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LGD 4033 SARM Liquid


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CAS Number 1165910-22-4
Other Names LGD4033, LGD 4033, Ligandrol, UNII-1EJT54415Am, VK-5211, 1EJT54415A, SCHEMBL221159, CHEMBL5170587
IUPAC Name 4-[(2R)-2-[(1R)-2,2,2-trifluoro-1-hydroxyethyl]pyrrolidin-1-yl]-2-(trifluoromethyl)benzonitrile
Molecular Formula C₁₄H₁₂F₆N₂O
Molecular Weight 338.25
Purity ≥99% Pure (LC-MS)
Liquid Availability sarms ligandrol for sale 30mL liquid Glycol (20mg/mL, 600mg bottle)

sarms ligandrol for sale 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)

sarms ligandrol for sale 60mL liquid Glycol (20mg/mL, 1200mg bottle)

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Powder Availability sarms ligandrol for sale 1 gram, 60 capsules (10mg/capsule, 600mg bottle)
Gel Availability sarms ligandrol for sale 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 LGD 4033 LIGANDROL SARM Liquid?

LGD-4033 is a selective androgen receptor modulator (SARM), commonly referred to as Ligandrol. The compound is currently being researched in order to determine its potential to reduce cases of muscle wasting and degeneration. LGD-4033 has been shown to selectively bind to the androgen receptors, indicating that it mimics the effects of testosterone without the occurrence of many of the associated side effects. Preclinical animal models of investigation have come to the conclusion that Ligandrol enhances anabolic activity, resulting in improved muscle mass and bone density.

Why Is It Called LGD 4033?

LGD-4033, commonly known as Ligandrol, is a selective androgen receptor modulator (SARM). The nomenclature “LGD-4033” is derived from the company that first developed it, Ligand Pharmaceuticals. In drug development, compounds often receive alphanumeric identifiers before they are given brand or common names.

In the case of LGD-4033:

  • “LGD” likely stands for “Ligand,” representing the company that developed it.
  • “4033” is a unique identifier for that particular compound within the company’s line of research.

When a compound progresses in research and development, it may receive a commercial name or be commonly referred to by its chemical structure or mechanism of action. In the case of LGD-4033, it became commonly known as Ligandrol after its development for potential therapeutic applications.


2 Main Research Findings

1) Results of the study report that the research team was able to identify the presence of the parent compound, LGD-4033, and 8 different metabolites in the plasma and urine collected from horses.

2) Muscle weight, capillary density, and muscle fiber size all increased in response to treatment with LGD-4033 administered to ovariectomized female rats.


Selected Data

1) Three female Thoroughbred houses were utilized in the experiment conducted by Hansson et. Al. The purpose of this study was to identify how the selective androgen receptor modulator, LGD-4033, is metabolized in the equine body. The horses ranged from 3-6 years of age and the weight of the horses varied from 447 to 587 kilograms. Prior to experimentation, the horses underwent physical examinations and complete blood counts in order to ensure they were healthy and free of disease. All blood and plasma analyses were performed according to standard procedure at the University of California, Davis in the Clinical Pathology Laboratory of the William R. Pritchard Veterinary Medical Teaching Hospital [1].

Two weeks before treatment began the subjects were not allowed any additional medication or supplements, however, food and water were provided for the subjects ad libitum. Prior to administration of the SARM, a 14-gauge catheter was placed bilaterally into the external jugular veins of the subjects. One side was used for drug administration while the other was used for sample collection. Following catheter placement the first 0.01 mg/kg dose of LGD-4033 was administered to the animals via intravenous bolus.

Blood samples were collected by the researchers immediately before the dose was administered, defined as hour 0, and again at 5, 10, 15, 30, and 45 minutes, followed by 1, 1.5, 2, 2.5, 3, 4, 5, 6, 8, 12, 18, 24, 48, 72, and 96 hours after LGD-4033 was administered. The samples were collected from the catheters according to standard procedure until 24 hours post-administration, all further samples were collected by direct venipuncture. The samples were then allowed to centrifuge at 1620 g for 10 minutes in order to properly separate compounds in the plasma [1].

Urine samples were gathered from the horses by free catch; collection took place at 3, 6, 8, 12, 24, 48, 72, and 96 hours after LGD-4033 was administered to the test subjects. For analytical purposes, after the samples were collected 100 uL of the urine was mixed with 100 uL of 0.1% formic acid in water. The research team completed a solid-phase extraction (SPE) through the use of an Oasis HLB 60 mg cartridge. Prior to extractions 2.0 mL of untreated urine were diluted with 2.0 mL of formic acid. A portion of the samples were then subjected to hydrolysis with beta-glucuronidase, while the remaining samples were further diluted [1].

For the samples subjected to hydrolysis, 2 mL of the untreated urine were mixed with 2 mL of a phosphate buffer and 100 uL of beta-glucuronidase. The samples were mixed and incubated for 2 hours in preparation for SPE. The samples were not diluted any further. The samples not subjected to hydrolysis were then conditioned with 2.0 mL MeOH, 2.0 mL of water, and 2.0 mL of formic acid. Further washing and elution occurred using 5% MeOH before the sample was allowed to evaporate to dryness. Once dry all samples were reconstituted in 200 uL of formic acid and prepared for final analysis.

In order to analyze plasma samples, 1.0 mL of the sample was added to 20 uL of the SARM, S22, in order to develop an internal standard sample. The next step the researchers took was to add 4 mL of ice cold acetonitrile to the samples. The samples were then put in the refrigerator for 20 minutes and centrifuged at 1000 g for 10 minutes. The resulting supernatant was put in new test tubes and allowed to evaporate to dryness. SImilar to the procedure followed with the urine samples, after drying the samples were reconstituted in 200 uL of formic acid and prepared for final analysis [1].

2) Three-month old female Sprague-Dawley rats were utilized by the research team of Roch et. Al in an attempt to determine the potential of LGD-4033 to enhance muscle tissue in cases of estrogen-deficient muscle wasting. Prior to treatment with LGD-4033, the first step of the study consisted of the animals undergoing an ovariectomy (OVX), the animals kept intact were marked as (non-OVX). Following surgery, the rats were left untreated for 9 weeks in order for sufficient levels of estrogen-deficient musculoskeletal degeneration to occur. During this time period the subjects were housed 3-4 rats per cage and were given ad libitum access to soy-free rodent food. Once treatment began, the different treatments were orally administered to the animals through their diet [2].

The dose of LGD-4033 administered to the animals was determined based on their food intake and body weight, which was measured weekly by the researchers. From there, LGD-4033 was administered in three different doses: 0.04 mg/kg, 0.4 mg/kg, and 4 mg/kg. The rats were then split into 5 different treatment groups with 4 animal housing cages per treatment group. The treatment groups included: non-OVX, OVX, OVX + LGD 0.04, OVX + LGD 0.4, and OVX + LGD 4. All treatments were administered to the subjects, daily, for 5 weeks [2]

Following 5 weeks of treatment, at week 13 post-OBVX, the animals were euthanized. Blood serum levels were collected in order to record levels of creatine kinase as an indicator of muscle damage. The uterus, gastrocnemius muscle, soleus muscle, and longissimus muscle were dissected from the animals and weighed in order to measure any muscular changes potentially due to LGD-4033 treatment. Intramuscular fat content was recorded in all treatment groups by dissecting a portion of the quadriceps femoris muscle and analyzing it according to proper procedure.

In addition to muscle weight, the research team observed changes in muscle fibers and capillary density by staining a 12 um prepared cross-section sample obtained from the harvested muscles. Capillaries in the muscle cross-sections were stained using a modified periodic acid-Schiff (PAS) reaction. On the other hand, muscle fibers were stained using adenosine-triphosphatase (ATPse). Prior to the staining method, fixative solution was applied to the cross-sections, followed by extensive washing with distilled water. Three ATPase-stained fields measuring 1 mm^2 each, were randomly selected and analyzed with a digital 10-fold magnification factor. This was performed in order to observe the stained capillaries and fibers, as well as to quantify the amount of fast and slow-twitch oxidative fibers and identify their distribution across the selected field [2]

Further analysis took place focused on the activity of muscle enzymes and changes to intramuscular fat content. Muscle activity was found to be linked to protein content. In order to solidify this finding the researchers collected sample serum levels of lactate dehydrogenase (LDH), citrate synthase (CS), and Complex I. Creatine kinase (CK) serum levels were measured prior to euthanasia as an indicator of muscle tissue damage. Additionally, the researchers noted that when observing changes in enzyme activity and protein content as a response to treatment, all analysis was performed according to standard procedure.

In order to measure intramuscular fat content, 5-10 grams of the homogenized quadriceps femoris sample was boiled in hydrochloric acid (HCl) in order to release any occluded lipid fragments that may be present in the muscle biopsy. The analysis of the intramuscular fat content was performed according to the method set by the International Organization for Standardization. After boiled the sample was dried and extracted. The fat content was defined as a percentage of the wet weight measured from the sample. Further statistical analysis was performed through a Tukey’s post-hoc test as well as a standard one-way ANOVA [2].



