Tramadol 100mg/2ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
Tramadol is a centrally acting synthetic opioid analgesic and SNRI (serotonin/norepinephrine reuptake-inhibitor) that is structurally related to [codeine] and [morphine].
Some safe custody exemptions; written records required
Legal requirements and restrictions
Schedule 3 medicines that do not require locked storage or register entries.
Legal requirements
- Prescriptions valid for 28 days
- No controlled drugs register required
- No safe custody (locked storage) required
Other medicines in this category
Safety information for pregnancy and breastfeeding
Pregnancy
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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Yellow Card reports
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Suspected adverse reactions reported for Tramadol
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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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Suspected adverse reactions reported for Tramadol
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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.
8 branded products available
Part of the Dromadol brand family (generic: Tramadol)
MHRA licensed products
View all licensed products for Tramadol on the MHRA register
Zydol 100mg/2ml solution for injection ampoules
Tramadol 100mg/2ml solution for injection ampoules
Tramadol 100mg/2ml solution for injection ampoules
Tramadol 100mg/2ml solution for injection ampoules
Tramadol 100mg/2ml solution for injection ampoules
Tramadol 100mg/2ml solution for injection ampoules
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.
WHO defined daily dose (DDD)
300 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
Tramadol
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Neuropathic pain in adults: pharmacological management in non-specialist settings (CG173)
Caesarean birth (NG192)
Aptiva for painful diabetic neuropathy (MIB119)
Osteoarthritis in over 16s: diagnosis and management (NG226)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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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. 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
238 found
Half-life
5-6 hours
Mechanism
Tramadol is a centrally acting μ-opioid receptor agonist and SNRI (serotonin/nor…
Food interactions
2 warnings
Human targets
15 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
75%
Tramadol is administered as a racemate, with both the [-] and [+] forms of both tramadol and the M1 metabolite detected in circulation.…
Half-life
5-6 hours
[A173980]
Protein binding
20%
Volume of distribution
2.6-2.9 L/kg
Metabolism
90-95%
Elimination
90%
Clearance
3.73 ml/min/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Tramadol differs from other traditional opioid medications in that it doesn't just act as a μ-opioid agonist, but also affects monoamines by modulating the effects of neurotransmitters involved in the modulation of pain such as serotonin and norepinpehrine which activate descending pain inhibitory pathways.[A182279] Tramadol's effects on serotonin and norepinephrine mimic the effects of other SNRI antidepressants such as [duloxetine] and [venlafaxine].
Tramadol exists as a racemic mixture consisting of two pharmacologically active enantiomers that both contribute to its analgesic property through different mechanisms and are also themselves metabolized into active metabolites: (+)-tramadol and its primary metabolite (+)-O-desmethyl-tramadol (M1) are agonists of the μ opioid receptor while (+)-tramadol inhibits serotonin reuptake and (-)-tramadol inhibits norepinephrine reuptake. These pathways are complementary and synergistic, improving tramadol's ability to modulate the perception of and response to pain.[A4269][A183842]
Tramadol has also been shown to affect a number of other pain modulators within the central nervous system as well as non-neuronal inflammatory markers and immune mediators.[A183728][A183734][A183761][A17159][A182300] Due to the broad spectrum of targets involved in pain and inflammation, it's not surprising that the evidence has shown that tramadol is effective for a number of pain types including neuropathic pain, post-operative pain, lower back pain, as well as pain associated with labour, osteoarthritis, fibromyalgia, and cancer. Due to its SNRI activity, tramadol also has anxiolytic, antidepressant, and anti-shivering effects which are all frequently found as comorbidities with pain.[A182300]
Similar to other opioid medications, tramadol poses a risk for development of tolerance, dependence and abuse. If used in higher doses, or with other opioids, there is a dose-related risk of overdose, respiratory depression, and death.[A183830,F4679] However, unlike other opioid medications, tramadol use also carries a risk of seizure and serotonin syndrome, particularly if used with other serotonergic medications.[A183836][A179926]
Tramadol is also used off-label in the treatment of premature ejaculation.
[A173986]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1977 interactions
[A174010]
In carcinogenic studies, there are reports of murine tumors which cannot be concluded to be carcinogenic in humans. On the other hand, tramadol showed no evidence to be mutagenic in different assays and does not have effects on fertility. However, there are clear reports of embryotoxicity and fetotoxicity.[L9257,F4679]
Tramadol exists as a racemic mixture consisting of two pharmacologically active enantiomers that both contribute to its analgesic property through different mechanisms: (+)-tramadol and its primary metabolite (+)-O-desmethyl-tramadol (M1) are agonists of the μ opioid receptor while (+)-tramadol inhibits serotonin reuptake and (-)-tramadol inhibits norepinephrine reuptake. These pathways are complementary and synergistic, improving tramadol's ability to modulate the perception of and response to pain.[A4269]
In animal models, M1 is up to 6 times more potent than tramadol in producing analgesia and 200 times more potent in μ-opioid binding.[L9257]
Tramadol has also been shown to affect a number of pain modulators including alpha2-adrenoreceptors, neurokinin 1 receptors, the voltage-gated sodium channel type II alpha subunit[A183728], transient receptor potential cation channel subfamily V member 1 (TRPV1 - also known as the capsaicin receptor)[A183734], muscarinic receptors (M1 and M3), N-methyl-D-aspartate receptor (also known as the NMDA receptor or glutamate receptor)[A17158], Adenosine A1 receptors[A183761], and nicotinic acetylcholine receptor.[A17159]
In addition to the above neuronal targets, tramadol has a number of effects on inflammatory and immune mediators involved in the pain response. This includes inhibitory effects on cytokines, prostaglandin E2 (PGE2), nuclear factor-κB, and glial cells as well as a change in the polarization state of M1 macrophages.[A182300]
Apart from analgesia, tramadol may produce a constellation of symptoms (including dizziness, somnolence, nausea, constipation, sweating and pruritus) similar to that of other opioids.
Central Nervous System
In contrast to [morphine], tramadol has not been shown to cause histamine release. At therapeutic doses, tramadol has no effect on heart rate, left-ventricular function or cardiac index. Orthostatic hypotension has been observed.[L9257]
Tramadol produces respiratory depression by direct action on brain stem respiratory centres. The respiratory depression involves both a reduction in the responsiveness of the brain stem centres to increases in CO2 tension and to electrical stimulation.
Tramadol depresses the cough reflex by a direct effect on the cough centre in the medulla. Antitussive effects may occur with doses lower than those usually required for analgesia.
Tramadol causes miosis, even in total darkness. Pinpoint pupils are a sign of opioid overdose but
are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origin may produce
similar findings). Marked mydriasis rather than miosis may be seen with hypoxia in the setting of
oxycodone overdose.F4679
Seizures have been reported in patients receiving tramadol within the recommended dosage range. Spontaneous post-marketing reports indicate that seizure risk is increased with doses of tramadol above the recommended range. Risk of convulsions may also increase in patients with epilepsy, those with a history of seizures
or in patients with a recognized risk for seizure (such as head trauma, metabolic disorders,
alcohol and drug withdrawal, CNS infections), or with concomitant use of other drugs known to reduce the seizure threshold.F4679
Tramadol can cause a rare but potentially life-threatening condition resulting from concomitant administration of serotonergic drugs (e.g., anti-depressants, migraine medications). Treatment with the serotoninergic drug should be discontinued if such events (characterized by clusters of symptoms such as hyperthermia, rigidity, myoclonus, autonomic instability with possible rapid fluctuations of vital signs, mental status changes including confusion, irritability, extreme agitation progressing to delirium and coma) occur and supportive symptomatic treatment should be initiated. Tramadol should not be used in combination with MAO inhibitors or serotonin-precursors (such as L-tryptophan, oxitriptan) and should be used with caution in combination with other serotonergic drugs (triptans, certain tricyclic antidepressants, lithium, St. John’s Wort) due to the risk of serotonin syndrome.F4679
Gastrointestinal Tract and Other Smooth Muscle
Tramadol causes a reduction in motility associated with an increase in smooth muscle tone in the antrum of the stomach and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, while tone may be increased to the point of spasm resulting in constipation. Other opioid-induced effects may include a reduction in gastric, biliary and pancreatic secretions, spasm of the sphincter of Oddi, and transient elevations in serum amylase.F4679
Endocrine System
Opioids may influence the hypothalamic-pituitary-adrenal or -gonadal axes. Some changes that can be seen include an increase in serum prolactin and decreases in plasma cortisol and testosterone. Clinical signs and symptoms may be manifest from these hormonal changes.F4679
Hyponatremia has been reported very rarely with the use of tramadol, usually in patients with predisposing risk factors, such as elderly patients and/or patients using concomitant medications that may cause hyponatremia (e.g., antidepressants, benzodiazepines, diuretics). In some reports, hyponatremia appeared to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and resolved with discontinuation of tramadol and appropriate treatment (e.g., fluid restriction). During tramadol treatment, monitoring for signs and symptoms of hyponatremia is recommended for patients with predisposing risk factors.F4679
Cardiovascular
Tramadol administration may result in severe hypotension in patients whose ability to maintain adequate blood pressure is compromised by reduced blood volume, or concurrent administration of drugs such as phenothiazines and other tranquillizers, sedative/hypnotics, tricyclic antidepressants or general anesthetics. These patients should be monitored for signs of hypotension after initiating or titrating the dose of tramadol.F4679
QTc-Interval Prolongation
The maximum placebo-adjusted mean change from baseline in the QTcF interval was 5.5 ms in the 400 mg/day treatment arm and 6.5 ms in the 600 mg/day mg treatment arm, both occurring at the 8h time point. Both treatment groups were within the 10 ms threshold for QT prolongation. Post-marketing experience with the use of tramadol containing products included rare reports of QT prolongation reported with an overdose. Particular care should be exercised when administering tramadol to patients who are suspected to be at an increased risk of experiencing torsade de pointes during treatment with a QTc-prolonging drug.F4679
Abuse and Misuse
Like all opioids, tramadol has the potential for abuse and misuse, which can lead to overdose and death. Therefore, tramadol should be prescribed and handled with caution.F4679
Dependence/Tolerance
Physical dependence and tolerance reflect the neuroadaptation of the opioid receptors to chronic exposure to an opioid and are separate and distinct from abuse and addiction. Tolerance, as well as physical dependence, may develop upon repeated administration of opioids, and are not by themselves evidence of an addictive disorder or abuse. Patients on prolonged therapy should be tapered gradually from the drug if it is no longer required for pain control. Withdrawal symptoms may occur following abrupt discontinuation of therapy or upon administration of an opioid antagonist. Some of the symptoms that may be associated with abrupt withdrawal of an opioid analgesic include body aches, diarrhea, gooseflesh, loss of appetite, nausea, nervousness or restlessness, anxiety, runny nose, sneezing, tremors or shivering, stomach cramps, tachycardia, trouble with sleeping, unusual increase in sweating, palpitations, unexplained fever, weakness and yawning.F4679
How the body processes this drug — absorption, distribution, metabolism, and elimination
Tramadol is administered as a racemate, with both the [-] and [+] forms of both tramadol and the M1 metabolite detected in circulation. Following administration, racemic tramadol is rapidly and almost completely absorbed, with a bioavailability of 75%. This difference in absorption and bioavailability can be attributed to the 20-30% first-pass metabolism.
Peak plasma concentrations of tramadol and the primary metabolite M1 occur at two and three hours, respectively.F4679 Following a single oral dose of 100mg of tramadol, the Cmax was found to be approximately 300μg/L with a Tmax of 1.6-1.9 hours, while metabolite M1 was found to have a Cmax of 55μg/L with a Tmax of 3 hours.
[A4269][L9257]
Steady-state plasma concentrations of both tramadol and M1 are achieved within two days of dosing. There is no evidence of self-induction.F4679 Following multiple oral doses, Cmax is 16% higher and AUC is 36% higher than after a single dose, demonstrating a potential role of saturable first-pass hepatic metabolism in increasing bioavailability.
[A4269]
Intramuscular Administration
Tramadol is rapidly and almost completely absorbed following intramuscular administration. Following injection of 50mg of tramadol, Cmax of 166μg/L was found with a Tmax of 0.75 hours.
[A4269]
Rectal Administration
Following rectal administration with suppositories containing 100mg of tramadol, Cmax of 294μg/L was found with a Tmax of 3.3 hours.
The absolute bioavailability was found to be higher than oral administration (77% vs 75%), likely due to reduced first-pass metabolism with rectal administration compared to oral administration.
