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Equipoise

Boldenone Undecylenate · EQ

Equipoise (boldenone undecylenate, "EQ") is a long-acting injectable anabolic-androgenic steroid (AAS) originally developed and marketed for veterinary use (chiefly horses); it has no approved human medical indication. It is a 17-beta esterified derivative of 1-dehydrotestosterone used non-medically to increase muscle mass. Because it is not 17-alpha-alkylated, it is thought to carry lower direct liver toxicity than oral AAS, but this must not be read as "safe": the primary human data are limited to forensic/autopsy case reports and small observational bodybuilder studies, and these plus animal models link boldenone (usually alongside other AAS) to dilated cardiomyopathy and heart failure, adverse lipid changes, kidney structural change and rising creatinine, suppression of the body's own testosterone/FSH, and multi-organ oxidative damage in rodents. No randomized human trials exist. The main risks are cardiac (heart-muscle dysfunction, sudden cardiac death in polypharmacy), suppression of natural hormone production, kidney strain, and estrogen-related effects from aromatization. This is educational information only, not medical advice, and does not create a doctor-patient relationship; these substances carry serious risks and any use warrants a physician and regular bloodwork. 21+ only.

Clinical readoutAAS · injectable-aas
Hepatic strainModerate
CardiovascularHigh
HPTA suppressionHigh
Half-life
Not formally esta…
Route
Intramuscular injection…
Evidence
C
Active
Long-acting depot
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not formally established in humans. The undecylenate ester creates a slow-release intramuscular oil depot with a prolonged duration of action; secondary sources commonly cite a multi-day to roughly two-week release window, but this is inferred from the ester and dosing intervals rather than from validated human pharmacokinetic studies. Boldenone and its metabolites can remain detectable in urine and hair for weeks to months.
Pharmacology

Mechanism of action

Boldenone is a synthetic anabolic-androgenic steroid, structurally 1-dehydrotestosterone (testosterone with an added double bond at the 1,2 position). Like other AAS it binds and activates the androgen receptor, promoting muscle protein synthesis and nitrogen retention. Boldenone is aromatizable, so it can be converted to estrogenic metabolites, giving it estrogen-related side-effect potential (a mechanistic/structural inference; robust human quantification is lacking). In non-medical products it is supplied as the undecylenate ester (boldenone undecylenate); the long undecylenate side-chain makes the molecule oil-soluble for a slow-release intramuscular depot, and tissue esterases cleave the ester to release active boldenone. Boldenone can also be produced endogenously at low levels in humans, which complicates interpretation of urine testing. In animal models the organ toxicity appears driven substantially by oxidative stress (increased reactive oxygen species via NADPH oxidase, lipid peroxidation) and inflammatory signaling.
Kinetics

Pharmacokinetics

Half-life

Not formally established in humans. The undecylenate ester creates a slow-release intramuscular oil depot with a prolonged duration of action; secondary sources commonly cite a multi-day to roughly two-week release window, but this is inferred from the ester and dosing intervals rather than from validated human pharmacokinetic studies. Boldenone and its metabolites can remain detectable in urine and hair for weeks to months.

Active duration

Long-acting depot; active over days to weeks after a single injection. Because washout is slow, cardiovascular, hormonal and lab abnormalities may persist for an extended period after the last dose.

Route

Intramuscular injection only (oil-based depot). Not orally active as marketed.

Metabolism & clearance

The undecylenate ester is hydrolyzed by esterases to free boldenone, which undergoes hepatic metabolism; metabolites (e.g., hydroxylated and reduced products) are excreted in urine, giving a long urinary detection window. PK values here are for monitoring and washout reasoning and clinician discussion only, never for evading drug testing.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Increased muscle mass and nitrogen retention via androgen-receptor activation (AAS class effect; no human efficacy trials for boldenone specifically)
  • Androgenic effects expected of an AAS
  • Estrogen-related effects possible because boldenone is aromatizable (e.g., potential for gynecomastia); human quantification is limited
  • In small human observational samples of bodybuilders using boldenone-containing regimens: adverse lipid shifts, rising kidney markers, and suppressed pituitary/gonadal hormones were reported
Safety

Adverse effects by system

Cardiovascular

Most serious documented harm. A human case report attributes fulminant heart failure with severe biventricular dilated cardiomyopathy (LV systolic function ~15%) to testosterone plus boldenone use over ~3 months. Multiple forensic/autopsy case reports describe sudden cardiac death with left ventricular hypertrophy where boldenone was among the AAS detected. Rodent studies show boldenone-induced cardiac oxidative stress, troponin I upregulation, adverse lipid profiles and histopathologic myocardial damage. Causation in humans is confounded by concurrent use of other AAS.

Hepatic

As a non-17-alpha-alkylated injectable, boldenone is expected to be less directly hepatotoxic than oral AAS, but this is not proven safe. A cross-sectional study of bodybuilders using AAS including boldenone found significantly elevated ALT. In rabbits, boldenone undecylenate caused hepatocellular vacuolation and disturbed hepatic architecture. Human liver data specific to boldenone are sparse and confounded by polypharmacy.

Endocrine / HPTA

Suppression of the hypothalamic-pituitary-gonadal axis is expected for any AAS and is supported by human observational data: bodybuilders using AAS including boldenone had significantly lower serum testosterone and FSH and higher prolactin versus controls, consistent with suppressed endogenous hormone production. Because boldenone aromatizes, estrogenic effects are mechanistically plausible.

Reproductive

Consistent with HPTA suppression, human AAS users including boldenone showed reduced testosterone and FSH. In rabbit and rodent models boldenone disrupted the spermatogenic cycle and testicular architecture. Reduced fertility/testicular suppression is therefore a plausible risk; dedicated human fertility outcome data for boldenone are lacking.

Neuropsychiatric

No boldenone-specific human data. AAS as a class are broadly associated with mood disturbance, irritability/aggression and dependence, but this cannot be attributed specifically to boldenone from the available literature.

Renal

An ultrasound study of bodybuilders found regimens containing boldenone undecylenate were associated with significantly increased renal cortical echogenicity, cortical thickness and renal volume, plus higher BUN and creatinine, versus other-AAS and non-user groups. A separate cross-sectional study reported elevated creatinine in AAS users including boldenone. Rabbit histopathology showed glomerular injury and glomerular mass reduction. High protein intake is a confounder in the human data.

Hematologic

No boldenone-specific human hematologic data located. Erythrocytosis (raised hemoglobin/hematocrit) is a recognized AAS class effect; monitoring hematocrit is a prudent general precaution, but a boldenone-specific effect size is not established.

Dermatologic

No boldenone-specific human dermatologic data located. Androgenic skin effects (acne, oily skin) are a general expectation of AAS and are not separately documented for boldenone in primary human sources.

Recovery

HPTA suppression & recovery

Suppression: Expected to be significant, as with any AAS. Human observational data in users of boldenone-containing regimens show reduced testosterone and FSH, consistent with meaningful suppression of endogenous hormone production.

Recovery of the hypothalamic-pituitary-gonadal axis after AAS is variable and individual, and the slow-release depot means suppression can outlast the last injection. Any recovery approach should be directed by an endocrinologist and guided by repeat bloodwork; where pharmacologic support is considered, only single-SERM approaches are within scope here. Dual-SERM protocols are out of scope and not described. Boldenone-specific human recovery data are not available; timelines cannot be promised.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Full lipid panel (HDL, LDL, triglycerides)Echocardiography / cardiac assessment where cardiac symptoms or long-term useBlood pressureRenal function: creatinine, BUN, urine albuminLiver function: ALT, AST, ALP, bilirubinHormonal panel: total testosterone, LH, FSH, estradiol, prolactinComplete blood count with hematocrit/hemoglobin (AAS class erythrocytosis precaution)

Cadence: Baseline before any use, then periodically during use (e.g., every few months) and after discontinuation until values normalize; more frequently if abnormalities or symptoms appear. All monitoring should be performed with and interpreted by a clinician.

Warning signs — seek care
  • Shortness of breath, exertional breathlessness, chest pain, palpitations, leg swelling, or reduced exercise tolerance (possible heart failure/cardiomyopathy - seek emergency care)
  • Fainting or collapse
  • Markedly reduced urine output, swelling, or rising creatinine
  • Jaundice, dark urine, right-upper-quadrant pain, or nausea (liver injury)
  • Breast tissue growth or tenderness (estrogenic effect)
  • Testicular shrinkage or loss of libido (HPTA suppression)
  • Severe mood change, aggression, or suicidal thoughts
Do not use if

Contraindications

  • No approved human use; it is a veterinary agent, so any human use is off-label with no established safety margin
  • Pre-existing cardiovascular disease, cardiomyopathy, heart failure, hypertension, or adverse lipid profile
  • Pre-existing kidney disease or elevated creatinine
  • Pre-existing liver disease or elevated transaminases
  • Hormone-sensitive conditions and prostate disease (androgen exposure)
  • Desire to preserve fertility or endogenous hormone production
  • Pregnancy or breastfeeding
  • Polypharmacy with other AAS or stimulants, which compounds cardiac risk
  • Age under 21 / not skeletally or endocrinologically mature
Combinations

Interaction profile

  • MajorWith another anabolic steroid: Additive cardiovascular strain
  • MajorWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith growth hormone: Additive cardiovascular strain
  • MajorWith another anabolic steroid: Blood / clotting
  • MajorWith a clot-promoting SERM: Blood / clotting
  • ModerateWith an aromatase inhibitor: Hormonal
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Educational information only, not medical advice; boldenone has no approved human use and no randomized human safety data exists.
  • The strongest human signal is cardiac: stop and seek emergency care for breathlessness, chest pain, palpitations, fainting, or leg swelling, which can indicate heart failure or cardiomyopathy.
  • Obtain baseline bloodwork before any use and repeat during and after use, with a clinician interpreting results (lipids, blood pressure, renal and liver panels, hormones, CBC).
  • Because it is a slow-release depot, harms and hormonal suppression can persist for weeks after the last dose; do not assume rapid recovery.
  • Combining boldenone with other AAS or stimulants compounds cardiovascular risk; most fatal case reports involved polypharmacy.
  • HPTA recovery is variable; any recovery plan should be directed by an endocrinologist and monitored with bloodwork. Only single-SERM approaches are in scope; dual-SERM protocols are not.
  • Seek prompt medical care for jaundice, dark urine, reduced urine output, breast tissue growth, or severe mood changes.
  • None of this is dosing guidance or a protocol; any use should be discussed with a qualified physician.
Evidence

Citations (10)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Testosterone plus boldenone use over ~3 months was attributed as the cause of fulminant heart failure with severe biventricular dilated cardiomyopathy (LV systolic function ~15%) in a weightlifter.

    Case reportAnabolic Androgenic Steroid Use as a Cause of Fulminant Heart Failure.PMID 30205989 ↗

  2. 02

    Regimens containing boldenone undecylenate in bodybuilders were associated with significantly increased renal cortical echogenicity, cortical thickness and renal volume and higher BUN and creatinine versus other groups.

    CohortEvaluation of anabolic steroid induced renal damage with sonography in bodybuilders.PMID 29148625 ↗

  3. 03

    Bodybuilders using AAS including boldenone had significantly lower testosterone and FSH, higher prolactin, elevated ALT, and elevated creatinine compared with non-using controls.

    CohortA hormonal side effect of anabolic steroids among a sample of Baghdad male bodybuilders.PMID 38945388 ↗

  4. 04

    A man died after self-injecting boldenone undecylenate; the paper documents postmortem boldenone concentrations, notes low-level endogenous boldenone in non-users, and states AAS abuse is associated with acute myocardial infarction, arrhythmia and sudden death.

    Case reportDetermination of boldenone in postmortem specimens including blood and urine samples using LC-MS/MS.PMID 30851513 ↗

  5. 05

    Sudden death in an AAS user with boldenone among the steroids detected; long-term AAS abuse is described as causing cardiac, hepatic and renal disease.

    Case reportThe Power of Keratinous Matrices (Head Hair, Body Hair and Nail Clippings) Analysis in a Case of Death Involving Anabolic Agents.PMID 36516229 ↗

  6. 06

    Sudden cardiac death in a former weightlifter with repetitive AAS abuse including boldenone detected in hair.

    Case reportIn a Case of Death Involving Steroids, Hair Testing is More Informative than Blood or Urine Testing.PMID 33991187 ↗

  7. 07

    Boldenone administration in rats caused myocardial oxidative stress, cardiac troponin I upregulation, adverse lipid profile changes and histopathologic cardiac damage.

    PreclinicalAssessment of inflammatory cytokines induced oxidative stress signalling, and troponin I gene dysregulation in cardiac tissue associated with chronic administration of boldenone and tramadol, alone or in combination.PMID 36932833 ↗

  8. 08

    Boldenone undecylenate induced cardiac toxicity in rats via increased reactive oxygen species and NADPH oxidase (NOX2/NOX4) expression.

    PreclinicalGrape Seed Proanthocyanidin Ameliorates Cardiac Toxicity Induced by Boldenone Undecylenate through Inhibition of NADPH Oxidase and Reduction in the Expression of NOX2 and NOX4.PMID 30116498 ↗

  9. 09

    Boldenone undecylenate in rabbits caused hepatocellular vacuolation, glomerular injury/reduced glomerular mass, disrupted spermatogenesis, and cardiac hypertrophy.

    PreclinicalHistopathological alterations after a growth promoter boldenone injection in rabbits.PMID 24097356 ↗

  10. 10

    Review of animal androgen studies including boldenone reports adverse effects on heart, kidney, liver and reproductive systems with variable and sometimes irreversible organ damage.

    ReviewExperimental studies on androgen administration in animal models: current and future perspectives.PMID 35943186 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice