Drug Database
TE

testosterone enanthate (Vibex QS T / QS T / Xyosted)

✓ Approved

Antares Pharma, Inc. · AR · Steroids

What is testosterone enanthate?

testosterone enanthate is a steroids developed by Antares Pharma, Inc.. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesVibex QS T, QS T, Xyosted
CompanyAntares Pharma, Inc.
Drug ClassSteroids, Small Molecule
Molecular TargetAR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Antares Pharma, Inc.

Mechanism of Action

Molecular Targets

testosterone enanthate acts on 1 molecular target:

ARandrogen receptor (DHTR, AR8)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

testosterone enanthate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Endocrine disordersHypogonadism✓ Approved

Related Research Articles

PubMedVeterinary medicine and science2026-07-17

The Combination of Nigella sativa Oil-Based Nanoemulsion and Quercetin Alleviates Oxidative Stress From Exogenous Testosterone Through Antioxidant and Anti-Inflammatory Mechanisms in Rats.

Najafi Majid M, Panahi Negar N, Hesaraki Saeed S, Akbari Ghasem G

Exogenous testosterone therapy induces testicular oxidative stress and inflammation, suppressing spermatogenesis. Chronic restraint and high-intensity exercise stress exacerbate reproductive dysfunction. Quercetin (Qu) and black seed oil (BSO) possess potent antioxidant and anti-inflammatory properties. This study evaluates the efficacy of Qu-loaded BSO (Qu-BSO) nanoemulsion in mitigating testosterone-induced testicular damage in rats subjected to exercise and restraint stress, as well as to testosterone and finasteride administration. A Qu-BSO nanoemulsion was prepared and characterized. Thirty-six male Wistar rats were divided into six groups (n = 6): control (C), testosterone (T) at 20 mg/kg weekly via subcutaneous injection, testosterone + finasteride (TF) at 1 mg/kg 5 days a week, testosterone + high-intensity treadmill exercise (TE) for 50 min daily, testosterone + chronic restraint stress (TI) for 3 h daily and testosterone + Qu-BSO (TQBSNE) for 6 weeks. Serum testosterone, LH, testicular antioxidants (SOD, CAT and GPx), lipid peroxidation (MDA), inflammatory cytokines (TNF-α and IL-1β mRNA), and histopathology were assessed. The T, TF and TI groups exhibited significant testicular damage with elevated oxidative stress and inflammation. The T and TF groups exhibited the highest serum testosterone. TE showed partial protection. The TQBSNE treatment group provided superior protection, with significantly higher SOD, CAT and GPx activities, the lowest MDA levels and reduced TNF-α and IL-1β expression. TQBSNE also partially restored LH levels. The high-intensity exercise group showed a partial protective effect. Chronic restraint stress exacerbated testicular damage caused by testosterone. Qu-BSO nanoemulsion effectively counteracted testosterone-induced testicular damage through antioxidant and anti-inflammatory mechanisms, representing a promising therapeutic strategy.

PMID 42464454
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PubMedAndrology2026-07-17

Follicle-Stimulating Hormone to Inhibin B Ratio Among Primary Infertile Men With Low Testosterone-A Biochemical Marker of Testicular Reserve.

Negri Fausto F, Pozzi Edoardo E, Raffo Massimiliano M, Boeri Luca L et al.

In adult males, Inhibin B (InhB) production depends on follicle-stimulating hormone (FSH)-which stimulates InhB as part of a negative feedback loop on the pituitary gland-and on spermatogenic activity, which reflects the functional state of the seminiferous epithelium. We aimed to (i) investigate the role of the FSH/InhB ratio in a homogeneous cohort of primary infertile men with low testosterone levels and (ii) evaluate its reliability as a marker of impairment severity. Data from 1568 consecutive primary infertile men, defined according to World Health Organization (WHO) criteria, were analyzed. Patients underwent thorough assessments comprising complete demographic, clinical, genetic, and laboratory investigations, including semen analysis and sperm DNA fragmentation index (SDF) testing. Low testosterone was defined as serum total testosterone (tT) < 3.5 ng/mL, according to the EAU threshold. Patients with any chromosomal alteration and history of cryptorchidism were excluded from the analysis. The final cohort was stratified into two groups based on the median FSH/InhB ratio (≤ 0.23 vs. > 0.23). Descriptive statistics were used to summarize baseline characteristics, and linear regression analysis was performed to evaluate the associations between the FSH/InhB ratio and sperm concentration. Overall, 360 men (23%) reported tT < 3.5 ng/mL. Of these, men with higher FSH/InhB ratio levels displayed lower mean testicular volume (TV) [13.5 (10, 20) vs. 17.5 (15, 22.5) mL, p < 0.001], anti-Müllerian hormone (AMH) [0.2 (0.16, 2.7) vs. 6 (3.5, 7.2) ng/mL, p = 0.01] and total motile sperm count (TMSC) [4.4 (0.4, 21.6) vs. 15.7 (2, 55), p < 0.001], along with higher rates of non-obstructive azoospermia (NOA) (31.7% vs. 12.8%, p < 0.001). No additional significant differences were observed between the groups. At multivariable linear regression analysis, smaller TV [β = 2.42 (95% CI 1.41, 2.86); p`0.01], higher BMI [β = -1.24 (95% CI -2.25, -0.23); p = 0.02] and higher FSH/InhB ratio [β = -0.53 (95% CI -1.04, -0.03); p = 0.04] were identified as independent predictors of lower sperm concentration, after adjusting for age and tT. Among primary infertile men with low tT levels, those with a higher FSH/InhB ratio exhibited a more severe phenotype, characterized by reduced TV, lower TMSC, and higher rates of NOA as compared with those with a lower ratio. These findings identify a distinct endocrine phenotype characterized by reduced InhB production at comparable FSH levels, which is associated with impaired gonadal function. The FSH/InhB ratio emerges as a useful biomarker to stratify gonadal dysfunction severity in men with primary infertility and hypogonadism.

PMID 42466593
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PubMedCureus2026-07-17

Urological Complications of Morbid Obesity and the Role of Bariatric Surgery and Glucagon-Like Peptide-1 Receptor Agonists in Their Management: A Systematic Review.

Khalil Waqas W, Bibi Khadija K, Fareed Tauheed T, Khan Sajad S et al.

Morbid obesity (body mass index (BMI) ≥40 kg/m² or ≥35 kg/m² with comorbidities) predisposes patients to multiple urological disorders, including urinary incontinence, overactive bladder, erectile dysfunction, hypogonadism, nephrolithiasis, obesity-related kidney disease, renal cell carcinoma, and aggressive prostate cancer. Bariatric surgery is the most effective durable treatment for severe obesity. Glucagon-like peptide-1 receptor agonists, including semaglutide and tirzepatide, have revolutionised obesity pharmacotherapy. This systematic review evaluates the urological complications of morbid obesity and the effects of bariatric surgery and glucagon-like peptide-1 receptor agonists on these outcomes. We searched MEDLINE, Embase, Scopus, and the Cochrane Library (January 2000 to June 2025) for studies reporting urological outcomes in adults with BMI ≥35 kg/m². Two reviewers independently screened and extracted data. We assessed risk of bias using the A Measurement Tool to Assess Systematic Reviews (AMSTAR) version 2 and the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE). Eighty-four studies (>165,000 participants) met the inclusion criteria. Obesity increases renal cell carcinoma risk (relative risk: 1.5-2.0) and prostate cancer mortality (hazard ratio: 1.19-1.24) but paradoxically reduces prostate cancer incidence. Urinary incontinence and overactive bladder improve or resolve in 50-70% of women after bariatric surgery. Erectile dysfunction and hypogonadism improve after bariatric surgery, with International Index of Erectile Function (IIEF) scores increasing 4-6 points and testosterone rising 30-50%. Glucagon-like peptide-1 receptor agonists increase testosterone (standardised mean difference: 1.39 ng/mL) and improve erectile function. Tirzepatide reduces urinary albumin-to-creatinine ratio by 19-47% and preserves estimated glomerular filtration rate. Roux-en-Y gastric bypass increases nephrolithiasis risk 2.5-4-fold via enteric hyperoxaluria, whereas sleeve gastrectomy does not. Robot-assisted surgery in obese patients achieves complication rates comparable to those of non-obese patients after comorbidity adjustment. Bariatric surgery improves obesity-related urological morbidity, but Roux-en-Y gastric bypass increases stone risk. Glucagon-like peptide-1 receptor agonists offer a promising alternative with evidence for testosterone restoration, improved erectile function, and renal protection. Preoperative urological assessment, procedure selection, and multidisciplinary care are essential.

PMID 42465136
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PubMedCureus2026-07-17

The Evidence-Practice Gap in Testosterone Therapy for Prostate Cancer: A Narrative Review.

Aly Mohammed M, Joseph Anisha A, Amer Tarik T

The contraindication to testosterone replacement therapy (TRT) in men with prostate cancer (PCa) has been progressively challenged by contemporary evidence. Over recent years, increasing data suggest that TRT does not increase biochemical recurrence, disease progression, or PCa-specific mortality in carefully selected men, including those managed by active surveillance and those treated with radical prostatectomy or radiotherapy. Despite this convergence in the evidence, clinical practice has lagged. Major society guidelines continue to describe the available data as inadequate; many clinicians decline TRT in any man with a history of PCa, and symptomatic hypogonadism in survivors remains undertreated. This narrative review synthesises the contemporary evidence and characterises the persistent gap between evidence and clinical practice. It examines the principal drivers of that gap, which include conservative interpretation of guideline language, medico-legal anxiety, concerns surrounding on-treatment biochemical monitoring, the absence of randomised trials in this specific population, multidisciplinary fragmentation, and limited exposure during training. A practical clinical framework for shared decision-making and on-treatment surveillance, relevant to the UK and European practice, is proposed. The review concludes that an absolute contraindication is no longer tenable in men with symptomatic hypogonadism and a history of treated PCa, and that this population deserves a contemporary, evidence-informed conversation about TRT.

PMID 42465160
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PubMedJournal of applied toxicology : JAT2026-07-17

Melatonin-Zinc MOFs Antimycotic, Molecular, and Antioxidant Protective Effects of Hepatic, Renal, and Testicular Dysfunctions Induced by Aflatoxin B1 in Rats.

Aly Mohamed S MS, Soliman Mona M H MMH, Balabel Esraa A EA, Abdelhameed Reda M RM et al.

Aflatoxin B1 causes renal, hepatic, and reproductive disorders. To investigate the protective effects of melatonin-zinc metal-organic frameworks (Mt-Zn-MOFs) nanoparticles against renal, hepatic, and reproductive toxicity induced by aflatoxins B1, male Sprague-Dawley rats (n = 40) were equally divided into control, Mt-Zn-MOFs, aflatoxins, and Mt-Zn-MOFs + aflatoxins groups. Blood and tissue samples were collected from the livers, kidneys, and testicles. Luteinizing hormone (LH), testosterone, estradiol (E2), interleukin-β (IL-β), transforming growth factor-β (TGF-β), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total antioxidants (TAC), nitric oxide (NO), AST, ALT, and creatinine were measured. Hepatic DNA fragmentation and the expression of CRAT, CYP39A1, and JunB genes were determined. Mt-Zn-MOFs have more antimycotic effects against A. flavus than A. parasiticus, with MIC and MFC of 3.125 and 6.25 mg/mL for A. flavus and 12.5 and 25 mg/mL for A. parasiticus, and 6.25 mg/mL inhibited A. flavus and A. parasiticus sporulation. Mt-Zn-MOFs rats had high (p < 0.001) testosterone, LH, E2, glucose, but low (p < 0.01) SOD, total proteins, albumin, globulin, AST, and ALT, compared to controls. Mt-Zn-MOFs-aflatoxin group had lower (p < 0.01) LH, SOD, GPx, total proteins, globulin, glucose, TGF-β (p < 0.022), DNA fragmentation, and the expressions of JunB, CYP39A1, and CRAT, but high (p < 0.01) NO, CAT, and total cholesterol than aflatoxin-treated rats. Mt-Zn-MOFs protected the liver, kidney, and spermatogenesis to a large extent. Mt-Zn-MOFs maintained normal testicular, hepatic, and renal histopathology in the aflatoxin treatment. Regardless, aflatoxin caused severe renal toxicity, Mt-Zn-MOFs reversed the effects of toxins and restored their normality, and are recommended to treat aflatoxicosis and mycotic infections.

PMID 42464561
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PubMedFrontiers in oncology2026-07-17

Adverse effects of systemic therapy in a patient with urothelial bladder cancer and chronic kidney disease - a case report.

Najmrocka Martyna M, Semeniuk Aleksandra A, Stec Rafał R

For patients with urothelial bladder cancer who are ineligible for cisplatin-based chemotherapy, particularly those with chronic kidney disease (CKD), immune checkpoint inhibitors (ICIs) have become an important therapeutic alternative. However, these agents may cause immune-related adverse events (irAEs) that can mimic CKD progression and complicate clinical management. We report the case of a 72-year-old man with type 2 diabetes mellitus and CKD who underwent cystoprostatectomy for locally advanced urothelial carcinoma. Following confirmation of PD-L1 positivity, adjuvant nivolumab was initiated at a dose of 240 mg every two weeks. After three treatment cycles, the patient developed diffuse myalgia, progressive weakness of all limbs, and paresthesia of the upper extremities. Laboratory results showed leukocytosis with neutrophilia and elevated alanine aminotransferase (100 U/L), C-reactive protein (119 mg/L), and troponin (113 ng/L), with normal creatine kinase activity. Electrocardiography and echocardiography excluded ischemia and myocarditis, while electromyography was unremarkable. High-dose intravenous glucocorticosteroids (1 mg/kg) led to clinical improvement, but symptom recurrence during tapering required re-escalation of immunosuppressive therapy. Multidisciplinary evaluation revealed chronic steroid toxicity and secondary testosterone deficiency. The patient continued on a gradual steroid taper combined with testosterone replacement and rehabilitation, achieving steady functional recovery under specialist follow-up. The presentation was consistent with ICI-induced muscular and endocrine toxicity, with no evidence of myocarditis or neuromuscular transmission disorder. This case underscores the diagnostic complexity of distinguishing irAEs from CKD progression and other comorbidities, highlighting the importance of coordinated input from oncology, nephrology, endocrinology, neurology, and cardiology teams. Adjuvant nivolumab remains a valuable therapeutic option for cisplatin-ineligible urothelial carcinoma patients with CKD, but its safe use requires vigilant monitoring, timely immunosuppression, and cautious steroid tapering. This report contributes to the limited body of evidence on ICI safety in patients with renal impairment and provides practical insights for multidisciplinary management in this challenging clinical context.

PMID 42465579
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