IngredientsTurkesterone is a naturally occurring phytoecdysteroid, a subclass of ecdysteroids, which are steroidal compounds structurally related to cholesterol. Its systematic IUPAC name is (2S,3R,5R,9R,10R,11R,13R,14S,17S)-2,3,11,14-tetrahydroxy-10,13-dimethyl-17-[(2R,3R)-2,3,6-trihydroxy-6-methylheptan-2-yl]-2,3,4,5,9,11,12,15,16,17-decahydro-1H-cyclopenta[a]phenanthren-6-one, and the compound is also described under the synonym (20R,22R)-2β,3β,11α,14α,20,22,25-heptahydroxy-5β-cholest-7-en-6-one. Its CAS Registry Number is 41451-87-0, its molecular formula is C₂₇H₄₄O₈, and it possesses an 11α-hydroxyl group that distinguishes it as a structural analogue of the insect steroid hormone 20-hydroxyecdysone. This C11 hydroxylation is a critical structural feature that influences receptor interaction and biological activity profiles.
Ecdysteroids are a class of invertebrate steroid hormones, first found in insects, in which they regulate activities such as molting, development, and reproduction, including the critical metamorphic phases in arthropods. Ecdysteroids are classified into three main groups based on their natural origin, including phytoecdysteroids (PEs), zooecdysteroids, and mycoecdysteroids. Phytoecdysteroids are a class of bioactive molecules produced by plants as a defense against herbivorous insects. Turkesterone has a polyhydroxylated structure with a cyclopentanoperhydrophenanthrene skeleton, resembling cholesterol-derived steroids. Its basic physicochemical properties include a molecular weight of 496.63 g/mol and limited aqueous solubility — it is practically insoluble in water, but soluble in ethanol and methanol.
Turkesterone is found in diverse plants, including Ajuga turkestanica, various Vitex species, Triticum aestivum, Cyanotis arachnoidea, and Rhaponticum acaule. The naturally occurring compounds ecdysterone and turkesterone are also present in plants including Rhaponticum carthamoides Willd. (Iljin), Spinacia oleracea L., and Chenopodium quinoa Willd. The most commercially significant botanical source is Ajuga turkestanica. Ajuga turkestanica is a perennial herb and member of the mint family Lamiaceae; there are over 300 species of the genus Ajuga found throughout Europe, Asia, Africa, Australia, and North America, and A. turkestanica is indigenous to Uzbekistan. The species is native to the Pamir-Alay mountain ranges of Central Asia, notably within Tajikistan, and grows in rocky clay conditions up to elevations of approximately 2,500 m (8,200 ft). It is a perennial herbaceous plant reaching heights between 40 and 60 cm.
A. turkestanica reportedly contains several phytoecdysteroids — including turkesterone, 20-hydroxyecdysone, cyasterone, cyasterone 22-acetate, ajugalactone, ajugasterone B, α-ecdysone, and ecdysone 2,3-monoacetonide — as well as the iridoids harpagide and related compounds. In R. carthamoides roots, a wide range of chemical classes has been found, including steroids (particularly ecdysteroids), flavonoids, lignans, and phenolic compounds. An examination of the phytoecdysteroid composition of R. carthamoides revealed the extraction of 20-hydroxyecdysone, inokosterone, leuzeasterone, polypodine B, rhapisterone, makisterone, carthamoleusterone, turkesterone, and their derivatives from its underground parts.
In the dietary supplement market, turkesterone is predominantly sold as a standardized extract derived from Ajuga turkestanica. The most common sources of ecdysterone and turkesterone in dietary supplements are plants such as Cyanotis arachnoidea, A. turkestanica, and R. carthamoides. Extracts are most commonly standardized to a stated percentage of turkesterone content — preparations at 10% standardization are frequently cited — and are delivered in encapsulated form. Turkesterone is a large, polar molecule with poor aqueous solubility and limited intestinal permeability; without delivery system enhancement, oral bioavailability is very low. Hydroxypropyl-β-cyclodextrin (HPβCD) complexation is one approach explored to address this limitation, as HPβCD forms an inclusion complex with turkesterone, potentially improving aqueous solubility and oral bioavailability. Cyclodextrins can massively improve the solubility of ecdysteroids — in some research, up to 100-fold — which increases the odds that turkesterone reaches circulation in meaningful amounts.
