OTR-AC (MK-2866 ESTER) SARM is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.


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OTR-AC (MK-2866 ESTER) SARM Liquid


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sarms mk 2866

CAS Number 1025658-44-9
Other Names OTR-AC, Ostarinyl Acetate (MK2886 acetate), Ostarine acetate (MK2886 acetate), Ostarine acetate ester (MK2886 acetate ester), Ostarine acetic acid ester (MK2886 Acetic acid ester)
IUPAC Name 5-(1H-pyrazol-5-yl)-1-[2-[4-(trifluoromethoxy)phenoxy]ethyl]indole-2-carboxylic acid
Molecular Formula C₂₁H₁₆F₃N₃O₄
Molecular Weight 431.37
Purity ≥99% Pure (LC-MS)
Liquid Availability sarms mk 2866 30mL liquid Glycol (20mg/mL, 600MG Bottle)
sarms mk 2866 30mL liquid Poly-Cell™ (20mg/mL, 600MG Bottle)
sarms mk 2866 60mL liquid Glycol (20mg/mL, 1200MG Bottle)
sarms mk 2866 60mL liquid Poly-Cell™ (20mg/mL, 1200MG Bottle)
Powder Availability sarms mk 2866 1 gram
Gel Availability sarms mk 2866 20mg
Storage Store in cool dry environment, away from direct sunlight.
Terms All products are for laboratory developmental research USE ONLY. Products are not for human consumption.



What is OTR-AC?

OTR-AC is a selective androgen receptor modulator (SARM) that is also commonly referred to as Ostarine-O-Acetate. This compound is an esterified version of the popular SARM, Ostarine, or MK-2866. While Ostarine and OTR-AC elicit similar benefits, the latter is considered to be the stronger of the two compounds following the esterification process.

Due to its ability to bind to androgen receptors, the SARM has been shown to mimic the action of testosterone. SARMs are becoming more popular and widely available for research purposes as evidence shows the compounds do not elicit negative androgenic side effects, like those observed with testosterone treatment.


Main Research Findings

1) The process of esterification leads to increased potency and improved efficacy of OTR-AC in comparison to its parent compound, MK-2866.

2) SARMs have been shown to promote various forms of functional therapy through tissue-selective activation of androgenic signaling

3) Ostarine has the potential to induce myogenic differentiation in the muscles of animal test subjects, as well as in C2C12 and L6 cells.


Selected Data

1) As it was previously mentioned, OTR-AC is the esterified form of MK-2866. MK-2866, like most SARMs, is typically known for its ability to promote anabolic activity in bone and muscle tissue. Current research examines the potential of MK-2866 to enhance neuroprotection and stimulate antitumor activity. As an esterified version of MK-2866, OTR-AC has been shown to elicit similar effects as its parent compound with far more potency. The esterification process proceeds by combining an organic acid (RCOOH) and an alcohol (ROH) to form water and an ester (RCOOR) [1].

sarms mk 2866
Figure 1: Chemical reaction for esterification

Furthermore, esterification reactions occur when a primary alcohol is treated with a carboxylic acid in the presence of sulphuric acid. The resulting compound tends to smell sweet and is generally classified as an ester compound. The chemical reaction typically takes place in 5 steps and follows the format:

The resulting ester compounds are organically found in oils and fats; due their pleasant smell they are widely used throughout the perfume, food, and cosmetics industries. Naturally occurring esters are detected in pheromones while phospho esters form the backbone of DNA molecules. Additionally, esters are frequently used in the manufacturing of surfactants like soap and detergent, polyesters on the other hand are used in the production of plastic compounds [1].

2) The research team of Shalender Bhasin, MD and Ravi Jasuja, PhD. examined the potential of selective androgen receptor modulators (SARMs) to promote various forms of functional therapy. Previous research has reported that SARMs bind to androgen receptors and display tissue-selective activation of androgenic signaling, leading to anabolism in skeletal muscles and bones. The actions of SARMs are compared to testosterone, the major ligand for androgen receptors. Testosterone is often supplemented to men and women of all ages suffering from androgen deficiency and decreased muscle and bone wasting. However, administration of androgenic compounds such as testosterone is often related to many dose-limiting adverse side effects such as prostate dysfunction, edema, and erythrocytosis. On the other hand, SARM administration has been shown to result in similar anabolic activity without the adverse side effects associated with typical androgen treatment [2].

In order to target functional limitations caused by osteoporosis, aging, and chronic disorders, researchers first attempted to develop a SARM with the desired activity profile and tissue selectivity. The second approach included elucidating the mechanisms of action of androgens on skeletal muscles and the prostate in order to identify signaling molecules downstream of the androgen receptors that are capable of activating hypertrophic pathways in skeletal muscles but not the prostate. When observing the structure of SARMs, the compounds can be categorized into two groups: steroidal and nonsteroidal. Steroidal SARMs are synthesized by modifying the chemical structure of testosterone molecules. For example, substitution of 7-alpha alkyl makes testosterone less susceptible to 5-alpha reduction, thus increasing tissue selectivity with respect to the prostate. This results in the increased anabolic activity in the levator ani muscle and a decreased rate of anabolism in the prostate and seminal vesicles [2].

Researchers at the University of Tennessee and Ligand Pharmaceuticals reported early data regarding the discovery of nonsteroidal SARMs. After publication of the initial findings various other structural categories of SARM pharmacophores were examined. These categories included: aryl-propionamide, bicyclic hydantoin, quinolones, tetrahydroquinoline analogs, benzimidazole, imidazolopyrozole, indole, pyrazoline derivatives, azasteroidal derivatives, and aniline, diaryl aniline, and benzoxazepinones derivatives. The first generation of SARMS was developed by manipulating the structure of aryl propionamide analogs, bicalutamide and hydroxyflutamide. This initial discovery led to copious amounts of research dedicated solely to modifying compound structures in order to promote tissue selectivity and further hone in on the beneficial anabolic activity [2].

3) The research team of Leciejewska et. Al examined how treatment with Ostarine affects myogenic differentiation in rats in order to observe how the treatment may be utilized to treat loss of muscle mass elicited by disease or age-related decline. Wistar rats were purchased from the Polish Academy of Science and all procedures were approved by the Local Ethical Commission for Investigation on Animals. The rats were initially acclimatized for 1 week followed by subcutaneous injections of Ostarine at a dose of 0.4 mg/kg of body weight. The rats received Ostarine treatment daily for 30 days while the animals in the control group were injected with the same dose of a vehicle compound [3].

All media and supplements used in this study were purchased from Corning located in Tewksbury, MA while 99.36% pure Ostarine was purchased from Selleck Chemicals. The primary antibodies used in the study included: anti-myogenin, anti-myh, anti-myoD, anti-vinculin, anti-phospho-ERK1/2, and anti-ERK1/2, all obtained from Santa Cruz Biotechnology in Dallas, TX. Sigma-Aldrich located in Taufkirchen, Germany supplied anti-GAPDH and all secondary antibodies that were utilized in the Western blot analysis. Additionally, both the C2C12 and L6 cell lines were grown under the same conditions and then purchased by the researchers from the European Collection of Authenticated Cell Cultures. The experimental medium used was DMEM with 0.2% bovine serum albumin (BSA) added instead of FBS [3].

In order to examine cell differentiation of the two cell lines, the cells were seeded on 6- or 12-well plated cultured in DMEM with 10% FBS. To initiate myogenic differentiation, the medium was changed to DMEM with 2% horse serum (HS) and varying concentrations of Ostarine added instead of FBS. For the early stage portion of the study the cells were collected 2 days after initiation of the differentiation process and 6 days after for the late stage portion of the study.

When examining the proliferation and viability of each cell line the cells were seeded onto a 96-well plate and cultured in standard medium for 24 hours. After 24 hours the cells were washed with PBS and cultured for another 24 hours with the experimental medium of DMEM with 0.2% BSA supplemented with Ostarine. In order to establish a positive control, some of the cells were grown in standard medium. After 24 hours the cells were treated with MTT solution for 1 hour in order to investigate viability. The medium was removed after an hour and replaced with 100 uL of DMSO in order to dissolve formazan crystals. From there, an ELISA BrdU colorimetric kit was used to test proliferation through evaluation of BrdU incorporation into new DNA strands of the proliferating cells. After 21 hours of incubation with Ostarine, 10 uM of BrdU solution was added for the remaining 3 hours of the incubation period [3].

In order to observe the effects of Ostarine on muscle tissue the quadriceps muscles were extracted from the animals after the treatment period. All samples were suspended in 10% paraformaldehyde while sections were prepared accordingly. The paraffin sections were then collected on microscope slides and stained using hematoxylin and eosin stain. Jenner-Giemsa staining then took place. The cells were seeded on 6-well plates until they reached 90% confluence; at that point the growth medium was replaced with the differentiation medium consisting of DMEM containing 2% HS supplemented with Ostarine in concentrations of 100 and 100 nM.

After 6 days of differentiation the cells were fixed by methanol. Following the removal of methanol the cell samples were incubated with Jenner staining solution prepared in a 1:3 ratio from stock solution and buffered sodium phosphate. After 10 minutes of incubation in the staining solution the cells were rinsed, followed by further staining with the Giemsa solution. Cells were washed twice with distilled water after an additional 10 minute incubation period. The fusion index was calculated by staining the fixed cells and determining the number of nuclei in a myotubule, compared to the total number in nuclei in the sample [3].



1) As an esterified version of Ostarine, OTR-AC is considered a superior version of its parent compound due to its improved bioavailability and potency, as well as a 10-fold increase in half-life. The esterification process also makes OTR-AC far more stable than Ostarine suggesting that it is more effective and safe. While the benefits of the two compounds are very similar, there is debate regarding how much stronger OTR-AC is compared to Ostarine. Further research is required in order to know exactly how much more potent the esterified compound is in comparison to the parent compound.

Multiple research-based studies have concluded that SARMs are able to increase muscle mass and reduce fat, however, researchers thought it was important to note that OTR-AC does not reduce fat by targeting fat directly, but rather by raising metabolic rate. The compound increases testosterone leading to improved metabolism and increased energy expenditure, ultimately resulting in fat loss. Additionally, evidence suggests that OTR-AC is capable of increasing libido, improving recovery from exercise by increasing protein synthesis, and enhancing physical performance by boosting muscle mass and raising metabolism. Treatment with OTR-AC has also been linked to improved cardiovascular health as the esterified compound is capable of lowering levels of low-density lipoprotein [4].

2) The research team of Bhasin and Jasuja were able to achieve selectivity of SARMs by elucidating the mechanism of testosterone’s action on the prostate, as well as how molecules farther downstream were associated with activation of AR signaling in skeletal muscle. Analysis of muscle biopsies collected from male test subjects treated with varying doses of testestore revealed that administration of the compound led to hypertrophy in type I and type II muscle fibers. In relation to testosterone dosage, both type I and type II fibers experienced significant changes in cross-sectional areas. It is important to note that there was no change observed in the absolute number or the relative proportion of type I and type II fibers in response to testosterone administration [2].

Hypertrophy of the skeletal muscle was further examined through observation of muscle satellite cells and the myonuclear number. These variables were assessed through the use of electron microscopy, using direct counting and spatial orientation methods at baseline and after 20 weeks of GnRH agonist and testosterone enanthate treatment. Results reported that absolute and percent satellite cell number was significantly greater than baseline after 20 weeks of the test subjects receiving supraphysiologic doses of testosterone. The observed changes in the number of satellite cells correlated with changes in total and free testosterone levels, indicating that muscle fiber hypertrophy induced by testosterone is correlated with an increase in the number of satellite cells and the myonuclear number.

Recent studies have found that both testosterone and DHT are able to promote association between liganded ARs and beta-catenin, its co-activator. Beta-catenin is stabilized by this interaction and enhances translocation into the nucleus and association with TCF-4, as well as the transcriptional activation of Wnt-target genes. Additionally, Testosterone upregulated the expression of follistatin, resulting in increased muscle mass and decreased fat mass. SMAD 7 is also upregulated by testosterone while TGF-beta-mediated SMAD signaling in TGF-beta target genes is downregulated. The connection between testosterone and follistatin expression indicates that the effects of testosterone are cross-communicated from the WNT pathway to the TGF-beta-SMAD pathway. These results further suggest that candidate molecules located downstream of AR and beta-catenin, such as follistatin, have the potential to mediate the effects of testosterone on the muscle and may provide desired selectivity of anabolism. The discovery of these candidate targets allows for further research to be conducted in order to develop selective anabolic drugs [2].

3) When observing the changes in cell proliferation and viability elicited by Ostarine, the research team reported increased proliferation and viability in both the C2C12 and L6 cell lines after incubation with an 1000 nM concentration of Ostarine. The SARM was also shown to have a stronger effect on the L6 cell line as there was a significant stimulation of proliferation identified. The next step of the study regarding mediation of the androgen receptor and ERK1/2 activation. The results reported that ERK1/2 was phosphorylated by different concentrations of Ostarine in both the C2C12 and L6 cell lines. The pharmacological blocker of ERK1/2 kinase, U0126, was applied in order to examine whether the proliferation stimulated effect was canceled after addition of the blocker. After treating cells with U0126, there was no observed stimulation of the proliferation process when the cell samples were supplemented with Ostarine [3].

The research team noted an interesting response when the ERK1/2 blocker was applied to the L6 cell line. Results reported that not only did the blocker eliminate all stimulating effects of Ostarine on the proliferation process, but actively inhibited the process. Furthermore, adding AR blockers to the L6 cell line completely abolished the stimulatory effects of Ostarine on cell viability. However, in C2C12 cells, when adding the AR blockers enzalutamide and cyproterone acetate, only enzalutamide blocked the stimulatory effects of Ostarine. Based on these results and previous experiments conducted, the researchers were able to confirm that the androgen receptors regulate the stimulation of ERK1/2 phosphorylation [3].

sarms mk 2866
Figure 2: (A,B) changes in ERK1/2 phosphorylation in both cell lines in response to different concentrations of Ostarine. (C,D) time activation of ERK1/2 phosphorylation by Ostarine in both cell lines. (E,F) Changes in proliferation of both cell lines in response to Ostarine and ERK1/2 inhibition. (G,H) changes in viability of both cell lines in response to Ostarine treatment and pharmacological AR blocking. (I,J) changes in Ostarine-induced ERK1/2 phosphorylation in both cell lines in the presence of the AR blockers.

Next, the research team investigated how Ostarine affects the differentiation in L6 and C2C12 cells. This portion of the study began by observing the mRNA expression of differentiation markers myogenin, myh, and myoD, in both early and late stages of differentiation. When examining the early stages of differentiation by removing cell samples from incubation after 2 days, the researchers reported that there was a significant increase in the mRNA expression of myogenin, myh, and myoD. In regards to the late stages of differentiation the cells were removed from incubation after 6 days, resulting in an increase of myogenin and myh, but not myoD. Additionally, after 6 days of differentiation there was a noticeable increase in protein content; this effect was not seen after only 2 days of differentiation. However, myogenin protein expression was successfully stimulated 2 days after differentiation when 100 or 1000 nM of Ostarine was added to the cell samples. The researchers also noted that the addition of 100 or 1000 nM of Ostarine led to increase in relative protein expression in the late stages of differentiation [3].

sarms mk 2866
Figure 3: changes in protein expression in L6 cells in response to the addition of varying concentrations of Ostarine in both the early stages (A-C) and late stages (D-F) of differentiation.

In a similar manner to the L6 cells, results reported that the C2C12 cells experienced an increase in mNA expression of the differentiation markers, myogenin, myh, and myoD in both the early and late stages of differentiation. After 2 days of differentiation there was a noticeable increase in the mRNA expression of myogenin and myh, while after 6 days of differentiation there was an increase in mRNA expression of myogenin, myh, and myoD. Furthermore, the researchers observed an increase in myogenin protein expression after 2 days when 100 nM of Ostarine was added; the addition of 100 and 10,000 nM of Ostarine increased myogenin protein expression after 6 days of differentiation [3].
sarms mk 2866
Figure 4: changes in protein expression in C2C12 cells in response to the addition of varying concentrations of Ostarine in both the early stages (A-C) and late stages (D-F) of differentiation.

The fusion index was calculated through Jenner-Giemsa staining of the L6 and C2C12 cells that were exposed to 100 and 1000 nM concentrations of Ostarine. Results of the staining found that both doses of the SARM increased the fusion index in L6 and C2C12 cells. Calculation of the fusion index was followed by the determination of the relationship between Ostarine-induced differentiation and activity of the androgen receptors in both L6 and C2C12 cell lines. Ostarine was administered in a dose of 1000 nM and in both early and late stages of differentiation the AR blocker enzalutamide inhibited the stimulatory effects of Ostarine.

The final portion of the experiment examined how Ostarine affected muscle differentiation in the rat test subjects. After 30 days administration of the SARM to the rats the research team observed an increase in the mass of the levator ani muscle. There was also an increase in the mRNA expression of myogenin and myh, as well as an increase in myH protein content. Staining revealed that there was an increase in the number of nuclei in the muscle cells following treatment with Ostarine. While the levator ani is typically used as an indicator of anabolic activity, the researchers also collected the quadriceps muscle to assess changes in protein expression in order to further solidify their data [3].

sarms mk 2866
Figure 5: Effects of 30-day treatment with Ostarine on (A) levator ani muscle mass, (B,C) myogenin and myh mRNA expression, and (D) protein levels of MyH.



*This information is for educational purposes only and does not constitute medical advice. THE PRODUCTS DESCRIBED HEREIN ARE FOR RESEARCH USE ONLY. All clinical research must be conducted with oversight from the appropriate Institutional Review Board (IRB). All preclinical research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).



[1] “Esterification (Alcohol & Carboxylic acid) – Reactions Mechanism & Uses with Videos.” Byju’s, https://byjus.com/chemistry/esterification/. Accessed 6 June 2023.

[2] Bhasin S, Jasuja R. Selective androgen receptor modulators as function promoting therapies. Curr Opin Clin Nutr Metab Care. 2009 May;12(3):232-40. doi: 10.1097/MCO.0b013e32832a3d79. PMID: 19357508; PMCID: PMC2907129.

[3] Leciejewska N, Kołodziejski PA, Sassek M, Nogowski L, Małek E, Pruszyńska-Oszmałek E. Ostarine-Induced Myogenic Differentiation in C2C12, L6, and Rat Muscles. Int J Mol Sci. 2022 Apr 15;23(8):4404. doi: 10.3390/ijms23084404. PMID: 35457222; PMCID: PMC9031805.

[4] Narayanan R, Mohler ML, Bohl CE, Miller DD, Dalton JT. Selective androgen receptor modulators in preclinical and clinical development. Nucl Recept Signal. 2008;6:e010. doi: 10.1621/nrs.06010. Epub 2008 Nov 26. PMID: 19079612; PMCID: PMC2602589.


OTR-AC (MK-2866 ESTER) SARM is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.

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Additional information

Weight 4 oz
Dimensions 3 × 3 × 5 in
Formula Option


Molar Mass

431.37 g·mol−1

Molecular Formula