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.
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Browse all Drug Analysis Profiles A–Z
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Silodosin
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
Clinical guidelines and formulary information
British National Formulary
Silodosin
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). 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.
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 medications. 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
Show
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
Patent information
All patents expired, 2 expired
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: