by YK11, could be undone by introducing an anti-Fst antibody. In simpler terms, the anti-Fst antibody counteracted the effects of YK11, reversing the muscle differentiation that had been previously initiated.

Gene expression 

In this research, investigators explored the selective mechanism through the administration of YK11, which demonstrated gene-selective transactivation mediated by the androgen receptors (AR) .

In AR-positive human breast cancer MDA-MB-453 cells, YK-11 showed distinct patterns of AR-mediated target gene expression and AR recruitment to the enhancer regions.

A docking study proposed that the sterically hindered C17-group of YK11 caused a movement in helices 11 and 12.

This method (docking study)  is used to predict the position and orientation of one molecule (often a small molecule or a compound like YK-11) when it binds to a specific site on another larger molecule (like a protein).

The term “sterically hindered C17-group of YK11” refers to a part of the YK11 molecule that is large or arranged in such a way that it may interfere with the molecule’s ability to interact with other molecules or structures. 

The “helices 11 and 12” likely refer to specific parts of the structure of a protein. Proteins are essentially composed of linked sequences of amino acids, and these chains can fold into helices (spiral-like structures) among other shapes.

The positions of these helices can change when a molecule like YK11 binds to the protein.

When YK11 binds to a certain protein, the C17-group on YK11 causes the positions of helices 11 and 12 in the protein to shift. This shifting could potentially influence how the protein functions.

The findings from this research imply that YK-11’s ability to selectively control certain genes could be due to its varying ability to bind to DNA and/or attract helper molecules when compared to other SARMs that bind to the same site.

These findings offer a new understanding of how YK-11 operates at a molecular level.

Osteoblast proliferation

In earlier research, we found that YK11 is a unique substance that selectively interacts with androgen receptors (a type of protein in cells), a characteristic of SARMs.

We also discovered that YK11 promotes the transformation of cells into muscle cells, promoting muscle growth and selectively controlling certain genes. 

Osteoblasts are cells that help promote bone growth and formation. Osteoblast proliferation refers to the process by which osteoblasts, the cells responsible for bone formation, multiply and increase in number.

This is a crucial part of bone growth and repair, as it allows for the expansion of the osteoblast cell population, facilitating the formation of new bone tissue.

In this study, researchers examined the effects of two substances – YK11 and dihydrotestosterone (DHT) – on a specific type of cell found in mice, known as MC3T3-E1 osteoblast cells.

Research demonstrated that using YK11 and dihydrotestosterone (DHT) sped up the process of cell division and mineralization of MC3T3-E1 osteoblast cells from mice.

Cell division is a biological process in which a single cell divides into two or more cells. This process is crucial for growth, development, and repair in living organisms. 

Mineralization in MC3T3-E1 cells is the process where these cells produce and deposit minerals into the extracellular matrix to form bone tissue.

Osteoblasts secrete collagen and proteins to create a structural framework, then release calcium and phosphate ions to form hydroxyapatite crystals. These crystals harden the matrix, resulting in mineralized bone tissue.

In addition, cells administered YK11 showed an increase in specific markers that indicate osteoblast differentiation, such as osteoprotegerin and osteocalcin, when compared to cells that were not treated.

To elaborate, osteoblast differentiation is the process where precursor cells transform into mature osteoblasts, which are essential for bone formation. This process can be tracked by monitoring certain marker proteins.

Osteoprotegerin and osteocalcin are two such markers that are produced in higher quantities when osteoblasts are differentiating and maturing.

The fact that these markers increased in YK11-administered cells suggests that YK11 may promote the differentiation process, leading to a greater number of mature osteoblasts capable of forming bone tissue.

This could potentially have implications for enhancing bone health and treating bone-related diseases

Muscle wasting 

As discussed before, research implies that YK11 could potentially counteract muscle deterioration occurring during sepsis and also mitigate the inflammatory conditions associated with it

It’s common to see muscle deterioration in patients with sepsis, which is often due to catabolic reactions happening in skeletal muscles. Myostatin, a substance that inhibits muscle growth, has been found to increase in diseases linked to muscle wasting.

However, the activity of myostatin during sepsis remains unclear. This study aimed to explore how the levels and control (expression and regulation) of myostatin, a protein that inhibits muscle growth and differentiation, changes in the skeletal muscle of mice.

These mice have been injected with gram-negative bacteria (a category of bacteria that, when subjected to the Gram staining technique used for bacterial differentiation, fail to hold onto the crystal violet stain. As a result, they display a red or pink color when viewed under a microscope). 

Elevation of Myostatin In Un-administered Septic Mice   

Researchers observed an elevated level of myostatin protein in the muscles of septic mice. This increase coincided with a rise in the levels of other proteins, including follistatin, NF-κΒ, myogenin, MyoD, p-FOXO3a, and p-Smad2.

  • Follistatin is a protein that influences muscle growth, inflammation, and fertility by binding and neutralizing certain proteins, and is found in almost all tissues of the body. 
  • Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a protein complex that regulates DNA transcription, cytokine production, and cell survival, playing a critical role in immune responses and inflammation.
  • Myogenin is a protein encoded by the MYOG gene in humans that plays a crucial role in muscle development and differentiation.
  • MyoD is a protein in humans that is encoded by the MYOD1 gene, playing a pivotal role in regulating muscle differentiation and development
  • Phosphorylated Forkhead box O3 (p-FOXO3a) is a post-translationally modified form of the FOXO3a protein, involved in regulating cellular processes such as apoptosis, cell cycle progression, and oxidative stress resistance.
  • Phosphorylated SMAD2 (p-SMAD2) is a modified form of the SMAD2 protein that plays a key role in cell proliferation, apoptosis, and differentiation by interacting with the transforming growth factor-beta (TGF-beta).
Post YK-11 Administration 

Additionally, when YK11 was administered as a myostatin inhibitor, it reduced the levels of pro-inflammatory cytokines and markers of organ damage in the blood and major organs of mice, which were initially elevated due to sepsis.

Therefore, the use of YK11 as a myostatin inhibitor resulted in a reduction in the death rate caused by sepsis.

Conclusively, the study’s findings imply that YK11 shows signs of muscle growth and lessening the inflammatory conditions associated with sepsis. This underscores its potential role as a protective measure against muscle wasting caused by sepsis.

Comparing YK-11 to Other SARMs

Where Does YK-11 Stand as a Selective Androgen Receptor Modulator? 

Relationship with the AR

YK-11 expresses one huge difference from conventional SARMs, the relationship between YK-11 and the AR. 

Conventional SARMs like Ostarine and LGD-4033 exhibit a strong binding affinity for the AR

However there are a small “sub-section” of SARMs that do not promote AR activation with the same intensity or at all. Some examples are MK677, SR9009, and GW501516.

YK11 is classified as a Selective Androgen Receptor Modulator (SARM) but functioning as a partial agonist for the AR. In simpler terms, YK11 doesn’t fully switch on the AR like full agonists do. Instead, it triggers a reaction in the receptor that doesn’t quite reach the highest possible response

Although YK-11 has conveyed outcomes like other traditional SARMs, the difference in how the outcomes are met relate more to the outliers of SARMs

Clinical Perspective 

YK-11 vs Traditional AR agonists 

Data on YK-11 suggests it has the potential to be studied for and produce the same effects as traditional AR agonists like LGD-4033 or Ostarine being muscle growth and promoting bone health

Ostarine has been immensely researched by investigators for its ability to promote muscle growth for subjects suffering from muscle wasting.

The limited data on YK-11 suggests the same thing. However, the difference is YK-11 does this by acting as a myostatin inhibitor, compared to the activation of androgen receptors. 

YK-11 is seen to promote bone formation, while Ostarine is seen to promote bone density. Although the pharmacodynamics of a traditional AR agonist and YK-11 are different, they relate by their effects in certain clinical situations

YK-11 vs Non-AR agonists 

These eccentric SARMs, like MK-677 and GW501516, have no relationship with the AR, yet they still express the same serviceable outcomes. 

