RAD-150 (TLB 150) SARM – 20MG/ML – 30ML/60ML BOTTLE


Rad-150 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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RAD-150 SARM (aka TLB-150 or RAD-140 Ester) Liquid


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CAS Number 29622-29-5
Other Names RAD150, RAD 150, TLB150, TLB-150, TLB 150, DTXSID40183806, 
IUPAC Name 2-[5-chloropentyl(methyl)amino]-N-(2,6-dimethylphenyl)acetamide
Molecular Formula C₁₆H₂₅ClN₂O
Molecular Weight 296.83
Purity ≥99% Pure (LC-MS)
Liquid Availability Buy RAD-150 SARMs 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)

Buy RAD-150 SARMs 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)

Powder Availability Buy RAD-150 SARMs 1 gram
Gel Availability Buy RAD-150 SARMs 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 RAD 150?

RAD 150, also known as TLB 150, is an esterified version of the popular selective androgen receptor modulator (SARM), RAD 140. While the benefits elicited by the two compounds are extremely similar, the esterification process results in enhanced potency and effectiveness. SARMs are able to bind to androgen receptors, suggesting that they are able to mimic the actions of testosterone. Because SARMs do not elicit the typical negative side effects observed with testosterone treatment, these compounds are becoming more popular and widely available for research purposes.


Main Research Findings

1) The process of esterification leads to increased potency and improved efficacy of RAD 150 in comparison to its parent compound, RAD 140.

2) SARMs have been shown promote various forms of functional therapy through tissue-selective activation of androgenic signaling

3) Treatment with RAD140 leads to enhanced neuroprotection in hippocampal cell cultures as well as improved anabolic activity in the levator ani muscle.


Selected Data

1) As it was previously mentioned, RAD 150 is the esterified form of RAD 140. RAD 140, like most SARMs, is typically known for its ability to promote anabolic activity in bone and muscle tissue. Current research examines the potential of RAD 140 to enhance neuroprotection and stimulate antitumor activity. As an esterified version of RAD 140, RAD 150 has been shown to elicit similar effects as its parent compound with far more potency. The esterification process proceeds by combining an organic acid (RCOOH) and an alcohol (ROH) to form water and an ester (RCOOR) [1].

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Figure 1: Chemical reaction for esterification

Furthermore, esterification reactions occur when a primary alcohol is treated with a carboxylic acid in the presence of sulphuric acid. The resulting compound tends to smell sweet and is generally classified as an ester compound. The chemical reaction typically takes place in 5 steps and follows the format:

The resulting ester compounds are organically found in oils and fats; due their pleasant smell they are widely used throughout the perfume, food, and cosmetics industries. Naturally occurring esters are detected in pheromones while phospho esters form the backbone of DNA molecules. Additionally, esters are frequently used in the manufacturing of surfactants like soap and detergent, polyesters on the other hand are used in the production of plastic compounds [1].

2) The research team of Shalender Bhasin, MD and Ravi Jasuja, PhD. examined the potential of selective androgen receptor modulators (SARMs) to promote various forms of functional therapy. Previous research has reported that SARMs bind to androgen receptors and display tissue-selective activation of androgenic signaling, leading to anabolism in skeletal muscles and bones. The actions of SARMs are compared to testosterone, the major ligand for androgen receptors. Testosterone is often supplemented to men and women of all ages suffering from androgen deficiency and decreased muscle and bone wasting. However, administration of androgenic compounds such as testosterone is often related to many dose-limiting adverse side effects such as prostate dysfunction, edema, and erythrocytosis. On the other hand, SARM administration has been shown to result in similar anabolic activity without the adverse side effects associated with typical androgen treatment [2].

In order to target functional limitations caused by osteoporosis, aging, and chronic disorders, researchers first attempted to develop a SARM with the desired activity profile and tissue selectivity. The second approach included elucidating the mechanisms of action of androgens on skeletal muscles and the prostate in order to identify signaling molecules downstream of the androgen receptors that are capable of activating hypertrophic pathways in skeletal muscles but not the prostate. When observing the structure of SARMs, the compounds can be categorized into two groups: steroidal and nonsteroidal. Steroidal SARMs are synthesized by modifying the chemical structure of testosterone molecules. For example, substitution of 7-alpha alkyl makes testosterone less susceptible to 5-alpha reduction, thus increasing tissue selectivity with respect to the prostate. This results in the increased anabolic activity in the levator ani muscle and a decreased rate of anabolism in the prostate and seminal vesicles [2].

Researchers at the University of Tennessee and Ligand Pharmaceuticals reported early data regarding the discovery of nonsteroidal SARMs. After publication of the initial findings various other structural categories of SARM pharmacophores were examined. These categories included: aryl-propionamide, bicyclic hydantoin, quinolones, tetrahydroquinoline analogs, benzimidazole, imidazolopyrozole, indole, pyrazoline derivatives, azasteroidal derivatives, and aniline, diaryl aniline, and benzoxazepinones derivatives. The first generation of SARMS was developed by manipulating the structure of aryl propionamide analogs, bicalutamide and hydroxyflutamide. This initial discovery led to copious amounts of research dedicated solely to modifying compound structures in order to promote tissue selectivity and further hone in on the beneficial anabolic activity [2].

3) The research team of Jayaraman et. Al examined the neuroprotective effects elicited by RAD 140 in response to normal age-related degeneration and dysfunction. Pregnant Sprague-Dawley rats were euthanized in order for researchers to collect the 17-18 day old pups in order to prepare neuronal cultures.The primary rat hippocampal cultures were prepared accordingly while the dissociated hippocampal neurons were plated in order to complete cell-viability assays. The cultures were prepared using a mix of approximately 12-14 both male and female in order to control for any differences based on sex. Experiments began 1-2 days in vitro and all experiments were completed at least three times with different cultures [3].

Data for this portion of the study was measured through cell-viability assays and Western blot analysis. Cell viability was assessed after the experimental treatment period was finished. Staining with vital dye calcein acetoxymethyl ester highlighted the number of viable hippocampal neurons present. The stained cells of each culture were counted in according to a predetermined, regular pattern separating the sample into 4 separate fields per well. Additionally, there were 3 wells per condition in each experiment that occurred; the amount of viable neurons in the treatment groups were compared to vehicle-treated control groups.

Using a reducing sample buffer, lysates were collected from the cultures in order for the researchers to perform a Western blot analysis. The lysates were boiled for 5 minutes and centrifuged for 10 minutes; all supernatants were analyzed by immunoblotting. Furthermore, the band densities were recorded through the use of Image J software, while the relative percent intensity of phospho-ERK bands were properly plotted on a graph [3].

The second portion of this study utilized 3 month-old male Sprague-Dawley rats that had previously been gonadectomized (GDX) or subjected to a sham-operation 14 days prior to treatment. The animals were housed in their own cage, stuck to a strict 12 hours dark, 12 hours light schedule, and given access to food and water ad libitum. The GDX animals receiving testosterone treatment received an implantation of a SILASTIC capsule packed with dry testosterone and capped with silicone glue. The same procedures were followed for the animals receiving a vehicle treatment with nothing packed into the capsule [3].

The GDX animals receiving SARM treatment were administered 1 mg/kg of RAD 140 suspended in 1 mg/mL of 0.5% methyl cellulose, via oral gavage. The treatment was administered to the different groups daily, over an experimental period of 2 weeks. On day 13 of treatment the test subjects were administered either 10 mg/kg of kainate or a sterile water control. On day 14, the final day of treatment, the SARM-treated rats were subcutaneously injected with a 1 mg/mL dose of RAD 140 suspended in safflower oil. This was due to the kainate lesion that made administration through oral gavage difficult. The animals were euthanized at the end of the treatment period; the researchers removed and hemisected the brains and prepared each half accordingly. The prostate, seminal vesicles, and levator ani muscle were then removed and dissected in order for the researchers to measure weight changes.

Results of this study were further measured through seizure assessment and immunohistochemistry tests. Behavior of the subjects was monitored by the researchers for 3 hours after administration of kainate in order to take note of aspects regarding the latency and severity of the seizures. The latency period occurs shortly after the kainate injection and is typically described as a “wet dog shake” and defined as the first appearance of stereotypic seizure-related behavior. The seizure severity of the animals was measured on a scale from 0-5, ranging from no seizure activity to seizure accompanied by rearing and falling [3].

