Loperamide 2mg oral lyophilisates_sugar free
Acute diarrhoea
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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.
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Suspected adverse reactions reported for Loperamide
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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.
EudraVigilance
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Suspected adverse reactions reported for Loperamide
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1 branded products available
Part of the Diocalm brand family (generic: Loperamide)
MHRA licensed products
View all licensed products for Loperamide on the MHRA register
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Loperamide
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Faecal incontinence in adults: management (CG49)
Irritable bowel syndrome in adults: diagnosis and management (CG61)
Clostridioides difficile infection: antimicrobial prescribing (NG199)
Teduglutide for treating short bowel syndrome (TA804)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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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
None known
Half-life
10.8 hours
Mechanism
Enteric neurons synthesize and release endogenous opioid peptides and other neur…
Food interactions
None known
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1%
Half-life
10.8 hours
[L42790]
Protein binding
95%
[L42790]
Volume of distribution
[A251610]
Although highly lipophilic, loperamide does not cross the blood-brain barrier [A6249] and generally acts peripherally.
[A251615]…
Metabolism
Elimination
1%
[A251625]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L42785]
As an off-label use, it is often used to manage chemotherapy-related diarrhea.
[A251610]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1020 interactions
[L42780]
Due to its actions on opioid receptors, loperamide has been misused and abused to self-manage opioid withdrawal symptoms and to induce euphoria.
[A251610][A251625]
However, loperamide is associated with a risk of experiencing a range of adverse effects, often life-threatening, if taken for non-therapeutic reasons or at doses higher than the recommended dose.
[L42790]
Loperamide overdose can lead to a range of cardiac and non-cardiac effects. Chronic ingestion of doses ranging from 70 mg to 1600 mg daily - which is four to 100 times the recommended dose - resulted in life-threatening cardiac adverse reactions, including QT/QTc and QRS interval prolongation, Torsades de Pointes, Brugada syndrome and other ventricular arrhythmias, syncope, cardiac arrest, and death. These cases included instances of loperamide misuse and abuse.
In case of cardiac effects, it is recommended that loperamide is discontinued and therapies to manage and prevent cardiac arrhythmias are initiated.
[L42790]
Cases of loperamide overdose may cause opioid toxic effects including CNS depression (e.g. altered mental status, stupor, coordination disorders, somnolence, miosis, muscular hypertonia, respiratory depression), hypotension, urinary retention, and paralytic ileus.
[L42790]
Naloxone may reverse the opioid-related toxicity, including CNS and respiratory depression, and hypotension, associated with loperamide overdosage.
[L42790]
Loperamide acts on the mu (μ)-opioid receptor expressed on the circular and longitudinal intestinal muscle.[A251610] Receptor binding leads to the recruitment of G-protein receptor kinases and the activation of downstream molecular cascades that inhibit enteric nerve activity.[A251630] By inhibiting the excitability of enteric neurons, loperamide suppresses neurotransmitter release, pre-synaptic and post-synaptic inhibition of transmission of excitatory and inhibitory motor pathways, and secretomotor pathways.[A251630] Loperamide inhibits the release of acetylcholine and prostaglandins,[L42790] thereby reducing propulsive peristalsis and increasing intestinal transit time.[A251615][L42790] Loperamide stimulates the intestinal absorption of water and electrolytes by inhibiting calmodulin.[A251615] Loperamide can bind to and hyperpolarize submucosal secretomotor neurons, promoting dry, hard stools.[A251630]
While loperamide is a potent mu-opioid receptor agonist,[A251615] it does not mediate significant analgesic activity at therapeutic and supratherapeutic doses.[A6249][A251615] However, at high doses of loperamide, inhibition of P-glycoprotein-mediated drug efflux may allow loperamide to cross the blood-brain barrier, where loperamide can exert central opioid effects and toxicity.[A251610]
At very high plasma concentrations, loperamide can interfere with cardiac conduction.[A251625] Because loperamide inhibits the Na+-gated cardiac channels [A251610] and ether-a-go-go–related gene potassium channels,[A251625] the drug can prolong the QRS complex and the QTc interval, which can lead to ventricular dysrhythmias, monomorphic and polymorphic ventricular tachycardia, torsade de pointes, ventricular fibrillation, Brugada syndrome, cardiac arrest, and death.[A251610]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A251615]
The drug bioavailability is less than 1%.
[A251610]
Following oral administration of a 2 mg capsule of loperamide, plasma concentrations of unchanged drug were below 2 ng/mL. Plasma loperamide concentrations are highest approximately five hours after administration of an oral capsule of loperamide and 2.5 hours after the liquid formulation of the drug.
[L42790]
[L42790]
[L42790]
[A251610]
Although highly lipophilic, loperamide does not cross the blood-brain barrier [A6249] and generally acts peripherally.
[A251615]
[L42790]
Metabolites of loperamide are pharmacologically inactive.
[A251625]
[A251625]
Excretion of the unchanged loperamide and its metabolites mainly occurs through the feces.
[L42790]
Only 1% of an absorbed dose excreted unchanged in the urine.
[A251625]
Proteins and enzymes this drug interacts with in the body
PMID:10529478 PMID:12589820 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone .
PMID:10529478 PMID:10836142 PMID:12589820 PMID:19300905 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors .
PMID:7905839
The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 .
PMID:12068084
They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity).
The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity).
The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation (By similarity). Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling (By similarity).
Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity)
Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine
Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain.
Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions
They are however insensitive to dihydropyridines (DHP)
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
ATC A07DA53
ATC A07DA03
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)
Loperamide
Additional database identifiers
Drugs Product Database (DPD)
2251
ChemSpider
3818
BindingDB
50017698
ZINC
ZINC000000537928
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8156
GenAtlas
OPRM1
GeneCards
OPRM1
GenBank Gene Database
L25119
GenBank Protein Database
452073
Guide to Pharmacology
319
UniProt Accession
OPRM_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8153
GenAtlas
OPRD1
GeneCards
OPRD1
GenBank Gene Database
U07882
GenBank Protein Database
27545517
Guide to Pharmacology
317
UniProt Accession
OPRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9201
GenAtlas
POMC
GeneCards
POMC
GenBank Gene Database
M38297
GenBank Protein Database
190188
UniProt Accession
COLI_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1388
GenAtlas
CACNA1A
GeneCards
CACNA1A
GenBank Gene Database
AF004884
GenBank Protein Database
2213913
UniProt Accession
CAC1A_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:1442
GeneCards
CALM1
UniProt Accession
CALM1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1445
GeneCards
CALM2
UniProt Accession
CALM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1449
GeneCards
CALM3
UniProt Accession
CALM3_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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
All patents expired, 3 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: