ACP 105 Vasculine SARMs Gel 20MG (Packs of 5, 10 or 30)


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 SARMs Gel


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  30mL liquid Glycol (20mg/mL, 600mg bottle)
 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)
 60mL liquid Glycol (20mg/mL, 1200mg bottle)
 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)
Powder Availability 1 gram
Gel Availability  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 by the biopharmaceutical company ACADIA Pharmaceuticals in 2008. 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) ACP-105 prevents age-related cognitive decline by enhancing rotarod performance and regulating MAP-2 immunoreactivity levels.

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


Selected Data

1) The study conducted by Dayger et. Al utilized two-month-old C56B1/6J female mice in order to assess how ACP-105 affects rotarod functioning and cued fear conditioning. The mice were provided food and water ad libitum and were kept on a strict 12 hour light/12 hour dark schedule with the lights first coming on at 6 am. The test subjects were then anesthetized with ketamine and xylazine, followed by sham-irradiation or irradiation using a dose of 10 Gy in a Mark 1 Cesium Irradiator. Lead was used to shield the eyes, body, and cerebellum of the mice. 24 hours after irradiation or sham-irradiation, the mice were implanted with mini-pumps full of ACP-105 (1 mg/kg/day) or a vehicle treatment (1.09 mg/200 uL) [1].

Behavioral testing began two weeks after irradiation, the mice were housed singly 3 days before testing was conducted in order to assess sensorimotor function of the rotarod during week 1. Living alone in the cage was not shown to affect any physiological indexes of stress or emotional behavior. The rotarod apparatus initially rotated at 4 RPM; every 15 seconds the rod accelerated by 15 RPM. Fall latency was recorded by a timer that stopped when the photobeams at the bottom of the chamber were broken by the mouse. Each test subject underwent three trials a day for three subsequent days.

Fear conditioning was tested during week 2 of the study. In order to stimulate fear conditioning the mice learned to associate the environment with an accompanying foot shock. On experimental day 1 the mice were placed in a conditioning chamber and allowed to habituate and explore for 2 minutes, followed by a 30 second tone and a 2 second foot shock. Two minutes later a second food shock was administered [1].

The next day the mice were placed in the same chamber without a loud tone or foot shock while hippocampus-dependent contextual freezing was monitored for 3 minutes. One hour later the test subjects were placed in a brand new conditional chamber with a different shape and odor. The mice were exposed to the fear conditioning tone for 3 minutes in order for the research team to assess hippocampus-independent cued fear conditioning.

After behavioral testing occurred the mice were euthanized while the brains were extracted and allowed to equilibrate in 30% sucrose overnight. Samples were then properly stored in order for future procession of MAP-2 and synaptophysin immunohistochemistry. Coronal brain sections were serially mounted on microscope slides, allowed to dry for 10 minutes and were then placed on a slide warmer for 45 minutes to promote adhesion to the slide. The slides were rehydrated and washed twice with PBS for 10 minutes at room temperature followed by a third wash with PBS containing 0.2% BSA + 0.2% Triton X-100 (PBT) for 15 minutes at room temperature [1].

Nonspecific binding was blocked with the application of 5% normal donkey serum and 1% fish skin gelatin. The slides were then incubated with mouse anti-synaptophysin or an anti-MAP-2 antibody overnight in a humidifying chamber. Slides were then washed and incubated with PBT several times followed by treatment with 10 mM CuSO4 in a 50 mM NH4OAc buffer and more washing with PBS. Anti-fade mounting media was then added to slides that were then sealed with enamel.

For each mouse 8 sections of the hippocampus were used while every 7th section was analyzed using an unbiased stereological approach. Immunoreactivity was assessed with an Olympus spinning disk confocal microscope in order to observe the dentate gyrus, CA1 and CA3 regions of the hippocampus, and the sensorimotor and entorhinal cortices. Each image was generated using a Z-stack which was then collapsed further into a single projection. The images were then analyzed for area occupied by MAP-2 and synaptophysin immunoreactivity through the use of Slidebook software [1].

2) 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 [2].

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.

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 [2].

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 [2].

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 [2].



1) The test subjects included in the study conducted by Dayger et. Al were first assessed for their sensorimotor functioning abilities using the rotarod apparatus. Vehicle-treated irradiated mice had lower fall latencies than the sham-irradiated mice treated with the vehicle. There was an observed day x irradiation interaction and an effect of irradiation exhibited in the vehicle-treated animals, however, these results were not seen when the test subjects were treated with ACP-105 [1].

Figure: rotarod performance of sham-irradiated versus irradiated animals treated with either a vehicle or ACP-105.

Fear conditioning in the mice was tested next. Neither ACP-105 or irradiation did not affect hippocampus-dependent contextual fear conditioning. The research team calculated % freezing each group: sham-irradiated, vehicle-treated mice: 41.51 ± 2.70, n = 7; sham-irradiated ACP-105-treated mice: 41.15 ± 4.39; irradiated, vehicle-treated mice: 38.81 ± 1.88, n = 8 mice; irradiated ACP-105-treated mice: 43.71 ± 4.40, n = 7 ACP-105-treated mice. Hippocampus-independent cued fear conditioning was affected by irradiation. Additionally, ACP-105 had the ability to enhance instances of freezing in both sham-irradiated and irradiated mice [1].

Figure: Cued fear conditioning in sham-irradiated and irradiated mice treated with either a vehicle or ACP-105.

MAP-2 and synaptophysin immunoreactivity was assessed in the CA1 and CA3 regions of the hippocampus as well as the sensorimotor and the entorhinal cortices. Results reported that there was an interaction observed between the cortex of the sham-irradiated mice and ACP-105. ACP-105 was found to reduce MAP-2 immunoreactivity in the sensorimotor cortex while MAP-2 immunoreactivity was slightly increased in the entorhinal cortex. In irradiated mice there was no interaction between ACP-105 and examined brain areas, as well as no effect of ACP-105 on MAP-2 immunoreactivity in the irradiated cortex or the irradiated and sham-irradiated hippocampus.

Additionally there was no interaction between brain area and ACP-105 or effect of ACP-105 on synaptophysin immunoreactivity. This was observed in the sham-irradiated and the irradiated cortex as well as the sham-irradiated and the irradiated regions of the hippocampus. Overall, the researchers were able to conclude that irradiation impaired sensorimotor function in mice treated with a vehicle compound, but not in the subjects treated with ACP-105. On the other hand, irradiation reduced fear conditioning in both sham-irradiated and irradiated mice but not in mice treated with ACP-105. Treatment with SARM also led to enhanced rotarod performance. This was further associated with reduced MAP-2 immunoreactivity in sham-irradiated mice. These results suggest that SARMs are capable of enhancing brain function after radiation [1].

2) 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 [2].

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 [2].

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.

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 [2].

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 [2].

Figure: Time profile for metabolites detected in hydrolyzed urine.



*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] Dayger C, Villasana L, Pfankuch T, Davis M, Raber J. Effects of the SARM ACP-105 on rotarod performance and cued fear conditioning in sham-irradiated and irradiated female mice. Brain Res. 2011 Mar 24;1381:134-40. doi: 10.1016/j.brainres.2010.12.088. Epub 2011 Jan 8. PMID: 21219889; PMCID: PMC3048897.

[2] 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.


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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