1) The primary focus of the study conducted by Hansson et. Al was to identify the presence of the parent compound, LGD-4033, or any related metabolites, in the plasma and urine samples collected from three female Thoroughbred horses. When LGD-4033 is ionized and fragmented, the main ion, [M+HCOO]-, is formed as an adduct of LGD-4033 and 0.1% formic acid. This ion was initially detected at m/z 383, however, it could be removed through the use of a higher cone voltage. Researchers thought it was important to mention that using a higher cone voltage led to in-source fragmentation at m/z 267. Additionally, retention time of LGD-4033 was measured at 10.77 minutes; the parent compound was only identified in plasma samples and hydrolyzed urine samples [1].

Additional metabolites of the parent compound were found through observing the mass and pattern of fragmentation of LGD-4033. 8 total metabolites were found when analyzing the horse urine samples. The metabolites ranged from M1a-M5b. Two of the identified metabolites were considered phase I metabolites while the other 6 had undergone phase II metabolism. Metabolites M1a-c were shown to have the same exact mass as well as the same product ions. The product ions of the three metabolites were all detected at different relative intensities, leading researchers to conclude that the metabolites they identified are isomers of each other.

Following beta-glucuronidase-induced hydrolysis of the urine samples, the metabolites M1a-c were no longer detectable in the urine samples. This led researchers to believe that M1a-c could be defined as glucuronides. However, results of the analysis of the samples emphasized the presence of three peaks representing mass values that correspond to the deprotonation of M2 aglycons. Retention times of the three peaks were measured as 7.5, 7.94, and 8.75 minutes, respectively, indicating to the research team that the metabolites could be represented as positional isomers or diastereomers. Furthermore, these results suggest that metabolites M1a-c were subjected to a hydroxylation reaction on the pyrrolidine ring [1].

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Figure 1: Ion chromatography for LGD-4033 and related metabolites found in horse urine samples.

The M2 metabolite identified in the urine sample had a recorded mass of m/z 545.0997. The mass of the metabolite is related to the deprotonation, dihydroxylation, and glucuronidation of LGD-4033. M2 exhibited the lowest intensity out of all observable metabolites; the compound was only identifiable after SPE was performed. Results of the analysis indicated that both of the hydroxyl groups had been positioned on the pyrrolidine ring. However, there was no peak detected for M2 suggesting that the metabolite was not found in the sample after hydrolyzation. Additionally, following hydrolysis via beta-glucuronidase administration, glucuronic acid was successfully removed from the samples.

Metabolite M3 was detected with an accurate mass of m/z 385.0625. Because the metabolite loses the C4H5F3O3 group, M3 is considered trihydroxylated. This is also due to the identification of product ions that coincide with the metabolite M1. The metabolite M4 was detected with an accurate mass similar to the mass of a dihydroxylated form of LGD-4033. After water, CO2, and an HCF3 fragment was removed from the sample, the main product ion was found at m/z 237 [1].

The last two metabolites identified by the researchers were M5a and M5b. They were detected with the same accurate mass of m/z 513.1105, as well as similar fragmentation patterns. The accurate mass of the metabolite corresponds to the conjugation of glucuronic acid to LGD-4033. This finding is supported by the presence of a product ion at m/z 337. Furthemore, the researchers noted that M5a was not detected in the urine samples following hydrolysis with beta-glucuronidase, however there was a peak detected that coincided with LGD-4033. In terms of the M5b metabolite, the researchers concluded it was capable of acting as a N-glucuronide considering that intensity levels were not reduced after administration of beta-glucuronidase. This suggests that M5b was not susceptible to hydrolysis [1].

Results of the plasma analysis reported that there were 6 metabolites, M1a-c, M4, and M5a-b identified in the sample as well as the parent compound, LGD-4033. All of the metabolites had the same accurate masses and retention times as the metabolites found in the urine, however, identifiable peaks displayed higher intensity in the plasma samples. This is interesting to note considering that plasma concentrations typically exhibit lower intensity than urine concentrations. When analyzing the plasma samples, the researchers were able to find product ions matching those observed in the urine samples. Overall, the results suggest a rapid transformation of LGD-4033 considering that the highest peak intensity was reached 15-45 minutes after the SARM was administered [1].

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Figure 2: Peak area ratio for LGD-4033 and metabolites observed in experimental horse 1

2) At the beginning of the experimental period all of the rats had a similar body weight of approximately 237 +/- 11.7 grams. Starting at week 2 of treatment the researchers noticed that rats in the non-OVX group weighed significantly less than all of the OVX animals. This weight difference was detected in the groups for the remainder of the experimental treatment period, regardless of which dose of LGD-4033 they were administered.

When comparing the weight of the uterus, the uterine weight in all four OVX groups was far lower than the non-OVX group, measured at 0.11 +/- 0.02 g and 0.58 +/- 0.11 g, respectively. There was no significant difference in uterine weight between the OVX + LGD 0.04 and the OVX + LGD 0.4, treatment groups. However, the OVX + LGD 4 group experienced a greater increase in uterine weight than the ODX, ODX + LGD 0.04, and ODX + LGD 0.4 treatment groups. In regards to weight of the calf muscles, all four ODX groups saw a significant increase in the weight of the gastrocnemius when comparing results to the non-ODX group. Additionally, administration of the 4 mg/kg dose of LGD-4033 elicited a larger increase in gastrocnemius muscle weight than the 0.04 and 0.4 mg/kg doses. The weight of the soleus muscle experienced inconsistent changes that were eventually deemed insignificant [2].

When analyzing muscle fibers the researchers concluded that LGD-4033 increases fiber size in ODX rats. This enhancement was specifically observed in the soleus muscle of the animals included in the OVX, OVX + LGD 0.4, and OVX + LGD 4 treatment groups. Improved muscle fibers were also observed in longissimus muscle of the subjects in the OVX + LGD 4 treatment group. The researchers mentioned that all changes observed in the experimental groups were compared to the control group, defined in this study as the non-OVX treatment group.

Treatment with LGD-4033 was also shown to elicit beneficial effects on muscle vascularization. This is important to note considering that enhanced vascularization leads to improved restoration of muscle contractility. Overall, results of the study found that treatment with LGD-4033 led to increased vascularization in the gastrocnemius, soleus, and longissimus muscles, in comparison to the non-OVX group [2].

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Figure 3: Changes in capillaries/muscle vascularization in muscle tissues in response to different treatments

The research team of Roch et. Al observed increased activation in several muscle enzymes in response to treatment with LGD-4033. The three main enzymes identified were lactate dehydrogenase (LDH), citrate synthase (CS), and Complex I. LDH is considered essential for cell metabolism in anaerobic conditions due to its ability to regulate glycolysis and catalyzes the oxidation process of lactate to pyruvate conversion. Under aerobic conditions, CS is a crucial mediator of the central metabolic pathway through its ability to act as a pace-making enzyme of the citric acid cycle. Finally, Complex 1 is deemed essential for cell functioning as it is the first enzyme in the respiratory chain found embedded in the mitochondrial membrane [2].

Results of this study reported that LGD-4033 led to higher CS activity in the gastrocnemius muscle of animals in the OVX and OVX + LGD 0.4 treatment groups, in comparison to the non-OVX group. The researchers also observed increased LDH activity in the longissimus muscle of animals in the OVX + LGD 0.4 treatment group. In regards to the soleus muscle, there were no identifiable differences in muscle enzyme activity between the treatment groups. Furthermore, serum CK levels were measured as an indicator to muscle damage, however, results were considered inconclusive as there were no significant changes in CK levels in response to treatment with LGD-4033 [2].

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Figure 4: Change in muscle enzyme activity in muscle tissue in response to different treatments

The researchers also thought it was important to mention that the quadriceps femoris of animals in the OVX + LGD 4 treatment group exhibited higher levels of intramuscular fat content in comparison to the non-OVX group. Additionally, the results reported that there was no significant variation between the intramuscular fat content measured in any OVX treatment group [2] .



*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] Hansson A, Knych H, Stanley S, Berndtson E, Jackson L, Bondesson U, Thevis M, Hedeland M. Equine in vivo-derived metabolites of the SARM LGD-4033 and comparison with human and fungal metabolites. J Chromatogr B Analyt Technol Biomed Life Sci. 2018 Feb 1;1074-1075:91-98. doi: 10.1016/j.jchromb.2017.12.010. Epub 2017 Dec 7. PMID: 29334634.

[2] Roch PJ, Henkies D, Carstens JC, Krischek C, Lehmann W, Komrakova M, Sehmisch S. Ostarine and Ligandrol Improve Muscle Tissue in an Ovariectomized Rat Model. Front Endocrinol (Lausanne). 2020 Sep 17;11:556581. doi: 10.3389/fendo.2020.556581. PMID: 33042018; PMCID: PMC7528560.

LGD-4033 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 4 oz
Dimensions 3 × 3 × 5 in
Formula Option

, ,

CAS Number‎

Molar Mass

338.253 g·mol−1

Molecular Formula



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1 review for LGD 4033 LIGANDROL SARM – 20MG/ML – 30ML/60ML BOTTLE

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