S-23 SARM – 20MG/ML – 30ML/60ML BOTTLE


S-23 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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S-23 SARM Liquid





CAS Number 1010396-29-8
Other Names S23, S 23, CCTH-methylpropionamide, UNII-XDK89456WM, SCHEMBL2816704, SSFVOEAXHZGTRJ-UHFFFAOYSA-N, BCP30652
IUPAC Name 3-(4-chloro-3-fluorophenoxy)-N-[4-cyano-3-(trifluoromethyl)phenyl]-2-hydroxy-2-methylpropanamide
Molecular Formula C₁₈H₁₃ClF₄N₂O₃
Molecular Weight 416.8
Purity ≥99% Pure (LC-MS)
Liquid Availability S-23 SARM 30mL liquid Glycol (20mg/mL, 600mg bottle)
S-23 SARM 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)
S-23 SARM 60mL liquid Glycol (20mg/mL, 1200mg bottle)
S-23 SARM 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)
Powder Availability S-23 SARM 1 gram, 60 capsules (18mg/capsule, 1080mg bottle)
Gel Availability S-23 SARM 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 S23?

(S)-N-(4-cyano-3-trifluoromethyl-phenyl)-3-(3-fluoro,4-chlorophenoxy)-2-hydroxy-2-methyl-propanamide, more commonly, referred to as S-23, is a potent selective androgen receptor modulator (SARM). S-23 is best known for its potential to increase libido, act as male contraceptive, promote anabolic activity in muscles and bones, and act as a partial agonist to the androgen receptor.


Main Research Findings

1) The partial agonistic actions of S-23 leads to a significant increase in sexual motivation in ovariectomized female rats.

2) Due to its pharmacokinetic profile and beneficial effects on muscle mass and tissue selectivity, S-23 has the potential to act as an effective form of male birth control.


Selected Data

1) Researchers Jones et. Al conducted a study examining the different qualities of the popular SARM, S-23, and how it can influence sexual motivation. Experimentation began by observing in vitro binding affinity of the androgen receptor. Initially, the ligand binding domain (LBD) of the androgen receptor was fused with glutathione S-transferase (GST); the results compound was expressed as a recombinant protein labeled as AR GST-LBD. Following proper preparation of all samples, chemical purities were determined through the use of nuclear magnetic resonance (NMR) and mass spectroscopy.

Increasing concentrations of the compounds were incubated with 4 nM [^3H]MIB and AR GST-LBD over an 18 hour period. In order to determine total and nonspecific binding, proteins were incubated with and without a high concentration of unlabeled MIB. All filter plates were harvested, washed three times with an ice-cold buffer solution, and allowed to dry to completion at room temperature. The specific binding of [^3H]MIB at varying concentrations was determined by subtracting nonspecific binding of [^3H]MIB and expressed as a percentage of specific binding in the absence of a competitor. The concentration of the compound of interest that reduced the specific binding of [^3H]MIB by 50% was determined by nonlinear regression using the standard four-parameter logistic curve. The research team was then able to calculate the equilibrium binding constant Ki while all binding affinities of the compounds of interests were recorded and compared to the results of dihydrotestosterone (DHT) [1].

The next step of the study was to examine in vitro transcriptional activation mediated by androgen and estrogen receptors in a cotransfection system. Human embryonic kidney (HEK) 293 cells (ER-alpha) or CV-1 cells (AR) were transfected in 15 cm dishes using Lipofectamine and maintained in serum-free Dulbecco’s minimal essential medium. Each dish of cells was transfected with 45 ug of GRELuc, I ug of CMVLuc, and 2.5 ug of CMVhAR, CMVhER-alpha, or CMVhER-beta expression vector. Following transfection the cells were allowed to recover over the course of 12 hours and were then seeded in 24-well plates in Dulbecco’s minimal essential medium containing 2% charcoal-stripped fetal bovine serum. The cells recovered for an additional 8 hours before drug treatment began.

The agonist activity of the test compounds was compared to the transcriptional activation induced by 1 nM of DHT or estradiol (E2). The cells were left untreated for 24 hours before being washed with Dulbecco’s phosphate-buffered saline (PBS) and lysed with 50 ul/well of passive lysis buffer for 30 minutes. Luciferase assays were completed using 25 ul of the cell lysate. Transcriptional activity was calculated in each well by determining the ratio of luciferase activity to Renilla luciferase activity; this calculation method was used in order to avoid variations in cell number and transfection efficiency [1].

The final in vitro examination allowed the research team to observe the interaction between the amino terminus and carboxyl terminus. The amino terminus-carboxyl terminus (N-C) interaction of the AR is identified by a mammalian two-hybrid assay. The AR cells were maintained and transfected while each cell dish was transfected with 45 ug of pG5Luc, 2.5 ug of pACT AR-N-terminal domain, 2.5 ug of pBind AR-LBD, and 1 ug of CMVLuc. Luciferase activity increases as a result of a facilitated interaction between the N-terminal domain and the LBD, as well as the close proximity of the activating domain to the DNA binding domain. The activity of the compounds were compared to the interaction induced by 10 nM of DHT. Luciferase assays were completed according to protocol while N-C interaction induced by each compound of interest was expressed as a percentage of the interaction induced by 10 nM of DHT [1].

The in vivo portion of the study conducted by Jones et. Al utilized male and female Sprague-Dawley rats. All subjects were given ad libitum access to food and water and were maintained on a 12 hour light and 12 hour dark schedule. All animal studies were conducted in accordance with the protocols approved by the Institutional Laboratory Animal Care and Use Committee and the University of Tennessee (male subject studies) or Ohio State University (female subject studies).

Castrated male rats were the first subjects observed by the research team in order to determine the in vivo pharmacologic activity of each AR ligand. The animals were orchidectomized 24 hours before the start of drug treatment, followed by 2 weeks of daily subcutaneous injection of 1 mg/kg of the test compound. Before daily administration each ligand was dissolved in a vehicle solution containing DMSO and PEG300. Two additional groups, one castrated one intact, received only a vehicle dose and were used as control groups. 24 hours after the last dose the animals were euthanized in order to extract the ventral prostate, seminal vesicles, and levator ani muscle. The three organ weights were recorded and normalized to total body weight while the weights of the prostate and seminal vesicles were used as an indicator of androgenic activity. The levator ani muscle was observed to determine the anabolic effects of the drug treatment [1].

In order to observe sexual motivation in female rats, ovariectomized female rats were treated with the SARM. The test subjects were ovariectomized via dorsal incision 24 hours before daily subcutaneous injection of the drug treatment began. Two additional groups, one ovariectomized one intact, received a vehicle treatment only to act as a control group. The compounds of interest were dissolved in a vehicle containing DMSO/PEG300 and administered for 14 days, daily at a dose of 3 mg/kg. Testosterone propionate was administered as a positive control and was coadministered with an antiandrogen in order to highlight the importance of AR activation [1].

A three-compartment chamber with wood shaving covering the floor was the primary apparatus used for behavioral testing. All testing was conducted 12 hours after the last treatment dose was given, typically taking place early during the 12 hour dark period under dim red light. Sexually experienced female rats were allowed to acclimate to the chamber in three 15-minute periods; two the week before behavioral testing and one immediately before testing. Exploration of the chamber took place in the absence of male rat stimulus. Four hours before behavioral testing the female rats were subcutaneously administered a 0.1 mg dose of progesterone to support and facilitate sensual behavior. After the last 15 minute acclimation period the female subjects were restricted to the central compartment while one intact and one castrated male rat were led into the lateral compartments.

Opaque partitions were put in place and the rats were allowed to habituate with each other for 5 minutes. After 5 minutes the partitions were removed and the female rat was able to roam freely for a 30 minute behavioral testing period. However, the males’ larger size forced them to remain in the lateral compartments. Duration of time and compartment entries were measured each time the female rat passed through to a different compartment of the chamber. Following the behavior testing the animals were euthanized 24 hours after the last treatment dose was injected while the uterus was extracted and weighed [1].

2) The initial portion of the study conducted by Jones et. Al assessed and confirmed the chemical purity of S-23 through the use of elemental analysis, mass spectrometry, and proton nuclear magnetic resonance. The first in vitro examination observed the transcriptional activation and AR binding affinity of the SARM through the use of a radiolabeled competitive binding assay and a cotransfection assay. 24 hours after castration took place cytosolic AR was obtained from the ventral prostate of male Sprauge-Dawley rats. AR-mediated transcription elicited by the agonist qualities of S-23 were compared to the control, defined in this study as the AR activation following treatment with 1 nM DHT [2].

The first in vivo experiment attempted to observe patterns in anabolic and androgenic activity following treatment with S-23 in castrated male rats. 30 male Sprague-Dawley rats weighing approximately 200 g were castrated via scrotal incision 24 hours prior to administration of the first drug treatment. 0.01, 0.05, 0;1, 0.5, 1, and 3 mg doses of S-23 were subcutaneously injected daily, over a treatment period of 2 weeks. Two additional groups were introduced, one castrated one intact, as control groups after receiving doses of a vehicle treatment. Animals were euthanized 24 hours after treatment; plasma samples were collected while the ventral prostate, seminal vesicles, and levator ani muscle were extracted and weighed. Androgenic activity was evaluated by weight changes in the prostate and seminal vesicles, and anabolic activity was measured by weight changes in the levator ani. In order to determine the maximal response (Emax) induced by S-23 the research team used nonlinear regression analysis [2].

The next portion of the study determined whether or not S-23 has the potential to act as a male contraceptive by observing the effects the SARM has on spermatogenesis and endocrine physiology in intact male rats. 42, 90-day-old male Sprauge-Dawley rats were assigned to seven different groups and subcutaneously administered different drug treatments. Group 1 was the intact control group that received only a vehicle composed of 5% DMSO and 95% PEG300. Group 2 was a control group that was hormone-primed with 5 ug/day of estradiol benzoate (EB). In addition to 5 ug/day of EB, groups 3-7 received doses of S-23 varying from 0.05, 0.1, 0.3, 0.5, and 0.75 mg/day, respectively.

The compounds were prepared accordingly and administered to the animals daily for 70 days. S-23 has high oral bioavailability, however, the research team used a subcutaneous method to reduce stress and morbidity in the animals while undergoing long-term treatment. Mating trials were conducted the last week of treatment, specifically in groups 1, 2, 4, and 5, to ensure the animals in each group were demonstrating proper mounting and copulatory behavior. Individual male rats from each group were cohabited with two sexually active females while the research team recorded the number of mounts, mount latency, intromissions, and intromission latency. After the female rats were impregnated they were allowed to carry to full term. The number of successful pregnancies was reported and male rats were only defined as fertile if he impregnated one or two female partners [2].

A secondary study was conducted with separate experimental groups where the animals were left untreated for 70 days following 70 days of drug treatment. On day 140 a second mating trial was performed and on day 168 a third mating trial was performed for the subjects that were deemed infertile on day 140. Whole body DEXA scans were taken one day before the end of treatment in order to record body weight, bone mineral density (BMD), percent fat mass (FM), and fat-free mass.

At the end of the treatment period the rats were anesthetized and euthanized. Body weight was recorded again at autopsy while the prostate, seminal vesicles, right testis, and right epididymis were extracted and weight. Blood samples were collected and maintained at room temperature followed by centrifugation for 10 minutes and preparation for further analysis. One testis was removed from each subject and weighed. Testicular parenchyma was then homogenized in order for each testicular homogenate to be used to count advanced spermatids. Remaining homogenates were centrifuged so the supernatant of each sample could be collected and used to quantify intratesticular testosterone concentrations. Statistical analysis was performed using single-factor ANOVA and Dunnett’s multiple comparison test [2].



1) The results of the initial in vitro examination regarding the AR binding affinity of the SARM revealed that the R-isomer of the SARM, S-23 bound to the AR very weakly with a relative binding affinity (RBA) of only 0.1% of DHT. This allowed researchers to confirm that this series of compounds engages in enantioselective binding. Additionally, the para-monosubstituted halogen derivatives bound to the AR with affinity that was directly related to, and varying with the electronegativity of the substituent.

Furthermore, the research team of Jones et. Al used an in vitro cotransfection assay in order to emphasize the ability of the S-23 to induce AR, ER-alpha, and ER-beta-mediated transcriptional activation. S-23 showed the most activity through the stimulation of AR-mediated transcriptional activation at 101% of that observed with 1 nM of DHT. S-23 also displayed weak partial agonistic activity on the ER-alpha receptors by stimulating ER-alpha-mediated transcription. S-23 was also the only SARM that exhibited minimal mediation of ER-beta transcription at 28.1% compared to that of the vehicle. Next, the two-hybrid assay used to observe N-C interactions revealed that S-23 led to a dose-dependent increase in interaction; the SARM induced the interaction to90% of 10 nM of DHT [1].

Figure 1: The ability of each SARM to induce N-C interactions.

In regards to the in vivo evaluations, the first sequence of studies examined the androgenic and anabolic activity of S-23 in castrated male rats treated for 14 days. After castration the rats experienced a depletion of endogenous testosterone leading to a significant decrease in the size of the prostate and levator ani muscle. When the rats were administered 0.75 mg/day the weights of the prostate and levator ani were restored to 121% and 70%, respectively. 2-23 also only displayed moderate tissue selectivity when the rats were administered 1 mg/day leading to maintenance of prostate size and the levator ani muscle at 110% and 136% of the control.

The in vivo pharmacological activity in the castrated male rats was compared to the activity of S-23 in ovariectomized female rats and how the SARM affected uterine weight. S-23 not only showed the most androgenic activity in the male castrated rats, but also elicited significant effects on the uterus in ovariectomized females. When 3 mg/kg/day were subcutaneously administered to the subjects, weight of the uterus was maintained at 98.9% of the control. Uterine weight responded in a dose-dependent manner, the researchers observed an increase in size from 37.8% when 0.05 mg/day were administered compared to 79.5% when 0.75 mg/day were administered [1].

Figure 2: Dose-dependent changes in pharmacological activity of S-23

Results of the behavioral testing reported that progesterone-primed, vehicle-treated, ovariectomized female rats showed no preference towards castrated or intact male rats. However, sexual motivation was significantly increased when the female rats were treated with TP; they displayed a preference for intact male rats at 22.6. When TP was administered with an androgen-antagonist sexual preference was noticeably reduced. The test subjects that were primed with progesterone and treated with varying doses of S-23, there was a significant increase in sexual motivation, primarily in the doses ranging from 0.05 mg/day to 3 mg/day. The researchers thought it was important to mention that the 0.3 mg/day dose did not lead to any increases in sexual motivation, however, this phenomenon was unexplained [1].

Figure 3: Time spent with castrated and intact male rats when given varying doses of S-23

2) The in vitro portion of the study conducted by Jones et. Al reported that S-23 led to a significant increase in transcription activation mediated by the androgen receptors when compared to the transcriptional activity elicited by 1 nM of DHT. The in vivo pharmacological portion of the study found that the weight of the prostate, seminal vesicles, and levator ani decreased after the animals were castrated. Additionally, androgen-dependent organs experienced a dose-dependent increase in weight when S-23 was administered to the castrated animals. When the animals were given 1.0 mg/day of S-23 the weight of the prostate and seminal vesicles were maintained at weights equal to or greater than that of intact animals. Weight of the levator ani was selectively maintained in doses as low as 0.1 mg/day. The Emax of S-23 in the prostate, seminal vesicles, and levator ani muscle was found to be 138 ± 21, 144 ± 1, and 129 ± 4%, respectively [2].

