Lidocaine 10mg/dose spray sugar free
Requires a prescription from a doctor or prescriber
Ever since its discovery and availability for sale and use in the late 1940s, lidocaine has become an exceptionally commonly used medication [T583].
Safety information for pregnancy and breastfeeding
Pregnancy
Breastfeeding
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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 Lidocaine
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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.
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Suspected adverse reactions reported for Lidocaine
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
2 branded products available
Part of the Xylocaine brand family (generic: Lidocaine)
MHRA licensed products
View all licensed products for Lidocaine on the MHRA register
Xylocaine 10mg/dose spray
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. 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
Lidocaine
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(9)
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Intrapartum care (NG235)
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
1 found
Half-life
1.5 to 2.0 hours
Mechanism
Lidocaine is a local anesthetic of the amide type [F4349, L5930, L5948].
Food interactions
None known
Human targets
8 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
35%
Half-life
1.5 to 2.0 hours
Protein binding
60 to 80%
Volume of distribution
0.7 to 1.5 L/kg
Metabolism
90%
Elimination
5%
Clearance
0.18 L
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Regardless, lidocaine is currently available as a relatively non-expensive generic medication that is written for in millions of prescriptions internationally on a yearly basis. It is even included in the World Health Organization's List of Essential Medicines [L6055].
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 2104 interactions
[L5930]
Patients may present initially with circumoral paraesthesia, numbness of the tongue, light-headedness, hyperacusis, and tinnitus .
[L5930]
Visual disturbance and muscular tremors or muscle twitching are more serious and precede the onset of generalized convulsions .
[L5930]
These signs must not be mistaken for neurotic behavior .
[L5930]
Unconsciousness and grand mal convulsions may follow, which may last from a few seconds to several minutes .
[L5930]
Hypoxia and hypercapnia occur rapidly following convulsions due to increased muscular activity, together with the interference with normal respiration and loss of the airway .
[L5930]
In severe cases, apnoea may occur. Acidosis increases the toxic effects of local anesthetics .
[L5930]
Effects on the cardiovascular system may be seen in severe cases .
[L5930]
Hypotension, bradycardia, arrhythmia and cardiac arrest may occur as a result of high systemic concentrations, with potentially fatal outcome .
[L5930]
Pregnancy Category B has been established for the use of lidocaine in pregnancy, although there are no formal, adequate, and well-controlled studies in pregnant women F4349. General consideration should be given to this fact before administering lidocaine to women of childbearing potential, especially during early pregnancy when maximum organogenesis takes place F4349.
Ultimately, although animal studies have revealed no evidence of harm to the fetus, lidocaine should not be administered during early pregnancy unless the benefits are considered to outweigh the risks .
[L5930]
Lidocaine readily crosses the placental barrier after epidural or intravenous administration to the mother .
[L5930]
The ratio of umbilical to maternal venous concentration is 0.5 to 0.6 .
[L5930]
The fetus appears to be capable of metabolizing lidocaine at term .
[L5930]
The elimination half-life in the newborn of the drug received in utero is about three hours, compared with 100 minutes in the adult .
[L5930]
Elevated lidocaine levels may persist in the newborn for at least 48 hours after delivery .
[L5930]
Fetal bradycardia or tachycardia, neonatal bradycardia, hypotonia or respiratory depression may occur .
[L5930]
Local anesthetics rapidly cross the placenta and when used for epidural, paracervical, pudendal or caudal block anesthesia, can cause varying degrees of maternal, fetal and neonatal toxicity F4349. The potential for toxicity depends upon the procedure performed, the type and amount of drug used, and the technique of drug administration F4349. Adverse reactions in the parturient, fetus and neonate involve alterations of the central nervous system, peripheral vascular tone, and cardiac function F4349.
Maternal hypotension has resulted from regional anesthesia F4349.
Local anesthetics produce vasodilation by blocking sympathetic nerves F4349. Elevating the patient’s legs and positioning her on her left side will help prevent decreases in blood pressure F4349. The fetal heart rate also should be monitored continuously, and electronic fetal monitoring is highly advisable F4349.
Epidural, spinal, paracervical, or pudendal anesthesia may alter the forces of parturition through changes in uterine contractility or maternal expulsive efforts F4349.
In one study, paracervical block anesthesia was associated with a decrease in the mean duration of first stage labor and facilitation of cervical dilation F4349. However, spinal and epidural anesthesia have also been reported to prolong the second stage of labor by removing the parturient’s reflex urge to bear down or by interfering with motor function F4349. The use of obstetrical anesthesia may increase the need for forceps assistance F4349.
The use of some local anesthetic drug products during labor and delivery may be followed by diminished muscle strength and tone for the first day or two of life F4349.
The long-term significance of these observations is unknown F4349. Fetal bradycardia may occur in 20 to 30 percent of patients receiving paracervical nerve block anesthesia with the amide-type local anesthetics and may be associated with fetal acidosis F4349. Fetal heart rate should always be monitored during paracervical anesthesia F4349.
The physician should weigh the possible advantages against risks when considering a paracervical block in prematurity, toxemia of pregnancy, and fetal distress F4349. Careful adherence to the recommended dosage is of the utmost importance in obstetrical paracervical block F4349. Failure to achieve adequate analgesia with recommended doses should arouse suspicion of intravascular or fetal intracranial injection F4349.
Cases compatible with unintended fetal intracranial injection of local anesthetic solution have been reported following intended paracervical or pudendal block or both. Babies so affected present with unexplained neonatal depression at birth, which correlates with high local anesthetic serum levels, and often manifest seizures within six hours F4349. Prompt use of supportive measures combined with forced urinary excretion of the local anesthetic has been used successfully to manage this complication F4349.
It is not known whether this drug is excreted in human milk F4349.
Because many drugs are excreted in human milk, caution should be exercised when lidocaine is administered to a nursing woman F4349.
Dosages in children should be reduced, commensurate with age, body weight and physical condition F4349.
The oral LD 50 of lidocaine HCl in non-fasted female rats is 459 (346-773) mg/kg (as the salt) and 214 (159-324) mg/kg (as the salt) in fasted female rats F4349.
In addition to blocking conduction in nerve axons in the peripheral nervous system, lidocaine has important effects on the central nervous system and cardiovascular system [F4349, L5930, L5948]. After absorption, lidocaine may cause stimulation of the CNS followed by depression and in the cardiovascular system, it acts primarily on the myocardium where it may produce decreases in electrical excitability, conduction rate, and force of contraction [F4349, L5930, L5948].
In particular, such cardiac effects are likely associated with the principal effect that lidocaine elicits when it binds and blocks sodium channels, inhibiting the ionic fluxes required for the initiation and conduction of electrical action potential impulses necessary to facilitate muscle contraction [F4349, L5930, L5948]. Subsequently, in cardiac myocytes, lidocaine can potentially block or otherwise slow the rise of cardiac action potentials and their associated cardiac myocyte contractions, resulting in possible effects like hypotension, bradycardia, myocardial depression, cardiac arrhythmias, and perhaps cardiac arrest or circulatory collapse [F4349, L5930, L5948].
Moreover, lidocaine possesses a dissociation constant (pKa) of 7.7 and is considered a weak base [L5948]. As a result, about 25% of lidocaine molecules will be un-ionized and available at the physiological pH of 7.4 to translocate inside nerve cells, which means lidocaine elicits an onset of action more rapidly than other local anesthetics that have higher pKa values [L5948]. This rapid onset of action is demonstrated in about one minute following intravenous injection and fifteen minutes following intramuscular injection [L5930]. The administered lidocaine subsequently spreads rapidly through the surrounding tissues and the anesthetic effect lasts approximately ten to twenty minutes when given intravenously and about sixty to ninety minutes after intramuscular injection [L5930].
Nevertheless, it appears that the efficacy of lidocaine may be minimized in the presence of inflammation [L5948]. This effect could be due to acidosis decreasing the amount of un-ionized lidocaine molecules, a more rapid reduction in lidocaine concentration as a result of increased blood flow, or potentially also because of increased production of inflammatory mediators like peroxynitrite that elicit direct actions on sodium channels [L5948].
How the body processes this drug — absorption, distribution, metabolism, and elimination
After injection into tissues, lidocaine is also rapidly absorbed and the absorption rate is affected by both vascularity and the presence of tissue and fat capable of binding lidocaine in the particular tissues F4468.
The concentration of lidocaine in the blood is subsequently affected by a variety of aspects, including its rate of absorption from the site of injection, the rate of tissue distribution, and the rate of metabolism and excretion [F4349, L5930, L5948]. Subsequently, the systemic absorption of lidocaine is determined by the site of injection, the dosage given, and its pharmacological profile [F4349, L5930, L5948]. The maximum blood concentration occurs following intercostal nerve blockade followed in order of decreasing concentration, the lumbar epidural space, brachial plexus site, and subcutaneous tissue [F4349, L5930, L5948].
The total dose injected regardless of the site is the primary determinant of the absorption rate and blood levels achieved [F4349, L5930, L5948]. There is a linear relationship between the amount of lidocaine injected and the resultant peak anesthetic blood levels [F4349, L5930, L5948].
Nevertheless, it has been observed that lidocaine hydrochloride is completely absorbed following parenteral administration, its rate of absorption depending also on lipid solubility and the presence or absence of a vasoconstrictor agent [F4349, L5930, L5948]. Except for intravascular administration, the highest blood levels are obtained following intercostal nerve block and the lowest after subcutaneous administration [F4349, L5930, L5948].
Additionally, lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion F4349.
[L5948]
[L5948]
In particular, lidocaine is distributed throughout the total body water .
[L5930]
Its rate of disappearance from the blood can be described by a two or possibly even three-compartment model .
[L5930]
There is a rapid disappearance (alpha phase) which is believed to be related to uptake by rapidly equilibrating tissues (tissues with high vascular perfusion, for example) .
[L5930]
The slower phase is related to distribution to slowly equilibrating tissues (beta phase) and to its metabolism and excretion (gamma phase) .
[L5930]
Lidocaine's distribution is ultimately throughout all body tissues .
[L5930]
In general, the more highly perfused organs will show higher concentrations of the agent .
[L5930]
The highest percentage of this drug will be found in skeletal muscle, mainly due to the mass of muscle rather than an affinity .
[L5930]
The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of lidocaine HCl [F4349, L5930]. Approximately 90% of lidocaine HCl administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged [F4349, L5930]. The primary metabolite in urine is a conjugate of 4-hydroxy-2,6-dimethylaniline [F4349, L5930].
[L5930]
This suggests by the latter that excretion of lidocaine occurs by non-ionic diffusion .
[L5930]
Proteins and enzymes this drug interacts with in the body
The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues .
PMID:15385606 PMID:16988069 PMID:17145499 PMID:17167479 PMID:19369487 PMID:24311784 PMID:25240195 PMID:26680203 PMID:7720699
Nav1.7 plays a crucial role in controlling the excitability and action potential propagation from nociceptor neurons, thereby contributing to the sensory perception of pain PMID:17145499 PMID:17167479 PMID:19369487 PMID:24311784
The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues .
PMID:1309946 PMID:21447824 PMID:23085483 PMID:23420830 PMID:25370050 PMID:26279430 PMID:26392562 PMID:26776555
Nav1.5 is the predominant sodium channel expressed in myocardial cells and it is responsible for the initial upstroke of the action potential in cardiac myocytes, thereby initiating the heartbeat .
PMID:11234013 PMID:11804990 PMID:12569159 PMID:1309946
Required for normal electrical conduction including formation of the infranodal ventricular conduction system and normal action potential configuration, as a result of its interaction with XIRP2 (By similarity)
PMID:10580103 PMID:12384689 PMID:24036948 PMID:24776970 PMID:25791876 PMID:26645915
Involved in membrane depolarization during action potential in nociceptors which function as key relay stations for the electrical transmission of pain signals from the periphery to the central nervous system .
PMID:24036948 PMID:24776970 PMID:25791876 PMID:26645915
Also involved in rapid BDNF-evoked neuronal depolarization PMID:12384689
PMID:10805725 PMID:27153536 PMID:2790960 PMID:35538033
Known ligands include EGF, TGFA/TGF-alpha, AREG, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF .
PMID:12297049 PMID:15611079 PMID:17909029 PMID:20837704 PMID:27153536 PMID:2790960 PMID:7679104 PMID:8144591 PMID:9419975
Ligand binding triggers receptor homo- and/or heterodimerization and autophosphorylation on key cytoplasmic residues. The phosphorylated receptor recruits adapter proteins like GRB2 which in turn activates complex downstream signaling cascades. Activates at least 4 major downstream signaling cascades including the RAS-RAF-MEK-ERK, PI3 kinase-AKT, PLCgamma-PKC and STATs modules .
PMID:27153536
May also activate the NF-kappa-B signaling cascade .
PMID:11116146
Also directly phosphorylates other proteins like RGS16, activating its GTPase activity and probably coupling the EGF receptor signaling to the G protein-coupled receptor signaling .
PMID:11602604
Also phosphorylates MUC1 and increases its interaction with SRC and CTNNB1/beta-catenin .
PMID:11483589
Positively regulates cell migration via interaction with CCDC88A/GIV which retains EGFR at the cell membrane following ligand stimulation, promoting EGFR signaling which triggers cell migration .
PMID:20462955
Plays a role in enhancing learning and memory performance (By similarity).
Plays a role in mammalian pain signaling (long-lasting hypersensitivity) (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:10454528 PMID:10525100 PMID:10966938 PMID:17509700 PMID:20722056 PMID:33124720
Also transports organic cations such as tetraethylammonium (TEA) without the involvement of sodium.
Relative uptake activity ratio of carnitine to TEA is 11.3 .
PMID:10454528 PMID:10525100 PMID:10966938
In intestinal epithelia, transports the quorum-sensing pentapeptide CSF (competence and sporulation factor) from B.subtilis which induces cytoprotective heat shock proteins contributing to intestinal homeostasis .
PMID:18005709
May also contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
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 S01HA07
ATC D04AB01
ATC R02AD02
ATC C01BB01
ATC S02DA01
ATC N01BB52
ATC C05AD01
ATC N01BB02
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)
Lidocaine
Additional database identifiers
Drugs Product Database (DPD)
10225
Drugs Product Database (DPD)
9471
ChemSpider
3548
BindingDB
50017662
PDB
LQZ
Guide to Pharmacology
2623
ZINC
ZINC000000020237
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10582
GenAtlas
SCN10A
GeneCards
SCN10A
GenBank Gene Database
AF117907
GenBank Protein Database
4838145
Guide to Pharmacology
585
UniProt Accession
SCNAA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10597
GenAtlas
SCN9A
GeneCards
SCN9A
GenBank Gene Database
X82835
GenBank Protein Database
758110
Guide to Pharmacology
584
UniProt Accession
SCN9A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10593
GenAtlas
SCN5A
GeneCards
SCN5A
GenBank Gene Database
M77235
GenBank Protein Database
184039
Guide to Pharmacology
582
UniProt Accession
SCN5A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10583
GenAtlas
SCN11A
GeneCards
SCN11A
GenBank Gene Database
AF188679
GenBank Protein Database
6572950
UniProt Accession
SCNBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3236
GenAtlas
EGFR
GeneCards
EGFR
GenBank Gene Database
X00588
GenBank Protein Database
757924
Guide to Pharmacology
1797
UniProt Accession
EGFR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10591
GenAtlas
SCN4A
GeneCards
SCN4A
GenBank Gene Database
M81758
GenBank Protein Database
338213
Guide to Pharmacology
581
UniProt Accession
SCN4A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_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: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:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_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:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_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:10969
GenAtlas
SLC22A5
GeneCards
SLC22A5
GenBank Gene Database
AF057164
GenBank Protein Database
3273741
UniProt Accession
S22A5_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
15 active patents, 16 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: