Diamorphine 240mg/5ml oral solution
Prescription only
Requires a prescription from a doctor or prescriber
Oral solution
240mg/5ml
Oral
Diamorphine (heroin) is a narcotic analgesic that may be habit-forming.
Active ingredients:
Diamorphine
CD Schedule 2
Strict controls: safe custody, register required
details
1 safety notice
Legal requirements and restrictions
These are medicines with high potential for misuse but with accepted medical uses. Subject to the strictest controls.
Legal requirements
- Must be stored in a locked controlled drugs cabinet
- Pharmacy must keep a controlled drugs register
- Prescriptions valid for 28 days only
- Prescriptions must include specific details (dose, form, strength, total quantity)
- Cannot be emergency supplied by pharmacists
Other medicines in this category
Morphine, Oxycodone, Fentanyl, Methylphenidate (Ritalin), Amphetamines
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
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 Diamorphine
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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
EMA
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 Diamorphine
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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
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Powder
500mg
Same therapeutic group
Buprenorphine 8.6mg / Naloxone 2.1mg sublingual tablets sugar free
Tablet
8.6mg
Same therapeutic group
Buprenorphine 1.4mg / Naloxone 360microgram sublingual tablets sugar free
Tablet
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Same therapeutic group
Buprenorphine 11.4mg / Naloxone 2.9mg sublingual tablets sugar free
Tablet
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Buprenorphine 2.9mg / Naloxone 710microgram sublingual tablets sugar free
Tablet
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Same therapeutic group
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
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Clinical guidelines and formulary information
British National Formulary
Diamorphine
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(7)
Caesarean birth (NG192)
NG192
NICE guideline
Updated Jun 2025Methadone and buprenorphine for the management of opioid dependence (TA114)
TA114
Technology appraisal
Updated Jan 2007Palliative care for adults: strong opioids for pain relief (CG140)
CG140
Clinical guideline
Updated Aug 2016Major trauma: assessment and initial management (NG39)
NG39
NICE guideline
Updated Feb 2016Spinal injury: assessment and initial management (NG41)
NG41
NICE guideline
Updated Feb 2016Sickle cell disease (QS58)
QS58
Quality standard
Updated Apr 2014Intrapartum care (NG235)
NG235
NICE guideline
Updated Nov 2025Source: 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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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
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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
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Searching UK clinical trials...
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
43 found
Half-life
Not available
Mechanism
When administered orally, diamorphine experiences extensive first-pass metabolis…
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
35%
Bioavailability is less than 35% when orally administered .
[A173668]
In particular, some studies have determined that the bioavailability of orally administered diamorphine could be as low as 22.9%…
[A173668]
In particular, some studies have determined that the bioavailability of orally administered diamorphine could be as low as 22.9%…
Half-life
In humans, administered diamorphine has a half-life of approximately two to three minutes .
[L4999]
[L4999]
Protein binding
20 to 35%
Diamorphine does not bind to plasma protein .
[L4999]
However, considering diamorphine is considered a prodrug for morphine, morphine itself…
[L4999]
However, considering diamorphine is considered a prodrug for morphine, morphine itself…
Volume of distribution
1 to 6 L/kg
Data regarding the volume of distribution specific to diamorphine is not readily accessible or available.…
Metabolism
Once administered into the body, diamorphine undergoes deacetylation via various esterase enzymes to generate active metabolites like 6-monoacetylmorphine and morphine .
[L4996,…
[L4996,…
Elimination
7-10 %
The majority of the drug is excreted via the kidney as glucuronides and to a much lesser extent as morphine .
[L4999]…
[L4999]…
Clearance
2.6 L
Some studies have determined a relatively high systemic diacetylmorphine clearance of about 8.7…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Illicit
Small molecule
About this compound
Diamorphine (heroin) is a narcotic analgesic that may be habit-forming. It is a controlled substance (opium derivative) listed in the U.S. Code of Federal Regulations, Title 21 Parts 329.1, 1308.11 (1987). Sale is forbidden in the United States by Federal statute. (Merck Index, 11th ed) Internationally, diamorphine is controlled under Schedules I and IV of the Single Convention on Narcotic Drugs. As heroin, it is illegal to manufacture, possess, or sell in the United States and the UK. However, under the name diamorphine, heroin is a legal prescription drug in the United Kingdom.
Properties:
solid
Avg. mass: 369.41 Da
DrugBank indication
Diamorphine, as a prescription medication in the United Kingdom, is indicated for use in the treatment of severe pain associated with surgical procedures, myocardial infarction or pain in the terminally ill and for the relief of dyspnoea in acute pulmonary edema .
[L4999]
[L4999]
Also known as(43)
(5α,6α)-7,8-Didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol diacetate (ester)
3,6-Diacetylmorphine
7,8-Dihydro-4,5-alpha-epoxy-17-methylmorphinan-3,6-alpha-diol diacetate
Diacetylmorphine
Diamorphine
Heroin
O,O'-Diacetylmorphine
hMOP
Dosage forms(4)
Powder, for solution (Intramuscular; Intravenous) — 200 mg / vial
Powder, for solution (Intramuscular; Intravenous) — 5000 mg / vial
Powder, for solution (Intramuscular; Intravenous; Subcutaneous) — 100 mg / mL
Powder, for solution (Intramuscular; Intravenous; Subcutaneous) — 30 mg / mL
Molecular properties(18)
Drug interactions(921)
Known interactions with other medications. Always consult a healthcare professional.
Buprenorphine
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Buprenorphine.
Doxylamine
Moderate
Doxylamine may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Dronabinol
Moderate
Dronabinol may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Droperidol
Moderate
Droperidol may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Hydrocodone
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Hydrocodone.
Hydroxyzine
Moderate
Hydroxyzine may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Magnesium sulfate
Moderate
The therapeutic efficacy of Diamorphine can be increased when used in combination with Magnesium sulfate.
Methotrimeprazine
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Methotrimeprazine.
Metyrosine
Moderate
Diamorphine may increase the sedative activities of Metyrosine.
Minocycline
Moderate
Minocycline may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Mirtazapine
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Mirtazapine.
Nabilone may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Orphenadrine
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Orphenadrine.
Paraldehyde
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Paraldehyde.
Perampanel
Moderate
Perampanel may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Pramipexole
Moderate
Diamorphine may increase the sedative activities of Pramipexole.
Ropinirole
Moderate
Diamorphine may increase the sedative activities of Ropinirole.
Rotigotine
Moderate
Diamorphine may increase the sedative activities of Rotigotine.
Rufinamide
Unknown severity
The risk or severity of adverse effects can be increased when Rufinamide is combined with Diamorphine.
Sodium oxybate
Unknown severity
The risk or severity of CNS depression can be increased when Diamorphine is combined with Sodium oxybate.
Suvorexant
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Suvorexant.
Tapentadol
Moderate
Tapentadol may increase the central nervous system depressant (CNS depressant) activities of Diamorphine.
Thalidomide
Moderate
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Thalidomide.
Diamorphine may increase the central nervous system depressant (CNS depressant) activities of Zolpidem.
The risk or severity of adverse effects can be increased when Diamorphine is combined with Alvimopan.
Desmopressin
Unknown severity
The risk or severity of hyponatremia can be increased when Diamorphine is combined with Desmopressin.
The risk or severity of adverse effects can be increased when Morphine is combined with Diamorphine.
The risk or severity of adverse effects can be increased when Codeine is combined with Diamorphine.
Hydromorphone
Unknown severity
The risk or severity of adverse effects can be increased when Hydromorphone is combined with Diamorphine.
Meperidine
Unknown severity
The risk or severity of adverse effects can be increased when Meperidine is combined with Diamorphine.
