Turkesterone
Also known as: Ajuga turkestanica extract, Phytoecdysteroid
Lower numbers = closer to natural. Higher numbers = more enhanced.
Why this rating?
A plant-derived ecdysteroid (most associated with Ajuga turkestanica) marketed aggressively as a "natural anabolic." Human evidence remains almost nonexistent: the first published human trial (Harris et al. 2024, a small acute single-dose crossover study, n=11) tested 1000mg and 2000mg doses and found no significant effect on serum IGF-1, resting metabolic rate, or substrate oxidation. Turkesterone’s pharmacokinetics and bioavailability in humans are still not formally established. It is structurally a steroid but is not an androgen: it does not bind the androgen receptor, does not aromatize, and does not suppress natural testosterone, so no PCT is involved. Rated 1 as an unproven, non-hormonal supplement.
Overview
A phytoecdysteroid (a subclass of ecdysteroids: steroidal compounds structurally related to cholesterol) found in plants such as Ajuga turkestanica, Vitex species and wheat. Heavily marketed as a natural muscle-building supplement, often with bigger claims than the better-studied ecdysterone. Human trial data specific to turkesterone is still minimal, the first published human trial (2024) tested only acute (single-dose) administration and found no significant anabolic signal.
Purpose & Use Cases
Claimed Muscle Building
Marketed as a non-hormonal anabolic to increase muscle mass and strength, a claim not backed by human trials.
Claimed Recovery
Promoted for recovery and protein synthesis based on cell/animal signalling data, not human outcomes.
Benefits
- Marketed as a non-hormonal "natural anabolic" (human evidence essentially absent)
- Does not bind the androgen receptor, aromatize, or suppress natural testosterone
- No PCT required
Good to Know
Human trial evidence is still almost nonexistent
Turkesterone is marketed as a natural anabolic, but until 2024 there were zero published human trials on it specifically, the anabolic story rested entirely on cell/animal signalling research (PI3K/AKT). The first human trial (Harris et al. 2024, n=11, acute single-dose crossover) found no significant effect on IGF-1, resting metabolism, or hypertrophy-relevant markers after single 1000mg or 2000mg doses, though it only tested acute dosing, not a full training cycle. Much of the hype is still extrapolated from the (also weak and disputed) ecdysterone literature.
A steroid by structure, but not an androgen
Ecdysteroids like turkesterone are steroidal in shape but do not bind the human androgen receptor, do not aromatize to estrogen, and do not shut down natural testosterone. That is why no PCT is needed, and also why it is not comparable to actual anabolic steroids or SARMs.
Not the same as ecdysterone
Turkesterone and ecdysterone are related ecdysteroids often conflated in marketing. Even ecdysterone, which has at least one human study, is disputed; turkesterone specifically has less than that.
Dosage Guidelines
| Experience Level | Dosage Range |
|---|---|
| Beginner | 500 – 1000 mg/day |
| Intermediate | 1000 – 1000 mg/day |
| Advanced | 1000 – 2000 mg/day |
These ranges reflect what supplement brands market, commonly as a "10% Ajuga turkestanica" extract. They are NOT clinically validated for muscle-building outcomes. Per the 2024 Harris et al. human trial, most manufacturers recommend around 1000mg/day and advise not exceeding 2000mg/day; that study used single acute doses of 1000mg and 2000mg and found no significant effect on IGF-1 or metabolic markers, though both doses were well tolerated with no cardiovascular or GI issues over the ~24h testing window. Turkesterone’s pharmacokinetics and bioavailability in humans remain otherwise unestablished. Product quality/label accuracy in this category is frequently poor.
Side Effects
Unknown long-term profile
uncommonLong-term human safety data remains essentially absent. The only published human trial (2024, single acute doses up to 2000mg) found no significant cardiovascular or GI issues, but that only covers one dose over ~24 hours, not sustained daily use. Users anecdotally report occasional mild GI upset, but nothing is well characterised over weeks/months.
Recognise the data gap; avoid megadosing.
Sourcing / purity risk
commonA poorly regulated, hype-driven supplement: actual turkesterone content and purity vary widely and products may be under-dosed or adulterated.
Buy third-party-tested product with a certificate of analysis; be sceptical of marketing claims.
General Mitigation Strategies
The honest position is that turkesterone’s human safety and efficacy are essentially unstudied. Treat marketing claims with scepticism, use third-party-tested product, and do not assume "natural" means proven or safe.
Post Cycle Therapy (PCT)
Not an androgen and does not suppress the HPTA. No PCT required.
How It Works
Turkesterone has a polyhydroxylated steroid structure (cyclopentanoperhydrophenanthrene skeleton) resembling cholesterol-derived steroids. It is under laboratory research to determine whether it has anabolic effects through activation of the phosphoinositide 3-kinase (PI3K) and AKT signalling pathways. Importantly, humans do not have the ecdysone receptor that these compounds act on in insects, and turkesterone does NOT act as an androgen (no androgen-receptor binding, no aromatization, no HPTA suppression). The proposed anabolic mechanism is non-hormonal and, in humans, unproven, a 2024 acute-dose human trial (Harris et al.) found no significant change in serum IGF-1, resting metabolic rate, or fat/carbohydrate oxidation after single 1000mg or 2000mg doses, though it was well tolerated with no reported cardiovascular or GI side effects.
Fundamentals
Reference on the practices relevant to Turkesterone: how they are done and where they go wrong. Not a recommendation to use it.
WADA Status
Turkesterone itself is not listed on the WADA Prohibited List. Note that the related ecdysteroid ecdysterone has been placed on WADA’s Monitoring Program (not prohibited). Turkesterone is not, but the ecdysteroid class is being watched.