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dutasteride + tamsulosin (Jalyn / Combodart / Duodart)

✓ Approved

GSK · ADRA1A · Small Molecule

What is dutasteride + tamsulosin?

dutasteride + tamsulosin is a small molecule developed by GSK. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesJalyn, Combodart, Duodart
CompanyGSK
Drug ClassSmall Molecule
Molecular TargetADRA1A, SRD5A1, SRD5A2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, GSK

Mechanism of Action

Molecular Targets

dutasteride + tamsulosin acts on 3 molecular targets:

ADRA1Aadrenoceptor alpha 1A (ALPHA1AAR, ADRA1C)
SRD5A1steroid 5 alpha-reductase 1 (S5AR 1)
SRD5A2steroid 5 alpha-reductase 2 ()
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

dutasteride + tamsulosin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Reproductive system and breast disordersBenign prostatic hyperplasia✓ Approved

Related Research Articles

PubMedCureus2026-06-09

Post-extracorporeal Membrane Oxygenation (ECMO) Bilateral Urolithiasis in an Adolescent With B-cell Acute Lymphoblastic Leukemia (ALL): A Case Report.

Tobia González Sebastian G SG, Raju Gaayana A GA, Smith-Harrison Leon I LI

Acute kidney injury and metabolic derangements are common after extracorporeal membrane oxygenation (ECMO), yet their potential contribution to urinary stone formation is rarely described. Critically ill patients may develop lithogenic conditions related to tubular injury, oliguria, prolonged immobilization, catabolism, infection, and alterations in urinary solute handling. We report the case of a 13-year-old girl with B-cell acute lymphoblastic leukemia undergoing induction chemotherapy who developed Pseudomonas septic shock requiring prolonged extracorporeal support with venoarterial ECMO followed by venovenous ECMO. Her course was further complicated by acute respiratory distress syndrome, bilateral pneumothoraces, and prolonged intensive care unit hospitalization. During recovery, computed tomography revealed bilateral renal and ureteral calculi with moderate left hydroureteronephrosis. Despite significant stone burden, the patient remained clinically stable without urinary tract infection, preserved renal function, and gradual radiographic improvement. Because of ongoing chemotherapy, immunosuppression, pulmonary risk, and fluctuating procedural candidacy, management required repeated multidisciplinary reassessment involving pediatric urology, oncology, pulmonology, nephrology, and the patient's family. Initial decompression and staged ureteroscopic intervention were considered; however, serial imaging demonstrated partial spontaneous migration of calculi, allowing temporary conservative management with tamsulosin and close surveillance. Persistent left-sided impaction and limited further migration ultimately supported definitive bilateral ureteroscopy with laser lithotripsy and short-term stenting once medically optimized. This case highlights the complex balance between surgical urgency and systemic risk in post-ECMO patients with urolithiasis. It also raises the possibility that ECMO-related renal injury and critical illness physiology may contribute to the formation of low-density or matrix-type stones. Individualized multidisciplinary decision-making is essential in medically fragile patients.

PMID 42261493
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PubMedMedicine2026-06-09

Drug-related pulmonary fibrosis: A real-world pharmacovigilance study of the FDA Adverse Event Reporting System.

Jian Ruonan R, Yang Lei L, Guo Jingjing J, Shi Erxia E et al.

Pulmonary fibrosis (PF) can lead to respiratory distress, persistent dry cough, and a decline in quality of life, and may be life-threatening in severe cases. The aim is to mine and analyze drug-related PF signals, summarize potential risk medications, and provide references for clinical medication safety. This research accessed data from the US Food and Drug Administration Adverse Event Reporting System covering reports from January 2004 to September 2024. Proportional disproportionality methods were utilized to explore the relationship between drugs and PF, and to assess demographic information, drug-related PF risks, and the timing of PF onset. The Food and Drug Administration Adverse Event Reporting System database contained reports of 830 drugs associated with PF. Through disproportionality analysis and subsequent filtering, 33 drugs were identified as having significant risks. Fifteen antitumor and immunomodulatory drugs (45.45%) were noted, including bleomycin (reporting odds ratio [ROR] = 41.68), interferon gamma-1B (ROR = 12.11), and anagrelide (ROR = 6.63). Four cardiovascular system drugs (12.12%) included amiodarone (ROR = 41.92), dronedarone (ROR = 10.25), and simvastatin (ROR = 6.94). Four respiratory system drugs (12.12%) included indacaterol (ROR = 6.87), salmeterol/fluticasone (ROR = 4.30), and olodaterol (ROR = 3.76). Four antipathogenic microbial drugs (12.12%) included nitrofurantoin (ROR = 22.92), sulfasalazine (ROR = 5.69), and hydroxychloroquine (ROR = 3.51). Six other drugs (18.18%) included iodine-131 (ROR = 19.72), calcium carbonate (ROR = 8.59), and tamsulosin (ROR = 7.48). Amiodarone (Bayesian confidence propagation neural network [BCPNN] = 5.26), bleomycin (BCPNN = 4.95), and nitrofurantoin (BCPNN = 4.40) were the 3 drugs characterized by the greatest associated PF risk. The time to PF onset from antitumor and immunomodulatory drugs was significantly shorter than that from other drug types (P = .0082). The study identified 33 drugs showing disproportionality signals suggestive of potential associations with PF, most notably among antitumor and immunomodulatory agents, which exhibited a significantly shorter time to PF onset compared with other drug classes. The 3 drugs associated with the greatest PF risk were amiodarone, bleomycin, and nitrofurantoin. These findings highlight potential pharmacovigilance signals that warrant clinical vigilance and further validation through prospective studies.

PMID 42260802
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PubMedFrontiers in pharmacology2026-06-08

Association of long-term 5α-reductase inhibitor use with survival in men with renal cell carcinoma: a nationwide population-based cohort study.

Lee Sieun S, Lee Jooyoung J, Min Kyungchan K, Tae Jong Hyun JH et al.

The incidence and mortality of renal cell carcinoma (RCC) exhibit marked sex-based differences, suggesting a potential role for androgen signaling in disease progression. Although 5α-reductase inhibitors (5-ARIs) are widely prescribed for benign prostatic conditions, their potential association with survival in patients with RCC remains poorly understood. We evaluated the association between long-term use of 5-ARIs and overall survival in men with RCC. This population-based retrospective cohort study used data from the Korean National Health Insurance Service database (2007-2020). Men aged ≥40 years with newly diagnosed RCC were included. Long-term 5-ARI use was defined as cumulative prescription of finasteride or dutasteride for ≥365 days prior to diagnosis. Propensity score matching (1:3 ratio) was employed to balance baseline characteristics, including age, year of diagnosis, income, comorbidity burden, and hypertension. The primary outcome was all-cause mortality, analyzed using Cox proportional hazards regression models. Subgroup analyses were stratified by treatment modality and Charlson comorbidity index (CCI). Among 31,927 eligible men, 1,803 5-ARI users were matched with 5,409 non-users (mean age 71.2 years). Long-term 5-ARI use was associated with significantly lower all-cause mortality (hazard ratio [HR]: 0.88; 95% CI: 0.79-0.94; p < 0.001). Although no significant associations were observed in patients undergoing surgery (HR: 0.94; 95% CI: 0.79-1.07) or systemic therapy (HR: 1.15; 95% CI: 0.82-1.55), a distinct survival benefit was evident in the no-surgery/no-systemic therapy group (HR: 0.82; 95% CI: 0.73-0.92; p < 0.001). Within this untreated subgroup, the benefit was most pronounced in patients with low comorbidity (CCI 0-1: HR: 0.78; 95% CI: 0.65-0.91) compared with those with high comorbidity (CCI ≥2: HR: 0.89; 95% CI: 0.76-1.03). Long-term 5-ARI use is associated with improved overall survival in men with RCC, particularly among those with low comorbidity who are managed without active oncological treatment. These findings suggest that androgen modulation may influence RCC progression and support the investigation of 5-ARIs as potential adjunctive agents in selected clinical settings.

PMID 42256393
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PubMedUrologia2026-06-05

A randomized controlled trial comparing alpha-blocker (tamsulosin) and a phyto-complex (Solidago virga-aurea, Phyllantus niruri, Epilobium angustifolium, Peumus boldus and Ononis spinosa) in the treatment of ureteral stent-related symptoms.

Gallo Giacomo G, Cicione Antonio A, Nacchia Antonio A, Lombardo Riccardo R et al.

Aim of our study is to compare phytotherapy (a combination of extracts of Solidago virga-aurea, Phyllantus niruri, Epilobium angustifolium, Peumus boldus and Ononis spinosa) versus Tamsulosin effect on double J stent-related symptoms. Between October 2021 and October 2022, 60 patients undergoing double J stent positioning were randomly divided into 2 (group 1, n: 30, group 2, n: 30). Each patient randomly received Tamsulosin 0.4 mg (one capsule per day, group 1) or phyto-complex (one capsule filled with extracts per day, group 2) for 1 month in an open label setting. Ureteral stent-related morbidity indices including urinary symptom, pain, general health, quality of work, sexual score and additional problems measured by Ureteral Symptom Score Questionnaire (USSQ) at the 1st, 7th and 21st (double J stent removal) day after stent positioning (labeled as Day 1, Day 7, and Day 21, respectively) were evaluated. Although both treatments resulted in an improvement from baseline in each USSQ parameter, the only statistically significant difference between the two groups was detected in terms of urinary symptoms domain of the USSQ at 7 and 21 days (respectively -6.1 ± 5.5 vs -4.6 ± 5.1 and -5.2 ± 6.7 vs -4.4 ± 5.9) in favor of the tamsulosin group, while no statistically significant differences were detected in terms of improvements in pain, general health, quality of work, sexual score and additional problems (p value >0.05). According to our results, we suggest that this combination of extracts could be as effective as Tamsulosin 0.4 mg to minimize stent-related urinary symptoms and improve general health in patients with double J stent.

PMID 42244389
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PubMedDrug delivery and translational research2026-05-31

Dual-drug nanostructured lipid carriers of spironolactone and 2-deoxy-D-ribose for targeted follicular delivery in androgenetic alopecia.

Kayal Pritam P, Mishra Manoj Kumar MK, Jawahar Natarajan N

Androgenetic alopecia (AGA) is a multifactorial condition driven by dihydrotestosterone (DHT)-induced follicular miniaturization and reduced perifollicular angiogenesis. Existing treatments such as finasteride, minoxidil, and dutasteride often show limited efficacy and systemic side effects like sexual dysfunction or cardiovascular issues, necessitating targeted approaches. The present study developed dual-drug nanostructured lipid carriers (NLCs) co-delivering spironolactone (SL), an anti-androgen, and 2-deoxy-D-ribose (2dDR), a pro-angiogenic agent, for synergistic follicular regeneration. NLCs were prepared by the hot microemulsion method, incorporating stearic acid as a solid lipid and fenugreek oil as a liquid lipid, with Span 80/Tween 80 surfactants. A Central Composite Design (CCD) was optimised to achieve minimal particle size and optimal zeta potential by varying lipid ratios and surfactant levels. The formulations were characterized by particle size analysis and zeta potential measurements, differential scanning calorimetry (DSC), X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), and in vitro drug release kinetics. Cytotoxicity and dihydrotestosterone (DHT)-protection assays were performed using human dermal papilla cells (hDPCs). Optimized SL-2dDR NLCs exhibited a particle size of 343.03 ± 9.0 nm, a PDI of 27.97 ± 2.84%, and a zeta potential of -20.13 ± 0.40 mV. Entrapment efficiency reached 99.00 ± 0.5% for SL and 98.75 ± 0.7% for 2dDR. DSC and XRD confirmed amorphous drug dispersion, while SEM revealed irregular, porous morphology favorable for follicular adhesion. In vitro release followed Higuchi kinetics for SL (R2 = 0.994) and Hixson-Crowell for 2dDR (R2 = 0.985). MTT assays demonstrated concentration-dependent cytoprotection against DHT-induced cytotoxicity, maintaining 82% cell viability at 50 µg/mL. The dual-drug NLC system represents a promising targeted therapy for AGA, combining anti-androgenic and pro-angiogenic mechanisms while minimizing systemic exposure.

PMID 42218358
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PubMedBMC medicine2026-05-28

Thyroid-stimulating hormone receptor mediates peripheral-central neuroimmune crosstalk in autoimmune thyroid diseases.

Zhang Haiyang H, Jiang Shufan S, Zhu Tianyi T, Liu Yuting Y et al.

Organ-specific autoimmune diseases, particularly Graves' disease (GD) and its extrathyroidal manifestation, Graves' orbitopathy (GO), are characterized by systemic autoimmunity that may extend its impact to the central nervous system (CNS). While thyroid-stimulating hormone receptor (TSHR) is the primary driver of pathological remodeling in the thyroid and orbital tissues, emerging evidence suggests it is also expressed in the brain and may participate in neuroimmune signaling. However, the molecular mechanisms linking peripheral TSHR-driven autoimmunity to these extended systemic features remain unclear. Thus, GD and GO provide a unique window to investigate how peripheral autoantibodies influence CNS involvement as part of its broader pathological spectrum. Genome-wide association studies (GWAS) and post-GWAS analyses were integrated with bulk RNA sequencing, single-cell and spatial transcriptomics, and brain imaging phenotypes to comprehensively characterize peripheral and central alterations in GD and GO. Mendelian randomization was applied to test causal relationships between genetic variants and brain signatures. Structural biology analyses were further conducted including protein-protein docking, small-molecule docking, and normal mode dynamics to identify prospective modulators of TSHR. Immunofluorescence staining was performed in a GO mouse model to validate the colocalization of potential interacted proteins in the specific brain region. Brain imaging-derived phenotypes (IDPs) alterations in GO and GO were systematically analyzed to identify neuroanatomical and functional alterations. TSHR was further identified as a shared genetic driver across peripheral and central compartments. TSHR was expressed in spiny projection neurons, microglia, and peripheral T cells, with cell-cell communication analyses highlighting TSHR-mediated interactions among neurons, endothelial cells, and microglia. Immunofluorescence staining in a GO mouse model confirmed the colocalization of TSHR with FN1 and GNAS in the basal ganglia, providing tissue-level validation of the computationally predicted ligand-receptor interactions. Immune profiling further showed immune alterations in GD and GO. Structural modeling supported plausible physical interfaces between TSHR and interacting proteins, and small-molecule screening identified three repurposable compounds - venetoclax, irinotecan, and dutasteride - with predicted favorable docking scores and stable binding poses in our simulations. These findings demonstrate that TSHR acts as a molecular hub mediating peripheral-central neuroimmune crosstalk in GD and GO. The results support a broader "disease-molecule axis" framework that links genetic susceptibility with multi-level immune and neural mechanisms. This work provides mechanistic insights relevant to the development of TSHR-targeted therapies, with implications for both peripheral immune modulation and central regulation. However, the limited sample size, lack of longitudinal follow-up, and absence of in vivo validation warrant cautious interpretation and further investigation.

PMID 42204533
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