Drug Monograph

Testosterone Cypionate

Depo-Testosterone · Azmiro · Generics

Androgen (Testosterone Ester) · Intramuscular injection · Schedule III Controlled Substance
Pharmacokinetic Profile
Half-Life
~8 days (IM)
Metabolism
Hepatic (to DHT, estradiol, 17-keto steroids)
Protein Binding
98% (40% SHBG, ~58% albumin, 2% free)
Bioavailability
IM depot (slow absorption from oil phase)
Excretion
90% urine (conjugates), 6% feces
Clinical Information
Drug Class
Androgen (Testosterone replacement)
Available Doses
100 mg/mL; 200 mg/mL (vials, PFS)
Route
Deep IM (gluteal) only
Renal Adjustment
No specific adjustment; caution with edema
Hepatic Adjustment
Use with caution; monitor LFTs
Pregnancy
Contraindicated (causes fetal virilization)
Lactation
Not recommended
Schedule / Legal Status
Schedule III Controlled Substance
Therapeutic Index
Dose-titrate to mid-normal testosterone
Generic Available
Yes (multiple manufacturers)
Rx

Indications for Testosterone Cypionate

IndicationApproved PopulationTherapy TypeStatus
Primary hypogonadism (congenital or acquired)Males with testicular failure (cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome, orchiectomy, Klinefelter syndrome, toxic damage)Replacement therapyFDA Approved
Hypogonadotropic hypogonadism (congenital or acquired)Males with gonadotropin or LHRH deficiency, or pituitary-hypothalamic injury from tumors, trauma, or radiationReplacement therapyFDA Approved

Testosterone cypionate is one of the most widely prescribed injectable testosterone preparations in the United States for male hypogonadism. The diagnosis must be confirmed by measuring serum testosterone on at least two separate mornings with levels below the normal range (generally <300 ng/dL per the Endocrine Society 2018 guideline). Testosterone cypionate is specifically indicated for conditions with documented deficiency or absence of endogenous testosterone, not for age-related declines in testosterone (“late-onset hypogonadism”), for which safety and efficacy have not been established in the FDA labeling.

Off-Label Uses

Gender-affirming hormone therapy (female-to-male transition): Testosterone cypionate is widely used for masculinizing hormone therapy per Endocrine Society 2017 guidelines. Typical starting doses are 50–100 mg IM every week or 100–200 mg every 2 weeks, titrated to male-range testosterone levels. Evidence quality: High (guideline-supported).

Delayed puberty in males: Used at lower doses (50–200 mg IM every 2–4 weeks) for limited courses to initiate puberty in adolescent boys with constitutional delay. Evidence quality: Moderate (longstanding clinical practice).

Dose

Dosing

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Male hypogonadism — initial replacement100 mg IM every 2 weeks50–400 mg IM every 2–4 weeks400 mg every 2 weeksIndividualize based on clinical response and testosterone levels; the Endocrine Society recommends 75–100 mg/week or 150–200 mg every 2 weeks
Administer deep into gluteal muscle; rotate injection sites
Male hypogonadism — dose titrationMeasure serum testosterone midway between injections (trough) at 3–6 months; target 400–700 ng/dLIf trough level is low, shorten interval or increase dose; if supraphysiologic, reduce dose
Check hematocrit at 3–6 months and then annually (Endocrine Society 2018)
Delayed puberty — male (off-label)50–100 mg IM every 2–4 weeks50–200 mg IM every 2–4 weeks200 mg every 2 weeksShort courses (4–6 months); monitor bone age every 6 months to avoid premature epiphyseal closure
Use lowest effective dose for shortest duration
Gender-affirming therapy (FTM, off-label)50–100 mg IM weekly50–100 mg IM weekly or 100–200 mg every 2 weeks100 mg/weekTitrate to male-range testosterone (320–1000 ng/dL); monitor hematocrit, lipids, liver function
Per Endocrine Society 2017 transgender guideline
Clinical Pearl: Confirming Diagnosis Before Treatment

The FDA label and the Endocrine Society both require that hypogonadism be confirmed by at least two morning serum testosterone measurements below the normal range before initiating therapy. Morning levels are preferred because testosterone follows a circadian rhythm, peaking in the early morning. The Endocrine Society 2018 guideline uses a threshold of 264–300 ng/dL (depending on assay) and recommends measuring total testosterone using a reliable assay (LC-MS/MS preferred). Confirming the diagnosis prevents inappropriate prescribing for non-hypogonadal men with age-related symptoms.

PK

Pharmacology

Mechanism of Action

Testosterone cypionate is a long-acting ester of the endogenous androgen testosterone, formulated in cottonseed oil for intramuscular depot injection. After IM injection, the ester is slowly released from the oil depot and hydrolyzed to free testosterone, which then enters the systemic circulation. Testosterone and its principal active metabolite, dihydrotestosterone (DHT, formed via 5-alpha reductase), bind to the intracellular androgen receptor. The steroid-receptor complex translocates to the nucleus, where it initiates gene transcription responsible for the development and maintenance of male sex characteristics, skeletal muscle mass, bone density, erythropoiesis, and libido. Testosterone also undergoes aromatization to estradiol via the aromatase enzyme, which mediates some of its effects on bone metabolism and contributes to feedback regulation of gonadotropins (LH and FSH) at the hypothalamic-pituitary level.

ADME Profile

ParameterValueClinical Implication
AbsorptionSlow IM depot release from cottonseed oil; Cmax ~758 ng/dL (SD 288.7) after single 200 mg dose; median Tmax ~72 hours (range 24–191 hours)Peak-trough variation is inherent; levels peak within 2–5 days and decline over 2–4 weeks; weekly dosing produces more stable levels than biweekly dosing
Distribution98% bound in plasma: ~40% to SHBG, ~58% to albumin, ~2% free; MW 412.61 DaFree testosterone concentration determines biological activity; SHBG levels (affected by age, obesity, thyroid status, liver disease) alter the free/bound ratio
MetabolismPrimarily hepatic; converted to DHT (5-alpha reductase) and estradiol (aromatase); inactivated to 17-keto steroids; not a 17-alpha-alkylated androgenLower hepatotoxicity risk than oral 17-alpha-alkyl androgens (methyltestosterone); aromatization to estradiol can cause gynecomastia; DHT mediates prostate and hair follicle effects
Eliminationt½ ~8 days (IM); ~90% excreted in urine as glucuronic and sulfuric acid conjugates; ~6% in feces (unconjugated)The 8-day half-life supports dosing every 1–4 weeks depending on desired trough level; longer intervals produce larger peak-trough swings
SE

Side Effects

Adverse reaction data below come from the Azmiro (testosterone cypionate) clinical trial (Study 1, N = 27 hypogonadal men, single-dose), class-effect data from the FDA PI, and the TRAVERSE cardiovascular safety trial (N = 5246, NEJM 2023). Testosterone cypionate shares the adverse effect profile common to all exogenous testosterone formulations.

≥10% Very Common (Azmiro Clinical Trial)
Adverse EffectIncidenceClinical Note
Injection site erythema26%All cases categorized as mild; typically transient; rotate injection sites
1–10% Common (Clinical Trial + Class Effects)
Adverse EffectIncidenceClinical Note
Injection site reaction (other)4%Mild; includes pain, swelling at site
Polycythemia (Hct elevation)Common (class effect)Most clinically important AE of TRT; monitor hematocrit; discontinue if persistently elevated (>54%)
Acne / SeborrheaCommon (class effect)DHT-mediated; dose-dependent; manage with topical treatments; reduce dose if severe
GynecomastiaCommon (class effect)Due to aromatization of testosterone to estradiol; may be dose-related; occasionally persistent
Edema (fluid retention)Common (class effect)Sodium and water retention; monitor in patients with cardiac, renal, or hepatic disease
Mood changes (irritability, anxiety, depression)Common (class effect)Can worsen with supraphysiologic levels or during trough periods; dose adjustment may help
HeadacheCommon (class effect)Usually transient
Male pattern alopeciaCommon (class effect)DHT-mediated; genetic predisposition determines susceptibility
Increased libidoCommon (class effect)Expected pharmacologic effect; may require dose adjustment if excessive
Serious Serious (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Polycythemia / Erythrocytosis (Hct >54%)Up to 20% develop elevated Hct; clinically significant in ~5–10%Months; cumulative effectMonitor hematocrit at baseline, 3–6 months, then annually; withhold if Hct >54%; resume at lower dose if normalized; increased VTE risk
Major adverse cardiovascular events (MACE)TRAVERSE trial: noninferior to placebo (7.0% vs 7.3%; HR 0.96)Variable; studied over mean 33 monthsInform patients of possible CV risk; epidemiologic data remain inconclusive; the TRAVERSE trial showed no increase in MACE but found more atrial fibrillation and PE in the testosterone group
Venous thromboembolism (DVT/PE)Postmarketing reports; TRAVERSE: PE higher in testosterone groupAny time during therapyEvaluate leg pain/swelling or acute dyspnea; discontinue and investigate if VTE suspected; use with caution in patients with thromboembolic history
Spermatogenesis suppression / InfertilityExpected at therapeutic doses; may be irreversibleWeeks to monthsCounsel about fertility impact BEFORE initiating; exogenous testosterone suppresses FSH/LH; consider alternatives (e.g., clomiphene, hCG) if fertility desired
Sleep apnea (new or worsened)Uncommon; higher risk with obesity or chronic lung diseaseWeeks to monthsScreen for OSA symptoms; consider sleep study if symptoms develop; may require dose reduction or discontinuation
Hepatic adverse effects (peliosis hepatis, neoplasms)Rare with injectable esters; primarily associated with oral 17-alpha-alkyl androgensMonths to years of continuous useTestosterone cypionate is NOT a 17-alpha-alkyl androgen and carries lower hepatotoxicity risk; nonetheless, report jaundice or hepatic dysfunction; monitor LFTs
Prostate cancer riskUncertain; TRAVERSE found no increase in prostate eventsN/AContraindicated in known/suspected prostate carcinoma; monitor PSA at baseline, 3–6 months, then annually; evaluate if PSA rises >1.4 ng/mL within 12 months or >4 ng/mL
DC Discontinuation Rates
TRAVERSE Trial (transdermal T, mean 33 months)
61.4% vs 61.7% placebo
Note: TRAVERSE used transdermal gel, not injectable cypionate; high discontinuation rate reflects long follow-up and elderly population with comorbidities
Real-World Injectable TRT
Variable
Top reasons: Injection burden, polycythemia requiring dose hold, mood changes, fertility concerns, cost
Managing Polycythemia — The Most Common Clinically Significant Side Effect

Testosterone stimulates erythropoiesis via erythropoietin and direct effects on bone marrow stem cells. Hematocrit elevation is dose-dependent and the most common reason for dose reduction or withholding. The Endocrine Society recommends withholding testosterone if hematocrit exceeds 54% and resuming at a lower dose once it normalizes. Strategies to reduce polycythemia risk include using lower doses, switching to shorter-acting preparations (e.g., weekly injections to reduce peaks), and considering therapeutic phlebotomy in refractory cases. Polycythemia increases VTE risk, which is why hematocrit monitoring is mandatory throughout therapy.

Int

Drug Interactions

Testosterone cypionate is metabolized by hepatic cytochrome P450 enzymes (primarily CYP3A4 for hydroxylation) and undergoes 5-alpha reduction and aromatization. Clinically relevant interactions are primarily pharmacodynamic.

ModerateOral Anticoagulants (warfarin, acenocoumarol)
MechanismAndrogens may increase sensitivity to oral anticoagulants by suppressing synthesis of clotting factors II, V, VII, and X
EffectPotentiation of anticoagulant effect; increased bleeding risk
ManagementMonitor INR/PT frequently at initiation and termination of testosterone therapy; adjust anticoagulant dose as needed
FDA PI
ModerateInsulin / Oral Hypoglycemics
MechanismTestosterone improves insulin sensitivity and may decrease blood glucose levels
EffectPotential hypoglycemia in diabetic patients on insulin or sulfonylureas
ManagementMonitor blood glucose more frequently when starting, adjusting, or stopping testosterone; reduce insulin/hypoglycemic doses if needed
FDA PI
ModerateCorticosteroids
MechanismBoth androgens and corticosteroids promote sodium and water retention
EffectAdditive fluid retention; risk of edema and CHF exacerbation
ManagementUse with caution, especially in patients with cardiac, renal, or hepatic disease; monitor weight and for signs of edema
FDA PI
MinorThyroid function tests
MechanismAndrogens decrease thyroxine-binding globulin (TBG) concentrations
EffectDecreased total T4 and T3 with increased T3 resin uptake; free thyroid hormone levels remain unchanged
ManagementNo clinical thyroid dysfunction; interpret total T4/T3 results with awareness of TRT; free T4 and TSH are unaffected
FDA PI
Minor5-alpha reductase inhibitors (finasteride, dutasteride)
MechanismBlock conversion of testosterone to DHT, reducing androgenic effects at target tissues
EffectMay reduce DHT-mediated side effects (acne, alopecia, prostate stimulation) but also reduce PSA levels, complicating prostate monitoring
ManagementIf used concurrently, adjust PSA threshold accordingly (double the measured PSA value); monitor for gynecomastia
Clinical practice
Mon

Monitoring

  • Serum Testosterone3–6 months after initiation; then annually
    Routine
    Measure midway between injections (trough level) for injections Q2W, or at any point for weekly injections. Target: 400–700 ng/dL (Endocrine Society). If supraphysiologic (>1000 ng/dL at peak), reduce dose or lengthen interval. If sub-therapeutic at trough, increase dose or shorten interval.
  • Hematocrit / HemoglobinBaseline; 3–6 months; then annually
    Routine
    Most important safety parameter. Withhold testosterone if hematocrit exceeds 54%. Restart at lower dose after normalization. Persistently elevated Hct requires permanent discontinuation or consideration of phlebotomy.
  • PSABaseline; 3–6 months; then per age-appropriate screening
    Routine
    Evaluate for prostate cancer if PSA >4.0 ng/mL or rises >1.4 ng/mL within 12 months of starting TRT (Endocrine Society). Digital rectal exam at baseline if clinically indicated. Refer to urology for PSA elevation.
  • Lipid PanelBaseline; 6–12 months
    Routine
    Testosterone may decrease HDL and increase LDL. Monitor and adjust lipid-lowering therapy if needed. Clinical significance debated; TRAVERSE showed no excess MACE despite lipid changes.
  • Liver Function TestsBaseline; periodically
    Trigger-based
    Testosterone cypionate is not a 17-alpha-alkyl androgen and carries low hepatotoxicity risk. Monitor LFTs if symptoms of hepatic dysfunction arise (jaundice, dark urine, abdominal pain).
  • Bone Density (DXA)Baseline (if osteoporosis risk); then 1–2 years
    Trigger-based
    Testosterone improves BMD in hypogonadal men. Monitor in patients treated for osteoporosis to assess response.
  • Bone Age (pediatric)Every 6 months during treatment
    Routine
    Testosterone accelerates skeletal maturation and may cause premature epiphyseal closure, compromising adult height. Wrist and hand X-ray every 6 months in pediatric patients.
  • Serum ProlactinBaseline; 3–4 months
    Routine
    Testosterone may increase serum prolactin. If prolactin remains elevated at 3–4 months, consider discontinuation and pituitary evaluation (per Azmiro PI).
CI

Contraindications & Cautions

Absolute Contraindications

  • Known or suspected prostate carcinoma: Exogenous testosterone may stimulate growth of androgen-sensitive prostate tumors.
  • Male breast carcinoma: Testosterone is contraindicated in men with breast cancer.
  • Pregnancy: Testosterone causes virilization of the female fetus. Contraindicated in pregnant women.
  • Known hypersensitivity: To testosterone cypionate or any excipient (cottonseed oil, benzyl benzoate, benzyl alcohol). Anaphylactoid reactions have been reported.

Relative Contraindications (Specialist Input Recommended)

  • Severe untreated sleep apnea: Testosterone may worsen obstructive sleep apnea. Screen and treat OSA before initiating TRT.
  • Uncontrolled heart failure: Fluid retention from androgens may exacerbate CHF.
  • Baseline hematocrit >50%: High pre-treatment hematocrit increases the risk of clinically significant polycythemia during TRT.
  • Desire for current fertility: Exogenous testosterone suppresses spermatogenesis and may cause irreversible infertility. Alternatives (clomiphene, hCG) should be considered in men planning conception.

Use with Caution

  • BPH: May worsen urinary symptoms; monitor for LUTS progression.
  • Pre-existing cardiac, renal, or hepatic disease: Risk of edema from sodium and water retention.
  • Patients on anticoagulants: Increased anticoagulant sensitivity; monitor INR closely.
  • History of thromboembolic events: Use with caution; TRAVERSE found higher PE incidence in the testosterone group.
  • Cancer patients at risk of hypercalcemia: Androgens may exacerbate hypercalcemia; monitor serum calcium.
FDA Class-Wide Regulatory Warning Cardiovascular Risk & Abuse Potential

In 2015, the FDA required all testosterone product labels to include a warning about the possible increased risk of MACE (MI, stroke, CV death) based on inconclusive epidemiologic data. The landmark TRAVERSE trial (NEJM 2023, N = 5246) subsequently demonstrated that TRT was noninferior to placebo for MACE in men with hypogonadism and pre-existing or high CV risk (HR 0.96; noninferiority margin met). However, the testosterone group had more nonfatal arrhythmias (including atrial fibrillation) and pulmonary embolism. Testosterone is also a Schedule III controlled substance with potential for abuse and dependence, particularly at supratherapeutic doses combined with other AAS.

Pt

Patient Counselling

Purpose of Therapy

Testosterone cypionate replaces the testosterone your body is not producing in adequate amounts. Treatment aims to restore testosterone levels to the normal male range, which can improve energy, mood, sexual function, muscle strength, and bone density. This medication is given as an injection into the buttock muscle, typically every 1 to 4 weeks, depending on your prescribed dose and schedule.

How to Take

Injections are administered deep into the gluteal (buttock) muscle by a healthcare provider. Some patients may be trained to self-inject at home. The medication should be stored at room temperature and protected from light. Do not inject intravenously. Keep all laboratory monitoring appointments, as regular blood tests are essential to ensure the medication is working safely.

Blood Thickness (Polycythemia)
Tell patientTestosterone can increase red blood cell counts, making blood thicker and raising the risk of blood clots, stroke, or heart attack. You will need regular blood tests to check this. If your levels are too high, you may need to temporarily stop treatment.
Call prescriberSudden headache, vision changes, chest pain, leg swelling or warmth, or shortness of breath.
Fertility Impact
Tell patientTestosterone therapy can significantly reduce or stop sperm production. This effect may be permanent in some men. If you plan to father children in the future, discuss this with your doctor BEFORE starting treatment. Alternative medications may be available that preserve fertility.
Call prescriberIf you are planning to have children or if your partner becomes pregnant.
Prostate Health
Tell patientTestosterone may affect the prostate gland. You will need periodic PSA blood tests and possibly prostate examinations. Testosterone cannot be used if you have or are suspected of having prostate cancer.
Call prescriberDifficulty urinating, weak urine stream, frequent nighttime urination, or blood in urine.
Mood & Sleep Changes
Tell patientTestosterone can affect mood and sleep. Some patients experience increased energy and improved mood, while others may notice irritability, anxiety, or worsened snoring and sleep apnea. Report any significant changes to your doctor.
Call prescriberNew or worsened snoring, daytime sleepiness, witnessed breathing pauses during sleep, or significant mood disturbances.
Controlled Substance & Abuse
Tell patientTestosterone is a controlled substance (Schedule III). Use only as prescribed. Taking more than your prescribed dose can lead to serious heart, liver, and psychiatric problems. Never share your medication with others. Selling or giving away this medicine is against the law.
Call prescriberIf you feel you are using more than prescribed or are experiencing withdrawal symptoms (fatigue, depression, irritability) after stopping.
Ref

Sources

Regulatory (PI / SmPC)
  1. Azmiro (testosterone cypionate) injection prescribing information. Slayback Pharma LLC. Revised February 2024. FDA LabelModern-format PI with comprehensive dosing, PK data (Table 1), adverse reactions, and updated warnings including CV risk, polycythemia, VTE, and prolactin increases.
  2. Depo-Testosterone (testosterone cypionate injection) prescribing information. Pharmacia & Upjohn/Pfizer. Revised 2018. FDA LabelOriginal brand label for Depo-Testosterone; provides legacy PK data, class-effect adverse reactions, and original dosing guidance.
Key Clinical Trials
  1. Lincoff AM, Bhasin S, Flevaris P, et al. Cardiovascular safety of testosterone-replacement therapy. N Engl J Med. 2023;389(2):107-117. DOI: 10.1056/NEJMoa2215025The landmark TRAVERSE trial (N = 5246): TRT noninferior to placebo for MACE in men with hypogonadism and CV risk; found more atrial fibrillation and PE in the testosterone group.
  2. Snyder PJ, Bhasin S, Cunningham GR, et al. Effects of testosterone treatment in older men. N Engl J Med. 2016;374(7):611-624. DOI: 10.1056/NEJMoa1506119The Testosterone Trials (TTrials): showed modest improvements in sexual function, physical function, and vitality in older men with low testosterone; informed the design of TRAVERSE.
  3. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2010;95(6):2536-2559. DOI: 10.1210/jc.2009-2354Prior version of the Endocrine Society guideline; established testosterone cypionate dosing standards and monitoring parameters widely adopted in clinical practice.
Guidelines
  1. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715-1744. DOI: 10.1210/jc.2018-00229Current gold-standard guideline for TRT: defines diagnostic criteria (2 morning T levels <300 ng/dL), recommends cypionate 75–100 mg/week or 150–200 mg Q2W, and details monitoring schedule.
  2. Hembree WC, Cohen-Kettenis PT, Gooren L, et al. Endocrine treatment of gender-dysphoric/gender-incongruent persons: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2017;102(11):3869-3903. DOI: 10.1210/jc.2017-01658Provides testosterone cypionate dosing recommendations for gender-affirming masculinizing hormone therapy (off-label use).
  3. Mulhall JP, Trost LW, Brannigan RE, et al. Evaluation and management of testosterone deficiency: AUA guideline. J Urol. 2018;200(2):423-432. DOI: 10.1016/j.juro.2018.03.115AUA guideline addressing diagnosis, treatment, and monitoring of hypogonadism; complements the Endocrine Society guideline with a urology-focused perspective.
Pharmacokinetics / Special Populations
  1. Nieschlag E, Behre HM, Bouchard P, et al. Testosterone replacement therapy: current trends and future directions. Hum Reprod Update. 2004;10(5):409-419. DOI: 10.1093/humupd/dmh035Comprehensive review of testosterone ester pharmacokinetics, including cypionate depot kinetics and peak-trough profiles.
  2. Morgentaler A, Zitzmann M, Traish AM, et al. Fundamental concepts regarding testosterone deficiency and treatment. Mayo Clin Proc. 2016;91(7):881-896. DOI: 10.1016/j.mayocp.2016.04.007Reviews the clinical pharmacology of testosterone replacement, including metabolism to DHT and estradiol, and the polycythemia dose-response.
Mechanistic / Basic Science
  1. Basaria S. Male hypogonadism. Lancet. 2014;383(9924):1250-1263. DOI: 10.1016/S0140-6736(13)61126-5Authoritative review of hypogonadism pathophysiology, testosterone mechanisms of action, and clinical management considerations.