Androgen receptor (AR); MK-2866 (GTx-024) showed high AR binding affinity with Ki = 3.8 ± 0.5 nM (determined by competitive radioligand binding assay using ³H-mibolerone). [1]
MK-2866 targets the androgen receptor (AR). It acts as a selective androgen receptor modulator (SARM), which means it binds to the AR and exerts tissue-specific effects. Ostarine binds to the androgen receptor with high affinity, with a Ki of 3.8 nM. In CV-1 cells co-transfected with human AR expression vectors, Ostarine modulates the transcriptional activity of the AR. It is designed to work like testosterone, promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength.

Ostarine at the concentration of 10 nM modulates the transcriptional activity of AR in CV-1 cells cotransfected with a human AR expression vector, a luciferase reporter vector, and a control β-galactosidase vector, with 94%-100% relative activity of the transcriptional activation observed for 1 nM DHT.
Kinase Assay: MK-2866 (aslo known as Enobosarm, GTx-024, Ostarine) is a selective androgen receptor modulator (SARM) with Ki of 3.8 nM, and is tissue-selective for anabolic organs. MK-2866 is developed by GTx Inc and was designed to work like testosterone, thus promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength.

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MK-2866 (GTx-024) bound to AR with high affinity (Ki = 3.8 ± 0.5 nM). [1]
In cotransfection assays using CV-1 cells co-transfected with human AR expression vector, luciferase reporter vector, and control β-galactosidase vector, MK-2866 (GTx-024) at a single concentration of 100 nM induced AR-mediated transcriptional activation to a level comparable to that induced by 1 nM dihydrotestosterone (DHT), indicating full agonist activity with no apparent difference from other cyano/nitro-substituted SARMs. [1]
In vitro, Ostarine exhibits the highest androgenic and anabolic activity among non-steroidal AR agonists. It is particularly effective in anabolic tissues, with ED50 values of 0.12, 0.39, and 0.03 mg/day for the prostate, seminal vesicles, and levator ani muscle, respectively. This makes it four times more effective on the levator ani muscle than testosterone propionate. At a low dose of 0.03 mg/day, Ostarine demonstrates effective and selective activity in anabolic tissues. In castrated male rats, it significantly stimulates the growth of the prostate, seminal vesicles, and levator ani muscle.

After intravenous administration of Ostarine at a single dose of 10 mg/kg, plasma concentration of Ostarine declines slowly, exhibiting a longer terminal half-life of 6.0 hours, as compared to that of other related cyano/nitro group-substituted SARMs with terminal halflives of 2.6-4.0 hours. Ostarine exhibits significantly androgenic and anabolic activity by stimulating the growth of prostate, seminal vesicles, and levator ani muscle when administered in castrated male rats; Ostarine is more potent than other cyano/nitro group-substituted SARMs. Ostarine restores the weight of the prostate to 39.2%, and seminal vesicle 78.8%, and stimulates the growth of levator ani muscle to a greater extent of 141.9% as compared with that of androgenic organs. Ostarine exhibits the highest in vivo androgenic and anabolic activity of any AR nonsteroidal agonist examined to date, with ED50 values of 0.12, 0.39 and 0.03 mg/day in prostate, seminal vesicles, and levator ani muscle, respectively, being 4 times as potent as testosterone propionate (TP) in levator ani muscle. At low dose of 0.03 mg/day, Ostarine is sufficient to exert efficacious and selective activity in anabolic tissues.
MK-2866 (GTx-024) exhibited potent in vivo anabolic and androgenic activity in castrated male rats after 14 days of daily subcutaneous administration. [1]
Dose-response analysis revealed ED50 values of 0.12 ± 0.05 mg/day for prostate, 0.39 ± 0.15 mg/day for seminal vesicles, and 0.03 ± 0.01 mg/day for levator ani muscle. [1]
The maximum pharmacological effects (Emax) as percentage of intact control were: prostate 51.1 ± 4.2%, seminal vesicles 98.0 ± 13.2%, and levator ani muscle 136.3 ± 3.5%. [1]
Relative potency in levator ani muscle was 4.41 compared to testosterone propionate (TP), and relative efficacy was 1.31, exceeding the anabolic activity of TP. [1]
Efficacious and selective anabolic activity was observed at dose rates as low as 0.03 mg/day. [1]
In vivo, Ostarine has been shown to facilitate recovery of prostate weight by 39.2%, seminal vesicle weight by 78.8%, and notably stimulated levator ani muscle growth to 141.9% in animal models. It is administered orally and has demonstrated anabolic activity, resulting in a dose-dependent decrease in LDL and HDL cholesterol levels, with the average LDL/HDL ratio remaining in the low-risk category. The compound has an ED50 of 0.44 mg/day in animal models. These in vivo findings support its potential for treating muscle-wasting conditions.

The AR binding affinity was determined using an in vitro competitive radioligand binding assay. Rat cytosol was incubated with increasing concentrations (10⁻² to 5000 nM) of each ligand, a saturating concentration of ³H-mibolerone (1 nM), and 1000 nM triamcinolone acetonide to prevent interaction with progesterone receptors. Incubation was carried out at 4°C for 18 hours. Free and bound ³H-mibolerone were separated using the hydroxyapatite method. IC50 values were determined by nonlinear regression analysis, and the apparent equilibrium dissociation constant (Ki) was calculated using the equation Ki = Kd × IC50 / (Kd + L), where Kd is the dissociation constant of ³H-mibolerone (0.19 ± 0.01 nM) and L is the concentration of ³H-mibolerone used (1 nM). [1]
Non-cellular binding assays for Ostarine typically involve measuring its affinity for the androgen receptor. These assays use purified AR or AR-containing preparations to determine the compound's ability to displace a labeled ligand, with its Ki value of 3.8 nM being a key parameter. Such studies are essential for characterizing its high-affinity binding and for comparing its potency to other SARMs.

The transcriptional activity of MK-2866 (GTx-024) was measured using a cotransfection assay in CV-1 cells. CV-1 cells were co-transfected with a human androgen receptor expression vector, a luciferase reporter vector, and a control β-galactosidase vector. Transcriptional activation was assayed using a single concentration (100 nM) of the ligand and expressed as a percentage of that induced by 1 nM dihydrotestosterone. [1]
In vitro cell-based assays for Ostarine commonly use CV-1 cells co-transfected with human androgen receptor expression vectors, a luciferase reporter vector, and a β-galactosidase control vector. In this system, the compound's ability to modulate AR transcriptional activity is measured by assessing luciferase activity, which serves as a readout of AR activation. These assays are crucial for confirming its mechanism of action as an AR modulator.

Dissolved in DMSO, and diluted in saline; 1 mg/kg; s.c. administration Immature castrated male Sprague-Dawley rats

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For in vivo pharmacodynamic studies: Immature male Sprague-Dawley rats (180-220 g) were castrated and randomly distributed into groups of five animals. MK-2866 (GTx-024) was administered via daily subcutaneous injection for 14 days at increasing doses (0.03, 0.1, 0.3, 0.5, 0.75, 1 mg/day). After 14 days, ventral prostates, seminal vesicles, and levator ani muscles were removed and weighed. Organ weights were normalized to body weight and compared with intact and castrated controls. [1]
For pharmacokinetic studies: Immature male Sprague-Dawley rats (approximately 250 g) were implanted with a jugular vein catheter one day before dosing. MK-2866 (GTx-024) was dissolved in a vehicle consisting of 5% DMSO and 95% PEG 300 and administered as a single intravenous bolus dose at 10 mg/kg via the jugular vein. Blood samples (250 μl) were collected via the jugular vein at predetermined time intervals. Plasma was separated by centrifugation and stored at -20°C until analysis. [1]
In vivo animal studies for Ostarine are typically conducted in castrated male rats. The compound is administered orally at various doses to evaluate its androgenic and anabolic activity. Endpoints often include measuring the weight of androgen-sensitive tissues such as the prostate, seminal vesicles, and the levator ani muscle. These studies demonstrate its tissue-selective anabolic effects and are key to its characterization as a SARM.

Pharmacokinetic parameters of MK-2866 (GTx-024) after a single intravenous dose (10 mg/kg) in male rats: terminal half-life (t1/2) = 6.0 h; plasma clearance (CL) = 1.4 ± 0.3 ml/min/kg; volume of distribution at steady state (Vss) = 635 ± 84 ml/kg; area under the plasma concentration-time curve from 0 to infinity (AUC∞) = 127 ± 27 μg·h/ml; mean residence time (MRT) = 475 ± 46 min. [1]
MK-2866 (GTx-024) showed the slowest clearance among the tested cyano/nitro-substituted SARMs, resulting in the highest systemic exposure. [1]
Ostarine is an orally active compound. Following a single intravenous injection of 10 mg/kg, it presents a slow decline in plasma concentration with a longer half-life of 6 hours, compared to the 2.6-4.0 hours half-life of other cyan/nitro-substituted SARMs. Its solubility is poor in water (< 1 mg/mL), but it is soluble in ethanol (72 mg/mL) and DMSO (55 mg/mL). For in vivo formulation, a mixture of 10% DMSO, 40% PEG300, 5% Tween 80, and 45% saline is recommended, achieving a solubility of 2 mg/mL.

Comprehensive toxicological data for Ostarine are not extensively detailed in standard summaries, as it is primarily a research compound. However, clinical studies have shown that it can result in a dose-dependent decrease in LDL and HDL cholesterol levels. As with all SARMs, its use is associated with potential hormonal side effects. Ostarine is not approved for clinical use and is strictly a research compound for laboratory use only.

J Pharmacol Exp Ther.2005 Oct;315(1):230-9;J Med Chem.2011 Jun 9;54(11):3973-6.

Enobosarm has been used in clinical trials investigating the treatment of stress urinary incontinence and triple-negative breast cancer. Enobosarm is a nonsteroidal anti-inflammatory drug with anabolic activity. The selective androgen receptor modulator (SARM) GTx-024 has a mechanism of action similar to testosterone, thereby promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength. By mimicking the effects of testosterone, this drug may increase lean body mass, thereby improving muscle atrophy in the hypermetabolic state of cancer cachexia.

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MK-2866 (GTx-024) is a selective androgen receptor modulator (SARM) with promising clinical potential for treating androgen deficiency-related disorders such as male hypogonadism, osteoporosis, muscle-wasting diseases, and for use in contraception. [1]
The compound demonstrated tissue-selective activity, with full maintenance of seminal vesicle weight (98.0% of intact control) and supra-maximal anabolic effect on levator ani muscle (136.3% of intact control) at higher doses, while prostate weight was restored to 51.1% of intact control. [1]
Relative potency in anabolic tissue (levator ani) was 4.41 times that of testosterone propionate, indicating high potency. [1]
Ostarine (MK-2866, Enobosarm) is a non-steroidal, orally active selective androgen receptor modulator (SARM) with high affinity for the androgen receptor (Ki = 3.8 nM). It was designed to provide the anabolic benefits of testosterone (such as increased muscle mass) with reduced androgenic side effects. Ostarine has been investigated for conditions like cancer cachexia and muscle wasting. It is not approved for clinical use and is available only as a research compound for studying androgen receptor biology and anabolic mechanisms.

C19H14F3N3O3

389.33

389.098

841205-47-8

11326715

White to off-white solid powder

1.4±0.1 g/cm3

632.3±55.0 °C at 760 mmHg

336.2±31.5 °C

0.0±2.0 mmHg at 25°C

1.578

4.83

2

8

5

28

658

1

C[C@](COC1=CC=C(C=C1)C#N)(C(=O)NC2=CC(=C(C=C2)C#N)C(F)(F)F)O

JNGVJMBLXIUVRD-SFHVURJKSA-N

InChI=1S/C19H14F3N3O3/c1-18(27,11-28-15-6-2-12(9-23)3-7-15)17(26)25-14-5-4-13(10-24)16(8-14)19(20,21)22/h2-8,27H,11H2,1H3,(H,25,26)/t18-/m0/s1

(2S)-3-(4-cyanophenoxy)-N-[4-cyano-3-(trifluoromethyl)phenyl]-2-hydroxy-2-methylpropanamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.42 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (6.42 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.42 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly..

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Solubility in Formulation 4: 1% DMSO +30% polyethylene glycol+1% Tween 80 :78 mg/mL (200.3 mM)

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 (Please use freshly prepared in vivo formulations for optimal results.)