ACP-105 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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ACP-105 SARM Liquid


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CAS Number 1048998-11-3
Other Names ACP105, ACP 105, 899821-23-9, SCHEMBL4469384, CHEMBL3084681, AMY32474, ZKB82123, AKOS040741043, MS-24152, HY-112256, CS-0044397
IUPAC Name 2-chloro-4-[(1R,5S)-3-hydroxy-3-methyl-8-azabicyclo[3.2.1]octan-8-yl]-3-methylbenzonitrile
Molecular Formula C₁₆H₁₉ClN₂O
Molecular Weight 290.79
Purity ≥99% Pure (LC-MS)
Liquid Availability sarm acp 105 30mL liquid Glycol (20mg/mL, 600mg bottle)
sarm acp 105 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)
sarm acp 105 60mL liquid Glycol (20mg/mL, 1200mg bottle)
sarm acp 105 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)
Powder Availability sarm acp 105 1 gram, 60 capsules (15mg/capsule, 900mg bottle)
Gel Availability sarm acp 105 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 ACP-105?

ACP-105 is a nonsteroidal selective androgen receptor modulator (SARM) that was originally developed in 2008 by the biopharmaceutical company ACADIA Pharmaceuticals. Like most SARMs, ACP-105 is capable of binding to androgen receptors in a manner similar to testosterone which ultimately results in enhanced anabolic activity in bones and muscles.

In addition to its anabolic effects, ACP-105 has also been shown to improve various aspects of cognition. Decreases in reproductive hormones like testosterone and estrogen lead to an increased risk for Alzheimer’s Disease and age-related cognitive decline. Current research has reported that ACP-105 can potentially combat deficits in cognitive functioning since the SARM acts a selective agonist to the androgen receptors.


Main Research Findings

1) Identification of in vivo and in vitro ACP-105 metabolites in the urine and plasma of horses.

2) In a mouse model of Alzheimer’s disease, ACP-105 was able to mediate amyloid-beta levels and cognitive deficits.


Selected Data

1) Researchers Broberg et. Al conducted a series of analyses on collected samples of equine urine and plasma in order to identify metabolites of the SARM, ACP-105. First, ACP-105 was purchased from the company ChemScene for administration purposes and the company MedChemExpress for analytical purposes. All chemicals and solvents purchased and involved in this study were of analytical grade or higher.

After the necessary chemicals were obtained, six adult Thoroughbred horses, 3 mares and 3 geldings, owned by the University of California were utilized for this study. Their ages ranged from 4-8 years old while weight varied from 515.5 to 569.5 kilograms. A physical examination was conducted in order to determine that the horses were healthy and free of disease, further solidified by the results of a complete blood count and a serum biochemistry panel. The horses were not administered any medication two weeks prior to the start of the study; the test subjects received food and water ad libitum throughout the study [1].

ACP-105 was orally administered into the back of the oral cavity at a dose of 0.05 mg/kg after the compound was weighed and suspended in DMSO and 0.9% NaCl. A catheter was aseptically placed into an external jugular vein into order to collect blood samples: collection occurred at time 0 (before ACP-105 administration) and at 15,30, and 45 minutes, as well as 1, 1.5, 2, 2.5, 3, 4, 5, 6, 8, 12, 24, 36, 48, 72, and 96 hours after administration of ACP-105. The catheter was flushed with 10 mL of a dilute heparinized saline solution after each sampling time and removed after 24 hours of sampling. All remaining collections occurred via direct venipuncture [1].

The samples were collected into EDTA-containing blood tubes and placed on ice prior to centrifugation. Plasma was then transferred and stored until ready for further analysis. Plasma precipitation was performed by the research team by initially transferring 200 uL of the plasma sample to an Eppendorg tube. 800 uL of ice cold acetonitrile was added to the Eppendorf tube, which was then mixed with a vortex mixer. Samples were then centrifuged for 10 minutes; 800 uL of the supernatant was transferred to a new tube and evaporated. The resulting products could be reconstituted in 200 uL of aqueous formic acid for further analytical purposes.

Urine samples were then collected from the horses. After administration of ACP-105 the samples were collected by free catch at 6, 24, 48, 72, and 96 hours. All urine samples were prepared with a generic method that includes diluting 2.0 mL of the sample with 2.0 mL of aqueous formic acid. Urine samples were loaded onto solid phase extraction cartridges and washed with 2.0 mL 5% MeOH in water, followed by elution using 3.0 mL MeOH. The solvent was evaporated in order to be reconstituted in 600 uL aqueous formic acid prior to centrifugation. The samples were centrifuged in Eppendorf tubes for 10 minutes; the supernatant was then diluted 1:1 with aqueous formic acid and was then transferred to vials for further analysis [1].

Additionally, the urine samples underwent hydrolysis with beta-glucuronidase. 2.0 mL of the sample were added to 2.0 mL of 0.1 M phosphate buffer, followed by 100 uL of beta-glucuronidase. The samples were placed in a heated bath and incubated for 2 hours, followed by cooling to room temperature and extraction using the SPE method. 200 uL of aqueous formic acid was used to reconstitute the samples for further analysis [1].

2) In order to investigate the effects of ACP-105 on cognitive deficits and amyloid-beta content, the research team of George et. Al utilized colonies of male homozygous 3xTg-AD and wild-type mice. The test subjects were established at Lund University in the Department of Experimental Medicine; all mice were provided food and water ad libitum and were maintained on a 12 hour light, 12 hour dark cycle. Once the mice reached 3 months of age, they were anesthetized using isoflurane gas and underwent gonadectomy to deplete endogenous testosterone levels. 10 mg/kg of ACP-105 was intraperitoneally injected either by itself or in combination with 10 mg/kg of the selective estrogen receptor beta1 agonist, AC-186 with 0.1 mg/day of DHT or a vehicle. Treatment took place 4 days a week over an experimental period of either 4 or 7 months [2].

The mice completed a Morris water maze assessment. The water maze consisted of a circular tank filled with water and opacified by painting the interior of the container white. Movement of the mice was recorded and analyzed with EthoVision 3.1 video-tracking software. The assessment was taken a step further and a hidden platform task was included. Both transgenic and wild-type test subjects were placed in the pool at one of four starting positions: NE, SE, SW, and NW, and were then required to locate the submerged platform in the NW quadrant. Each mouse was subject to 24 trials in total. Intervals between trials averaged approximately 24 minutes while the maximum trial length was 90 seconds; the mice were guided to the hidden platform if they did not find it after 90 seconds.

The time to reach the platform was recorded for each mouse. 6 days after the cue trials the platform was removed and the test subjects were subject to a recall task. On this day, all mice were placed in the NE quadrant of the pool while the researchers recorded the amount of time the subjects spent in the NW quadrant where the platform was previously located. Next, working memory was measured using a reversal learning protocol that included placing the mice in the water maze where the hidden platform had been re-installed in a new location. Additionally, vision tests took place by placing the platforms in a position visible above the water line, from there the mice were placed in the four corners and timed on how long it took to identify the newly raised platform [2].

Spontaneous alternation and spontaneous locomotor activity were the next variables assessed by the research team. Alternation was measured by recording the arm choices of the mice entering the arm. The subjects were then allowed to explore the maze for 8 minutes while their movement was monitored. Mice that made fewer than 10 arm choices were excluded from this portion of the study. The score of spontaneous alternation was calculated as the proportion of alternation to the total number of opportunities for alternation. Spontaneous locomotor behavior was assessed through an open field test. Individual test subjects were placed in a 42 cm x 42 cm box and the research team monitored behavior and activity for 10 minutes and analyzed using EthoVision 3.1 video-tracking software.

Anxiety in the mice was investigated by placing the mice in the middle of an opaque maze raised 30 cm off the floor; the maze included two open and two closed arms, each measuring 5 cm wide by 28.5 cm long and 20 cm high. The total session duration was 5 minutes for each mouse and the number of entries into each arm was recorded by the research team. Additionally, when examining rotarod activity, the mice were placed on a 4.5 cm rod facing the opposite direction to that of the rotation. Pretraining consisted of walking for 30 seconds on the rod turning at a speed of 5 RPM. Over a 4 minute period, four trials were conducted and the rotation speed gradually increased to 40 RPM. Total time spent on the rotarod was recorded and averaged by the researchers for each mouse [2].

After the specified treatment period had passed, the animals were euthanized and their brains were extracted and the hemispheres were dissected in half. The tissue was then subjected to Western blotting and ELISA analysis. Protein levels were also determined through the use of bicinchoninic acid assay. The resulting homogenates were mixed with an SDS-PAGE sample buffer, heated for 5 minutes, and electrophoresed. The tissue membranes were incubated with primary antibodies as well as HRP-conjugated secondary antibodies while signals were detected through the use of chemiluminescence. ELISA assays were also used to determine the levels of amyloid-beta 1-40 as well as amyloid-beta 1-42. Samples of the mouse brain hemispheres were homogenized in ice-cold PBS; all homogenates were then centrifuged for 20 minutes prior to quantification with ELISA [2].



1) When identifying in vivo metabolites the research team of Broberg et. Al tentatively reported 21 phase I and phase II metabolites in the place and urine samples. Chromatographic peaks that were developed consisted of a minimum of five scans as well as MS/MS spectrum with product ions that match the suggested metabolite structure. Additional structural isomers of various metabolites were identified, however, the data did not meet the required criteria and was eventually deemed insignificant [1].

sarm acp 105
Figure: Extracted ion chromatogram of ACP-105 metabolites

Three mono-hydroxylated metabolites M1a-c (C16H19ClN2O2) were detected in hydrolyzed urine with the longest reported detection time. M1a and M1c were also found in the plasma, however they were not found in the untreated urine samples. These results indicated the conjugation of glucuronic acid had taken place. Furthermore, two hydroxylated metabolites, M2a-b (C16H19ClN2O2) were detected in hydrolyzed urine while M2a was found in both plasma and untreated urine samples. Metabolites M3a-b could be identified in hydrolyzed urine while only M3b was found in untreated urine.

The phase I metabolic transformations that occurred successfully resulted in mono-, di-, and tri-hydroxylated forms of the compound, in addition to a net loss of two hydrogen molecules. The loss of the two hydrogen molecules were observed in an aliphatic structure. This suggests the presence of a double formation. Additionally, several phase I metabolites were formed through the combination of various different metabolic transformations. For example, two mono-hydroxylated metabolites with a net loss of two hydrogens, M4a-b (C16H17ClN2O2), could be found in hydrolyzed urine in addition to M5a-c. M5b was found in all three samples, however, the detection time was shortest in the plasma samples. Metabolites M6a-c (C16H17ClN2O4) were all detected in untreated and hydrolyzed urine [1].

Additionally, 7 glucuronides were observed, one of which was the directly glucuronidated parent compound, metabolite M7, most commonly identified in untreated urine. M8a-M8d were categorized as four glucuronidated forms of mono-hydroxylated metabolites. M8A and M8d were found in all three samples while M8b and M8c could only be detected in untreated urine. Two glucuronidated di-hydroxylated metabolites, M9a and M9 were found in both untreated and hydrolyzed urine samples. These results allowed the researchers to confirm the tentative identification and presence of these metabolites. Tentative identification was also used to match the expected polarity differences to the retention order of the metabolites and parent compounds.

All major metabolites were selected by the research team based on how easily detected they were in each sample. In plasma samples the highest reported intensities belonged to the mono-hydroxylated metabolite M1c and the mono-hydroxylated glucuronides M8a and M8d. The di-hydroxylated metabolites M5b, M8a, and M8d were detected with the highest intestines in untreated urine. Finally, the highest reported metabolite intensity detected 96 hours post-administered in hydrolyzed urine samples were mono-hydroxylated metabolites M1a, M1c, and M5b. Using these results the researchers decided to select the metabolites M1a, M1c, M5b, M8a, and M8d to further characterize the structure of the metabolites [1].

sarm acp 105
Figure: Time profile for metabolites detected in hydrolyzed urine.

2) The results of the study conducted by George et. Al reported that gonadectomized 3xTg-AD mice treated with ACP-105 for 4 months displayed improved results in the Morris water maze, indicating that the SARM can enhance long-term spatial memory. The experimental and the control groups of mice were trained to find a hidden platform over the course of 6 days. There were no significant differences between the mice treated with ACP-105 versus the vehicle-treated animals. However, it is important to note that all mice learned the task by the sixth day. On day 7 the hidden platform was removed. The gonadectomized male 3xTg-AD treated with ACP-105 displayed increased frequency in platform crossings as well as more time spent in the platform zone [2].

In order to test working memory, the mice underwent a reversal learning trial where the mice were placed in the water maze after the hidden platform was moved to a new location. The mice were treated with ACP-105 or a vehicle and trained to identify the platform in its new location. No significant differences were seen between the SARM-treated and vehicle-treated animals. The swim speed was also analyzed to further control for possible confounds in movement sores, again, no significant differences were noticed between the experimental and control groups.

sarm acp 105
Figure: E) frequency of platform crossing in response to different treatment, F) time in platform zone in response to different treatments

This study also assessed the anxiety-like behavior in the male gonadectomized 3xTg-AD treated with ACP-105 through the use of an elevated plus maze. In the subjects treated with ACP-105 alone, anxious behavior was significantly reduced, however, there was no significant difference between the experimental and control groups in terms of time spent in the open arms of the maze. In the mice treated with both ACP-105 and AC-186, there was a significant increase in the percentage of total number of open arm entries compared to total arm entries [2].

Anxious behavior was also measured by assessing the frequency of entries into the closed arms of the elevated plus maze. Following treatment with ACP-105 anxious behavior was significantly reduced. Additionally, there was no dramatic difference between the treatment groups in terms of the total number of arms visited. This suggests that there was similar locomotor behavior between the treatment groups. Instances of stretching postures were correlated to stress and anxiety in the test subjects, following treatment, stretching behavior in the elevated maze was analyzed. However, results reported that there were no significant differences between treatment and control groups [2].

sarm acp 105
Figure: changes in A) time spent in open arms, B) % open entries/total entries, C) frequency in closed arms, D) total number of arm visits, E) stretching frequency in the center of the maze, in response to different treatments

Spontaneous locomotor activity was also linked to anxiety-like behavior in the test subjects. Locomotor activity was analyzed over the course of 10 minutes and did not exhibit significant changes between the treatment groups. Locomotor activity was increased over the first 2 minutes of the assessment and gradually decreasing suggesting habituation to the environment. To further assess anxiety in an open field, stretching frequency was analyzed and revealed a dramatic decrease in the mice treated with ACP-105. The amount of time the mice spent on the rotarod apparatus further confirmed that there were no locomotor impairments identified in any of the treatment groups. Overall, the results of the study found combination treatment with ACP-105 and AC-186 led to reduced anxiety, this claim was further supported by the observed decrease in stretch frequency [2].

The results of this study have also reported that both treatment with ACP-105 alone, and in combination with AC-186 led to significant differences in the frequency of entries to the closed arms of the maze. While there was a large jump from baseline, there was no significant difference between the treatment groups in terms of frequency of entries. This allowed the researchers to conclude that SARM treatment results in reduced anxiety in the elevated plus maze and the open field utilized in this study [2].

In addition to its effects on anxiety-like behavior, the research team of George et. Al hypothesized that ACP-105 has the potential to regulate levels of amyloid-beta, the deposition of which is highly associated with the development of Alzheimer’s Disease. The results of the ELISA assay performed suggests that treatment with ACP-105 and AC-186 leads to decreased levels of amyloid-beta-40 and amyloid-beta-42. The ratio between the two compounds was also significantly decreased after 7 months of treatment with the SARM, the same results were not observed after only 4 months of treatment. Immunohistochemistry was used to analyze amyloid-beta levels after 4 or 7 months of treatment with ACP-105. The assay revealed a decrease in amyloid beta/c99 immunoreactivity [2].

sarm acp 105
Figure: Levels of amyloid-beta 42 after four or seven months of different treatments.



*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] Broberg MN, Knych H, Bondesson U, Pettersson C, Stanley S, Thevis M, Hedeland M. Investigation of Equine In Vivo and In Vitro Derived Metabolites of the Selective Androgen Receptor Modulator (SARM) ACP-105 for Improved Doping Control. Metabolites. 2021 Feb 1;11(2):85. doi: 10.3390/metabo11020085. PMID: 33535528; PMCID: PMC7912737.

[2] George S, Petit GH, Gouras GK, Brundin P, Olsson R. Nonsteroidal selective androgen receptor modulators and selective estrogen receptor β agonists moderate cognitive deficits and amyloid-β levels in a mouse model of Alzheimer’s disease. ACS Chem Neurosci. 2013 Dec 18;4(12):1537-48. doi: 10.1021/cn400133s. Epub 2013 Sep 25. PMID: 24020966; PMCID: PMC3867967.

ACP-105 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 2 oz
Dimensions 3 × 3 × 5 in
Formula Option

, ,

CAS Number‎

Molar Mass

290.79 g·mol−1

Molecular Formula



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