LGD 4033 SARM POWDER – 1000MG / 1 GRAM


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.



  • One (~10mg – 15mg) Red Micro Scoop

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LGD 4033 SARM Powder


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Image showing the formula LGD 4033 SARM


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 LGD 4033 30mL liquid Glycol (20mg/mL, 600mg bottle)

LGD 4033 30mL liquid Poly-Cell™ (20mg/mL, 600mg bottle)

LGD 4033 60mL liquid Glycol (20mg/mL, 1200mg bottle)

LGD 4033 60mL liquid Poly-Cell™ (20mg/mL, 1200mg bottle)

Powder Availability LGD 4033 1 gram
Gel Availability LGD 4033 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.


  • One (~10mg – 15mg) Red Micro Scoop

10mg - 15mg Micro Scoop - 5 Pack

What is LGD-4033?

The potent selective androgen receptor modulator (SARM), LGD-4033, commonly referred to as Ligandrol, is known for its potential to mimic the mechanism of action of testosterone by selectively binding to androgen receptors. However, while many of the same benefits elicited by testosterone are seen with LGD-4033 treatment, many adverse side effects, such as prostate growth, are avoided through use of the SARM. Previous preclinical data has determined that Ligandrol shows potential in enhancing anabolism in the muscles and bones. Current research is being conducted in order to examine the ability of LGD-4033 to combat cases of muscle wasting and degeneration.


2 Main Research Findings

1) Researcher Roch et. Al demonstrated how LGD-4033 is capable of enhancing various aspects of muscle tissue in ovariectomized rats.

2) Results of this study reported that LGD-4033 treatment was considered safe and tolerable with the potential to improve overall body composition.


Selected Data

1) Researchers Roch et. Al examined the potential of LGD-4033 to enhance muscle tissues, specifically in ovariectomized female rats. Three-month old Sprague-Dawley rats were obtained from Janvier Labs in Saint-Berthevin, France. The subjects underwent an ovariectomy (OVX) or were left intact (non-OVX), prior to treatment with the SARM. The rats were left untreated for 9 weeks following surgery in order to elicit musculoskeletal changes as a result of estrogen deficiency [1].

Throughout the experiment, rats were housed 3-4 rats per cage and 4 cages were in each treatment group. The subjects ate a soy-free rodent diet supplied with LGD-4033 and provided to the rats ad libitum. Food intake and body weight of the animals were strictly measured and recorded on a weekly basis in order to calculate the dose of LGD-4033 that needed to be administered. The researchers administered LGD-4033 in three different doses, 0.04 mg/kg, 0.4 mg/kg, and 4 mg/kg. Rats were then split into 5 different treatment groups: non-OVX, OVX, OVX + LGD 0.04, OVX + LGD 0.4, and OVX + LGD 4. Treatment was administered to the subjects daily for up to 5 weeks.

13 weeks after OVX all of the animals were euthanized: blood serum was collected in order to record creatine kinase levels. The uterus, gastrocnemius muscle, soleus muscle, and longissimus muscle were extracted and weighed in order to observe muscular changes in response to treatment. Intramuscular fat content was measured in the animals by observing and dissecting the quadriceps femoris muscle from different treatment groups, including: non-OVX, OVX, and OVX + LGD-4033 [1].

Both the muscle fibers and the muscle capillaries of the test subjects were stained in order to identify and analyze treatment-related changes. A cryotome was used to cut 12 um cross sections from the middle of the extracted muscles; samples were then air-dried and stored for further staining to take place. Muscle capillaries were stained through the use of a modified periodic acid-Schiff (PAS) reaction. Muscle fibers were stained through a modified method of staining using adenosine-triphosphatase (ATPase); staining of the fibers occurs after the application of a fixative solution and extensive washing with distilled water. Capillaries and fibers were digitally analyzed at a 10-fold magnification of three randomly chosen, ATPase-stained, fields measuring 1 mm^2. This was performed in order to identify the number of fast and slow- twitch oxidative fibers, and how they are distributed in the selected field [1].

Further results of the study were determined by a standard statistical analysis, as well as, an analysis of muscle enzyme activity and intramuscular fat content. The research team determined that muscle enzyme activity was related to protein content. That being said, the first step of this analysis was to obtain sample serum levels of lactate dehydrogenase (LDH), citrate synthase (CS), and Complex I. As it was previously mentioned, creatine kinase levels were collected prior to euthanasia in order to indicate levels of muscle tissue damage. Protein content and levels of enzyme activity found in the samples were analyzed according to standard procedure.

Intramuscular fat content was measured according to the method set in place by the International Organization for Standardization. 5-10 grams of the homogenized quadriceps femoris was boiled in HCl in order to release occluded lipid fractions. The sample was properly dried and extracted; the fat content was quantified as a percentage of the wet weight taken from the sample for analysis purposes. Finally, statistical analysis was performed through one-way ANOVA as well as Tukey’s post-hoc test [1].

2) The effects of varying doses of LGD-4033 in healthy men were examined by the research team of Basaria et. Al. This study, approved by the Institutional Review Board of Boston University, was double-blind and controlled while all test subjects provided written, informed consent. Eligible subjects were nonsmoking, healthy men, aged 21-50 years old. The subjects were then randomly assigned to the placebo treatment or active SARM treatment. In comparison to the placebo, three dose levels of LGD-4033 were administered; level 1 started at 0.1 mg, level 2 was 0.3 mg, and level 3 was 1 mg. The initial dose of 0.1 mg was given over a set period of time. If the dose level was completed by a subject that the safety and tolerability data was reviewed by a Safety Panel and Data and Safety Monitory Board in order to determine if the next dose level should be administered [2].

Each dose of LGD-4033 was administered after an overnight fast with 8 ounces of water; the SARM was given to the subjects daily over the course of 21 days. Pharmacokinetic sampling was conducted 48 hours after the first dose; this indicates that the subjects received 20 doses despite there being 21 treatment days.The dose of LGD-4033 administered to the subjects increased if the compound met specific safety criteria with no significant symptoms of toxicity. The same procedures were followed for the second dose level and the same Safety Panel determined if the 0.3 mg dose was safe and tolerable before moving to the third dose level of 1.0 mg. After 3 weeks of treatment the subjects were monitored for an additional 5 weeks [2].

The secondary goal of the study was to observe changes in lean body mass and overall body composition elicited by LGD-4033. LBM and body composition changes were recorded through DEXA scans as well as a 1 repetition maximum test and an evaluation of stair climbing power. 1RM was measured through leg press strength. The subjects went through a full body warm up, one set of 5-10 repetitions at 40%-60% of the estimated maximum, followed by progressively heavier sets until the subject reached failure. The last lift completed successfully was recorded as the 1 RM.

Stair climbing power was assessed by the 12-step stair-climb test. As fast as they could, the subjects would ascend a staircase, with a step rise of 17 cm. Motion-activated switch-mats were placed on the 8th and 12th steps in order to record time. Power was calculated from the time elapsed during the recorded trials, the subjects body weight, and the vertical distance.The researchers thought it was important to acknowledge that 3 weeks may not be a long enough time period to accurately measure anabolic effects of the SARM [2].

Blood samples were collected at different points throughout the treatment period in order to measure the rate of protein synthesis. In order to collect blood samples and complete tracer infusion, an 18-gauge catheter was placed bilaterally into the forearms of the subjects. One side was for collection of blood samples while the other was utilized for a consistent infusion of phenylalanine to be maintained over a 6 hour period All sample collection and infusion took place on day 1 and day 20 of the 3 week treatment. Two additional muscle biopsies were obtained from the vastus lateralis muscle; the biopsies were collected 3 and 6 hours into the phenylalanine infusion

The research team determined that enrichment of intracellular phenylalanine was dependent on extraction with gas and cation exchange chromatography. Additionally, muscle samples were weighed out so the proteins could be precipitated through the use of 800 uL of 10% sulfosalicylic acid. Once the mixed-muscle proteins were washed, dried, and hydrolyzed, all remaining amino acids were extracted and analyzed in order to calculate the mixed-muscle fractional synthesis rate (FSR). This was followed by a final hormone assay measuring serum levels of testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex hormone-binding globulin (SHBG). Variations in the levels of serum LH, FSH, and SHBG were measured through the use of two site-directed immunofluorometric assays while all changes in serum testosterone were observed using liquid chromatography-tandem mass spectrometry.



1) When starting the experiment all of the rats had a similar body weight of approximately 237 +/- 11.7 grams. At the beginning of week 2, the researchers noticed that rats in the non-OVX group weighed significantly less than all of the OVX animals. This difference in weight difference was seen in the groups for the remainder of the experimental treatment period. These results were independent of the dose of LGD-4033 they were administered. The research team initially reported that treatment with LGD-4033 was shown to elicit beneficial effects on muscle vascularization and capillary density in the muscles that were harvested. This is important to note considering that enhanced vascularization leads to improved restoration of muscle contractility. Overall, the study concluded that treatment with LGD-4033 led to increased vascularization and enhanced capillary density in the gastrocnemius, soleus, and longissimus muscles, in comparison to the non-OVX group [1].

LGD 4033
Figure 1: Muscle enzyme activity in response to different treatments

When comparing weight of the uterus, all four OVX treatment groups experienced lower uterine weight than the non-OVX group; the weights averaged at 0.11 +/- 0.02 g and 0.58 +/- 0.11 g, respectively. There was a significant difference in uterine weight between the OVX + LGD 4 group and the ODX, ODX + LGD 0.04, and ODX + LGD 0.4 treatment groups. However, no dramatic changes were noticed when comparing the OVX + LGD 0.04 and the OVX + LGD 0.4, treatment groups.

When observing changes in the weight of the gastrocnemius and soleus muscles, the research team reported that all four ODX groups saw a significant increase in the weight of the gastrocnemius muscle in comparison to the results of the non-ODX group. A larger increase in muscle weight of the gastrocnemius was reported when the subjects were administered the 4 mg/kg dose of LGD-4033, in comparison to the 0,04 and 0.4 mg/kg doses of the SARM. Weight changes measured in the soleus muscle were deemed insignificant due to the inconsistent changes observed by the research team [1].

Furthermore, when analyzing muscle fibers the researchers determined that LGD-4033 increases fiber size in ODX rats. Improved muscle fibers were observed in longissimus muscle of the subjects in the OVX + LGD 4 treatment group. The soleus muscle of the animals also saw significant enhancement, primarily in the OVX, OVX + LGD 0.4, and OVX + LGD 4 treatment groups. The researchers mentioned that all changes observed in the experimental groups were compared to the non-OVX treatment group [1].

LGD 4033
Figure 2: Changes in muscle vascularization in different muscle tissues in response to various treatments

When examining any changes in intramuscular fat content, the researchers also mentioned that the quadriceps femoris of animals in the OVX + LGD 4 treatment group exhibited higher levels of fat content in comparison to the non-OVX group. Results of this portion of the study reported that there was no significant variation in recorded levels of intramuscular fat content seen between any OVX treatment group.

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

Results of this study also indicated that in comparison to the non-OVX control group, treatment with LGD-4033 led to higher LDH activity in the longissimus muscle of animals in the OVX + LGD 0.4 treatment group. The researchers also detected higher rates of CS activity in the gastrocnemius muscle of animals in the OVX + LGD 0.4 and OVX + LGD 4 treatment groups. However, there were no observed differences in muscle enzyme activity in the soleus between any of the treatment groups. Serum CK levels were measured by the research team as an indicator to muscle damage. Results of the enzyme analysis were considered inconclusive as there were no significant changes in CK levels in response to treatment with LGD-4033 [1].

2) Results of this study reported that LGD-4033 was safe and well-tolerated by the subjects included in the study. Any reported side effects were similar between the experimental and the placebo group. Infections of the upper respiratory tract were seen at the LGD-4033 1.0 mg level, however, researchers were able to determine these side effects were not related to the drug study. Pharmacokinetic characterizations determined LGD-4033 displayed a half-life of approximately 24-36 hours. Additionally, there was a dose-proportional accumulation of LGD-4033 when comparing days 1 and 21. This observation was supported by serum measurements of LGD-4033 that were reported to have experienced a three-fold increase in concentrations from day 1 to day 21 [2].

Furthermore, results of the hormonal assay revealed that there was a dose-dependent suppression of total testosterone and SHBG when comparing day 1 to day 21. The researchers noted that suppression of free testosterone was only seen in the subjects receiving a 1.0 mg dose of LGD-4033. There were no significant changes observed in serum LH levels, however, levels of FSH were found to be suppressed in subjects receiving the 1.0 mg dose of LGD-4033. Hormone levels returned to their baseline values after treatment with LGD-4033 was discontinued.

In addition to determining the safety and tolerability of the SARM, the second goal of the study conducted by researchers Basaria et. Al was to examine how LGD-4033 affects various aspects of body composition. This study is specifically viewing variations in plasma lipids, lean body mass (LBM), skeletal muscle mass, and fat mass. Results found that total cholesterol and low density lipoprotein (LDL) cholesterol did not exhibit any significant changes from baseline. However, high density lipoprotein (HDL) exhibited a reduction from baseline levels when the subjects were administered doses greater than 0.3 mg. HDL levels returned to baseline after treatment stopped while triglyceride levels significantly decreased in response to all three of the different treatment doses [2].

There were also significant changes observed in LBM, fat mass, and skeletal muscle mass in response to treatment. Increases in LBM was primarily noted in subjects being administered the 1.0 mg dose of LGD-4033; this treatment group experienced an average increase of 1.21 kg LBM. There were no significant changes in fat mass in response to treatment. There were slight increases observed in skeletal muscle mass, however, all experimental values were similar to the placebo group so all differences between treatment groups were deemed insignificant [2].

Increases in strength in response to LGD-4033 treatment was measured by 1RM test and a stair-climbing test. Average strength increased in the test subjects by approximately 68.3 N; these results were typically seen with the 1.0 mg treatment group. While there was a slight improvement in strength, the difference from baseline strength levels was not statistically significant. The stair-climbing speed and power test showed an elevation that seemed to be trending towards dose-related improvements, however, similar to the 1RM max test, changes from baseline were insignificant.

When observing fractional mixed-muscle protein synthesis rats through phenylalanine infusion, results of the study reported that there was no change in plasma phenylalanine concentrations at the 3 hour or 6 hour mark. When determining the FSR, baseline levels averaged 6% an hour, but in terms of the study, changes in FSR from baseline in a fasted state displayed no significant differences when comparing the 0.3 mg dose of LGD-4033 and the placebo groups [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] 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.

[2] Basaria S, Collins L, Dillon EL, Orwoll K, Storer TW, Miciek R, Ulloor J, Zhang A, Eder R, Zientek H, Gordon G, Kazmi S, Sheffield-Moore M, Bhasin S. The safety, pharmacokinetics, and effects of LGD-4033, a novel nonsteroidal oral, selective androgen receptor modulator, in healthy young men. J Gerontol A Biol Sci Med Sci. 2013 Jan;68(1):87-95. doi: 10.1093/gerona/gls078. Epub 2012 Mar 28. PMID: 22459616; PMCID: PMC4111291.

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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LGD 4033

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