The immunohistochemistry test examined the number of immunoreactive cells present in the fixed brain samples. Every eighth brain section was immunostained with NeuN antibody, mounted on slides, and allowed to dry overnight prior to further analysis. 2-dimensional cell counts of random sampling were used to estimate the number of immunoreactive NeuN cells present in the CA2/3 region of the hippocampus. Every eighth hippocampal section had the CA2/CA3 region of the hippocampus outlined in order to organize an oriented counting frame. Only positively stained nuclei were recorded, and to control for variability throughout the analyzed sections, the number of immunoreactive nuclei counted was divided by the number of sections. The resulting figure was defined as the control variable and expressed as the percentage of neurons counted in the sham-GDX, non-lesioned group. All statistical analyses that occurred to compare the treatment groups were performed using ANOVA and Fisher’s least significant difference test [3].



1) As an esterified version of RAD 140, RAD 150 is considered a superior version of its parents compound due to its increased potency and improved bioavailability. The esterification process also makes RAD 150 far more stable than RAD 140 suggesting that it is more effective and safe. While the benefits of the two compounds are very similar, there is debate regarding how much stronger RAD 150 is compared to RAD 140. Recent evidence suggests that RAD 150 is approximately 10-15% more potent.

Multiple research-based studies have concluded that SARMs are able to increase muscle mass and reduce fat, however, researchers thought it was important to note that RAD 150 does not reduce fat by targeting fat directly, but rather by raising metabolic rate. RAD 150 increases testosterone leading to improved metabolism and a calorie deficit, ultimately resulting in fat loss. Additionally, evidence suggests that RAD 150 is capable of increasing libido, improving recovery from exercise by increasing protein synthesis, and enhancing physical performance by boosting muscle mass and raising metabolism.

2) The research team of Bhasin and Jasuja were able to achieve selectivity of SARMs by elucidating the mechanism of testosterone’s action on the prostate, as well as how molecules farther downstream were associated with activation of AR signaling in skeletal muscle. Analysis of muscle biopsies collected from male test subjects treated with varying doses of testestore revealed that administration of the compound led to hypertrophy in type I and type II muscle fibers. In relation to testosterone dosage, both type I and type II fibers experienced significant changes in cross-sectional areas. It is important to note that there was no change observed in the absolute number or the relative proportion of type I and type II fibers in response to testosterone administration [2].

Hypertrophy of the skeletal muscle was further examined through observation of muscle satellite cells and the myonuclear number. These variables were assessed through the use of electron microscopy, using direct counting and spatial orientation methods at baseline and after 20 weeks of GnRH agonist and testosterone enanthate treatment. Results reported that absolute and percent satellite cell number was significantly greater than baseline after 20 weeks of the test subjects receiving supraphysiologic doses of testosterone. The observed changes in the number of satellite cells correlated with changes in total and free testosterone levels, indicating that muscle fiber hypertrophy induced by testosterone is correlated with an increase in the number of satellite cells and the myonuclear number.

Recent studies have found that both testosterone and DHT are able to promote association between liganded ARs and beta-catenin, its co-activator. Beta-catenin is stabilized by this interaction and enhances translocation into the nucleus and association with TCF-4, as well as the transcriptional activation of Wnt-target genes. Additionally, Testosterone upregulated the expression of follistatin, resulting in increased muscle mass and decreased fat mass. SMAD 7 is also upregulated by testosterone while TGF-beta-mediated SMAD signaling in TGF-beta target genes is downregulated. The connection between testosterone and follistatin expression indicates that the effects of testosterone are cross-communicated from the WNT pathway to the TGF-beta-SMAD pathway. These results further suggest that candidate molecules located downstream of AR and beta-catenin, such as follistatin, have the potential to mediate the effects of testosterone on the muscle and may provide desired selectivity of anabolism. The discovery of these candidate targets allows for further research to be conducted in order to develop selective anabolic drugs [2].

3) Initial results of the study conducted by Jayaraman et. Al determined that RAD140 elicited neuroprotective effects. Cell cultures exposed to A-beta for 24 hours experienced a 50% decrease in the number of viable neurons found in the cell culture. Pretreating the cultures with 10 nM of testosterone of a DHT an hour before exposure led to a dramatic decrease in cell death. Similar reductions in cell death were seen when the cultures were pretreated with 30 nM of RAD140 an hour before A-beta exposure.
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Figure 2: Changes in neuron viability in A) testosterone and C) RAD140

Further analysis of the conducted data revealed that the MAPK/ERK is associated with androgen-mediated neuroprotection against cell death. Initially, the neuronal cultures were pretreated with the presence or absence of a MEK inhibitor and exposed to 100 nM of RAD140. It was determined by the research team that RAD140 protects against apoptosis induced by A-beta exposure. That being said, the next step in the study was to observe the inhibitory effects elicited by U0126 MAPK/ERK signaling in RAD140-treated cell cultures. Researchers came to the conclusion that the neuroprotective effects of RAD140 are blocked when cells are pretreated with the inhibitor, U0126 [3].

Researchers turned their focus to the neuroprotective effects of RAD140 in vivo following the results of previous experimentation. Male rats underwent gonadectomy or a sham gonadectomy (referred to as GDX and sham-GDX, respectively). Androgen treatment took place over the course of two weeks and on day 13 the subjects were administered a single dose of kainate. Initial results reported that the weight of the prostate, seminal vesicles, and levator ani muscles were all significantly diminished following GDX. However, following treatment with testosterone the weight of each three tissues increased to a weight similar to those recorded in the sham-GDX groups.

In comparison to testosterone, treatment with RAD140 increased the weight of the prostate and seminal vesicles to a level considered insignificant. When treated with the SARM, both the weight of the prostate and seminal vesicles measured significantly lower than the weights collected from the sham-GDX and GDX+testosterone groups. Additionally, the levator ani muscle also exhibited a drastic increase in weight after treatment with RAD140. Records of weights collected from the RAD140 treatment groups were similar to the weight of the levator ani in the sham-GDX and GDX + testosterone treatment groups [3].
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Figure 3: Changes in the weight of A) seminal vesicles, B) prostate, and C) levator ani muscle, in response to the different treatments

When observing kainate-induced neuron death, the neuroprotective effects of RAD140 were thoroughly examined through immunostaining and assessing cell cultures gathered from the CA2/CA3 hippocampal regions. Initial results reported that kainate injected in sham-GDX vehicle-treatment led to a 20% cell loss, however, cell loss was significantly reduced after the androgen treatment was administered. Overall the research team concluded that testosterone and RAD140 elicited potent neuroprotective effects in GDX rats injected with a single-dose of kainate [3].

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Figure 4: Percentage of cell survival in response to different treatments.

The research team examined how the latency and severity of kainate-induced seizures responded to hormonal manipulations. The initial step was to determine how seizure behavior was measured; the intensity of the seizure behavior was determined by the degree of hippocampal neuron loss. All animals were observed by the research team for 3 hours. The animals treated with kainate had at least one seizure, while the vehicle-treated animals did not exhibit any seizure behavior. The kainate lesioned animals did not result in significant changes or variations in seizure latency or severity between the treatment groups. It is important to note that the GDX + testosterone and GDX + RAD 140 treatment groups experienced a slight reduction in seizure severity, but the change was considered insignificant [3].

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Figure 5: Changes observed in latency and severity of kainate-induced seizures in response to different treatment groups



*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] “Esterification (Alcohol & Carboxylic acid) – Reactions Mechanism & Uses with Videos.” Byju’s, https://byjus.com/chemistry/esterification/. Accessed 31 May 2023.

[2] Bhasin S, Jasuja R. Selective androgen receptor modulators as function promoting therapies. Curr Opin Clin Nutr Metab Care. 2009 May;12(3):232-40. doi: 10.1097/MCO.0b013e32832a3d79. PMID: 19357508; PMCID: PMC2907129.

[3] Anusha Jayaraman, Amy Christensen, V. Alexandra Moser, Rebekah S. Vest, Chris P. Miller, Gary Hattersley, Christian J. Pike, Selective Androgen Receptor Modulator RAD140 Is Neuroprotective in Cultured Neurons and Kainate-Lesioned Male Rats, Endocrinology, Volume 155, Issue 4, 1 April 2014, Pages 1398–1406, https://doi.org/10.1210/en.2013-1725

Rad-150 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.

RAD-150 for sale Buy RAD-150 SARMs Buy RAD-150 SARMs

RAD-150 for sale Buy RAD-150 SARMs Buy RAD-150 SARMs

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Additional information

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

CAS Number‎

Molar Mass

497.93 g·mol−1

Molecular Formula