Figure 4: Androgenic and anabolic activity of S-23 in intact male rats

Mating trials took place at the end of the treatment period in order to assess the efficacy of S-23 as a male contraceptive. Estradiol benzoate was administered in addition with the SARM in order to ensure sufficiently restored mating behavior in the castrated male rats. Results reported that the weight of the levator ani muscle in castrated male rats was maintained at doses between 0.1 and 0.3 mg/day. Researchers observed groups 1, 2, 4, and 5: vehicle, EB only, EB + 0.1 mg S-23, and EB + 0.3 mg S-23, respectively. There were no observed differences in the number of mounts, mount latency, number of intromissions, or intromission latency between the four groups, allowing the research team to conclude that EB alone and EB + S-23 were able to maintain normal sexual behavior relative to the control group.

Contraception efficacy was measured by the fertility rate of the male rat included in the mating trials. Results found that all male rats treated with EB + 0.1 mg of S-23 were infertile while only one of six male rats treated with EB + 0.3 mg of S-23 was fertile. In terms of spermatogenesis, it was first evaluated by counting the number of homogenization-resistant advanced spermatids from control and experimental rats. There were no differences in mean sperm count between the intact control animals and the EB-treated animals. When EB was administered with S-23, the SARM elicited a biphasic effect on sperm count in the testis. This response is directly related to the androgenic activity of drug treatment in the sexual organs. Spermatogenesis was significantly inhibited in the treatment group receiving EB + 0.1 mg/day of S-23. Four out of the six animals in the treatment group exhibited no sperm in the testis while sperm count was barely detectable in the other two animals [2].

Figure 5: Testicular sperm concentrations

After the test subjects were euthanized the body weight of each animal was recorded. All EB-treated groups exhibited significantly lower body weight and prostate weight, however, total body BMD was greater than that in the intact, vehicle-treated group. The animals that received S-23 experienced a decrease in the weight of the testis while weight of the levator ani muscle remained unchanged. Treatment with EB alone did not significantly change fat mass in comparison to the intact control group. When EB was administered with S-23 fat mass was shown to decrease in a dose-dependent manner; doses of 0.3 mg/day of S-23 and higher, led to a significant diminishment of fat mass in comparison to the intact control group. Overall, the researchers were able to conclude that S-23 treatment in addition to EB administration, effectively decreases fat mass [2].

Figure 6: dose-dependent changes in fat mass elicited by S-23



*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] Jones A, Hwang DJ, Duke CB 3rd, He Y, Siddam A, Miller DD, Dalton JT. Nonsteroidal selective androgen receptor modulators enhance female sexual motivation. J Pharmacol Exp Ther. 2010 Aug;334(2):439-48. doi: 10.1124/jpet.110.168880. Epub 2010 May 5. PMID: 20444881; PMCID: PMC2913771.

[2] Jones A, Chen J, Hwang DJ, Miller DD, Dalton JT. Preclinical characterization of a (S)-N-(4-cyano-3-trifluoromethyl-phenyl)-3-(3-fluoro, 4-chlorophenoxy)-2-hydroxy-2-methyl-propanamide: a selective androgen receptor modulator for hormonal male contraception. Endocrinology. 2009 Jan;150(1):385-95. doi: 10.1210/en.2008-0674. Epub 2008 Sep 4. PMID: 18772237; PMCID: PMC2630904.

S-23 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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04-28-2023-Umbrella-Labs-S23-Certificate-Of-Analysis-COA.pdf S-23 SARM




Additional information

Weight 4 oz
Dimensions 3 × 3 × 5 in
Formula Option

, ,

CAS Number‎

PubChem CID

ChemSpider ID

Molar Mass

416.76 g·mol−1

Molecular Formula



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