Silodosin 8mg capsules
Requires a prescription from a doctor or prescriber
Silodosin is a selective antagonist of alpha(α)-1 adrenergic receptors that binds to the α<sub>1A</sub> subtype with the highest affinity.
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EudraVigilance
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Suspected adverse reactions reported for Silodosin
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1 branded products available
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 23 · Randomised trials: 26 · 2006–2026
Showing the 50 most relevant studies, sorted by most relevant.
Adhoni MZU, Haider M, Somani B, et al.
2024
- Indoles
- Ureteroscopy
- Postoperative Complications
M. Adhoni, Muhammad Haider, A. Almushatat, et al.
European Urology Open Science, 2024
Steven Sapta Putra
Journal of Advanced Research in Medical and Health Science (ISSN 2208-2425), 2023
Gopal Sharma
Indian Journal of Urology, 2023
Luciano A. Favorito
International Brazilian Journal of Urology, 2026
Murilo Ribeiro Sanches, Lucas Guimarães Campos Roriz de Amorim, Marcus Vinícius Barbosa Moreira, et al.
Urology Research and Practice, 2025
Dexing Wen, Huan Guo, Ying Wang, et al.
2026
Li J, Ai C, Yuan C, et al.
2025
Ramadhan M, Benzouak T, Ali Y, et al.
2025
- Ureteral Calculi
- Indoles
- Ureteroscopy
Ramanah M, Banerjee I, Nunkoo S, et al.
2025
Urolithiasis is a common urinary tract disease. This systematic review and meta-analysis aim to evaluate the effectiveness of alpha-blockers compared to novel therapies. The objective of this systematic review and meta-analysis was to compare the efficacy and safety of emerging pharmacologic therapies, namely tadalafil and mirabegron, with traditional alpha-blockers, such as tamsulosin and silodosin, as medical expulsive therapies (METs) for distal ureteric stones measuring ≤10 or <5 mm. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines were implemented during the conduct of this systematic review. A systematic review and meta-analysis of randomized controlled trials was conducted involving adult patients with distal ureteric stones. A total of six studies have been included, and quality assessment has been performed individually. Subgroup analyses were made using forest plots and funnel plots to study the odds ratios (ORs), confidence intervals (CIs), and heterogeneity of the articles. The studies included patients treated with various agents (tamsulosin, silodosin, tadalafil, and mirabegron) for up to four weeks. The primary outcome was the expulsion rate of the stones. Secondary outcomes included stone expulsion time (SET), analgesic use, hospital visits, and adverse effects. For the stone expulsion rate (SER), in the mirabegron subgroup, an overall pooled OR of 0.98 (95% CI: 0.26-3.66) with high heterogeneity was obtained (I² = 79%, p = 0.02), indicating substantial variability among the included studies. This could be due to the limited number of studies that require further investigation through a sensitivity analysis. In the tadalafil subgroup, an overall pooled OR of 1.79 (95% CI: 0.62-5.14) was obtained with tadalafil showing a better trend toward outcomes compared to alpha-blockers, but the result was not statistically significant. For the secondary outcomes, the tadalafil subgroup showed a significant reduction in the SET compared to alpha-blockers, with a pooled mean difference (MD) of -2.08 days (95% CI: -3.14 to -1.02), indicating no heterogeneity. However, the mirabegron subgroup obtained a pooled MD of 0.16 days (95% CI: -6.06 to 6.38) with very high heterogeneity (I² = 97%, p < 0.0001), suggesting large variability between the studies and no statistically significant difference in expulsion time between mirabegron and alpha-blockers. For the amount of analgesia used, an overall MD of 4.54 mg (95% CI: -53.19 to 62.27) was obtained, indicating no statistically significant difference in analgesic use between the newer drugs and alpha-blockers (p = 0.88). The frequency of adverse effects was noted more in the alpha-blocker group, with significant ejaculation and orthostatic hypertension noted in silodosin only, and insignificant side effects in both the mirabegron and tadalafil groups. It is concluded from this study that tadalafil is clinically better than alpha-blockers in the MET of distal ureteric stones of <10 mm. Tadalafil has a higher SER and a lower expulsion time, and requires a reduced amount of analgesia. However, given that pooled results are not statistically significant, the following require further evaluation. On the contrary, alpha-blockers are still better than mirabegron, but again, this is not statistically significant enough to prove their supremacy.
Abstract licence: CC BY
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
213 found
Half-life
8.07 hours
Mechanism
The pathogenesis of benign prostatic hyperplasia is not fully understood: it is…
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
32%
Half-life
8.07 hours
[L32368]
…
Protein binding
97%
[L32368]
Volume of distribution
49.5 L
[L32368]
Metabolism
Elimination
10 days
Clearance
10 L/h
[L32368]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Silodosin was first approved by the FDA in October 2008 [A231159] and it is also approved in Europe and Canada. Silodosin is available as oral capsules with common trade names Rapaflo and Urorec. It is indicated for the symptomatic treatment of benign prostatic hyperplasia in adults.[L32368] Most commonly affecting males over the age of 40 years, benign prostatic hyperplasia is the non-malignant enlargement of the prostate gland, associated with lower urinary tract symptoms that have a negative impact on the quality of life of patients.[A231159] Silodosin works by binding to α1A-adrenoceptors with high affinity and relaxing the lower urinary tract, thereby improving urinary symptoms and alleviating bladder outlet obstruction.[A231229]
[L32368]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 679 interactions
[L32393]
In clinical trials, postural hypotension was the most common dose-limiting adverse event. In case of drug overdose leading to hypotension, the patient should be placed in a supine position to restore blood pressure and normalize heart rate. Further measures, such as administration of intravenous fluids, may be initiated.
In case of the use of vasopressors, renal function should be monitored and supported as needed. Since silodosin is highly bound to plasma proteins, dialysis is unlikely to be beneficial.
[L32368]
α1-adrenoceptors are G protein-coupled receptors: upon binding of its natural ligand, norepinephrine and epinephrine, leads to the activation of phospholipase C and downstream signalling molecules, including inositol triphosphate and diacylglycerol. Ultimately, there is an increase in intracellular calcium levels and, consequently, smooth muscle contraction. Silodosin is an antagonist of α1-adrenoceptors, with the highest selectivity for the α1A-adrenoceptor subtype. By blocking the α1A-adrenoceptor signalling pathway, silodosin promotes prostatic and urethral smooth muscle relaxation, thereby improving lower urinary tract symptoms such as voiding. Silodosin also targets afferent nerves in the bladder, relieving bladder overactivity and storage symptoms.[A231159]
Silodosin inhibited the human ether-a-go-go-related gene (HERG) tail current; however, it has weak cardiovascular effects.[A231199] As with all α1-adrenoceptor antagonists blocking α1-adrenoceptors in the iris dilator muscle, silodosin may cause intraoperative floppy iris syndrome (IFIS), which is characterized by small pupils and iris billowing during cataract surgery in patients taking α1-AR antagonists.[A231229]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L32368]
Silodosin glucuronide or KMD-3213G, the main metabolite of silodosin, has an AUC three- or four fold higher than for the parent compound.
[A231159]
A moderate fat or calorie meal reduces Cmax by 18% to 43% and AUC by 4% to 49%, as well as Tmax by about one hour.
However, the US prescribing information recommends drug intake with meals to avoid the potential adverse effects associated with high plasma drug concentrations.
[L32368]
[L32368]
[L32368]
[L32368]
KMD-3293 has negligible pharmacological activity and reaches plasma exposures similar to that of silodosin. Silodosin is also metabolized by CYP3A4, which catalyzes the oxidation reaction.
[L32368]
Other than glucuronidation, dehydrogenation, and oxidation as its main metabolic pathways, silodosin can also undergo dealkylation (KMD-3289), N-dealkylation, hydroxylation, glucosylation, and sulfate conjugation. Metabolites of silodosin can undergo a series of further metabolic pathways.
[A231179]
[L32368]
[L32368]
Proteins and enzymes this drug interacts with in the body
PMID:32723862
Exhibits faster activation and deactivation kinetics and slow inactivation at membrane potentials positive to 240 mV, resulting in the weakest inward rectification PMID:32723862
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:17523162 PMID:21820390 PMID:23468132 PMID:24594635 PMID:24723470 PMID:24806754 PMID:31873305 PMID:7957936 PMID:8898203 PMID:9366571
Plays a role in the recruitment of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and sphingomyelin (SM) molecules to nonraft membranes and to further enrichment of SM and cholesterol in raft membranes in hepatocytes .
PMID:23468132
Required for proper phospholipid bile formation (By similarity).
Indirectly involved in cholesterol efflux activity from hepatocytes into the canalicular lumen in the presence of bile salts in an ATP-dependent manner .
PMID:24045840
Promotes biliary phospholipid secretion as canaliculi-containing vesicles from the canalicular plasma membrane .
PMID:28012258 PMID:9366571
In cooperation with ATP8B1, functions to protect hepatocytes from the deleterious detergent activity of bile salts .
PMID:21820390
Does not confer multidrug resistance (By similarity)
ATC G04CA04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Silodosin
Additional database identifiers
Drugs Product Database (DPD)
20659
ChemSpider
4471557
BindingDB
50160154
PDB
A1EMV
ZINC
ZINC000003806063
HUGO Gene Nomenclature Committee (HGNC)
HGNC:277
GenAtlas
ADRA1A
GeneCards
ADRA1A
GenBank Gene Database
D25235
GenBank Protein Database
433201
Guide to Pharmacology
22
UniProt Accession
ADA1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:280
GenAtlas
ADRA1D
GeneCards
ADRA1D
GenBank Gene Database
M76446
GenBank Protein Database
177807
Guide to Pharmacology
24
UniProt Accession
ADA1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:278
GenAtlas
ADRA1B
GeneCards
ADRA1B
GenBank Gene Database
M99589
Guide to Pharmacology
23
UniProt Accession
ADA1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6251
GenAtlas
KCNH2
GeneCards
KCNH2
GenBank Gene Database
U04270
GenBank Protein Database
487738
Guide to Pharmacology
572
UniProt Accession
KCNH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18862
GenAtlas
KCNH6
GeneCards
KCNH6
GenBank Gene Database
AF311913
GenBank Protein Database
11878259
Guide to Pharmacology
573
UniProt Accession
KCNH6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18863
GenAtlas
KCNH7
GeneCards
KCNH7
GenBank Gene Database
AF032897
GenBank Protein Database
4104136
UniProt Accession
KCNH7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:404
GenAtlas
ALDH2
GeneCards
ALDH2
GenBank Gene Database
X05409
GenBank Protein Database
28606
Guide to Pharmacology
2595
UniProt Accession
ALDH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:380
GeneCards
AKR1A1
GenBank Gene Database
J04794
GenBank Protein Database
178481
UniProt Accession
AK1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:45
GeneCards
ABCB4
GenBank Gene Database
M23234
GenBank Protein Database
307181
UniProt Accession
MDR3_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72