Skip to main content

Testosterone Replacement Therapy

Testosterone replacement therapy (TRT) is the standard treatment for symptomatic men with confirmed testosterone deficiency (TD). FDA-approved indications are limited to primary hypogonadism (testicular failure) and hypogonadotropic hypogonadism from established hypothalamic-pituitary disease.[1][2] The safety landscape has been fundamentally reshaped by the TRAVERSE trial (2023, NEJM, n = 5,246) establishing cardiovascular non-inferiority, and by the 2025 NEJM review that reframes the benefit–risk conversation around consistent benefit for libido, body composition, bone density, and anemia alongside a narrower list of genuine concerns — erythrocytosis, pulmonary embolism, atrial fibrillation, and (unexpectedly) clinical fractures.[2][3]

For related classes, see PDE5 inhibitors, Intracavernosal injection agents, and Androgen adjuncts.

Diagnosis — confirm the biochemical defect before prescribing​

The AUA uses compatible symptoms/signs plus two early-morning total testosterone (TT) measurements, with <300 ng/dL as a reasonable diagnostic threshold; it does not require fasting. The Endocrine Society recommends two fasting morning measurements showing consistently low testosterone. Its 264 ng/dL lower reference limit applies to CDC-standardized assays in healthy, nonobese young men; it is not a universal cutoff for every assay or clinical situation.[1][4]

Interpret SHBG correctly: low SHBG can produce low TT with normal free T, whereas high SHBG can conceal low free T behind normal or high TT. When TT is borderline or SHBG is altered, use equilibrium dialysis or a validated free-T calculation with TT, SHBG and albumin; do not use an inaccurate direct analog free-T assay.[1]

Core diagnostic workup​

TestPurpose
Total testosterone (morning; fasting per Endocrine Society)Confirm on a separate morning with a reliable assay[1][4]
Free testosterone (equilibrium dialysis or calculated)Confirmatory when TT is borderline or when SHBG-altering conditions are present (obesity, aging, liver disease, thyroid disorders)[1]
LH and FSHPrimary (elevated) vs secondary (low / normal) hypogonadism[5]
ProlactinIf LH is low or low-normal — evaluate for pituitary adenoma[5]
Secondary-cause workupPituitary MRI (hyperprolactinemia, panhypopituitarism), iron studies (hemochromatosis), karyotype (Klinefelter)[6]

When to measure testosterone even without classic sexual symptoms[4]​

Unexplained anemia, low bone density, type 2 diabetes, chemotherapy or radiation exposure, HIV/AIDS, chronic opioid use, infertility, pituitary dysfunction, chronic corticosteroids.

Validated symptom questionnaires (ADAM, AMS) are NOT recommended as screening tools or as surrogates for laboratory testing.[4]

Indications and contraindications​

Indication: symptomatic men with confirmed low TT, after shared decision-making regarding benefits and risks.[1]

Reasons to defer treatment or obtain specialist assessment[1][4]​

CategorySpecific
OncologicBreast cancer or known/suspected prostate cancer per product labels; distinguish this from individualized specialist discussion after definitive treatment[29][31]
Prostate evaluation pendingPalpable prostate nodule or induration without urologic evaluation; PSA >4 ng/mL (>3 ng/mL in high-risk men) without urologic evaluation
HematologicAUA: baseline hematocrit >50% warrants withholding treatment while investigating the cause. Endocrine Society identifies >48% (>50% at altitude) as increased risk and recommends against starting with elevated hematocrit or thrombophilia. These are not the on-treatment intervention thresholds below.
RespiratoryUntreated severe OSA
LUTSEndocrine Society recommends against starting with severe LUTS (IPSS >19); evaluate and manage the outlet problem first.
CardiovascularEndocrine Society: uncontrolled heart failure or MI/stroke within 6 months. Follow product-specific blood-pressure warnings.
FertilityCurrent or future fertility interest — exogenous testosterone should not be prescribed under AUA/ASRM guidance (see below).[8]

Formulations — detailed comparison​

FormulationTypical doseKey features
Testosterone cypionate / enanthate (IM, short-acting)Endocrine Society starting regimens: 75–100 mg IM weekly or 150–200 mg every 2 weeksInexpensive, widely available; supraphysiologic peaks and symptom troughs; monitor mid-interval TT and titrate to response[1]
Testosterone undecanoate (IM, long-acting — Aveed)750 mg IM, repeat at 4 wk, then every 10 wk10-week maintenance interval after loading; Boxed warning for POME and anaphylaxis; 30-minute observation after each injection and Aveed REMS enrollment remain required[29]
Testosterone gel 1.62% (AndroGel)40.5 mg (2 pumps) to shoulders / upper arms daily; range 20.25–81 mgSteady-state levels; secondary transfer risk to women and children — wash hands, cover application site[9]
Other gels / solutionsUse the individual product labelConcentrations, application sites, starting doses and titration tests are not interchangeable.[9]
Subcutaneous pellets (Testopel)Label: 150–450 mg SC every 3–6 months (2–6 pellets, 75 mg each); individualized higher regimens described in guidelines are off-label for TestopelLess easily adjusted than daily treatment; infection/extrusion and possible pellet removal require counseling.[1][33]
Oral undecanoate (Jatenzo)Start 237 mg BID with food; titrate 158–396 mg BID using product-specific testingCurrent label has a blood-pressure warning, not the former cardiovascular boxed warning[28][30]
Other oral undecanoate — Tlando / KyzatrexFollow the individual label; formulations are not dose-interchangeableKyzatrex starts at 200 mg BID with food; its titration range extends from 100 mg each morning to 400 mg BID[32]
Nasal gel (Natesto)5.5 mg per nostril (11 mg total per dose), three times dailyOne actuation per nostril; 33 mg/day total. Nasal adverse effects; spermatogenesis may be suppressed[31]

Selection principles: injection for cost and efficacy; gel for steady physiology (watch transfer); pellets for adherence-challenged men; IM undecanoate for long dosing intervals with POME/anaphylaxis precautions; oral products require daily product-specific dosing and BP monitoring. Do not present nasal testosterone as a proven fertility-preserving alternative.[8][28]

FDA’s February 2025 labeling change removed adverse-cardiovascular-outcome boxed-warning language and required blood-pressure warnings. It did not remove Aveed’s POME/anaphylaxis boxed warning. Check BP before and during treatment.[28][29]

Treatment goals and monitoring​

Target: AUA recommends the minimum dose needed to reach approximately 450–600 ng/dL, with symptom improvement. Endocrine Society recommends the mid-normal range, not a blanket target of 300–900 ng/dL. Apply the individual product's sampling and titration instructions.[1][4]

Monitoring — distinguish guideline and product instructions[1][4]​

ParameterTimingAction thresholds
Serum testosteroneProduct-specific titration, then reassessment at 3–6 mo; AUA every 6–12 mo once stableSampling timing varies by formulation; reassess continued treatment if testosterone normalizes without symptom benefit.
HematocritBaseline, 3–6 mo, then annually (earlier when indicated)AUA: ≥54% requires intervention, with dose adjustment first when on-treatment T is high. Endocrine Society: >54%, stop until safe, investigate hypoxia/OSA, then restart at reduced dose.
PSAAUA: baseline in men over 40. Endocrine Society: shared prostate-monitoring decisions at 55–69, or 40–69 with increased risk; if chosen, baseline and 3–12 moConfirm a rise before acting. Endocrine Society: urologic evaluation for confirmed increase >1.4 ng/mL above baseline during the first 12 mo, confirmed PSA >4 ng/mL, or abnormal examination.
DRE / prostate monitoringAccording to the chosen guideline and shared screening planInvestigate abnormality or substantial LUTS worsening; thereafter follow routine screening guidance.
BMD (DXA)After 1–2 y in men with osteoporosisAssess response
Symptoms and AEsEvery visitClinical response and formulation-specific effects

The 2025 Eur Urol review recommends follow-up at 3 months and every 6–12 months thereafter.[10]

Benefits​

Sexual function​

Consistent improvement in libido and sexual activity. Effect on erectile function is small but statistically significant (SMD 0.16–0.27).[1][11] The 2025 NEJM review is explicit: TRT may not be effective if the main symptom is ED.[3] The Cochrane review (Lee 2024) concluded TRT produces little to no clinically important difference in erectile function vs placebo.[12] Adding testosterone to an optimized PDE5i regimen has not been shown to further improve erectile function in RCTs.[1] See PDE5 inhibitors.

Body composition​

Consistently increases lean mass and decreases fat mass. Buratto 2023 meta-analysis (16 RCTs) — significant gains in hip BMD and total lean mass at 6 months; effects less clear at 12 months.[13]

Bone mineral density​

Increases areal and volumetric BMD at spine and hip; improves cortical density and thickness.[1][14]

TRAVERSE fracture substudy: Snyder 2024 reported more clinical fractures with testosterone (91/2,601 [3.50%] vs 64/2,603 [2.46%]; HR 1.43, 95% CI 1.04–1.97) over a median 3.19 years. The mechanism is uncertain; increased activity is a hypothesis, not an established explanation. Improved BMD must not be presented as demonstrated fracture prevention.[15]

Anemia​

TRT corrects unexplained anemia in hypogonadal men; significantly greater proportion achieved hemoglobin increments >1 g/dL in the TTrials.[1]

Mood and energy​

Slight improvements in depressive symptoms, mood, and energy; effect sizes are small and not consistently significant across trials.[1][3]

Glycemic outcomes — the T4DM / TRAVERSE contrast​

  • T4DM (Wittert 2021, n = 1,007) — 2 years of testosterone undecanoate + a structured lifestyle program reduced progression to T2D by 40% (RR 0.59) in overweight men with IGT, independent of baseline testosterone[16]
  • TRAVERSE diabetes substudy (Bhasin 2024) — testosterone gel without a structured lifestyle program showed no significant difference in prediabetes-to-diabetes progression and no glycemic improvement in established T2D[17]
  • Interpretation: these trials differ in population, formulation and co-intervention; their contrast does not prove that lifestyle modification is the cause of their different results. Do not prescribe TRT as established diabetes prevention or glucose-lowering therapy.[1][16][17]

Cardiovascular safety — TRAVERSE​

TRAVERSE 2023 (Lincoff, NEJM, n = 5,246 men 45–80 y with hypogonadism and established or high CV risk) is the first adequately powered RCT of CV safety:[2]

EndpointTestosteronePlaceboInterpretation
MACE (primary)7.0%7.3%Non-inferior; HR 0.96 (95% CI 0.78–1.17; p < 0.001 for non-inferiority)
Pulmonary embolism0.9%0.5%Higher on testosterone
Atrial fibrillation3.5%2.4%Higher on testosterone
Acute kidney injury2.3%1.5%Higher on testosterone[5]
Clinical fractures3.50% (91/2,601)2.46% (64/2,603)Higher on testosterone[15]
Prostate cancer / LUTSNo significant between-group difference in the separately reported prostate safety outcomes—Men at high prostate-cancer risk or with severe LUTS were excluded; this is not a lifetime safety guarantee.[19]

The Androgen Society 2024 position paper interprets the cardiovascular evidence as reassuring. Keep the stronger practical claim bounded by TRAVERSE's randomized population, formulation and follow-up; absence of excess MACE in this trial does not resolve all other harms.[2][18]

Genuine residual signals: pulmonary embolism, atrial fibrillation, and the unexplained fracture signal. Counsel accordingly.

Prostate safety​

Prostate cancer risk​

AUA 2018 — Strong Recommendation, Grade B: clinicians should inform patients of the absence of evidence linking TRT to prostate cancer development.[4]

  • TRAVERSE prostate substudy (Bhasin 2023) — high-grade PCa occurred in 5/2,596 vs 3/2,602 men (HR 1.62, 95% CI 0.39–6.77); low event counts and wide uncertainty do not establish equivalence[19]
  • Baik 2025 Medicare cohort (n = 546,964) — TRT was associated with 16% reduction in PCa hazard (HR 0.84)[20]
  • García-Becerra 2026 meta-analysis of 41 RCTs (n = 11,161) — no statistically significant increase in PCa events (OR 0.88, 95% CI 0.52–1.51)[21]

TRT after prostate cancer​

The AUA states there is inadequate evidence to quantify the risk-benefit ratio in men with PCa history (Expert Opinion). Observational reports after treatment or during active surveillance remain subject to selection bias and do not establish oncologic safety for every risk group.[4][22][23][24]

SPIRIT 2026 randomized 136 men with symptomatic low testosterone, organ-confined Gleason 3+3 or 3+4 disease treated by radical prostatectomy, and undetectable PSA for at least 2 years, to testosterone cypionate 100 mg IM weekly or placebo for 12 weeks. Sexual activity and desire improved; erectile function did not. No biochemical recurrence was observed, but the trial was too small and short to determine long-term cancer safety. Its findings do not cover active surveillance, high-grade disease, radiation or androgen-deprivation recipients. A subsequent correction concerned baseline testosterone units, not the reported treatment outcomes.[34][35]

The saturation model offers a biological hypothesis; it does not prove that replacement cannot stimulate residual or recurrent cancer in an individual patient.[22][25]

BPH / LUTS​

Trials have not shown significant LUTS worsening in their selected populations, but severe LUTS was generally excluded. Continue symptom monitoring. A retrospective association with BPH diagnosis cannot establish causation or be dismissed as proven detection bias.[1][19][20]

Erythrocytosis — the most common dose-limiting AE​

Highest risk with injectable formulations and in older men.[1][6] In T4DM, hematocrit >54% was triggered in 22% of testosterone-treated men (vs 1% placebo).[16]

AUA: hematocrit ≥54% requires intervention; reduce dose when on-treatment T is high. If T is low/normal, reassess SHBG/free T and investigate other causes, with hematology input when indicated. Endocrine Society: if hematocrit >54%, stop until safe, evaluate hypoxia/OSA, then restart at reduced dose. Routine phlebotomy is not an automatic substitute for reassessing the dose and cause. Oral formulations do not eliminate erythrocytosis risk.[1][4][30]

Fertility — exogenous TRT suppresses spermatogenesis​

AUA / ASRM Male Infertility Guideline — Clinical Principle: exogenous testosterone should not be prescribed to men interested in current or future fertility.[8]

Recovery after discontinuation is variable and can take months or longer. Estimates from healthy-men contraceptive studies should not be promised to a previously infertile or chronically treated patient; some men do not recover adequately.[4]

AUA/ASRM allows selected use of hCG, SERMs or aromatase inhibitors for infertile men with low testosterone (conditional, Grade C). Selection depends on the endocrine defect and fertility evaluation; an increase in serum T is not proof of improved sperm production or live birth. The Habous 2018 trial (282 men) compared short-term testosterone and symptom outcomes, not demonstrated preservation of spermatogenesis.[8][26]

See the Androgen adjuncts hub for agents, label/off-label distinctions and dosing considerations.

Special populations​

Older men — age-related decline vs pathologic hypogonadism​

The 2025 NEJM review — benefit most likely in men with unequivocal hypogonadism (TT <200 ng/dL with classic symptoms); marginal in age-related decline without consistent symptoms.[3] EMAS position statement 2023 — offer TRT in symptomatic older men with confirmed low testosterone only after explaining uncertainties about long-term safety, and prefer short-acting transdermal preparations for initiation.[7]

Obesity​

The most common cause of functional hypogonadism. Weight loss through lifestyle modification is first-line — it raises endogenous testosterone. T4DM showed testosterone augmented a structured lifestyle program, but TRT for diabetes prevention in men without pathologic hypogonadism is premature.[7][10][16]

Cancer survivors (non-prostate)​

Per the NCCN Survivorship Guidelines, survivors of non-prostate malignancies who develop hypogonadism after radiation, chemotherapy, or surgery should be evaluated and treated for hormone-related symptoms.[27]

Evidence Summary​

DomainEffectStrengthKey source
Libido / sexual desireConsistently improvedStrongMultiple RCTs; Endocrine Society 2018[1]
Erectile functionSmall improvement; inadequate if ED is dominantModerate (Cochrane-moderate)Lee 2024[12]
Body composition↑ Lean mass, ↓ fat massStrongBuratto 2023[13]
Bone mineral densityIncreased at spine and hipStrongNg Tang Fui 2021[14]
Clinical fracturesUnexpectedly increased (43%)Moderate (single large RCT)Snyder 2024 TRAVERSE[15]
AnemiaCorrectedStrongTTrials / Endocrine Society[1]
Mood / depressionSlight improvementLow–Moderate2025 NEJM review[3]
MACENo increase (non-inferiority established)StrongTRAVERSE 2023[2]
Pulmonary embolismIncreasedModerateTRAVERSE[2]
Atrial fibrillationPossibly increasedLow–ModerateTRAVERSE[2]
Prostate cancerNo significant excess in selected short–mid-term trials; long-term and post-cancer uncertainty remainsLimited for rare events and cancer survivorsTRAVERSE; SPIRIT 2026[19][34]
ErythrocytosisDose-dependent; most common AEStrongMultiple sources[1][16]
Fertility (spermatogenesis)SuppressedStrongAUA/ASRM 2024[8]

