OTR-AC (MK-2866 Ester) SARMs Gel 20MG (Packs of 5, 10 or 30)


OTR-AC 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) SARMs Gel


OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels OTR-AC SARMs Gels,sarms gels


OTR-AC SARMs Gels,sarms gels

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 OTR-AC SARMs Gels,sarms gels 30mL liquid Glycol (20mg/mL, 600MG Bottle)
OTR-AC SARMs Gels,sarms gels 30mL liquid Poly-Cell™ (20mg/mL, 600MG Bottle)
OTR-AC SARMs Gels,sarms gels 60mL liquid Glycol (20mg/mL, 1200MG Bottle)
OTR-AC SARMs Gels,sarms gels 60mL liquid Poly-Cell™ (20mg/mL, 1200MG Bottle)
Powder Availability OTR-AC SARMs Gels,sarms gels 1 gram
Gel Availability OTR-AC SARMs Gels,sarms gels 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, also referred to as Ostarine-O-Acetate, is a selective androgen receptor modulator (SARM) that is an esterified version of the popular compound, Ostarine. The benefits of OTR-AC and Ostarine are very similar, however, OTR-AC is considered to be the more effective compound following the esterification process.

SARMs have been shown to mimic the action of testosterone by effectively binding to androgen receptors. These compounds are becoming more popular and widely available for research purposes as evidence shows SARMs do not elicit negative androgenic side effects, such as increased prostate weight, that are typically associated 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-treated male Wistar rats experienced a regulation of lipid metabolism and endocrine functioning throughout the subjects’ mature adipocytes.


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].

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 esterification process occurs one of three ways: 1) from acid anhydride and alcohol, 2) from acid chloride and alcohol, or 3) from carboxylic acid and alcohol. The reaction between acid anhydride and alcohol is slower than the reaction between acid chloride and alcohol. In order to effectively produce ester compounds the mixture requires the addition of a reagent to warm the fixture. For example 2,6-diiodophenol is commonly used in the acid anhydride reaction to form the ester. The esterification process between acid chloride and alcohol can be performed at room temperature. Finally, the production of esters from carboxylic acid and alcohol requires heating in the presence of an acid catalyst like sulphuric acid [1].

OTR-AC SARMs Gels,sarms gels
Figure 1: acid anhydride and alcohol

OTR-AC SARMs Gels,sarms gels
Figure 2: acid chloride and alcohol

OTR-AC SARMs Gels,sarms gels
Figure 3: carboxylic acid and alcohol

The resulting ester compounds typically have a pleasant smell, leading to widespread usage in the perfume, food flavoring, and cosmetics industries. They are also organic compounds typically found in oils and fats that are able to be used and an organic solvent.

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) In order to examine how Ostarine treatment affects adipocyte metabolism, the research team of Leciejewska et. Al began their study by purchasing male Wistar rats from Brwinow, Warsaw, Poland. All test subjects were housed in standard conditions and kept on a 12 hour dark/12 hour light schedule. The rats were euthanized via decapitation in order for the researchers to quickly dissect and transfer epididymal fat tissue into a plastic beaker with PBS. After the blood vessels were removed the fat pads were sectioned off and digested in Krebs-Ringer bicarbonate buffer supplemented with 10 mM HEPES (KRBH), collagenase type II (3 mg/1 g tissue), 3% BSA, and 5 mmol/L glucose for 45 in a shaking water bath. The cells were then filtered through nylon mesh and rushed with warm KRBH [3].

The next step of the study was to incubate the isolated rat adipocytes in KRBH in the presence of Ostarine for 480 minutes in a shaking water bath. A portion of the adipocytes were preincubated in the presence of specific inhibitors of AR-cyproterone acetate and flutamide in order to observe the effects of the inhibitors on the expression of the androgen receptor. There was also a group of adipocytes incubated with testosterone that acts as a natural ligand. The next step of the study was to examine the lipolytic activity. Isolated rat adipocytes were incubated in KRBH in the presence of Ostarine, doses varying from 0.001, 0.01, 0.1, 1, and 10 um, over the course of 120 or 480 minutes. Isoproterenol was used as the positive control and the adipocytes were incubated with testosterone as a natural ligand for the androgen receptors. The adipocytes were preincubated in the presence of AR inhibitors, cyproterone acetate and flutamide. The intensity of lipolysis was defined as the concentration of glycerol released from adipocytes into the incubation medium through the use of free glycerol reagents [3].

The concentration of adiponectin (ADP) and leptin in the incubation medium was measured using species-specific ELISA and RIA kits. ADP was measured using a Rat Adiponectin/Acrp30 ELISA kit while the leptin concentration was measured in the incubation medium using Multi-Species Leptin RIA kit. The intensity of lipogenesis was measured by incorporating glucose into the isolated rat adipocytes. The mature adipocytes were transferred into polystyrene tubes and incubated with varying doses of Ostarine in KRBH. 500 nM of insulin was used as a positive control and after 120 minutes Dole’s extraction mixture was added to stop all reactions. Heptin and water were added and the upper phase of the lipid fraction was transferred to scintillation liquid in order for beta counting to take place [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) The researchers reported that the preincubation of the adipocytes with AR inhibitors flutamide and cyproterone acetate helped to confirm the effect of Ostarine on the adipocyte metabolism via the androgen receptor. Incubation took place for 30 minutes followed by the addition of Ostarine and testosterone to the medium and incubation for another 8 hours. The results found that adding 1 uM of Ostarine upregulated the AR mRNA expression, while 0.1uM concentration of the SARM did not elicit any significant changes in mRNA expression. Addition of testosterone was also shown to increase the level of AR mRNA expression Additionally, specific antagonists of androgen receptors were used to examine the resulting effects on the expression of the Ostarine receptor. The data that was collected shows that preincubation with cyproterone acetate and flutamide did not result in significant effects of Ostarine on the AR mRNA expression [3].

The next portion of the study investigated how Ostarine affects lipolytic activity in the isolated rat adipocytes after 120 and 480 minutes of incubation. Isoproterenol was used as the positive control while testosterone was used as the natural AR agonist. 1 uM of Ostarine as well as 1 uM of testosterone was able to stimulate lipolysis after 120 minutes of incubation. 480 minutes of incubation led to an increase in glycerol concentration in the incubation medium. Furthermore, when preincubating the adipocytes with the AR antagonists, Ostarine has been shown to stimulate lipolysis via the androgen receptor.

OTR-AC SARMs Gels,sarms gels
Figure 4: Effects of Ostarine on lipolysis intensity after (A) 120 minutes incubation and (B) 480 minutes of incubation as well as the inhibitory effects of flutamide and cyproterone acetate on lipolysis stimulated by both Ostarine and testosterone after (C) 120 minutes of incubation and (D) 480 minutes of incubation

Next, the effects of Ostarine on biotransformation of glucose to lipids in the isolated adipocytes was evaluated by the research team. In contrast to the results of lipolysis assay, low concentrations of Ostarine was found to have the greatest effects on the cell. In fact, when high concentrations of Ostarine were added to the medium, the rate of lipogenesis was inhibited [3].

OTR-AC SARMs Gels,sarms gels
Figure 5: Effects of varying doses of Ostarine and testosterone on the intensity of lipogenesis

The final portion of the experiment examined how treatment with Ostarine changes mRNA expression and secretion of ADP and leptin throughout the isolated rat adipocytes. The results of the study reported that leptin gene expression was downregulated in the presence of 0.01 and 0.1 uM of Ostarine, as well as 1 and 100 uM of testosterone. Expression of the ADP gene experienced similar results in response to treatment with Ostarine. The primary difference between the expression of the two genes is that ADP was downregulated with all concentrations of Ostarine and testosterone [3].

Secretion of leptin and ADP in the isolated rat adipocytes in response to Ostarine treatment, was examined by the research team. After 120 minutes of incubation Ostarine was shown to decrease leptin secretions at concentrations of 0.001 and 1 uM, as well as 1 uM of testosterone. After 480 minutes of incubation, leptin secretion was decreased following administration of 0.01 uM concentration of Ostarine. Similar to leptin, the expression of ADP content significantly decreased in the presence of Ostarine and testosterone. After 120 minutes of incubation Ostarine was shown to decrease ADP secretions at concentrations of 0.001 and 1 uM, as well as 1 uM of testosterone. After 480 minutes of incubation, there was a noticeable difference between ADP secretion in the presence of 0.1 and 1 uM of Ostarine treatment as well as testosterone administered at a concentration of 100 nM [3].

OTR-AC SARMs Gels,sarms gels
Figure 6: Effects of Ostarine on adiponectin secretion from isolated rat adipocytes after (A) 120 minutes and (B) 480 minutes of incubation, as well as (C) adiponectin mRNA expression after 480 minutes of incubation.



*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, Pruszynska-Oszmalek E, Bien J, Nogowski L, Kolodziejski PA. Effect of ostarine (enobosarm/GTX024), a selective androgen receptor modulator, on adipocyte metabolism in Wistar rats. J Physiol Pharmacol. 2019 Aug;70(4). doi: 10.26402/jpp.2019.4.04. Epub 2019 Oct 19. PMID: 31642815.

[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 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.


OTR-AC SARMs Gels,sarms gels

OTR-AC SARMs Gels,sarms gels

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