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dutasteride + tamsulosin (Jalyn / Combodart / Duodart)

✓ Approved

GSK · ADRA1A · 小分子

什么是 dutasteride + tamsulosin？

dutasteride + tamsulosin 是一种小分子，由GSK研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Jalyn, Combodart, Duodart
公司GSK
药物类别小分子
分子靶点ADRA1A, SRD5A1, SRD5A2
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, GSK

作用机制

分子靶点

dutasteride + tamsulosin 作用于 3 个分子靶点：

ADRA1Aadrenoceptor alpha 1A (ALPHA1AAR, ADRA1C)
SRD5A1steroid 5 alpha-reductase 1 (S5AR 1)
SRD5A2steroid 5 alpha-reductase 2 ()
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

dutasteride + tamsulosin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Reproductive system and breast disordersBenign prostatic hyperplasia✓ Approved

相关研究文献

PubMedDiabetes, obesity & metabolism2026-08-04

Absence of Interaction Between 5α-Reductase Inhibitors and Glucocorticoids on Incidence of Myocardial Infarction in People With Type 2 Diabetes.

Tu Haolan H, Ju Chengsheng C, McGurnaghan Stuart J SJ, Blackbourn Luke A K LAK et al.

People with Type 2 diabetes experience higher cardiometabolic risk, and both synthetic glucocorticoids and use of 5α-reductase inhibitors have been individually linked to increased risk of myocardial infarction. We tested whether the increase in risk is exacerbated by co-prescription of both drugs. We performed a population-based cohort study in the Scottish Diabetes Research Network-National Diabetes Dataset (SDRN-NDS) and IQVIA Medical Research Data-UK (IMRD-UK). Patients with Type 2 diabetes aged ≥ 40 years receiving 5α-reductase inhibitors or tamsulosin, who were incident users of systemic glucocorticoids during 2006-2021 were included. We modelled the joint effect of 5α-reductase inhibitors and cumulative exposure to glucocorticoids on the risk of myocardial infarction using a time-varying Cox proportional hazards model. A total of 13 161 patients with Type 2 diabetes were included in SDRN-NDS and 15 084 in IMRD-UK. Mean age was 71.4 ± 9.6 and 72.3 ± 9.4 years, with mean follow-up of 4.7 (3.6) and 5.6 (4.0) years, respectively. Median (IQR) total glucocorticoids exposure was 210 (96-630) and 420 (200-1240) prednisolone-equivalent milligram. Risk for myocardial infarction was increased among users of 5α-reductase inhibitors (HR [95% CI]: SDRN-NDS, 1.21 [1.02-1.43]; IMRD-UK, 1.27 [1.02-1.59]) and per SD increase in cumulative glucocorticoid exposure (HR [95% CI]: SDRN-NDS, 1.09 [1.03-1.14]; IMRD-UK, 1.08 [1.01-1.15]). We did not observe a multiplicative interaction (SDRN-NDS, p = 0.44; IMRD-UK, p = 0.68) between the use of the two drugs. People with Type 2 diabetes exposed to 5α-reductase inhibitors or glucocorticoids are at an increased risk of myocardial infarction, although a multiplicative interaction between the use of the two drugs was not found.

PMID 42547757
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PubMedCureus2026-08-02

Painless Ischemic Priapism Associated With Tamsulosin Use: A Case Report and Literature Review.

Rector Caitlin E CE, Lei Kevin K, Hubbard Lael L, Ovasapians Navasard N et al.

Tamsulosin, a selective α1-adrenergic antagonist prescribed for benign prostatic hyperplasia and expulsion of ureteral stones, carries a rare risk of priapism. We present a 59-year-old male with hypogonadism, hypertension, and hyperlipidemia who developed painless priapism 72 hours after initiating tamsulosin for ureterolithiasis. Despite the atypical absence of pain, penile blood gas analysis confirmed ischemic priapism. Initial treatment with intracavernosal phenylephrine (1000 mcg) failed, requiring bilateral corpus spongiosum shunts for resolution. A literature review revealed that many of the 14 existing cases identified occurred within 24 hours of drug initiation in middle-aged or older patients without additional risk factors. Approximately half responded to intracavernosal vasoconstrictors, while refractory cases required surgical intervention. To our knowledge, this is the first reported case of painless tamsulosin-induced ischemic priapism, emphasizing the importance of patient counseling and prompt evaluation of persistent erections regardless of pain intensity.

