IngredientsEcdysterone is the most widely used common name for the compound formally designated 20-hydroxyecdysone (abbreviated 20E or 20HE). It is a naturally occurring steroid hormone belonging to the ecdysteroid class and is also encountered in the scientific literature under the synonyms crustecdysone and beta-ecdysone. Its molecular formula is C27H44O7 and its full systematic name is 2β,3β,14α,20β,22R,25-hexahydroxy-5β-cholest-7-en-6-one.
Chemically, ecdysteroids are a group of polyhydroxylated ketosteroids that are structurally similar to androgens. The carbon skeleton is termed cyclopentanoperhydrophenanthrene with a β-side chain at carbon-17. Despite this structural similarity to androgens, ecdysterone behaves very differently in mammalian systems. Phytoecdysteroids are classed as triterpenoids, the group of compounds that includes triterpene saponins, phytosterols, and phytoecdysteroids.
Ecdysteroids are polyhydroxylated sterols, and are widespread in the plant and animal world. To date, over 520 ecdysteroids have been isolated from natural sources. Within this large family, 20-hydroxyecdysone is the most abundant and the most pharmacologically studied member.
Phytoecdysteroids are a class of chemicals that plants synthesize for defense against phytophagous (plant-eating) insects. These compounds are mimics of hormones used by arthropods in the molting process known as ecdysis. It is presumed that these chemicals act as endocrine disruptors for insects, so that when insects eat the plants containing these chemicals they may prematurely molt, lose weight, or suffer other metabolic damage and die.
Plants, but not animals, synthesize phytoecdysteroids from mevalonic acid in the mevalonate pathway of the plant cell using acetyl-CoA as a precursor. Many more plants have the ability to "turn on" the production of phytoecdysteroids when under stress, animal attack, or other conditions.
The principal botanical sources of commercial significance include:
The first ecdysteroid, named ecdysone, was isolated by Butenandt and Karlson in 1954 from the silkworm pupae; its structure was elucidated in 1965 by Huber and Hoppe using X-ray crystallography. Some ecdysteroids, including ecdysone and 20-hydroxyecdysone (20E), are produced by both plants and arthropods.
The use of R. carthamoides for medicinal purposes dates back to ancient times, and traditional Siberian medicine has long praised the plant for its ability to treat weariness and debility after sickness. More broadly, phytoecdysteroids are a group of naturally occurring ecdysteroid hormones found in certain plant families and used for centuries for their adaptogenic, tonifying, and antioxidant properties.
The use of natural adaptogens by humans has a rich history — they are used in recovery from illness, physical weakness, memory impairment, and other conditions. Ecdysterone is also historically prescribed for various metabolic, renal, cardiovascular, respiratory, and digestive ailments.
Although plant adaptogens have been used by people since ancient times, the term "adaptogen" is relatively young — it was introduced in 1947 by the Soviet scientist Lazarev. It defines adaptogens as substances that cause non-specific resistance of the living organisms.
Research over the last century has shown R. carthamoides's muscle- and strength-building capabilities, resulting in widespread use among elite athletes in Soviet and Russian sports. In 1969, Brekhman and Dardymov classified R. carthamoides as an adaptogen, now widely used in herbal medicine to promote recovery. Extracts from Panax ginseng, Eleutherococcus senticosus, Rhaponticum carthamoides, Rhodiola rosea, and Schisandra chinensis are considered to be naturally occurring adaptogens.
Long before Russians were caught doping their athletes with steroids, the former Soviet Union spent decades secretly searching for energy-enhancing plants that would help their Olympians, as well as their soldiers and astronauts, perform better. The Soviets were looking for what they called "adaptogens" — plant species that would encourage the body to adapt to physical and mental stress without major side effects.
About 50 years ago, plant adaptogens were first used in professional sports due to their high potential to increase the body's resistance to stress and to improve physical endurance.
In 1961, Rhaponticum carthamoides liquid extract (1:1) was officially recognized and included in the Soviet Pharmacopoeia as a natural remedy for overcoming fatigue, improving physical and mental productivity performance, and for shortening recovery time after illness.
While ecdysterone is the primary pharmacologically studied constituent, the plants from which it is extracted contain a broader array of bioactive molecules. Various medicinal preparations from R. carthamoides rhizomes and roots have been reported to possess not only adaptogenic effects but also antioxidant, immunomodulatory, anticancerogenic, antimicrobial, antiparasitic, and repellent activities. The main isolated chemical classes include not only phytodysones but also phenolics such as flavonoids and phenolic acids.
The ecdysteroid profile of R. carthamoides includes 20-hydroxyecdysone (the dominant ecdysteroid), ponasterone A, and turkesterone. Besides the widely shared ecdysone and 20-hydroxyecdysone, over 250 ecdysteroid analogs have been identified so far in plants, and it has been theorized that there are over 1,000 possible structures which might occur in nature.
Emerging evidence indicates that, unlike traditional anabolic steroids that act primarily via the Androgen Receptor (AR), ecdysterone's anabolic effects may be mediated through Estrogen Receptors (ERs), particularly Estrogen Receptor beta (ERβ). This distinction is mechanistically important because it separates ecdysterone's anabolic activity from classical androgenic pathways.
A key 2014 preclinical study published in a peer-reviewed journal established this pathway experimentally: ecdysterone and ERβ-selective ligand treatment, but not ERα-selective treatment, induced myotube hypertrophy. The effect of ecdysterone and ERβ could be antagonized by an ERβ-selective antagonist. In summary, results indicate that ERβ is involved in the mediation of the anabolic activity of ecdysterone. Furthermore, hypertrophy induced by estradiol and ecdysterone could be antagonized with an antiestrogen but not by an antiandrogen.
A 2025 in-silico study using all-atom molecular dynamics simulations corroborated this: ecdysterone preferentially binds to ERβ, forming stable and compact complexes characterized by minimal per-residue fluctuations. These findings underscore the pivotal role of ERβ in mediating ecdysterone's anabolic effects, distinguishing it from traditional androgenic steroids, and provide critical insights into its unique mechanism of action. This work lays the foundation for further exploration of ecdysterone as a potential anabolic agent.
Despite these insights, the precise molecular mechanisms underlying ecdysterone's biological activity remain poorly characterized.
Current evidence proposes that the stimulation of a putative membrane-associated G protein-coupled receptor (GPCR) triggers the activation of phospholipase C (PLC), the enzyme responsible for generating inositol trisphosphate (IP3). The latter activates its own receptor (IP3R), releasing intracellular calcium reserves in the cytoplasm. Furthermore, ecdysterone has the capacity to trigger the opening of extracellular calcium channels. The subsequent influx of calcium ions promotes the phosphorylation of Akt, ultimately driving an upregulation in protein synthesis.
In vitro, ecdysterone (1 μM) induced a significant increase of myotube diameter comparable to dihydrotestosterone (1 μM) and IGF-1 (1.3 nM) in C2C12 myotubes.
A further mechanistic pathway identified in pharmaceutical research is activation of the MAS receptor, part of the protective arm of the renin-angiotensin-aldosterone system (RAAS). MAS receptor, as the protective arm of the renin–angiotensin system (RAS), appeared feasible to interpret pleiotropy; a cooperative activity between MAS and a palmitoylated (membrane-bound) estrogenic receptor has been proposed for the mechanism of 20E action. BIO101 (20-hydroxyecdysone), developed as a pharmaceutical candidate, is described as an activator of the MAS receptor, and is being investigated as safe and capable of improving muscle function and physical performance of community-dwelling older sarcopenic patients.
It has been shown that 20E exerts its effect through SIRT6-mediated deacetylation of NF-κB p65 (nuclear factor kappa of B cells) to inhibit CD40 expression in 3-D human endothelial cell culture (HUVEC).
When administered orally, ecdysterone has been shown to alleviate induced hyperglycemia in rat models and enhance overall tissue glucose uptake, likely by upregulating cellular insulin sensitivity.
The most cited human study is by Isenmann et al. (2019), funded by WADA and published in Archives of Toxicology. A 10-week intervention study of strength training in young men (n = 46) was carried out. Different doses of ecdysterone-containing supplements were administered to evaluate the performance-enhancing effect. This study showed that 10-week supplementation of ecdysterone at 12 mg daily and 48 mg daily in young men contributed to the improvement of anthropometric and performance parameters. Significantly higher increases in muscle mass were observed in participants dosed with ecdysterone. Specifically, research participants supplemented with high-dose ecdysterone (48 mg of ecdysterone) showed a significant increase in muscle mass (2.0 kg delta). The results strongly suggested the inclusion of ecdysterone in the list of prohibited substances and methods in sports in class S1.2 "other anabolic agents."
However, the actual amount of ecdysterone in the capsule used was only 6 mg, whereas the declared amount was 100 mg. This labeling discrepancy complicates interpretation of the dose-response relationship established in that study.
A separate study examined the effects of asparagus extract (containing 20E) on muscle mass and strength following resistance training. When comparing muscle mass development after the resistance training period, that study found no significant differences between the placebo and the 20E groups. These results contrasted with those of Isenmann et al., who discovered differences between the groups receiving high doses (48 mg/day) of ecdysterone and a placebo group. The contrasting observations can be attributed to the varying concentrations of ecdysterone and leucine.
An earlier study published in the Journal of the International Society of Sports Nutrition (Wilborn et al., 2006) assessed ecdysterone supplementation in resistance-trained males (referenced in multiple later studies). A dose-dependent effect was observed in muscle mass and performance across these human studies.
In comparison with prohibited anabolic agents (e.g., metandienone and others), ecdysterone revealed to be even more effective in a recent study performed in rats. However, scientific studies in humans are very rarely accessible.
Evidence strength: Human evidence is preliminary, limited to a small number of trials with small sample sizes. Findings are mixed — one trial reported significant muscle mass gains while at least one other showed no significant effect versus placebo. Methodological heterogeneity (varying doses, training protocols, and supplement purity) prevents robust conclusions.
Ecdysterone under the pharmaceutical designation BIO101 (a ≥97% pure 20E preparation) has been investigated in formal clinical trials for sarcopenia. Sarcopenia is an age-related skeletal muscle disorder characterized by loss of muscle mass and strength leading to mobility disability. 20-Hydroxyecdysone (20E) is a polyhydroxylated plant steroid that demonstrates pharmacological effects in many disease animal models including ageing/sarcopenia. BIO101 demonstrated good toxicology profiles in rat and dog.
A Phase 1 study (Dioh et al., 2023, published in Journal of Cachexia, Sarcopenia and Muscle) assessed the safety and pharmacokinetics of BIO101 in healthy young and older adults. In addition to studies involving healthy and trained individuals, 20E is currently being investigated as a phytopharmaceutical in preliminary clinical pilot trials (phases 1 and 2).
A Phase 2b randomized, double-blind trial (SARA-INT, published in Journal of Cachexia, Sarcopenia and Muscle, 2025, Fielding et al.) assessed BIO101 in sarcopenic seniors at risk of mobility disability. After 6 to 9 months of treatment, BIO101 350 mg twice daily showed strong trends consistent with a clinically relevant effect on the 400-meter walk test gait speed, close to the minimal clinically important difference (MCID) in sarcopenia (0.1 m/s).
Evidence strength: Early-stage clinical (Phase 1 and Phase 2b). Results are promising but not yet sufficient to establish clinical efficacy for sarcopenia treatment; larger Phase 3 trials are needed.
In vivo studies suggest that ecdysterone possesses effects on lipid metabolism, as well as anti-obesity and anti-diabetic effects. It has been highlighted that ecdysterone is correlated with an increased cell immunity, and that it is also endowed with adaptogenic, anti-diabetic, hepatoprotective, and anti-tumour properties.
Other interesting metabolic effects include hypolipidemic, antidiabetic, hepatoprotective, and adaptogenic effects. When administered orally, ecdysterone has been shown to alleviate induced hyperglycemia in rat models and enhance overall tissue glucose uptake, likely by upregulating cellular insulin sensitivity.
A controlled randomized study investigated the utilization of 20HE in metabolic syndrome.
Evidence strength: Preclinical (animal and in vitro) evidence is substantial. Direct human clinical trial evidence for antidiabetic effects is very limited. Claims cannot yet be extrapolated to humans without further controlled trials.
Ecdysterone exhibited anti-oxidative and scavenging and neuroprotective properties; these antioxidant properties could alleviate neuronal loss and behavioral deficits in neurologic patients. Combining ecdysterone supplementation with high-intensity interval training (HIIT) has emerged as a promising therapeutic strategy to ameliorate physiological brain function during the cognitive decline associated with Alzheimer's disease. This dual intervention has been shown to drive synaptic refinement alongside noticeable behavioral improvements.
In vivo studies suggest that ecdysterone possesses effects on Alzheimer's disease. Some of the in vivo studies confirm the in vitro studies about neuroprotective and cytotoxic effects, as well as the prevention of Alzheimer's disease.
Evidence strength: Preclinical only. No published randomized controlled trials in human populations have evaluated ecdysterone specifically for neurological outcomes.
Diverse bioactivities reported for phytoecdysteroids include hepatoprotective properties. Ecdysterone is also endowed with hepatoprotective properties in the broader pharmacological literature.
Evidence strength: Despite the copious amount of phytoecdysteroid research performed over the past two decades, most results cited are based on in vitro studies; data associated with in vivo and clinical studies are very limited.
Phytoecdysteroids have shown a wide range of biological, pharmacological, and medicinal properties implicated in the prevention and therapy of acute and chronic diseases. Phytoecdysteroids are effective against different types of cancer due to their anti-inflammatory and antioxidant mechanisms.
Ecdysterone can inhibit breast cancer growth by suppressing glycolytic and mitochondrial bioenergetics and induction of cell autophagy and apoptosis of cancer cells but not of control cells.
Evidence strength: In vitro only. No human clinical evidence exists for anticancer applications of ecdysterone supplementation.
In vivo studies suggest that ecdysterone possesses effects on osteoblast differentiation and bone regeneration, joint morphology, and osteoporosis.
Evidence strength: Animal model data only. No controlled human trials have been published specifically evaluating ecdysterone for bone or joint outcomes.
Based on the peer-reviewed literature, ecdysterone has been associated with the following body systems and health domains:
Only a few studies on the pharmacokinetics of ecdysterone in humans have been reported. In one study, post-administration urine samples in twelve volunteers (single dose of 50 mg of ecdysterone) were analyzed. Ecdysterone was the most abundant analyte present in post-administration urine samples, detected for more than 2 days, with a maximum concentration (Cmax) in the 2.8–8.5 h urine (Cmax = 4.4–30.0 μg/mL).
In human urine, excretion of deoxy-ecdysterone metabolites has been reported as 2-deoxyecdysterone, deoxyecdysone, and 14-deoxy-ecdysterone. Two metabolites — 14-deoxy-ecdysterone and 14-deoxy-poststerone — have been identified and quantified following oral administration.
Ecdysterone and 14-deoxy-ecdysterone were excreted following first-order kinetics with half-lives calculated at three hours, while pharmacokinetics of 14-deoxy-poststerone needs further evaluation. In total, up to 50.3% (mean = 21.1%, n = 12) of the administered dose was recovered in urine (as a parent drug and metabolites).
The low distribution of ecdysteroids in skeletal muscle tissue may limit their effects for athletic purposes, especially since the effects of ecdysteroids are typically concentration-dependent. The largest concentrations of ecdysteroids are typically located in the human liver and the kidneys. In addition, ecdysteroids are typically metabolized rapidly and excreted through bile and urine. Being very hydrophilic molecules, their urine excretion may be further increased.
Within 30 minutes after ingestion in rodent models, 20E reaches the large intestine, where microorganisms firstly remove the 14-hydroxyl group and reduce the 6-one. The breakdown of ecdysterone differs considerably between species, generating different metabolites.
Ecdysterone is commercially available in a variety of forms, including standardized powdered plant extracts (most commonly from Rhaponticum carthamoides, Cyanotis arachnoidea, or spinach), capsules, and tablets. Commercially available dietary supplements are labeled as containing extracts of Rhaponticum carthamoides, Cyanotis arachnoidea, Ajuga turkestanica, or ecdysteroids.
The following doses appear in the peer-reviewed research:
After ingestion of a low-dose supplement, the parent compound and metabolite were detectable in urine for 70 and 48 hours respectively, while following a higher dose they were detectable for 96 and 48 hours.
In short-term human clinical trials, ecdysterone has demonstrated a favorable safety profile compared to prohibited anabolic agents. A 10-week study in young men found that daily supplementation did not result in significant increases in biomarkers for liver or kidney toxicity. Participants in these controlled settings did not report typical hormonal side effects, such as changes in libido or mood, often seen with traditional steroids.
The most frequently reported adverse effect is mild gastrointestinal distress, including nausea or an upset stomach. This reaction is usually transient and dose-dependent, often resolving as the body adjusts to the supplement.
Ecdysterone does not appear to possess any severe side effects across the reviewed literature, and these data suggest that ecdysterone supplementation is safe.
The long-term safety of ecdysteroid supplementation remains undetermined due to the limited duration of current human studies. A significant concern arises from mechanistic animal research suggesting potential kidney damage over time. The pharmaceutical candidate BIO101 previously demonstrated good toxicology profiles in rat and dog, providing some additional preclinical safety data.
The World Anti-Doping Agency (WADA) added ecdysterone to its Monitoring List in 2020 due to its demonstrated anabolic potency. This action signifies that the substance is being closely tracked to determine if it should be moved to the Prohibited List. Analysis of urines from athletes (n = 1,000) confirmed four positives for 20-hydroxyecdysone, suggesting a prevalence of use of 0.4%. Prevalence of its use by elite athletes was relatively low, however, this needs to be confirmed in other populations.
Supplementation with ecdysterone by professional athletes has raised some concerns about its safety and quality, leading to its inclusion in the World Anti-Doping Agency monitoring program.
Research consistently identifies a serious problem with commercial supplement quality. It was found that most commercially tested products do not meet the desired quality and safety standard concerning the correspondence of their actual ecdysterone content with the value reported on the labeling. A validated method was successfully applied to 12 different dietary supplements labelled to contain ecdysterone, showing an actual content generally much lower than the labelled one.
In one comprehensive analysis, in all cases the measured ecdysterone content was much lower than labelled, and 20% of the samples contained a prohibited substance. The concentration of ecdysterone and contaminations varied randomly from batch to batch.
Independent testing frequently reveals that the actual amount of ecdysterone in commercial products is far lower than the quantity declared on the label, or that the product is contaminated. This lack of purity and standardization means consumers may not be taking the intended substance or dose, introducing unpredictable safety risks. Contamination with undisclosed and prohibited substances, including actual anabolic steroids, is a serious concern for athletes.
Because ecdysterone's mechanism of action involves ERβ rather than the androgen receptor, it does not suppress endogenous testosterone production via the classical hypothalamic-pituitary-gonadal axis. The 10-week Isenmann study found no adverse hormonal signal on the safety biomarkers measured. Nevertheless, the precise molecular mechanisms underlying ecdysterone's biological activity remain poorly characterized, meaning potential interactions with sex steroid signalling pathways require continued study. No significant sex-specific differences were observed for ecdysterone and 14-deoxy-ecdysterone excretion, while for 14-deoxy-poststerone, a significant difference between female and male was observed.
Health conditions that Ecdysterone may help support.
Ecdysterone (beta-ecdysterone, 20-hydroxyecdysone) is a phytoecdysteroid studied for anabolic and ergogenic effects. A 2019 double-blind RCT found significant improvements in muscle mass and strength with ecdysterone supplementation. WADA has considered banning it. Evidence suggests it may act via estrogen receptor beta to stimulate muscle protein synthesis.
Ecdysterone (20-hydroxyecdysone) is the most studied phytoecdysteroid for physical performance. A 2019 double-blind RCT found it significantly improved muscle mass and strength in resistance-trained men. It activates estrogen receptor beta and mTOR signaling to enhance protein synthesis, supporting both muscle endurance and stamina. WADA monitored it for potential performance-enhancing classification.
Body systems that Ecdysterone may help support.
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