The risk or severity of adverse effects can be increased when Oxycodone is combined with Diamorphine.
Dextropropoxyphene
Unknown severity
The risk or severity of adverse effects can be increased when Dextropropoxyphene is combined with Diamorphine.
Naltrexone
Moderate
The therapeutic efficacy of Diamorphine can be decreased when used in combination with Naltrexone.
Sufentanil
Unknown severity
The risk or severity of adverse effects can be increased when Sufentanil is combined with Diamorphine.
Alfentanil
Unknown severity
The risk or severity of adverse effects can be increased when Alfentanil is combined with Diamorphine.
The risk or severity of adverse effects can be increased when Fentanyl is combined with Diamorphine.
Levorphanol
Unknown severity
The risk or severity of adverse effects can be increased when Levorphanol is combined with Diamorphine.
Remifentanil
Unknown severity
The risk or severity of adverse effects can be increased when Remifentanil is combined with Diamorphine.
Diphenoxylate
Unknown severity
The risk or severity of adverse effects can be increased when Diphenoxylate is combined with Diamorphine.
Oxymorphone
Unknown severity
The risk or severity of adverse effects can be increased when Oxymorphone is combined with Diamorphine.
The risk or severity of adverse effects can be increased when Dezocine is combined with Diamorphine.
Methadyl acetate
Unknown severity
The risk or severity of adverse effects can be increased when Methadyl acetate is combined with Diamorphine.
Dihydroetorphine
Unknown severity
The risk or severity of adverse effects can be increased when Dihydroetorphine is combined with Diamorphine.
Bezitramide
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Bezitramide.
Ethylmorphine
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Ethylmorphine.
The risk or severity of adverse effects can be increased when Diamorphine is combined with Etorphine.
Dextromoramide
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Dextromoramide.
Desomorphine
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Desomorphine.
Carfentanil
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Carfentanil.
Dihydrocodeine
Unknown severity
The risk or severity of adverse effects can be increased when Diamorphine is combined with Dihydrocodeine.
Showing 50 of 921 interactions
Food & lifestyle interactions
Avoid Alcohol
Avoid alcohol.
Toxicity & overdose
Overdosage with diamorphine well characterised by a number of symptoms including respiratory depression, pulmonary oedema, muscle flaccidity, coma or stupor, constricted pupils, cold, clammy skin and occasionally bradycardia and hypotension .
[L4996][L4999]
The antidote for heroin overdose or poisoning is naloxone .
[L4996]
[L4996][L4999]
The antidote for heroin overdose or poisoning is naloxone .
[L4996]
How it works
Mechanism of action
When administered orally, diamorphine experiences extensive first-pass metabolism by way of deacetylation to generate the active metabolites 6-monoacetylmorphine (6-MAM) and morphine [L4996][L4999]. Alternatively, when given as an injection the acetyl groups present in the diamorphine/diacetylmorphine compound confer the substance lipophilicity that facilitates diamorphine's rapid crossing of the blood-brain-barrier [L4996][L4999]. Once in the brain, diamorphine is metabolised via deacetylation to the active 6-MAM and morphine metabolites as well [L4996][L4999]. Despite diamorphine possessing little to no opioid agonist activity itself, its rapid transit across the blood-brain-barrier elicits a far faster onset of activity in comparison to the extensive first-pass metabolism of oral administration [L4996][L4999]. Regardless, the metabolism of diamorphine to morphine makes heroin a prodrug for the delivery of morphine [L4996][L4999].
Morphine is subsequently a mu-opioid agonist. It acts on endogenous mu-opioid receptors that are spread in discrete packets throughout the brain, spinal cord and gut in almost all mammals [A2476]. Morphine, along with other opioids, are agonists to four endogenous neurotransmitters [A2476]. They are beta-endorphin, dynorphin, leu-enkephalin, and met-enkephalin [A2476]. The body responds to morphine in the brain by reducing (and sometimes stopping) production of the endogenous opioids when morphine is present [A2476]. Endorphins are regularly released in the brain and nerves, attenuating pain. Their other functions are still obscure, but are probably related to the effects produced by morphine besides analgesia (antitussin, anti-diarrheal) [A2476].
Nevertheless, morphine ultimately elicits the majority of its analgesic activity by binding to mu opioid receptors in both the central and peripheral nervous systems [L5005]. The overall effect of morphine is activation of descending inhibitory pathways of the central nervous system as well as inhibition of nociceptive afferent neurons of the peripheral nervous system, which results in an overall reduction of the nociceptive pain transmission [L5005].
Morphine is subsequently a mu-opioid agonist. It acts on endogenous mu-opioid receptors that are spread in discrete packets throughout the brain, spinal cord and gut in almost all mammals [A2476]. Morphine, along with other opioids, are agonists to four endogenous neurotransmitters [A2476]. They are beta-endorphin, dynorphin, leu-enkephalin, and met-enkephalin [A2476]. The body responds to morphine in the brain by reducing (and sometimes stopping) production of the endogenous opioids when morphine is present [A2476]. Endorphins are regularly released in the brain and nerves, attenuating pain. Their other functions are still obscure, but are probably related to the effects produced by morphine besides analgesia (antitussin, anti-diarrheal) [A2476].
Nevertheless, morphine ultimately elicits the majority of its analgesic activity by binding to mu opioid receptors in both the central and peripheral nervous systems [L5005]. The overall effect of morphine is activation of descending inhibitory pathways of the central nervous system as well as inhibition of nociceptive afferent neurons of the peripheral nervous system, which results in an overall reduction of the nociceptive pain transmission [L5005].
Pharmacodynamics
The onset of heroin's effects is dependent on the method of administration. Taken orally, heroin is totally metabolized in vivo via extensive first-pass metabolism into morphine before crossing the blood-brain barrier; so the effects are the same as orally administered morphine [L4996][L4999]. Take by injection, diamorphine's acetyl groups facilitate rapid crossing into the brain [L4996][L4999]. Once in the brain, heroin is rapidly metabolized into morphine by removal of the acetyl groups, therefore making it a prodrug for the delivery of morphine [L4996][L4999]. Subsequently, whether eliciting actions peripherally (on smooth muscle, skeletal muscle, kidney, lung, liver, or spleen tissue [L4996], for example) or on the central nervous system, it is ultimately the morphine metabolite of heroin that then binds with opioid receptors and produces the narcotic opioid effects commonly associated with the substance [L4996][L4999].
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Bioavailability is less than 35% when orally administered .
[A173668]
In particular, some studies have determined that the bioavailability of orally administered diamorphine could be as low as 22.9% (16.4-29.4%) on average in opioid-naive subjects .
[A173683]
Nevertheless, diamorphine administered by any many medically indicated routes of administration leads to a rapid absorption .
[L4996]
Peak serum levels are achieved five to ten minutes subcutaneously, three to five minutes intranasally and intramuscularly, and less than one minute intravenously .
[L4996]
[A173668]
In particular, some studies have determined that the bioavailability of orally administered diamorphine could be as low as 22.9% (16.4-29.4%) on average in opioid-naive subjects .
[A173683]
Nevertheless, diamorphine administered by any many medically indicated routes of administration leads to a rapid absorption .
[L4996]
Peak serum levels are achieved five to ten minutes subcutaneously, three to five minutes intranasally and intramuscularly, and less than one minute intravenously .
[L4996]
Half-life
In humans, administered diamorphine has a half-life of approximately two to three minutes .
[L4999]
[L4999]
Protein binding
Diamorphine does not bind to plasma protein .
[L4999]
However, considering diamorphine is considered a prodrug for morphine, morphine itself is about 20 to 35% reversibly bound to human plasma proteins [L4999, F2857].
[L4999]
However, considering diamorphine is considered a prodrug for morphine, morphine itself is about 20 to 35% reversibly bound to human plasma proteins [L4999, F2857].
Volume of distribution
Data regarding the volume of distribution specific to diamorphine is not readily accessible or available. However, considering diamorphine is considered a prodrug for morphine, the volume of distribution of morphine has been determined to be approximately 1 to 6 L/kg F2857.
Metabolism
Once administered into the body, diamorphine undergoes deacetylation via various esterase enzymes to generate active metabolites like 6-monoacetylmorphine and morphine .
[L4996][L4999]
In particular, when administered orally, diamorphine undergoes extensive first pass metabolism .
[L4996][L4999]
[L4996][L4999]
In particular, when administered orally, diamorphine undergoes extensive first pass metabolism .
[L4996][L4999]
Route of elimination
The majority of the drug is excreted via the kidney as glucuronides and to a much lesser extent as morphine .
[L4999]
About 7-10 % is eliminated via the biliary system into the faeces .
[L4999]
[L4999]
About 7-10 % is eliminated via the biliary system into the faeces .
[L4999]
Clearance
Some studies have determined a relatively high systemic diacetylmorphine clearance of about 8.7 +/- 2.6 L/min, suggesting that the intestine, liver, and blood might all collectively take part in the first pass metabolism of diacetylmorphine to morphine [A173683], although such clearance observations were made only in opioid-addicted individuals .
[A173695]
However, considering diamorphine is considered a prodrug for morphine, the mean adult plasma clearance of morphine is approximately 20 to 30 mL/min/kg F2857.
[A173695]
However, considering diamorphine is considered a prodrug for morphine, the mean adult plasma clearance of morphine is approximately 20 to 30 mL/min/kg F2857.
Drug targets(4)
Proteins and enzymes this drug interacts with in the body
Mu-type opioid receptor
OPRM1
agonist
Specific functionbeta-endorphin receptor activity
Cellular location
Cell membrane
General function & pharmacology
Receptor for endogenous opioids such as beta-endorphin and endomorphin .
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: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)
Kappa-type opioid receptor
OPRK1
agonist
Specific functiondynorphin receptor activity
Cellular location
Cell membrane
General function & pharmacology
G-protein coupled opioid receptor that functions as a receptor for endogenous alpha-neoendorphins and dynorphins, but has low affinity for beta-endorphins. Also functions as a receptor for various synthetic opioids and for the psychoactive diterpene salvinorin A. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase.
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
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
Delta-type opioid receptor
OPRD1
agonist
Specific functionG protein-coupled enkephalin receptor activity
Cellular location
Cell membrane
General function & pharmacology
G-protein coupled receptor that functions as a receptor for endogenous enkephalins and for a subset of other opioids. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. 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 and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine
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
Liver carboxylesterase 1
CES1
Specific functioncarboxylesterase activity
Cellular location
Endoplasmic reticulum lumen
General function & pharmacology
Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs .
PMID:18762277 PMID:7980644 PMID:9169443 PMID:9490062
Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acyl-CoA ester .
PMID:18762277 PMID:7980644 PMID:9169443 PMID:9490062
Hydrolyzes the methyl ester group of cocaine to form benzoylecgonine .
PMID:7980644
Catalyzes the transesterification of cocaine to form cocaethylene .
PMID:7980644
Displays fatty acid ethyl ester synthase activity, catalyzing the ethyl esterification of oleic acid to ethyloleate .
PMID:7980644
Converts monoacylglycerides to free fatty acids and glycerol. Hydrolyzes of 2-arachidonoylglycerol and prostaglandins .
PMID:21049984
Hydrolyzes cellular cholesteryl esters to free cholesterols and promotes reverse cholesterol transport (RCT) by facilitating both the initial and final steps in the process .
PMID:11015575 PMID:16024911 PMID:16971496 PMID:18762277
First of all, allows free cholesterol efflux from macrophages to extracellular cholesterol acceptors and secondly, releases free cholesterol from lipoprotein-delivered cholesteryl esters in the liver for bile acid synthesis or direct secretion into the bile PMID:16971496 PMID:18599737 PMID:18762277
PMID:18762277 PMID:7980644 PMID:9169443 PMID:9490062
Hydrolyzes aromatic and aliphatic esters, but has no catalytic activity toward amides or a fatty acyl-CoA ester .
PMID:18762277 PMID:7980644 PMID:9169443 PMID:9490062
Hydrolyzes the methyl ester group of cocaine to form benzoylecgonine .
PMID:7980644
Catalyzes the transesterification of cocaine to form cocaethylene .
PMID:7980644
Displays fatty acid ethyl ester synthase activity, catalyzing the ethyl esterification of oleic acid to ethyloleate .
PMID:7980644
Converts monoacylglycerides to free fatty acids and glycerol. Hydrolyzes of 2-arachidonoylglycerol and prostaglandins .
PMID:21049984
Hydrolyzes cellular cholesteryl esters to free cholesterols and promotes reverse cholesterol transport (RCT) by facilitating both the initial and final steps in the process .
PMID:11015575 PMID:16024911 PMID:16971496 PMID:18762277
First of all, allows free cholesterol efflux from macrophages to extracellular cholesterol acceptors and secondly, releases free cholesterol from lipoprotein-delivered cholesteryl esters in the liver for bile acid synthesis or direct secretion into the bile PMID:16971496 PMID:18599737 PMID:18762277
Carriers(1)
Proteins that carry this drug through the body
Thyroxine-binding globulin
SERPINA7
inducer
Specific functionserine-type endopeptidase inhibitor activity
Cellular location
Secreted
General function & pharmacology
Major thyroid hormone transport protein in serum
Biological pathways(2)
Scientific references(4)
Tschacher W., Haemmig R., Jacobshagen N.
Time series modeling of heroin and morphine drug action.
Psychopharmacology
2003165(2):188-193. doi: 10.1007/s00213-002-1271-3
Rook E.J., van Ree J.M., van den Brink W., Hillebrand M.J., Huitema A.D., Hendriks V.M., Beijnen J.H.
Pharmacokinetics and pharmacodynamics of high doses of pharmaceutically prepared heroin, by intravenous or by inhalation route in opioid-dependent patients.
Basic & Clinical Pharmacology & Toxicology
2006 Jan98(1):86-96. doi: 10.1111/j.1742-7843.2006.pto_233.x
Halbsguth U., Rentsch K.M., Eich-Hochli D., Diterich I., Fattinger K.
Oral diacetylmorphine (heroin) yields greater morphine bioavailability than oral morphine: bioavailability related to dosage and prior opioid exposure.
British Journal of Clinical Pharmacology
2008 Dec66(6):781-91. doi: 10.1111/j.1365-2125.2008.03286.x
Rentsch K.M., Kullak-Ublick G.A., Reichel C., Meier P.J., Fattinger K.
Arterial and venous pharmacokinetics of intravenous heroin in subjects who are addicted to narcotics.
Clinical Pharmacology Therapeutics
2001 Sep70(3):237-46. doi: 10.1067/mcp.2001.117981
ATC classification(1 code)
ATC N07BC06
Affected organisms(1)
Humans and other mammals
Salt forms(1)
Diamorphine hydrochloride(DBSALT000095)
Experimental properties(5)
External resources(1)
Commercial products(4)
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)
Diamorphine
Additional database identifiers
Drugs Product Database (DPD)
8283
ChemSpider
4575379
ZINC
ZINC000004097183
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: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:1863
GenAtlas
CES1
GeneCards
CES1
GenBank Gene Database
M73499
Guide to Pharmacology
2592
UniProt Accession
EST1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11583
GenAtlas
SERPINA7
GeneCards
SERPINA7
GenBank Gene Database
M14091
GenBank Protein Database
338697
UniProt Accession
THBG_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)