Urapidil 60mg capsules
Requires a prescription from a doctor or prescriber
Urapidil has been investigated for the treatment of Hypertension During Pre-Eclampsia.
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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.
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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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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: 16 · Randomised trials: 2 · Trials: 3 · 1979–2026
Showing the 50 most relevant studies, sorted by most relevant.
Theodorou A, Melanis K, Palaiodimou L, et al.
2026
- Hypertension
- Antihypertensive Agents
- Blood Pressure
IntroductionElevated blood pressure (BP) in acute hemorrhagic stroke has been associated with adverse clinical outcomes. Limited data from randomized controlled clinical trials (RCTs) indicate that early BP management, in the prehospital setting, may be safe and beneficial. We sought to evaluate the efficacy and safety of prehospital BP-lowering in acute hemorrhagic stroke when compared to usual care.Patients and methodsWe conducted a systematic review and meta-analysis including available RCTs evaluating prehospital BP-lowering among acute hemorrhagic stroke patients. The pooled risk ratio (RR) of a 3-month good functional outcome, defined as modified-Rankin-Scale scores of 0-2 and all-cause 3-month mortality were the primary efficacy and safety outcomes, respectively. Secondary outcomes included the pooled RR of hematoma expansion (HE) and serious adverse events (SAEs).ResultsA total of four RCTs were included, comprising 642 patients treated with prehospital BP-lowering therapies and 617 patients receiving usual care. Prehospital BP-lowering was associated with similar rates of good functional outcome (RR: 1.07; 95% CI, 0.52-2.19) and all-cause mortality (RR: 0.90; 95% CI, 0.60-1.35) at 3 months, compared to usual care. The risk of SAEs (RR: 0.97; 95% CI, 0.74-1.26) and HE (RR: 1.05; 95% CI, 0.45-2.46) did not significantly differ between the two groups. Subgroup analyses revealed the superiority of the α-adrenoreceptor blocker urapidil compared to glyceryl trinitrate in terms of reducing SAE risk and HE.ConclusionOur meta-analysis indicates that prehospital BP-lowering in acute hemorrhagic stroke does not improve functional outcome and survival. Future RCTs conducted in mobile stroke units, and exclusively focusing on patients with acute hemorrhagic stroke, are required.
Abstract licence: CC BY
Cui YK, Shang XJ
2023
- Prostatic Hyperplasia
- Lower Urinary Tract Symptoms
- Piperazines
Zhao Q, Liu S, Zhou Y, et al.
2026
BackgroundThe effect of vasodilators in the management of heart failure (HF) remains inconclusive. This study aims to evaluate and compare the overall benefits of vasodilators to patients with HF.MethodsPubMed, Embase, Cochrane Library, and Web of Science were searched from database inception to December 27th, 2021. Randomized controlled trials (RCTs) assessing the efficacy of vasodilators in the treatment of HF were included. The Cochrane risk of bias assessment tool was applied to assess the risk of bias of included studies. Meta-analysis was performed using R and Stata 15.0 software.ResultsA total of 5517 articles were retrieved, and 18 eligible RCTs were finally included, with 9188 participants. Network meta-analysis showed no difference in the mortality, readmission rate, incidence of adverse cardiovascular events, and serum creatinine (Scr) among different vasodilators. Urapidil was more effective in reducing NT-pro-BNP, compared with nitroglycerin [WMD=-975.64, 95%CI (-1558.32, -320.14)].ConclusionThere are no differences in the efficacy and safety among vasodilators in the management of HF. Especially, although nitroprusside may be the most effective in reducing mortality, there is no significant difference between other drugs. Given the low certainty of the evidence, current evidence suggests that vasodilators have limited efficacy in the routine management of HF. More well-designed RCTs are needed to validate these findings.Trial registrationPROSPERO (CRD42022351231).
Abstract licence: CC BY
Yan-zhong Xie, Jian-ming Ni, Shan-jing Zhang, et al.
Medicine, 2019
Jiaxiao M. Shi, Yulin Li, Cong Xing, et al.
Drug Design Development and Therapy, 2018
- Acute Disease
- Nitroglycerin
- Heart Failure
Gertraud Hanft, Gerhard Groß
British Journal of Pharmacology, 1989
- Tetralones
- Adrenergic alpha-Antagonists
- Antihypertensive Agents
Gerhard Groß, Gertraud Hanft, Christian-U. Rugevics
European Journal of Pharmacology, 1988
- Adrenergic alpha-Antagonists
- Binding Sites
- Binding, Competitive
Wei Yang, Yujie Zhou, Yan Fu, et al.
Yonsei Medical Journal, 2016
- Acute Disease
- Antihypertensive Agents
- Blood Pressure
Wei Yang, Qi Hua, Yu-Jie Zhou, et al.
The American Journal of the Medical Sciences, 2015
- Echocardiography
- Nitroglycerin
- Heart Failure
Wang W, Zhu D, Liu X, et al.
2026
- Hypertension
- Ischemic Stroke
- Brain Ischemia
RationaleHypertensive emergency complicated by acute ischemic stroke (AIS) represents a life-threatening clinical condition. Abrupt elevations in blood pressure not only increase the risk of stroke-related complications but also predispose patients to cerebral perfusion imbalance and target-organ injury. However, there is no consensus regarding the optimal antihypertensive strategy or individualized management protocol in this setting.Patient concernsThree individuals with preexisting chronic hypertension developed acute ischemic stroke in the context of a hypertensive emergency, posing challenges in evaluating disease evolution, optimizing individualized treatment strategies, and assessing long-term prognosis.DiagnosesBased on clinical manifestations and imaging examinations, all 3 cases were diagnosed as hypertensive emergencies with concomitant AIS.InterventionsIn the emergency department, all patients were managed with urapidil administered through a continuous microinfusion pump to achieve blood pressure control. Following stabilization, intravenous thrombolysis was performed in case 1, whereas mechanical thrombectomy was undertaken in cases 2 and 3.OutcomesAfter therapeutic intervention, all patients achieved blood pressure stabilization within the target range and demonstrated significant neurological recovery in the acute phase. Cases 1 and 2 demonstrated favorable clinical recovery without major complications during follow-up. Case 3 underwent successful emergency thrombectomy but was transferred to another institution shortly thereafter and was subsequently lost to follow-up.LessonsTreating hypertensive emergency in the setting of AIS demands careful appraisal of the patient's condition, hemodynamic profile, and cerebral perfusion needs to guide individualized therapy. Effective yet safe blood pressure reduction is critical to avoid cerebral hypoperfusion. Long-term prognosis can be further optimized through a multidisciplinary team (MDT), close follow-up, strict medication compliance, and targeted lifestyle interventions.
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
Investigational
Major interactions
49 found
Half-life
Not available
Mechanism
Not available
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1183 interactions
Proteins and enzymes this drug interacts with in the body
PMID:22957663 PMID:3138543 PMID:33762731 PMID:37935376 PMID:37935377 PMID:8138923 PMID:8393041
Also functions as a receptor for various drugs and psychoactive substances .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:38552625 PMID:8138923 PMID:8393041
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:8138923 PMID:8393041
HTR1A is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission: signaling inhibits adenylate cyclase activity and activates a phosphatidylinositol-calcium second messenger system that regulates the release of Ca(2+) ions from intracellular stores .
PMID:33762731 PMID:35610220
Beta-arrestin family members regulate signaling by mediating both receptor desensitization and resensitization processes .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of 5-hydroxytryptamine release and in the regulation of dopamine and 5-hydroxytryptamine metabolism .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of dopamine and 5-hydroxytryptamine levels in the brain, and thereby affects neural activity, mood and behavior .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the response to anxiogenic stimuli PMID:18476671 PMID:20363322 PMID:20945968
ATC C02CA06
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)
Urapidil
Additional database identifiers
ChemSpider
5437
BindingDB
50237617
ZINC
ZINC000001544805
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5286
GenAtlas
HTR1A
GeneCards
HTR1A
GenBank Gene Database
M28269
GenBank Protein Database
189928
Guide to Pharmacology
1
UniProt Accession
5HT1A_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