Ajuga turkestanica, a perennial herb native to Central Asia, has a rich tradition of medicinal use dating back centuries. Revered in traditional Uzbek and Tajik herbal medicine, A. turkestanica was prized for its ability to restore strength and vitality, especially after illness or intense physical activity. Folk healers often prescribed infusions or decoctions made from its aerial parts to aid in the recuperation of warriors and laborers, attributing to it rejuvenating properties for both body and spirit.
It has been used in traditional medicine in Central Asia for centuries to treat a range of conditions, such as inflammation, muscle pain, gut, heart, and respiratory issues, and is prized as a general tonic and for its stress-relieving and antioxidant properties. Its extracts were commonly used to address fatigue, support muscle recovery, and promote general wellness, and some records suggest it was also used to soothe digestive complaints and bolster immune resilience.
Turkesterone was first isolated in 1975 by Russian scientists, and gained attention in the 1970s and 1980s when Russian athletes were suspected of using it to enhance their performance. Much of the early experimental pharmacology was conducted within the Soviet research tradition, examining phytoecdysteroids from Central Asian flora as potential anabolic and adaptogenic agents. This body of work, published primarily in Russian-language pharmaceutical and medical chemistry journals, established foundational data on ecdysteroid effects on protein metabolism in animal models, though formal translation and integration into the Western literature occurred much later.
It is important to note that although A. turkestanica, alongside many other Ajuga species, is claimed to have uses in folk medicine, there is no clinical evidence that A. turkestanica compounds have effects as a therapeutic in humans.
The phytochemical profile of Ajuga turkestanica is dominated by ecdysteroids, of which turkesterone is the principal and most characterized compound. HPLC chromatographic analysis has confirmed the identities of phytoecdysteroids present in A. turkestanica extracts, including turkesterone, 20-hydroxyecdysone (20E), cyasterone, ajugasterone, ajugalactone, and cyasterone 22-acetate. Ajuga turkestanica is a wild plant native to Uzbekistan and other regions of Central Asia and contains an array of bioactive phytochemicals, in particular phytoecdysteroids; these phytoecdysteroids are plant-produced analogues of ecdysteroids (insect molting hormones that control cell proliferation, growth, and development), and the phytoecdysteroids from A. turkestanica are reported to have anabolic, analgesic, anti-inflammatory, antihypertensive, antioxidant, antibacterial, and hepatoprotective properties.
Turkesterone is a phytoecdysteroid possessing an 11α-hydroxyl group, and it is an analogue of the insect steroid hormone 20-hydroxyecdysone. The structural distinction between turkesterone and 20-hydroxyecdysone — its closest chemical relative — resides in this additional 11α-hydroxyl group. The first ecdysteroid, ecdysone, was isolated from silkworm pupae by Butenandt and Karlson in 1954, and its structure was elucidated in 1965; nowadays, over 550 ecdysteroids are known. They possess a tetrahydroxylated four-ring structure, a cyclopentanoperhydrophenanthrene skeleton consisting of 27–30 carbon atoms with a β-side chain at C17, originating from cholesterol or alternative sterols.
A defining characteristic that separates turkesterone from synthetic anabolic-androgenic steroids is its apparent lack of activity at the androgen receptor. Animal research demonstrated that turkesterone's latent anabolic effects were comparable to those of traditional androgenic anabolic steroids in terms of acute muscle protein synthesis (MPS) through increased muscle weight and total protein level. Although AAS-mediated anabolic effects are facilitated through androgen receptor activation and subsequent nuclear translocation, phytoecdysteroid mechanisms of action are not fully understood; they are currently believed to impact signal transduction pathways through molecules binding to various receptor interactions. From a biochemical perspective, turkesterone is structurally similar to insect molting hormones (ecdysteroids), but in humans, it differs from androgens or synthetic anabolic steroids, with proposed mechanisms involving signaling pathways such as PI3K/Akt/mTOR rather than direct binding to classical androgen receptors.
Muscle protein synthesis and muscle protein breakdown are allosterically controlled by the phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway, which is a predominant mediator of load-induced skeletal muscle hypertrophy. Turkesterone is postulated to have a signaling effect via membrane-bound estrogen receptor beta (ERβ) binding and subsequent activation of the PI3K/Akt/mTORC1 pathway. Turkesterone is under laboratory research to determine if it has anabolic effects through the activation of the phosphoinositide 3-kinase and AKT signaling pathways.
An in vitro study reported that turkesterone may augment this postulated anabolic environment through increased circulating IGF-1 concentrations and reducing myostatin gene expression. An investigation in aged rats supplemented orally with turkesterone observed increased protein synthesis, cross-sectional skeletal muscle area, and mitochondrial biogenesis. These findings are derived from preclinical models; direct confirmation in humans is lacking (see Section 6).
Turkesterone, isolated from Ajuga turkestanica, is a potent ecdysteroid and acts as an ecdysteroid receptor (EcR) agonist in some insect systems. Whether a functional mammalian ecdysteroid receptor homolog exists and mediates the reported effects in humans remains an active area of investigation. Mammalian ecdysteroid receptors are an area of ongoing research; the evidence suggests ecdysteroids may interact with nuclear receptors — possibly ERRγ (estrogen-related receptor gamma) — that activate anabolic gene expression programs through PI3K/Akt/mTOR without requiring androgen receptor engagement.
Protein biosynthesis in liver tissue, both in vivo and in vitro, was enhanced following the administration of phytoecdysterone or turkesterone (0.5 mg/100 g) and the anabolic steroid compound nerobol (1 mg/100 g) to mice in early Soviet-era pharmacological studies. Previous ecdysteroid QSAR and molecular modelling studies predicted that the cavity of the ligand binding domain of the ecdysteroid receptor would possess space in the vicinity of C-11/C-12 of the ecdysteroid; a series of turkesterone 11α-acyl derivatives have been synthesized to explore this possibility.
Researchers believe turkesterone may influence muscle growth through the PI3K/Akt/mTOR signalling pathway, which regulates protein synthesis and cell growth. In vitro experiments suggest turkesterone might upregulate insulin-like growth factor-1 (IGF-1) and reduce myostatin, a protein that inhibits muscle growth — but these findings are preliminary. Studies in castrated rats found that turkesterone supplementation increased muscle mass and total protein content, and similar experiments on cultured muscle cells showed improved protein synthesis rates; while encouraging, these results do not guarantee the same effects in humans.
In a rodent study, treatment with 50 mg/kg of turkesterone significantly increased grip strength, muscle fiber diameter, and force without the need for resistance training. Another investigation reported that supplementing for as little as 5 days was able to elicit similar results in muscle mass in young mice and rats.
Studies on how phytoecdysteroids alter myostatin, IGF-1, and lipid and carbohydrate metabolism are almost entirely based on isolated muscle cell cultures or animal models; translating these inferences to humans may not adequately represent the beneficial effects of turkesterone supplementation.
The human evidence base for turkesterone specifically is very limited and has, as of mid-2026, consistently failed to demonstrate statistically significant benefits.
Antonio et al. (randomized, double-blind, placebo-controlled trial; 2024): This study examined the effects of turkesterone supplementation among a cohort of healthy young men and women; thirty-one active individuals (14 male, 17 female) volunteered for this randomized, double-blind, placebo-controlled trial. Daily supplementation with 500 mg of turkesterone for four weeks did not produce any significant changes in lean body mass, fat mass, or overall body mass compared to the placebo group. There were no significant differences pre versus post for the turkesterone group across body mass, lean body mass, fat mass, and body fat percentage.
Harris et al. (preliminary investigation; Baylor University/Muscles, 2024): This study investigated whether turkesterone enhances IGF-1 and resting metabolic rate (RMR); eleven apparently healthy males (mean age 23.3 ± 2.2 years) volunteered, with samples collected pre-, 3 hours post-, and 24 hours post-ingestion. Doses of 1000 mg and 2000 mg of turkesterone were tested. Subsequent analyses failed to reveal any significant main condition, time, or interaction main effects for serum IGF-1, RMR, lipid, and carbohydrate metabolism (p > 0.05), although non-significant serum IGF-1 concentrations increased with both turkesterone conditions and remained elevated compared with placebo. Acute supplementation did not adversely impact resting heart rate, blood pressure, or subjective gastrointestinal tolerability; the authors concluded that doses up to 2000 mg appear well tolerated with acute consumption.
A second short-term randomized, double-blind trial assessing a turkesterone-containing product over 4 weeks, tracking body composition, handgrip strength, mood, and sleep, similarly found no significant differences between treatment and placebo groups across any of those measures. The most direct turkesterone supplementation studies available are short (4 weeks) and generally show no meaningful advantage versus placebo.
Although these data fail to fully support turkesterone as a potent anabolic supplement, the authors note the findings are foundational to persistent future inquiry.
Because turkesterone-specific human RCTs are scarce, some researchers draw on data for its close structural relative, 20-hydroxyecdysone (ecdysterone). A WADA-commissioned study (Isenmann et al., 2019, published in Archives of Toxicology) found that ecdysterone supplementation in resistance-trained men produced significant increases in muscle mass compared to placebo, which prompted WADA to commission a broader review of ecdysteroids. These ecdysterone data cannot be directly extrapolated to turkesterone given the distinct structural and possible bioavailability differences; the two should be treated as separate compounds from an evidence standpoint.
The evidence for turkesterone's effects on muscle mass and athletic performance in humans is currently weak. Available human RCTs are small in sample size, short in duration (4 weeks), and have produced null results for body composition endpoints. Mechanistic and animal data provide a biological rationale but have not translated to demonstrated human benefit in controlled trials. Even if turkesterone has anabolic effects in vitro or in animal studies, it may not be effectively absorbed or utilized by the human body, and the bioavailability of turkesterone in humans is unclear.
A comparative study of multiple phytoecdysteroids identified ecdysterone and turkesterone as the most active compounds, producing a pronounced hypoglycemic effect in rats with hyperglycemia induced by glucose, adrenalin, and alloxan; the study explicitly ranks it among the top two most potent compounds from a panel that included alpha-ecdysone, 2-deoxy-alpha-ecdysone, 2-deoxyecdysterone, integristerone A, and 22-acetylcyasterone. A 2012 medical review reported that turkesterone has a "pronounced hypoglycemic effect" in animal studies, suggesting it may have favorable effects on blood sugar in individuals with diabetes or pre-diabetes. These data are entirely from animal models.
In research examining anti-adipogenic effects, HPTLC analysis confirmed the presence of 20-hydroxyecdysone, ponasterone A, and turkesterone in R. carthamoides extract; the results of the study demonstrated that the extract and 20E exhibit anti-obesity potential by reducing adipogenesis and promoting lipolysis in human adipocytes, while turkesterone showed only anti-adipogenic (reduced adipogenesis) properties without the lipolytic effect. This in vitro finding highlights a potentially divergent metabolic profile between turkesterone and ecdysterone. No human clinical trials have examined turkesterone's metabolic effects.
The phytoecdysteroids from A. turkestanica are reported to have anabolic, analgesic, anti-inflammatory, antihypertensive, antioxidant, antibacterial, and hepatoprotective properties based on preclinical and in vitro research. The therapeutic potential of phytoecdysteroid-rich extracts extends beyond sports nutrition, with promising applications in treating chronic fatigue, cardiovascular diseases, and neurodegenerative disorders as discussed in reviews of the broader ecdysteroid literature. These are described as promising applications requiring further investigation, not established clinical outcomes.
Turkesterone most commonly comes in capsule form. Extracts are standardized to varying concentrations; 10% standardization is one commonly cited specification in commercial products.
The following dosages have been used or reported in identified studies and reviews:
No established therapeutic dose has been validated in adequately powered human clinical trials. There is no established "typical dose" due to variations between how different turkesterone supplements are created, including differences in extract concentration and delivery form.
Studies in both mice and rabbits demonstrated both 20-hydroxyecdysone and turkesterone to exhibit very low acute toxicity when administered orally (LDâ‚…â‚€ > 6 g/kg). Furthermore, it was revealed that there were no adverse consequences such as atrophy of the testes or enlargement of other tissues commonly associated with anabolic steroid use.
A medical review published in the Archives of Toxicology journal examined the safety of ecdysteroids, a class of compounds that includes turkesterone; the researchers concluded that no toxic effects were noted after testing liver and kidney biomarkers. However, this review did not examine turkesterone specifically — only chemically similar compounds.
Acute supplementation (up to 2000 mg) in a small human study did not adversely impact resting heart rate, blood pressure, or subjective gastrointestinal tolerability; the authors concluded that doses up to 2000 mg are well tolerated, posing little-to-no risk to general population consumption with acute consumption. Long-term human safety data are absent.
Turkesterone is a naturally occurring plant steroid described as having no reported adverse side effects compared with traditional anabolic androgenic steroids. However, its potential enhancement of muscle protein synthesis and thermogenesis remains undescribed despite widespread consumption. Anecdotal reports from consumers and some clinical observation protocols have documented nausea as a possible effect when the compound is taken on an empty stomach.
A key safety feature distinguishing turkesterone from synthetic anabolic steroids, based on available preclinical data, is its apparent lack of interaction with the hypothalamic-pituitary-gonadal (HPG) axis. Unlike anabolic steroids, turkesterone does not bind to androgen receptors and does not appear to interfere with the hypothalamic-pituitary-gonadal (HPG) axis. This profile has not been formally confirmed in controlled human pharmacological studies.
The bioavailability of turkesterone is unclear; furthermore, despite turkesterone having a similar structure to other steroids, it may not interact with human androgen receptors in the same way. Its pharmacokinetics, bioavailability, and possible effects in humans remain to be determined. Poor and variable bioavailability means that effective internal exposure may differ substantially from the stated dose on a supplement label, complicating both safety and efficacy assessment.
As of 2025, turkesterone is legal to purchase and use as a dietary supplement in the United States and most other countries, and it is not classified as a controlled substance. Ecdysteroids are not currently prohibited by WADA, but they are on the monitoring list; athletes should stay updated and use third-party tested supplements. Athletes should understand that ecdysteroids are on WADA's monitoring list, meaning they are being tracked and the status could change in the future. A. turkestanica extracts are marketed with the presumption of usefulness as bodybuilding supplements; however, ecdysteroid compounds have no proven anabolic effects on muscle in mammals and no approval as a drug in any country.
Supplement quality is highly variable; many products are under-dosed or poorly standardized, and third-party testing is essential. Because turkesterone lacks a pharmacopoeial monograph and is sold as a dietary supplement (not a regulated drug in most jurisdictions), purity, potency, and actual ecdysteroid content can vary substantially between manufacturers. No government health body (NIH ODS, FDA, EFSA, EMA) has issued a formal monograph or comprehensive safety review specifically for turkesterone as of the date of this article.
Turkesterone presents a well-characterized chemical identity and a theoretically compelling set of proposed mechanisms rooted in ecdysteroid biology. The preclinical evidence — from cell culture and animal models — provides a plausible rationale for effects on muscle protein synthesis, metabolic function, and antioxidant activity. However, the translation of these findings to humans remains unestablished. Muscle gain is not convincingly supported by current short-term human trials, there are no clear improvements in strength or performance in the direct turkesterone trials, and the most direct supplementation studies available are short (4 weeks) and generally show no meaningful advantage versus placebo. Even if turkesterone has anabolic effects in vitro or in animal studies, it may not be effectively absorbed or utilized by the human body, and the bioavailability of turkesterone is unclear. Longer, adequately powered, well-characterized human RCTs examining a range of outcomes and addressing bioavailability are needed before definitive conclusions can be drawn.
Health conditions that Turkesterone may help support.
Turkesterone is an ecdysteroid found in Ajuga turkestanica studied for anabolic and ergogenic effects. It is proposed to stimulate muscle protein synthesis via estrogen receptor beta, similar to ecdysterone. While human RCT evidence is limited, it is among the most discussed phytoecdysteroids for athletic performance.
Turkesterone is a phytoecdysteroid from Ajuga turkestanica with structural similarity to ecdysterone but with proposed higher anabolic potency. Preclinical studies show superior muscle protein synthesis effects compared to ecdysterone. While human RCT data are limited, it is increasingly studied for physical endurance and strength based on phytoecdysteroid mechanisms and traditional Central Asian use.
Body systems that Turkesterone may help support.
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