Clinical Positioning​

  • Confirm symptoms plus consistently low testosterone on two mornings; fasting is the Endocrine Society recommendation, not an AUA requirement. Interpret assay limits and altered SHBG.[1][4]
  • TRAVERSE established MACE non-inferiority within its studied population and follow-up. It does not establish lifelong safety for every formulation, dose or population.[2][18]
  • Pulmonary embolism, atrial fibrillation, and the unexplained fracture signal remain genuine — counsel patients on these, particularly men with prior VTE, paroxysmal AF, or falls risk.[2][15]
  • For isolated ED as the chief complaint, TRT is not the answer. Libido responds; erectile function does not meaningfully improve on its own, and adding T to PDE5i has not improved ED in RCTs.[3][12]
  • Monitor hematocrit. Separate the AUA baseline >50% investigation threshold from its on-treatment ≥54% intervention threshold; follow the guideline-specific actions above.[1][4]
  • Do not prescribe exogenous testosterone for men interested in current or future fertility. Refer to the androgen-adjuncts hub and select alternatives after endocrine and fertility assessment.[8]
  • Nasal testosterone remains exogenous testosterone. Limited short-term semen studies do not establish long-term reproductive safety or override fertility counseling.[8][31]
  • Known or suspected prostate cancer remains a product-label contraindication. Observational use after treatment or during surveillance must not be presented as routine label-approved care; specialist selection and explicit discussion of uncertainty are essential.[22][23][24]
  • Obesity first — in men with functional hypogonadism from obesity, lifestyle modification is first-line before TRT; T4DM shows TRT can augment a structured program but does not replace it.[10][16]
  • For older men with age-related decline and mild symptoms, prefer transdermal formulations and short courses with explicit reassessment windows — EMAS 2023 framing.[7]
  • Confirm PSA changes. A confirmed rise >1.4 ng/mL above baseline during the first treatment year is an Endocrine Society trigger for urologic evaluation, alongside absolute PSA and examination findings.[1]
  • Prevent gel transfer: wash hands immediately, cover the site after drying, and wash the application site before anticipated skin contact. Drying alone does not eliminate transfer risk.[9]

See Also​

References​

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.2018-00229

2. Lincoff AM, Bhasin S, Flevaris P, et al. "Cardiovascular safety of testosterone-replacement therapy (TRAVERSE)." N Engl J Med. 2023;389(2):107–117. doi:10.1056/NEJMoa2215025

3. Bhasin S, Snyder PJ. "Testosterone treatment in middle-aged and older men with hypogonadism." N Engl J Med. 2025;393(6):581–591. doi:10.1056/NEJMra2404637

4. 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.2018.03.115

5. Heidelbaugh JJ, Belakovskiy A. "Testosterone replacement therapy for male hypogonadism." Am Fam Physician. 2024;109(6):543–549.

6. De Silva NL, Papanikolaou N, Grossmann M, et al. "Male hypogonadism: pathogenesis, diagnosis, and management." Lancet Diabetes Endocrinol. 2024;12(10):761–774. doi:10.1016/S2213-8587(24)00199-2

7. Kanakis GA, Pofi R, Goulis DG, et al. "EMAS position statement: testosterone replacement therapy in older men." Maturitas. 2023;178:107854. doi:10.1016/j.maturitas.2023.107854

8. Brannigan RE, Hermanson L, Kaczmarek J, et al. "Updates to male infertility: AUA/ASRM guideline (2024)." J Urol. 2024;212(6):789–799. doi:10.1097/JU.0000000000004180

9. AndroGel 1.62% prescribing information. DailyMed. Accessed September 12, 2026.

10. Boeri L, Masterson T, Antonio L, et al. "Testosterone therapy in adult males with hypogonadism." Eur Urol. 2025. doi:10.1016/j.eururo.2025.12.015

11. Diem SJ, Greer NL, MacDonald R, et al. "Efficacy and safety of testosterone treatment in men: an evidence report for a clinical practice guideline by the American College of Physicians." Ann Intern Med. 2020;172(2):105–118. doi:10.7326/M19-0830

12. Lee H, Hwang EC, Oh CK, et al. "Testosterone replacement in men with sexual dysfunction." Cochrane Database Syst Rev. 2024;1:CD013071. doi:10.1002/14651858.CD013071.pub2

13. Buratto J, Kirk B, Phu S, Vogrin S, Duque G. "Safety and efficacy of testosterone therapy on musculoskeletal health and clinical outcomes in men: a systematic review and meta-analysis of randomized placebo-controlled trials." Endocr Pract. 2023;29(9):727–734. doi:10.1016/j.eprac.2023.04.013

14. Ng Tang Fui M, Hoermann R, Bracken K, et al. "Effect of testosterone treatment on bone microarchitecture and bone mineral density in men: a 2-year RCT." J Clin Endocrinol Metab. 2021;106(8):e3143–e3158. doi:10.1210/clinem/dgab149

15. Snyder PJ, Bauer DC, Ellenberg SS, et al. "Testosterone treatment and fractures in men with hypogonadism." N Engl J Med. 2024;390(3):203–211. doi:10.1056/NEJMoa2308836

16. Wittert G, Bracken K, Robledo KP, et al. "Testosterone treatment to prevent or revert type 2 diabetes in men enrolled in a lifestyle programme (T4DM): a randomised, double-blind, placebo-controlled, 2-year, phase 3b trial." Lancet Diabetes Endocrinol. 2021;9(1):32–45. doi:10.1016/S2213-8587(20)30367-3

17. Bhasin S, Lincoff AM, Nissen SE, et al. "Effect of testosterone on progression from prediabetes to diabetes in men with hypogonadism: a substudy of the TRAVERSE randomized clinical trial." JAMA Intern Med. 2024;184(4):353–362. doi:10.1001/jamainternmed.2023.7862

18. Morgentaler A, Dhindsa S, Dobs AS, et al. "Androgen Society position paper on cardiovascular risk with testosterone therapy." Mayo Clin Proc. 2024;99(11):1785–1801. doi:10.1016/j.mayocp.2024.08.008

19. Bhasin S, Travison TG, Pencina KM, et al. "Prostate safety events during testosterone replacement therapy in men with hypogonadism: a randomized clinical trial." JAMA Netw Open. 2023;6(12):e2348692. doi:10.1001/jamanetworkopen.2023.48692

20. Baik SH, Baye F, Fung KW, Xian H, McDonald CJ. "Association between testosterone replacement therapy and prostatic disorders in elderly hypogonadal men." J Clin Endocrinol Metab. 2025. doi:10.1210/clinem/dgaf504

21. García-Becerra CA, Arias-Gallardo MI, Juárez-García JE, et al. "Cardiovascular and prostate cancer risk associated to testosterone replacement therapy — a systematic review and meta-analysis of 41 randomized controlled trials." Int J Impot Res. 2026. doi:10.1038/s41443-026-01237-4

22. Kaplan AL, Hu JC, Morgentaler A, et al. "Testosterone therapy in men with prostate cancer." Eur Urol. 2016;69(5):894–903. doi:10.1016/j.eururo.2015.12.005

23. Gibson J, George M, Grice P, et al. "Testosterone replacement therapy following definitive treatment for prostate cancer: a scoping review of safety and efficacy." Int J Impot Res. 2025. doi:10.1038/s41443-025-01206-3

24. Santucci J, Stapleton P, Perera M, et al. "Oncological safety of testosterone replacement therapy in men with localised prostate cancer: a systematic review of observational studies." BJU Int. 2025. doi:10.1111/bju.16870

25. Morgentaler A, Caliber M. "Safety of testosterone therapy in men with prostate cancer." Expert Opin Drug Saf. 2019;18(11):1065–1076. doi:10.1080/14740338.2019.1666103

26. Habous M, Giona S, Tealab A, et al. "Clomiphene citrate and human chorionic gonadotropin are both effective in restoring testosterone in hypogonadism: a short-course randomized study." BJU Int. 2018;122(5):889–897. doi:10.1111/bju.14401

27. National Comprehensive Cancer Network. NCCN clinical practice guidelines in oncology: survivorship. Updated 2026-04-08.

28. US Food and Drug Administration. FDA issues class-wide labeling changes for testosterone products. February 28, 2025.

29. Endo USA. Aveed prescribing information, revised July 2025. DailyMed. Accessed September 11, 2026.

30. Tolmar. Jatenzo prescribing information. DailyMed. Accessed September 11, 2026.

31. Acerus Pharmaceuticals. Natesto prescribing information, revised July 2025. DailyMed. Accessed September 11, 2026.

32. Marius Pharmaceuticals. Kyzatrex prescribing information. Accessed September 11, 2026.

33. Endo USA. Testopel prescribing information, revised July 2025. Accessed September 12, 2026.

34. Bhasin S, et al. "Testosterone treatment in prostate cancer survivors with hypogonadism: a randomized clinical trial." JAMA Intern Med. 2026. doi:10.1001/jamainternmed.2026.1343. SPIRIT; PMID 42113507.

35. "Errors in units of measure in Table 1." JAMA Intern Med. 2026. doi:10.1001/jamainternmed.2026.3289.