PMID 42540804
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PubMedAmerican journal of men's health2026-07-30

Concurrent Jackstone Calculus and Prostate Cancer: Should They Be Treated Concurrently or Sequentially?

Tian Shuo S, Li Huijuan H, Jiang Yuliang Y, Wang Cheng C et al.

Jackstone calculus is a rare urinary stone morphology with a distinctive spiculated appearance, most often reported in the bladder and usually associated with urinary stasis or outlet obstruction. We report a 70-year-old man with 1 year of progressive dysuria and intermittent interruption of urinary stream despite tamsulosin and finasteride. Urinalysis showed pyuria, hematuria, and bacteriuria. Ultrasonography and pelvic computed tomography identified an irregular star-shaped bladder stone and marked prostatic enlargement, with an estimated prostate volume of approximately 125 mL on ultrasonography. Serum total prostate-specific antigen was 16.2 ng/mL, with a free-to-total ratio of 0.138. Systematic transrectal biopsy showed adenocarcinoma in 2 of 12 cores, Gleason score 3 + 3 = 6 (Grade Group 1). After multidisciplinary discussion, the patient underwent laparoscopic radical prostatectomy with concomitant intact stone removal. The 3.1-cm stone showed classic jackstone morphology. Final pathology showed Gleason 3 + 4 = 7 adenocarcinoma (Grade Group 2), upgraded from biopsy, with negative surgical margins. Telephone follow-up at 1, 3, and 12 months showed sustained improvement of lower urinary tract symptoms without recurrent urinary tract infection-related symptoms. Postoperative imaging and prostate-specific antigen data were unavailable. This case is relevant to men's health because a visually distinctive bladder stone may coexist with clinically relevant prostatic disease. In men with lower urinary tract symptoms and abnormal prostate-specific antigen values, bladder outlet obstruction, infection, or bladder stones should not preclude further oncologic evaluation. In selected patients in whom definitive prostate surgery is chosen, combined stone removal can be a practical single-stage approach.

PMID 42531155
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PubMedInternational journal of urology : official journal of the Japanese Urological Association2026-07-29

The Impact of Dutasteride Treatment on Subsequent Multiparametric Prostate Magnetic Resonance Imaging Sequences and PI-RADS Score in Patients With PI-RADS 3 Lesions in the Transitional Zone.

Sekkeli Sami S, Erbin Akif A, Erdal Feyzi Sinan FS, Gursoy Ezgi E et al.

The effect of dutasteride on benign prostate lesions and Prostate Imaging-Reporting and Data System (PI-RADS) scores remains uncertain. We evaluated its impact on pathologically benign transition zone (TZ) PI-RADS 3 lesions. We reviewed 3104 multiparametric magnetic resonance imaging (mp-MRI) scans (March 2019-November 2023). Patients undergoing MRI-ultrasound fusion biopsy for PI-RADS 3 lesions with ≥ 2 mp-MRI scans were evaluated. After exclusions, dutasteride users formed the study group (n = 24) and non-users the control group (n = 60). Demographics, prostate-specific antigen (PSA), PSA density, prostate volume, pre-biopsy/control mp-MRI characteristics and PI-RADS scores were compared. Mean dutasteride use was 12.1 months. Lesion size decreased in both groups, more so in the study group. Within the study group, mean lesion apparent diffusion coefficient (ADC) increased and the T2-weighted (T2WI) lesion/transition-zone ROI ratio decreased whereas neither changed in controls; on between-group comparison, the ADC increase was significantly greater but the T2WI ratio change was not. Complete lesion disappearance was significantly more frequent in the study group and remained an independent predictor on multivariable analysis; PI-RADS up/downgrading and new-lesion rates were similar. In benign TZ PI-RADS 3 lesions, dutasteride did not affect PI-RADS up-/downgrading of persistent lesions but was independently associated with a higher rate of complete lesion disappearance, a greater reduction in lesion size, and a greater increase in lesion ADC; the T2WI ratio change did not differ between groups. Because these changes can make benign lesions appear less conspicuous, dutasteride use should be conveyed to the radiologist interpreting follow-up mp-MRI.

PMID 42522546
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PubMedGalen medical journal2026-07-25

Effect of Tamsulosin on Osteopontin Gene Expression in Preventing Ethylene Glycol-Induced Kidney Stone in Male Wistar Rats : Short title: Effect of Tamsulosin on Osteopontin Gene Expression.

Parvizrad Ramin R, Ghorbani Marghamlki Elahe E, Nikfar Somayeh S, Khalili Dermani Sara S

Tamsulosin, an α1-adrenergic receptor antagonist, has been proposed as a potential therapeutic agent against urolithiasis-induced renal damage. However, limited in vivo evidence exists regarding its renoprotective mechanisms. Forty male Wistar rats were randomly allocated into four groups (n=10/group): positive control, negative control (ethylene glycol-induced urolithiasis), prevention (tamsulosin administered simultaneously with ethylene glycol), and treatment (tamsulosin administered after model induction). Biochemical parameters including serum creatinine, urea, uric acid, calcium, and phosphorus were measured using rat-validated commercial kits (Pars Azmun, Iran). Normal ranges were defined based on published reference values. Gene expression was analyzed by qPCR using the 2^-ΔΔCt method. Study design and reporting followed the ARRIVE checklist. At day 30, the prevention group exhibited significantly lower serum creatinine (0.60 ± 0.08 mg/dL) compared to the negative control (0.98 ± 0.12 mg/dL, P0.01). Although urea levels were slightly higher in the prevention group (4.0 ± 0.7 mg/dL) versus the negative control (3.22 ± 0.6 mg/dL), the calculated BUN/creatinine ratio was significantly improved (46.7 vs. 33.0, P0.05). No significant changes were observed in serum calcium or phosphorus. Gene expression analysis showed upregulation of protective markers in the prevention group. In vivo findings on the beneficial effects of tamsulosin on the renal profile in ethylene glycol-induced urolithiasis illustrate its protective effects on the renal system through improvement of creatinine clearance and BUN/creatinine balance. This underscores its probable use as a protective therapeutic agent against renal injury of crystallization origin.

PMID 42499366
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PubMedFrontiers in neuroendocrinology2026-07-24

Steroid 5α-reductases in the brain: From neurosteroidogenesis to therapeutic implications.

Braccagni Giulia G, Branca Caterina C, Bortolato Marco M

Steroid 5α-reductases (5αRs) catalyze the irreversible, NADPH-dependent reduction of Δ4-3-ketosteroids. This process regulates major steroid signaling pathways, including neurosteroid biosynthesis, androgen activation, and glucocorticoid metabolism. By governing these processes, 5αRs influence GABAergic and dopaminergic neurotransmission, and behavioral responses to stress and reward. Although the two principal isoenzymes, 5αR1 and 5αR2, have overlapping functions, they are increasingly recognized as functionally distinct. 5αR1 supports constitutive neurosteroid synthesis in several brain regions. Conversely, 5αR2, long known for converting testosterone to dihydrotestosterone during male sexual differentiation, has emerged as the enzyme that mediates rapid allopregnanolone production in the prefrontal cortex of males during acute stress. These advances may provide a framework for understanding the complex neurobehavioral profile of 5αR inhibitors such as finasteride and dutasteride. These drugs have been associated with depression, anxiety, suicidality, sexual dysfunction, and, in some individuals, persistent sexual, somatic, and neuropsychiatric symptoms after discontinuation. At the same time, 5αR inhibition may have therapeutic value in conditions characterized by excessive or maladaptive neurosteroid signaling, including tic disorders, impulse-control disorders, and substance use disorders. In this comprehensive review, we synthesize pharmacological, genetic, and behavioral evidence on the distinct contributions of 5αR1 and 5αR2 to steroid signaling across stress, sex, and development. Finally, we outline several open questions in the biology of 5αRs, the resolution of which will be essential to advancing toward mechanistically precise and clinically actionable interventions.

PMID 42492846
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