Morphine (Opium tincture) 10mg/ml oral drops sugar free
Requires a prescription from a doctor or prescriber
Opium is the first substance of the diverse group of the opiates.
Strict controls: safe custody, register required
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
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MHRA alerts for Opium
Safety monitoring data
Yellow Card reports
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Opium
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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
MHRA licensed products
View all licensed products for Opium on the MHRA register
Dropizol 10mg/ml oral drops
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
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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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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 13 · 2018–2026
Showing the 50 most relevant studies, sorted by most relevant.
Hefteh N, Welch O, Sheikh M, et al.
2025
- Neoplasms
- Analgesics, Opioid
- Cell Proliferation
BackgroundThe International Agency for Research on Cancer (IARC) monographs recently classified opium consumption as carcinogenic to humans in certain organs, raising concerns regarding the effects of pharmaceutical opioids. This systematic review (Open Science Framework osf.io/xyg9p) evaluated whether opioid exposure causes organ-specific modulation of malignant processes in cancer cell culture studies.MethodsWe identified all research articles evaluating tumour modulation by opioids in vitro through 28/02/2024. Data on the organ of origin of cancer cells, opioid activity, opioid exposure, and cancer outcomes (tumour cell growth, metastasis, clonogenicity) were extracted. Statistical analyses were performed using Fisher's exact tests and multivariable logistic regression.ResultsThe anti-cancer outcome was the most prevalent (57%) while only 11% of experiments reported pro-cancer outcomes. A total of 230 publications, comprising 1465 experiments, were included. Low opioid concentrations (p = 0.0005), short exposure durations (p = 0.0035), and organs where cancer risk increases with opium use (p = 0.002), were associated with reporting of pro-cancer effects for opioid agonists.ConclusionThe findings support a positive association between opioid exposure and growth of cancer cells from lung, bladder, larynx, pancreas, pharynx, stomach, or oesophagus and further reveal duration and concentration as critical factors in experiments evaluating the effects of opioids on cultured cancer cells.
Abstract licence: CC BY
Schofield J, Conti AA, Khan F, et al.
2025
AimChronic opioid exposure (COE) is linked to adverse health outcomes, but its relationship with cardiovascular disease (CVD) remains unclear. This systematic review and meta-analysis aimed to summarise published evidence on CVD risk associated with COE, including prescription opioids, opium use, and opioid use disorder (OUD).MethodsFollowing PRISMA guidelines and PROSPERO registration (CRD42024573206), we searched multiple databases for relevant human studies reporting associations between COE and CVD. Random-effects meta-analysis estimated pooled odds ratios (OR) with 95% confidence intervals. Subgroup analyses and meta-regression explored associations by COE type, CVD outcome, and potential moderators. Risk of bias was assessed using ROBINS-E.ResultsSeventeen studies (1,676,000 participants) met inclusion criteria, with 13 studies contributing 22 effect sizes to meta-analysis. COE was associated with increased CVD risk (pooled OR: 1.74, 95% CI: 1.12-2.70), though substantial heterogeneity was observed. Cerebrovascular accidents (OR: 1.84, 95% CI: 1.45-2.35) and ischaemic heart disease (OR: 1.51, 95% CI: 1.40-1.63) showed the strongest associations. Opium use had a significant association with CVD, while findings for OUD and prescription opioids were less consistent. Meta-regression identified study design as a key moderator.ConclusionCOE is associated with increased risk of CVD, particularly cerebrovascular accidents and ischaemic heart disease. Given the global opioid and CVD burden, targeted interventions and integrated care approaches are needed. Findings are limited by heterogeneity and risk of bias in published studies. Further high-quality research should explore pathophysiological mechanisms, causality, dose-response relationships, and the potential reversibility of CVD risk following opioid cessation.
Abstract licence: CC BY
Cheraghi Z, Azmi-Naei B, Azmi-Naei N, et al.
2025
- Neoplasms
- Opium
- Analgesics, Opioid
ObjectiveThe existing literature on the direct effects of opioid use on cancer is limited. The goal of our systematic review and meta-analysis is to consolidate the findings of previous studies and provide a pooled effect size regarding the association between opioid usage and cancer.MethodsThe PRISMA guidelines were employed to construct a framework for conducting this systematic review and meta-analysis. A systematic search was conducted in international and national databases. A search of PubMed, Web of Science, Scopus, and national electronic databases was conducted up to May 2024. The random effects model was employed for the presentation of results with a 95% confidence interval. The statistical analysis was conducted using Stata 11.ResultsOut of 1674 articles were retrieved 38 studies remained in the final analysis (six cohort study and 32 case-control studies). The pooled adjusted odds ratio of opium on esophageal cancer was 1.68 (95% CI: 1.36, 2.08), for bladder cancer was 5.00(95% CI: 3.76, 6.66), for head and neck cancer was 4.93 (95% CI: 2.41, 10.06) for pancreatic cancer was 2.4 (95% CI: 1.62, 2.56) for lung cancer was 2.89(95% CI: 2.14, 3.30) for laryngeal cancer was 6.76 (95% CI: 3.77, 11.80) for gastric cancer was 3.13 (95% CI: 1.92, 5.11) and for colorectal cancer was 2.51 (95% CI: 1.04, 6.07).All association were statistically significant.ConclusionThe findings underscore the potential carcinogenic effects of opium on cancers. Public health organizations should work collaboratively to mitigate opioid exposure while promoting alternative pain management strategies to protect community health and reduce the burden of cancer.
Abstract licence: CC BY-NC-ND
Semnani K, Ghoreshi B, Mehrpour O, et al.
2026
Opium use has been suggested as a possible risk factor for several cancers. While increased risk may be attributable to adulterants or smoking by-products, direct effects for opium alkaloids remains a possibility. Considering the overlap between natural and semi-synthetic or synthetic opioids, such an effect may entail increased risk in a broader population. We reviewed reports on associations between opium or opioid use and cancer. MEDLINE, Scopus, and Web of Science were searched. Epidemiological studies were included. Two researchers performed screening, data extraction, and quality assessment independently. Meta-analysis was carried out using a random-effects model. 82 publication (from 78 studies) contributed to the meta-analysis. Opium use was associated with increased cancer odds (OR = 3.55; 95% CI 2.94, 4.29; 95% PI 1.07, 11.82), particularly for bladder, laryngeal, and oesophageal cancers. In contrast, opioids use showed a modest association in case-control studies (OR 1.04; 95% CI 1.00, 1.07, 95% PI 0.94, 1.15), and a non-significant trend in cohort studies (HR = 1.44; 95% CI 0.98, 2.11; 95% PI 0.25, 8.32). Opioid use was also associated with increased cancer mortality (HR = 1.69; 95% CI 1.16, 2.46; 95% PI 0.36, 7.98). However, high heterogeneity, residual confounding, and the paucity of longitudinal evidence preclude causal inferences.
Abstract licence: CC BY-NC-ND
Ardeshir M, Rafiemanesh H, Rostam-Abadi Y, et al.
2026
- Opioid-Related Disorders
- Opium Dependence
- Opium
Zanjiri F, Mohammadi Y, Ravanjo L, et al.
2025
- Opium
- Blood Glucose
- Glycemic Index
Keykha E, Shabanpour MJ, Tahmasebi E, et al.
2025
- Mouth Neoplasms
- Opium
- Opium Dependence
Alhifany AA, Alsaab HO
2025
Mancon S, Matsukawa A, Cadenar A, et al.
2025
- Opium
- Urinary Bladder Neoplasms
- Opium Dependence
Kambiz Soltaninejad, Shahin Shadnia
International Journal of Preventive Medicine, 2018
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
53 found
Half-life
3-10 hours
Mechanism
Opium produces its effects by activating specific G protein-coupled receptors in…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
16-24 mg/ml
Half-life
3-10 hours
Protein binding
20-60%
Volume of distribution
Metabolism
[L1780]
…
Elimination
2-12 hours
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Opium is extracted from Papaver somniferum, which is more known as poppies. This plant is an integrant of the Papaveraceae family, and it is characterized by solitary leaves and capsulated fruits. Therefore, opium is a sticky brown resin obtained by collecting and drying the latex that exudes from the poppy pods.[L1761]
Once extracted, opium contains two main groups of alkaloids; the psychoactive constituents which are in the category of phenanthrenes and alkaloids that have no central nervous system effect in the category of isoquinolines. Morphine is the most prevalent and principal alkaloid in opium, and it is responsible for most of the harmful effects of opium.[L1762]
Opium has gradually been superseded by a variety of synthetic opioids and general anesthetics. Some of the isolated derivatives of opium are morphine, noscapine, strychnine, veratrine, colchicine, codeine, and quinine.[A32175] Opium is a prohibited drug of abuse in most countries, but the illegal production of this drug and its derivatives keeps being registered. There is some legal production of opium in different countries for the obtention of alkaloids by extraction.[L1766]
Illegal use of opium has been registered to be for both recreational and medicinal purposes.
[A32182]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1663 interactions
[L1802]
The addictive character of opium is related to the binding to the μ-opioid receptors, which will activate dopaminergic neurons in the ventral tegmental area of the midbrain and thus, enhance the dopamine release in the nucleus accumbens. This mechanism involves the reward activity of the mesolimbic dopaminergic pathway.[T137]
In the cardiovascular system, there are reports of peripheral vasodilatation, including cutaneous causing flushing of the face, neck, and thorax, impaired sympathetic reflexes and postural hypotension. In the gastrointestinal and urogenital system, the increase in smooth muscle tone has been shown to produce reduced peristalsis, delayed gastric emptying and urinary retention.[T136]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A32183]
[A32195]
[L1780]
Opioids are metabolized vastly by the enzyme CYP 2D6 and any mutation in this kind of enzyme or coadministration with drugs that interfere with this enzyme may generate a change in the metabolism speed.
[L1807]
For years, because of this metabolism pathway, it was very hard to differentiate between illicit heroin users and involuntary exposure to poppy seeds. The original tests for this differentiations were based in the presence of morphine in urine without evidence of 6-monoacetylmorphine.
Now it is known the presence of a glucuronide metabolite only in the consumption of heroin called ATM4G and this allows a clear differentiation of the consumption of illegal heroin and poppy seed ingestion.
[A32197]
The urinary excretion of morphine and codeine seems to be longer as the dose of opium is increased. After multiple dosages of opium, the presence of codeine and morphine in urine could be detected even after 48 and 84 hours post administration, respectively.
[A32198]
After ingestion of poppy seeds, it is possible to collect morphine and codeine in urine 3-25 hours and 3-22 hours after administration, respectively.
[A32199]
Proteins and enzymes this drug interacts with in the body
Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine
Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain.
Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions
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)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC A07DA02
ATC N02AA02
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)
Opium
Additional database identifiers
Drugs Product Database (DPD)
6897
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8153
GenAtlas
OPRD1
GeneCards
OPRD1
GenBank Gene Database
U07882
GenBank Protein Database
27545517
Guide to Pharmacology
317
UniProt Accession
OPRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC: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: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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:914
GeneCards
B2M
GenBank Gene Database
AY187687
GenBank Protein Database
27763813
UniProt Accession
B2MG_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72