[A4269]
[A173980]
[A182300]
Tramadol crosses the blood-brain barrier with peak brain concentrations occurring 10 minutes following oral administration. It also crosses the placental barrier with umbilical concentrations being found to be ~80% of maternal concentrations.
[A4269]
The wide variability in the pharmacokinetic properties between patients can partly be ascribed to polymorphisms within the gene for CYP2D6 that determine its enzymatic activity.
CYP2D6\*1 is considered the wild-type allele associated with normal enzyme activity and the "extensive metabolizer" phenotype; 90-95% of Caucasians are considered "extensive metabolizers" (with normal CYP2D6 function) while the remaining 5-10% are considered "poor metabolizers" with reduced or non-functioning enzyme.
[A182294]
CYP2D6 alleles associated with non-functioning enzyme include *3, *4, *5, and *6 while alleles associated with reduced activity include *9, *10, *17, and *41.
[A183812]
Poor metabolizers have reduced activity of the CYP2D6 enzyme and therefore less production of tramadol metabolites M1 and M2, which ultimately results in a reduced analgesic effect as tramadol interacts with the μ-opioid receptor primarily via M1.
[A4269]
There are also large differences in the frequency of these alleles between different ethnicities: \*3, \*4, \*5, \*6, and \*41 are more common among Caucasians while \*17 is more common in Africans for example.
[A183812]
Compared to 5-10% of Caucasians, only ~1% of Asians are considered poor metabolizers, however Asian populations carry a much higher frequency (51%) of the CYP2D6\*10 allele, which is relatively rare in Caucasian populations and results in higher exposure to tramadol.
[A182294]
Some individuals are considered "ultra-rapid metabolizers", such as those carrying CYP2D6 gene duplications (CYP2D6*DUP) or multiplications. These individuals are at risk of intoxication or exaggerated effects of tramadol due to higher concentrations of its active metabolite (M1).
[A182297]
The occurrence of this phenotype is seen in approximately 1% to 2% of East Asians (Chinese, Japanese, Korean), 1% to 10% of Caucasians, 3% to 4% of African-Americans, and may be >10% in certain racial/ethnic groups (ie, Oceanian, Northern African, Middle Eastern, Ashkenazi Jews, Puerto Rican). The FDA label recommends avoiding the use of tramadol in these individuals.[L9257,F4679]
[A174010]
The mean terminal plasma elimination half-lives of racemic tramadol and racemic M1 are 6.3 ± 1.4 and 7.4 ± 1.4 hours, respectively. The plasma elimination half-life of racemic tramadol increased from approximately six hours to seven hours upon multiple dosing.[L9257,F4679]
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)
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Essential for serotonin homeostasis in the central nervous system. In the developing somatosensory cortex, acts in glutamatergic neurons to control serotonin uptake and its trophic functions accounting for proper spatial organization of cortical neurons and elaboration of sensory circuits.
In the mature cortex, acts primarily in brainstem raphe neurons to mediate serotonin uptake from the synaptic cleft back into the pre-synaptic terminal thus terminating serotonin signaling at the synapse (By similarity). Modulates mucosal serotonin levels in the gastrointestinal tract through uptake and clearance of serotonin in enterocytes. Required for enteric neurogenesis and gastrointestinal reflexes (By similarity).
Regulates blood serotonin levels by ensuring rapid high affinity uptake of serotonin from plasma to platelets, where it is further stored in dense granules via vesicular monoamine transporters and then released upon stimulation .
PMID:17506858 PMID:18317590
Mechanistically, the transport cycle starts with an outward-open conformation having Na1(+) and Cl(-) sites occupied. The binding of a second extracellular Na2(+) ion and serotonin substrate leads to structural changes to outward-occluded to inward-occluded to inward-open, where the Na2(+) ion and serotonin are released into the cytosol. Binding of intracellular K(+) ion induces conformational transitions to inward-occluded to outward-open and completes the cycle by releasing K(+) possibly together with a proton bound to Asp-98 into the extracellular compartment.
Na1(+) and Cl(-) ions remain bound throughout the transport cycle .
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Additionally, displays serotonin-induced channel-like conductance for monovalent cations, mainly Na(+) ions. The channel activity is uncoupled from the transport cycle and may contribute to the membrane resting potential or excitability (By similarity)
PMID:1325650 PMID:17021166 PMID:28256214 PMID:29844171
Implicated in the regulation of hippocampal replay occurring within sharp wave ripples (SPW-R) important for memory (By similarity)
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
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N02AJ16
ATC N02AJ13
ATC N02AJ14
ATC N02AX02
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)
Tramadol
Additional database identifiers
Drugs Product Database (DPD)
13904
ChemSpider
5322
BindingDB
50176259
ZINC
ZINC000000000853
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:11048
GenAtlas
SLC6A2
GeneCards
SLC6A2
GenBank Gene Database
M65105
GenBank Protein Database
189258
Guide to Pharmacology
926
UniProt Accession
SC6A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11050
GenAtlas
SLC6A4
GeneCards
SLC6A4
GenBank Gene Database
X70697
GenBank Protein Database
36433
Guide to Pharmacology
928
UniProt Accession
SC6A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10588
GenAtlas
SCN2A
GeneCards
SCN2A
GenBank Gene Database
M94055
GenBank Protein Database
457879
Guide to Pharmacology
579
UniProt Accession
SCN2A_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: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:4584
GenAtlas
GRIN1
GeneCards
GRIN1
GenBank Gene Database
D13515
GenBank Protein Database
219920
Guide to Pharmacology
455
UniProt Accession
NMDZ1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4585
GenAtlas
GRIN2A
GeneCards
GRIN2A
GenBank Gene Database
U09002
GenBank Protein Database
558749
Guide to Pharmacology
456
UniProt Accession
NMDE1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4586
GenAtlas
GRIN2B
GeneCards
GRIN2B
GenBank Gene Database
U90278
GenBank Protein Database
1899202
Guide to Pharmacology
457
UniProt Accession
NMDE2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4587
GenAtlas
GRIN2C
GeneCards
GRIN2C
GenBank Gene Database
L76224
GenBank Protein Database
1196449
Guide to Pharmacology
458
UniProt Accession
NMDE3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4588
GenAtlas
GRIN2D
GeneCards
GRIN2D
GenBank Gene Database
U77783
GenBank Protein Database
2444026
UniProt Accession
NMDE4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16767
GenAtlas
GRIN3A
GeneCards
GRIN3A
GenBank Gene Database
AJ416950
GenBank Protein Database
20372905
UniProt Accession
NMD3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16768
GenAtlas
GRIN3B
GeneCards
GRIN3B
GenBank Gene Database
AC004528
GenBank Protein Database
3025446
UniProt Accession
NMD3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:262
GenAtlas
ADORA1
GeneCards
ADORA1
GenBank Gene Database
S45235
GenBank Protein Database
256155
Guide to Pharmacology
18
UniProt Accession
AA1R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:282
GenAtlas
ADRA2B
GeneCards
ADRA2B
GenBank Gene Database
M34041
GenBank Protein Database
178198
Guide to Pharmacology
26
UniProt Accession
ADA2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:283
GenAtlas
ADRA2C
GeneCards
ADRA2C
GenBank Gene Database
J03853
GenBank Protein Database
178194
Guide to Pharmacology
27
UniProt Accession
ADA2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5295
GenAtlas
HTR2C
GeneCards
HTR2C
GenBank Gene Database
M81778
GenBank Protein Database
338028
Guide to Pharmacology
8
UniProt Accession
5HT2C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1960
GenAtlas
CHRNA7
GeneCards
CHRNA7
GenBank Gene Database
X70297
GenBank Protein Database
496607
Guide to Pharmacology
468
UniProt Accession
ACHA7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1952
GenAtlas
CHRM3
GeneCards
CHRM3
GenBank Gene Database
X15266
GenBank Protein Database
32324
Guide to Pharmacology
15
UniProt Accession
ACM3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1950
GenAtlas
CHRM1
GeneCards
CHRM1
GenBank Gene Database
X52068
GenBank Protein Database
34451
Guide to Pharmacology
13
UniProt Accession
ACM1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11526
GenAtlas
TACR1
GeneCards
TACR1
GenBank Gene Database
S62045
GenBank Protein Database
8176544
Guide to Pharmacology
360
UniProt Accession
NK1R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12716
GenAtlas
TRPV1
GeneCards
TRPV1
GenBank Gene Database
AJ277028
GenBank Protein Database
8977866
Guide to Pharmacology
507
UniProt Accession
TRPV1_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:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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
9 active patents, 8 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: