AC-262,536 Accadrine SARMs Gel 20MG (Packs of 5, 10 or 30)


AC-262,536 Accadrine 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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AC-262,536 Accadrine SARMs Gel


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CAS Number 870888-46-3
Other Names AC-262536, AC 262, AC262, AC 262536, AC262536, U8VS41J5O6, UNII-U8VS41J5O6, SCHEMBL4879625, SCHEMBL4881906, CHEMBL3084525, DTXSID701336168, EX-A4672, EX-A7097, MFCD24386408, AKOS040747750
IUPAC Name 4-[(1R,5S)-3-hydroxy-8-azabicyclo[3.2.1]octan-8-yl]naphthalene-1-carbonitrile
Molecular Formula C₁₈H₁₈N₂O
Molecular Weight 278.355
Purity ≥99% Pure (LC-MS)
Liquid Availability sarms gels,yk-11 myobol 30mL liquid Glycol (20mg/mL, 600mg bottle)
sarms gels,yk-11 myobol 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)
sarms gels,yk-11 myobol 60mL liquid Glycol (20mg/mL, 1200mg bottle)
sarms gels,yk-11 myobol 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)
Powder Availability sarms gels,yk-11 myobol 1 gram
Gel Availability sarms gels,yk-11 myobol 20 milligrams
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 AC 262,536 Gel?

Originally developed by Acadia Pharmaceuticals, AC 262,536 is a selective androgen receptor modulator (SARM) typically used to treat various cognitive disorders and prostate cancer. Additionally, AC 262,536 treatment has the potential to support the reproductive system as well as enhance muscle growth, bone density, and fat loss.


Main Research Findings

1) Research reports that AC 262,536 promotes anabolism in the levator ani muscle and supports pituitary functioning by lowering levels of luteinizing hormone (LH) at a rate similar to testosterone without eliciting negative side effects on the seminal vesicles and prostate.

2) The purpose of this study was to determine the metabolism of AC 262,563 in urine, plasma, and hair samples obtained from two equine test subjects.


Selected Data

1) Researchers Piu et. Al utilized male Sprague-Dawley rats as their test subjects. The research team was attempting to examine the effects of AC 262,536 on the weight of the levator ani muscle, prostate, seminal vesicles and plasma LH levels. The test subjects were randomly placed in groups and underwent castration or a sham-operation. After surgery the rats were given 5 days to assimilate to the research setting and recover. Over the course of 14 days all castrated animals were administered a vehicle, a 1 mg/kg dose of testosterone propionate (TP), or a dose of AC 262,536 of either 3, 10, or 30 mg/kg on a daily basis.

24 hours after the final injection, the rats were euthanized. In order to record results plasma samples were taken while the levator ani muscle, seminal vesicles, and prostate were harvested. Each organ was dissected away from all excess adipose tissue and blotted dry so their weights could be accurately measured. Receptor selection and amplification technology (R-SAT) is a cell-based assay that allows for observation of receptor-dependent proliferative responses found throughout various different receptor classes.

The R-SAT data was normalized to the response that is typically elicited by testosterone. The dose-response curve defined the minimum and maximum efficacy values throughout the study. All animal data was analyzed by one-way ANOVA and an unpaired-t test. Following the 2-week rat study the data was normalized to testosterone, clarifying that effects of the vehicle in castrated rats were marked as 0% while the castrated rats treated with 1 mg/kg of TP were defined as 100%. Additionally, plasma LH levels were recorded by using an ELISA kit.

2) The study that was conducted by Cutler et. Al investigated how AC 262,536 is metabolized in the equine body. Two Thoroughbred horses were obtained and exercised in a manner similar to the training that takes place in British training yards. Horse 1 was a 6-year-old gelding weighing 518 kg and Horse 2 was a 5-year-old mare weighing 498 kg. The subjects were fed a typical racehorse diet and housed at the British Horseracing Authority’s Centre for Racehorse Studies in Newmarket UK.

Blood samples were obtained daily for 3 days while urine samples were obtained daily for 4 days preceding administration of dosing. A 50 mg dose of AC 262,536 was orally administered with food at 9 am, 3 days in a row. An IV catheter was placed in the left jugular vein of each horse on the first day of the study in order to obtain blood samples throughout the experimentation period. Blood samples were collected both before and after the dose was administered; samples following dosing were collected at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 18 hours. Blood samples were obtained 7 hours after the first dose and at varying points in time over the 12 days following the final dose.

Before extraction, plasma was spiked with a 50 ng/mL concentration of ACP 105, collected blood samples were analyzed via sample hydrolysis. A conditioning solution composed of 30 g trichloroacetic acid, 24.5 g Trizma base, and 0.05 g sodium azide in 250 mL RG h20 pH 7.1, was applied to the samples and left for 5 minutes. This took place prior to the addition of ACN in order to promote protein precipitation. Non-spiked and samples spiked with 0.5, 1, 2, and 5 ng/mL concentrations of AC 262,536 were prepared and extracted along with post-administration samples. Blank samples were spiked with a concentration of 5 ng/mL of AC 262,536 following extraction for the purpose of comparing extracted spikes to estimations made of extraction recovery.

For the first day of dosing all naturally voided urine was collected for the samples. After the second dosing urine samples were collected twice the following day, while all voided urine was collected for 48 hours after the third dose. After the final dose, one urine sample was collected every other day for up to 13 days. Hair samples were gathered from multiple sections of the mane by pulling the hair out directly at the root. Hair samples were taken for analysis at 0.1, 168, 629, 1805, and 5065 hours following the final dose administration. All samples were collected post-exercise while all but the 0.1 hour measurement took place post-washing and drying.

During extraction, urine samples were spiked with a 50 ng/mL concentration of ACP-105 as an internal marker. Samples were analyzed through the use of enzyme hydrolysis. Following spiking with an 80 ug/mL dose of E. coli, a liquid-liquid extraction was conducted through the addition of 1.5 mL NaOH (2 M). Samples spiked at a concentration of 2, 5, 10, 25, and 50 ng/ml, as well as non-spiked samples, of AC 262,536 were prepared and extracted along with post-administration samples BLank samples were spiked with aa concentration of 5 ng/mL post-extraction in order to compare extracted spikes to estimates of extraction recovery .

Hair samples were obtained in accordance with published methodology for prohibited substances found in equine mane hair. The researchers compared dry hair samples to post-wash hair samples in order to gain a full understanding of the internal and external deposition of AC 262,536. Hair samples were segmented and washed twice with 4 mL of DCM, followed by a 4 mL 10% IPA wash in order to compare the amount of drug in the hair versus the amount in the wash, before drying the hair at 40 degrees Celsius. Dried hair was ground into a fine powder in order to be weighed for analysis. All washes were retained and prepared in order to evaporate to dryness in order to be compared to the hair samples. This was adjusted to account for how much hair was weighed out for analysis versus the amount of hair that was washed. Following extraction, blank hair samples were spiked so researchers could compare extracted spikes to estimations of extraction recovery.



1) The preliminary R-SAT data found that AC 262,536 exhibited increased androgen receptor activity at a level similar to the natural ligand testosterone. Researchers also noted that AC 262,536 acted as a partial agonist relative to testosterone. Through the use of cell extracts expressing the androgen receptor, binding assays revealed that AC 262,536 physically interacted with the androgen receptors with an affinity of 5 nM.

The partial agonist properties of AC 262,536 were further evaluated through the generation of known androgen receptor mutants meant to display either improved or impaired activity in a manner relative to the wild-type receptors (WT). The R-SAT data found that the agonistic nature of AC 262,536 is enhanced in receptors with impaired activity. In the WT androgen receptors, AC 262,536 behaved as an agonist in a manner comparable to testosterone (64% versus 100%).

The T877A mutant exhibited greater levels of testosterone activity (122%) when compared to the mutants G743A and A748T (87% and 27%, respectively). The researchers thought it was important to know that in the T877A mutant there was very little AC 262,536 activity; the compound was completely inactive in the G742A and A748T mutants. The use of the mutants allowed the research team to confirm that AC 262,536 acts as a partial agonist.

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Figure 1: Comparing the efficacy of the mutant androgen receptors in comparison to the control group.

The research reported that AC 262,563 promoted anabolism in a manner similar to that of TP without the instance of adverse androgenic-related side effects.14 days of treatment with TP led to a significant increase in the weight of the prostate. In vehicle-treated animals the prostate was measured at 23 ± 3 mg while the prostates of TP-treated subjects were measured at 223 ± 14 mg. However, results of the study showed that the rats administered AC 262,563 experienced very little prostate growth. Average prostate weight was 12 ± 2 mg in subjects that received the 3 mg/kg dose, while the average prostate weight of the subjects being administered 10 and 30 mg/kg doses were measured at 55 ± 6 mg and 54 ± 5 mg, respectively.

Similar growth patterns were identified in the seminal vesicles. Compared to the vehicle group, the weight of the seminal vesicle experienced a 14-fold growth increase. The two groups weighed in at 52 ± 5 mg to 748 ± 48 mg, respectively. The weight of the seminal vesicles slightly increased in the subjects administered AC 262,563. Weight of the seminal vesicles in the 3 mg/kg group increased to 67 ± 4 mg. Weight of the seminal vesicles in the 10 and 30 mg/kg groups were found to be 150 ± 12 mg and 208 ± 15 mg, respectively. Additionally, comparison of the anabolic effects of AC 262,536 and TP was performed by weighing the levator ani muscle of the subjects. Test subjects administered AC 262,536 experienced a 70% restoration of the maximum effect seen in subjects in the TP-treatment group. In addition to these promising results, it is important to note that instances of androgenic side effects were greatly decreased in the AC 262,563 treatment groups in comparison to the TP-treatment group. That being said, the research team was able to come to the conclusion that AC 262,536 is capable of acting as a partial agonist of androgen receptors [1].

sarms gels,yk-11 myobol
Figure 2: Changes in prostate and seminal vesicle weight based on different experimental treatments.

In terms of pituitary functioning, results of this study found that AC 262,536 reduced LH levels, in a dose-dependent manner, to a greater extent than TP. Treatment with TP led to a significant decrease in LH levels, when compared to the vehicle treatment; LH levels measured at 3.12 ± 0.69 ng/ml vs 9.95 ± 0.60 ng/ml, respectively, Initial results found that the 3 mg/kg dose of AC 262,536 results in a reduction in LH levels at 40% of the maximum effects exhibited by TP-treatment. However, the 10 mg/kg and 30 mg/kg dose of AC 262,536 led to a greater decrease in LH levels at a more significant rate than TP-treatment. The 10 mg/kg dose led to a 1.53 ± 0.34 ng/ml decrease in plasma LH levels, while the 30 mg/kg led to a 3.12 ± 0.69 ng/ml. The research team found that after the animals were castrated, AC 262, 536 elicits a greater reduction in LH levels when compared to TP-treatment without the associated adverse side effects. Further analysis was conducted in order to determine the dose needed in order to reach 50% of the displayed effects of TP (ED50). For this study the ED50 was reported to be approximately 2.8 mg/kg of AC 262,356 [1].


sarms gels,yk-11 myobol
Figure 2: Changes in plasma LH levels based on different experimental treatments.

2) After oral administration of AC 262,536 to two Thoroughbred horses, urination samples were collected for 13 days and examined different metabolites: All pre-administration urine samples did not report any evidence suggesting the presence of AC-262,536 or any metabolites in the urine. Post-administration samples identified significant levels of M2, M3b, M3c, and M4d in the urine samples of both horses. Increased levels of M1, M4b, and M4c were also reported, however, the peak intensities elicited by the presence of the metabolites did not raise high enough to be considered significant.

In respect to FS signal intensity the compound that was most abundantly found in the urine samples of both horses was the postulated epi-AC-262,635 metabolite (M2), displaying a signal 5-times greater than the parent compound. M2 also exhibited the longest duration of detection in the samples collected from both horses, compared to other metabolites present. The second most abundant compound found in the sample was the parent compound, AC 236,536.

In Horse 1 the maximal concentrations of AC 262,536 were observed in the urine sample for approximately 4 hours after final dose administration. The maximal concentrations of the compound were observed for approximately 1 hour following the final dosing in Horse 2. Maximal concentrations of AC 262,536 were 494 ng/mL and 285 ng/mL, respectively. While there was no accumulation of metabolites in the subjects, AC 262,536 and metabolites did not completely clear out of circulation [2].

sarms gels,yk-11 myobol
Figure 3: Signal intensities of AC 262,536 and primary metabolites found in post-administration urine samples collected up to 120 hours after final administration

After administering AC 262,536 to two Thoroughbred horses, pre- and post-administration plasma samples were collected up to 12 days after the final dose in order to identify any metabolites. Pre-administration samples did not report any observations of the presence of AC-262,536 or any related metabolites in the plasma. Post-administration samples collected from both horses found that parent AC 262,536, the M2 metabolite, and the M3c metabolite were present in the sample. It is important to note that the researchers identified very low signal intensity levels in selected samples from both subjects. Furthermore, without the use of enzyme sample hydrolysis M3c and AC 262,536 were only found in the samples at very low levels. However, once enzyme sample hydrolysis was used there was a 5-fold increase in detection of AC 262,536 and a 3-fold increase in detection of M3c.

With respect to FS signal intensity, M2 was the most frequently detected metabolite found in plasma samples obtained from both horses. M2 was detected with 3-times greater signal intensity than parent AC 262,536 with the longest recorded duration of detection period in plasma compared to other metabolites and the parent compound. The parent compound, AC 262,536 was the second most abundant compound found in both subjects. Concentrations reached maximum level in Horse 1, 2 hours after the last administration and 0.5 hours after final dosing for Horse 2. Appropriate maximal concentrates were determined to be approximately 7.5 ng/mL and 2.8 ng/mL, respectively, in the two horses. There was a reported 79% recovery rate based on spikes that occurred pre-and post-extraction. Furthermore, the research team reported that there was no accumulation of the parent compound; AC 262,536 was cleared from the plasma after dose 1, however, after dose 2 only Horse 2 experienced full clear out of the compound [2].

The M3c metabolite was found in the plasma samples collected from both horses. It was determined to be the least abundant metabolite that the researchers could still reliably detect in the plasma samples. Like the parent compound, M3c was cleared from the serum in both subjects after receiving the first dose. The metabolite clearing from the serum was only observed in the samples from Horse 2 after dose 2. The researchers notably mentioned that Horse 1 experienced a longer duration of detection of M3c than the parent compound; the opposite was true in Horse 2 as the duration of detection was significantly shorter.

sarms gels,yk-11 myobol
Figure 4: Signal intensities of AC 262,536 and primary metabolites found in post-administration plasma samples

Pre- and post-administration hair samples were analyzed in an attempt to identify the presence of AC 262,536 or any related metabolites in the sample. In negative controls and pre-administration samples there was no detection of AC 262,536. The extraction recovery of the compound was determined to be approximately 70% based on the spikes occurring before and after dose administration. Preliminary analysis conducted of the hair samples of both horses indicated the presence of the parent compound, AC 262,536, in the post-administration hair samples collected at 5 min, 7 days, and 26 days after final dosing. At the 75 day post-administration sample collection, AC 262,536 was detected in Horse 1 after 3 SRM transitions, however, the compound was detected in Horse 2 after only 1 SRM transition [2].

sarms gels,yk-11 myobol
Figure 5: SRM chromatogram displaying concentrations of AC 262,563 present in a) the preadministration hair sample, b) a spiked hair sample, c) a sample collect 5 minutes after final administration, and d) a sample collected 7 days after the last dose was given.



*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] Piu F, Gardell LR, Son T, Schlienger N, Lund BW, Schiffer HH, Vanover KE, Davis RE, Olsson R, Bradley SR. Pharmacological characterization of AC-262536, a novel selective androgen receptor modulator. J Steroid Biochem Mol Biol. 2008 Mar;109(1-2):129-37. doi: 10.1016/j.jsbmb.2007.11.001. Epub 2007 Nov 22. PMID: 18164613.

[2] Cutler C, Viljanto M, Taylor P, Habershon-Butcher J, Muir T, Biddle S, Van Eenoo P. Equine metabolism of the selective androgen receptor modulator AC-262536 in vitro and in urine, plasma and hair following oral administration. Drug Test Anal. 2021 Feb;13(2):369-385. doi: 10.1002/dta.2932. Epub 2020 Oct 15. PMID: 32959959


AC-262,536 Accadrine SARMs Gels are a highly stable, durable storage and delivery matrix. Sarms Gels are a brand new way to store, transport and deliver SARMS in precise dosages. These AC-262,536 Accadrine SARMs Gels are individually packaged for your convenience and offer key benefits over liquid and powder alone.

SARMS Gels are a gel base media with a specific SARMS compound and quantity embedded into each gel. This dissolvable matrix is able to be accurately concentrated while remaining highly durable along with being far more portable and storage stable than liquids and powders. AC-262,536 Accadrine SARMs Gels promote greater testing compliance and more consistent test results.

At UMBRELLA Labs we strive to be a step above the rest and will continue to be the most innovative and trusted research company on the planet.

AC-262,536 Accadrine SARMs Gel 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.


sarms gels,yk-11 myobol

Additional information


Packs of 5, Packs of 10, Packs of 30