MK-677 promotes muscle growth by activating the ghrelin receptor and therefore increasing pulsate growth hormone content. Growth hormone also holds a significant role in the processes of growth and development. Instead, YK-11 leads to muscle mass incarceration through myogenic differentiation and the production of a protein called follistatin

Comparison Conclusion 

YK-11 is somewhere in the middle of acting as a “regular” SARM. It has a partial affinity for the AR, like traditional SARMs, and the applicable outcomes being from the unique pharmacodynamics as MK-677 does. 

Whether it is gene expression or myogenic differentiation, the end result of each study has been seen to promote the same idea. YK-11 appears to have advantageous outcomes for future research. 

Whether it is more or less of a SARM is a separate question for future research to answer. With limited data on YK-11 being left to the interpretation of the researcher and not concrete, it wouldn’t be outlandish to suggest there will be more research and studies in the near future. 

It is important to prepare for your research by reading up on what you need to know before buying SARMs like RAD 140 and YK 11.

How Can Sports Technology Labs Help? 

We encourage you to continue reading for more information on YK11. If you’ve got questions or concerns about YK 11 or any other research chemicals, don’t be a stranger – Sports Technology Labs is here to help! We offer an expansive selection of 3rd party tested SARMs and peptides, each guaranteed to have at least 98% purity. Buy YK-11 from Sports Technology Labs today to experience the difference that quality makes in your research.


SARMs are investigational compounds still awaiting FDA approval and are not dietary supplements. At Sports Technology Labs we are chemical suppliers, not medical doctors, and our expertise is sourcing and quality control.

 Sports Technology Labs does not encourage or condone consumer use of SARMs products, they are for research purposes only. Anecdotal reports and guides may not match those used in carefully designed medical research protocols and may pose a serious risk of adverse effects on users. 

Individual variables, comorbidities, and polypharmacy can also contribute significantly to the risk of health problems.

Scientific References:

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2. Yatsu T, Kusakabe T, Kato K, Inouye Y, Nemoto K, Kanno Y. Selective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1 Cells. Biol Pharm Bull. 2018;41(3):394-398. doi: 10.1248/bpb.b17-00748. PMID: 29491216.

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4. Zboray L, Pluciennik A, Curtis D, Liu Y, Berman-Booty LD, Orr C, Kesler CT, Berger T, Gioeli D, Paschal BM, Merry DE. Preventing the Androgen Receptor N/C Interaction Delays Disease Onset in a Mouse Model of SBMA. Cell Rep. 2015 Dec 15;13(10):2312-23. doi: 10.1016/j.celrep.2015.11.019. Epub 2015 Dec 7. PMID: 26673324; PMCID: PMC4684905.

5. Lee SJ, Gharbi A, Shin JE, Jung ID, Park YM. Myostatin inhibitor YK11 as a preventative health supplement for bacterial sepsis. Biochem Biophys Res Commun. 2021 Mar 5;543:1-7. doi: 10.1016/j.bbrc.2021.01.030. Epub 2021 Feb 12. PMID: 33588136.

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9. Basaria S, Collins L, Dillon EL, Orwoll K, Storer TW, Miciek R, Ulloor J, Zhang A, Eder R, Zientek H, Gordon G, Kazmi S, Sheffield-Moore M, Bhasin S. The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men. J Gerontol A Biol Sci Med Sci. 2013 Jan;68(1):87-95. doi: 10.1093/gerona/gls078. Epub 2012 Mar 28. PMID: 22459616; PMCID: PMC4111291.

10. Dierickx P, Emmett MJ, Jiang C, Uehara K, Liu M, Adlanmerini M, Lazar MA. SR9009 has REV-ERB-independent effects on cell proliferation and metabolism. Proc Natl Acad Sci U S A. 2019 Jun 18;116(25):12147-12152. doi: 10.1073/pnas.1904226116. Epub 2019 May 24. PMID: 31127047; PMCID: PMC6589768.

11. Dressel U, Allen TL, Pippal JB, Rohde PR, Lau P, Muscat GE. The peroxisome proliferator-activated receptor beta/delta agonist, GW501516, regulates the expression of genes involved in lipid catabolism and energy uncoupling in skeletal muscle cells. Mol Endocrinol. 2003 Dec;17(12):2477-93. doi: 10.1210/me.2003-0151. Epub 2003 Oct 2. PMID: 14525954.

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