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BHuman cohort / observational
CardiotoxicNeuropsychiatric

Sustanon 250

Testosterone blend

Sustanon 250 is a brand of injectable testosterone consisting of a blend of four testosterone esters (propionate, phenylpropionate, isocaproate, and decanoate) totaling 250 mg per mL. In legitimate medicine it is a testosterone-replacement product for diagnosed male hypogonadism; it is also widely misused at supraphysiologic doses as an anabolic-androgenic steroid (AAS) to increase muscle mass and strength. Once injected, the mixed esters are hydrolyzed to testosterone, so its biology is simply that of exogenous testosterone delivered as a long-acting depot. The main risks are: (1) marked rise in red-cell mass (hemoglobin/hematocrit) that thickens blood and can raise thrombotic risk; (2) cardiovascular strain — long-term illicit AAS use is associated with impaired heart muscle function and accelerated coronary plaque; (3) shutdown of the body's own testosterone production (HPTA suppression), infertility, and testicular shrinkage that may not fully reverse; (4) mood and aggression changes in a subset of users; and (5) estrogen-related effects such as gynecomastia. It is not medical advice — these are prescription-only substances that require physician supervision and regular bloodwork. This monograph reports doses only as they appear in the literature, attached to their risks, and never as a recommendation.

Clinical readoutAAS · injectable-testosterone
Hepatic strainLow
CardiovascularModerate
HPTA suppressionVery high
Half-life
24 h
Route
Deep intramuscular inje…
Evidence
B
Active
On the order of 2-3 wee…
24 h2 d3 d4 d5 d
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ No single value: the blend combines a short-acting ester (propionate, on the order of ~1 day) with progressively longer-acting esters up to decanoate (long-chain, multi-day), so the long ester dominates terminal elimination. The best available human time-course data for a comparable testosterone-ester mixture come from a study of female-to-male transgender adolescents newly starting testosterone-ester therapy, not adult male AAS/TRT users, so baseline physiology differs; with that caveat, salivary/free testosterone peaked supraphysiologically within days of injection and fell back into the male reference range by about day 9 (PMID 23123742), suggesting an effective composite action on the order of 2-3 weeks per injection. A directly equivalent time-course study in adult men has not been identified.
Pharmacology

Mechanism of action

Sustanon 250 delivers testosterone, an endogenous androgen, as four esters of differing chain length that dissolve the same active molecule into a sustained-release depot. After deep intramuscular injection, serum and tissue esterases cleave the ester bonds to liberate free testosterone. Testosterone binds the androgen receptor in muscle, bone, CNS, and other tissues to drive anabolic and androgenic effects; it is also converted by 5-alpha-reductase to the more potent androgen dihydrotestosterone (DHT) and by aromatase to estradiol, which mediates estrogenic effects such as gynecomastia and also feedback. Exogenous testosterone exerts negative feedback on the hypothalamus and pituitary, suppressing gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone, which shuts down endogenous testicular testosterone production and spermatogenesis. Supraphysiologic androgen exposure additionally stimulates erythropoiesis (raising red-cell mass) and adversely remodels the myocardium and vasculature.
Kinetics

Pharmacokinetics

Half-life

No single value: the blend combines a short-acting ester (propionate, on the order of ~1 day) with progressively longer-acting esters up to decanoate (long-chain, multi-day), so the long ester dominates terminal elimination. The best available human time-course data for a comparable testosterone-ester mixture come from a study of female-to-male transgender adolescents newly starting testosterone-ester therapy, not adult male AAS/TRT users, so baseline physiology differs; with that caveat, salivary/free testosterone peaked supraphysiologically within days of injection and fell back into the male reference range by about day 9 (PMID 23123742), suggesting an effective composite action on the order of 2-3 weeks per injection. A directly equivalent time-course study in adult men has not been identified.

Active duration

On the order of 2-3 weeks of meaningfully elevated testosterone per injection, extrapolated from the adolescent transgender-therapy ester time-course above (PMID 23123742) rather than a study in adult male AAS/TRT users; with 250 mg every 4 weeks, levels in that study fell below the male reference range by the end of the interval, illustrating the peak-and-trough pattern this ester mixture produces. Documented here for washout/monitoring and clinician discussion only, never for evading testing.

Route

Deep intramuscular injection (oil depot).

Metabolism & clearance

Esters are hydrolyzed by esterases to free testosterone; testosterone is metabolized peripherally to DHT (via 5-alpha-reductase) and to estradiol (via aromatase), and cleared mainly by hepatic metabolism to inactive 17-ketosteroids (androsterone, etiocholanolone) with renal excretion of conjugates. Relevant for washout reasoning and lab-timing discussions with a clinician, not for test evasion.

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

Reported effects

Physiological & performance effects

  • Raises serum testosterone into or above the physiologic range, correcting symptoms of true hypogonadism (improved sexual function, energy, and quality of life in hypogonadal men) (PMID 39248210)
  • Increases lean/muscle mass and, at supraphysiologic doses, muscle size and strength — this is the reason for non-medical misuse (context: PMID 10665615)
  • Increases red-cell mass (hemoglobin and hematocrit) (PMID 20525906; PMID 16339333; a larger rise is reported in a different, transgender-hormone-therapy population, PMID 38457996)
  • Suppresses endogenous testosterone production and spermatogenesis, reducing sperm counts to oligo-/azoospermia (PMID 21651568; PMID 26908067)
  • Can elevate manic/aggressive symptom ratings in a subset of users at supraphysiologic doses (PMID 10665615)
Safety

Adverse effects by system

Cardiovascular

Long-term illicit AAS use is associated with reduced left-ventricular systolic and diastolic function and accelerated, dose-dependent coronary atherosclerosis in a cross-sectional cohort of weightlifters (PMID 28533317). Case reports/series link AAS to cardiomyopathy, left-ventricular thrombus, myocardial infarction, and aortic dissection (PMID 35972452; PMID 33083037). Testosterone lowers HDL cholesterol (PMID 20525906). In therapeutic-dose RCTs of hypogonadal men, testosterone therapy was noninferior to placebo for major adverse cardiac events but showed higher rates of atrial fibrillation and pulmonary embolism (PMID 37326322); supraphysiologic misuse is not represented by those trials.

Hepatic

Injectable testosterone esters are not 17-alpha-alkylated, and testosterone-therapy RCT meta-analyses did not identify significant hepatotoxicity as an adverse effect (PMID 20525906); the classic AAS liver injuries (cholestasis, peliosis hepatis, hepatic tumors) are chiefly associated with oral 17-alpha-alkylated steroids rather than injectable testosterone. Direct human data specifically quantifying liver injury from injectable testosterone esters are limited.

Endocrine / HPTA

Exogenous testosterone suppresses the hypothalamic-pituitary-gonadal axis (lowering LH/FSH), shutting down endogenous testosterone production; recovery after cessation is variable and may be incomplete or prolonged (PMID 26908067). Aromatization to estradiol can cause gynecomastia and estrogenic effects (context: PMID 26908067).

Reproductive

Testosterone suppresses spermatogenesis, producing oligozoospermia or azoospermia and impaired fertility, with testicular atrophy; in controlled studies sperm counts recovered to baseline after discontinuation in most men over months, but recovery can be delayed or incomplete (PMID 21651568; PMID 26908067).

Neuropsychiatric

In a randomized controlled trial, supraphysiologic testosterone (up to 600 mg/week) significantly increased manic and aggressive symptom ratings; effects were highly variable, with most men minimally affected but a minority becoming hypomanic (PMID 10665615). Observational data associate AAS use with aggression, though confounded by pre-existing personality traits (PMID 12762541).

Renal

A higher incidence of acute kidney injury was observed in the testosterone group versus placebo in a large therapeutic-dose RCT (PMID 37326322). Direct data on renal effects of supraphysiologic Sustanon use specifically are limited.

Hematologic

Testosterone significantly increases hemoglobin and hematocrit in meta-analyses of male hypogonadal/AAS populations (+0.80 g/dL hemoglobin, +3.18% hematocrit; ~4-fold increased odds of hematocrit >50%), raising blood viscosity and potential thrombotic risk (PMID 20525906; PMID 16339333). A larger hemoglobin/hematocrit rise (+1.48 g/dL, +4.39%) has been reported in a meta-analysis of gender-affirming testosterone therapy in transgender people assigned female at birth (PMID 38457996) — a population with a very different hematologic baseline than adult male AAS users, so that specific magnitude should not be read as an estimate for this monograph's male-use audience, though it is directionally consistent.

Dermatologic

Androgenic skin effects — acne and oily skin — are expected androgen effects; hematocrit-driven facial plethora may occur. Formal quantification specific to Sustanon is limited; androgenic dermatologic effects are consistent with testosterone's androgen-receptor and DHT activity (context: PMID 10665615).

Recovery

HPTA suppression & recovery

Suppression: Marked — exogenous testosterone reliably and strongly suppresses the HPTA (LH/FSH and endogenous testosterone/spermatogenesis)

Recovery of the axis and of spermatogenesis after stopping is variable: many men recover over months, but some experience prolonged or incomplete recovery, and older/longer/heavier use predicts slower recovery (PMID 26908067; PMID 21651568). Any recovery strategy should be individualized and directed by an endocrinologist; where pharmacologic assistance is considered, only single-agent selective estrogen receptor modulator approaches are within scope here, and management belongs with a specialist. Dual-SERM protocols are out of scope. This is not a recommendation to use or to self-manage cessation.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Hematocrit and hemoglobin (baseline and periodically; a leading, predictable adverse effect) (PMID 20525906; PMID 16339333)Total testosterone (and estradiol where clinically indicated)Lipid panel including HDL (PMID 20525906)Prostate-specific antigen (PSA) with digital rectal exam in older men (PMID 16339333)Blood pressureLiver function tests (baseline/periodic, though hepatotoxicity risk is low for injectable esters)Semen analysis if fertility is a concern (PMID 21651568)

Cadence: Baseline before any use, then commonly at ~3 and 6-12 months and at least annually thereafter under a clinician; sooner if symptoms or abnormal results arise. Hematocrit warrants particular vigilance because elevation is frequent (PMID 16339333).

Warning signs — seek care
  • Chest pain, shortness of breath, leg swelling/pain, or signs of stroke — seek emergency care (possible thrombosis, MI, PE, or cardiomyopathy) (PMID 28533317; PMID 35972452)
  • Severe headache, flushing, or visual changes (possible marked hematocrit rise/hyperviscosity) (PMID 20525906)
  • New or worsening mood instability, mania, or aggression (PMID 10665615)
  • Breast tenderness/enlargement (gynecomastia)
  • Testicular shrinkage or new infertility (PMID 26908067)
  • Severe acne or rapid blood-pressure rise
Do not use if

Contraindications

  • Known or suspected prostate cancer or male breast cancer
  • Polycythemia / elevated hematocrit (e.g., hematocrit >50-54%) until corrected
  • Men seeking to preserve fertility (suppresses spermatogenesis)
  • Untreated severe obstructive sleep apnea
  • Poorly controlled heart failure or recent major cardiovascular event
  • Active thrombophilia or prior venous thromboembolism (risk of further raised viscosity/thrombosis)
  • Pregnancy (teratogenic virilization) and women generally, given virilizing effects
  • Hypersensitivity to testosterone esters or the oil vehicle (e.g., arachis/peanut or benzyl components)
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

  • This is educational information, not medical advice, and not an endorsement of use; these substances are prescription-only and carry serious risks. Anyone using or considering them should be under a physician's care with regular bloodwork. 21+ only.
  • Do not use without baseline and ongoing labs: hematocrit/hemoglobin, testosterone, lipids, PSA (older men), blood pressure, and liver panel; rising hematocrit is the most predictable dangerous change (PMID 20525906; PMID 16339333).
  • Stop and seek urgent medical care for chest pain, breathlessness, unilateral leg swelling, sudden severe headache, or stroke-like symptoms — these may signal thrombosis, MI, pulmonary embolism, or cardiomyopathy (PMID 28533317; PMID 35972452).
  • If hematocrit becomes elevated, this must be addressed with a clinician before continuing anything; hyperviscosity raises clotting risk (PMID 38457996).
  • Be aware that suppression of your own testosterone and fertility is expected and may not fully reverse; if fertility matters, discuss it with a specialist before any use and consider sperm evaluation (PMID 26908067; PMID 21651568).
  • Watch for and report mood changes, new aggression, or hypomania — a minority of users are strongly affected (PMID 10665615).
  • Any decision to stop, and any post-cessation recovery plan for the HPTA, should be directed by an endocrinologist; only single-SERM approaches are within scope here and self-management is discouraged.
  • This monograph does not provide sourcing, dosing-to-maximize, or protocol design; dose figures appear only as reported in studies and are always paired with their risks.
Evidence

Citations (13)

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

  1. 01

    In female-to-male transgender adolescents newly starting testosterone-ester mixture therapy (not adult male AAS/TRT users), intramuscular injection produced supraphysiologic testosterone peaks within days that fell into the male reference range by ~day 9 and below range by 4 weeks (PK/washout time-course used here as the best available human ester-blend data; no equivalent study in adult men was identified).

    CohortSalivary testosterone in female-to-male transgender adolescents during treatment with intra-muscular injectable testosterone esters.PMID 23123742 ↗

  2. 02

    In hypogonadal men, testosterone therapy improves sexual function and quality of life; individual-participant-data meta-analysis found no difference versus placebo in cardiovascular/cerebrovascular events.

    Meta-analysisThe effects and safety of testosterone replacement therapy for men with hypogonadism: the TestES evidence synthesis and economic evaluation.PMID 39248210 ↗

  3. 03

    Testosterone therapy was noninferior to placebo for major adverse cardiac events in high-CV-risk hypogonadal men, but showed higher rates of atrial fibrillation, acute kidney injury, and pulmonary embolism (therapeutic doses).

    RCTCardiovascular Safety of Testosterone-Replacement Therapy.PMID 37326322 ↗

  4. 04

    Testosterone significantly increases hemoglobin (+0.80 g/dL) and hematocrit (+3.18%) and decreases HDL cholesterol.

    Meta-analysisClinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysisPMID 20525906 ↗

  5. 05

    Testosterone replacement roughly quadruples the odds of hematocrit >50% and increases prostate events; hematocrit, PSA, and prostate exam should be monitored.

    Meta-analysisAdverse events associated with testosterone replacement in middle-aged and older men: a meta-analysisPMID 16339333 ↗

  6. 06

    In a meta-analysis of gender-affirming hormone therapy with testosterone in transgender people assigned female at birth (a different baseline population than adult male AAS/TRT users), testosterone therapy increased hemoglobin (+1.48 g/dL) and hematocrit (+4.39%), raising blood viscosity.

    Meta-analysisEffects of gender affirming hormone therapy with testosterone on coagulation and hematological parameters in transgender people assigned female at birth: A systematic review and meta-analysis.PMID 38457996 ↗

  7. 07

    Long-term illicit AAS use is associated with reduced LV systolic and diastolic function and dose-dependent accelerated coronary atherosclerosis.

    CohortCardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid UsePMID 28533317 ↗

  8. 08

    AAS use is associated with cardiomyopathy and left-ventricular thrombus, with partial recovery after cessation (case report).

    Case reportFor the love of muscles: a bodybuilder with complicated left ventricular heart failure.PMID 35972452 ↗

  9. 09

    AAS abuse is associated with aortic dissection, myocardial infarction, and cardiomyopathy (case series).

    Case seriesAnabolic Steroid Use and Aortic Dissection in Athletes: A Case Series.PMID 33083037 ↗

  10. 10

    Supraphysiologic testosterone (up to 600 mg/week) significantly increased manic and aggressive symptom ratings in an RCT, with highly variable individual response and a minority becoming hypomanic.

    RCTEffects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized controlled trial.PMID 10665615 ↗

  11. 11

    Supraphysiologic testosterone concentrations in weightlifters were associated with increased aggression, though confounded by pre-existing personality traits.

    CohortMeasures of aggression and mood changes in male weightlifters with and without androgenic anabolic steroid use.PMID 12762541 ↗

  12. 12

    Exogenous testosterone/AAS suppress the HPG axis and spermatogenesis; recovery after cessation is variable and may be incomplete or prolonged.

    ReviewRecovery of spermatogenesis following testosterone replacement therapy or anabolic-androgenic steroid use.PMID 26908067 ↗

  13. 13

    Testosterone alone suppresses spermatogenesis to oligo-/azoospermia, and sperm counts returned to baseline range after discontinuation in controlled study.

    CohortHormonal male contraception in men with normal and subnormal semen parameters.PMID 21651568 ↗

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