Hydromorphone 24mg modified-release capsules
Hydromorphone is a pure opioid,[A176468] a semi-synthetic hydrogenated ketone derivative of [morphine] that has been available clinically since 1920.
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
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).
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Hydromorphone
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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
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Suspected adverse reactions reported for Hydromorphone
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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.
1 branded products available
Part of the Palladone brand family (generic: Hydromorphone)
MHRA licensed products
View all licensed products for Hydromorphone on the MHRA register
WHO defined daily dose (DDD)
20 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 the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
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
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Supply & safety information
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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 code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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: 10 · Randomised trials: 34 · 1996–2026
Showing the 50 most relevant studies, sorted by most relevant.
Li Wang, B. Johnston, Alka Kaushal, et al.
Canadian Journal of Anesthesia/Journal canadien d'anesthésie, 2016
- Hydromorphone
- Drug Combinations
- Ketamine
Columba Quigley
Journal of Pain and Symptom Management, 2003
- Acute Disease
- Analgesics, Opioid
- Chronic Disease
Lisa Felden, Carmen Walter, S. Harder, et al.
British Journal of Anaesthesia, 2011
- Analgesics, Opioid
- Hydromorphone
- Morphine
Yihang Li, Xinying Yue, Shuang Liang, et al.
Pain physician, 2024
S. Grape, K. El‐Boghdadly, C. Jaques, et al.
Journal of clinical anesthesia, 2024
STUDY OBJECTIVE Neuraxial hydromorphone provides postoperative pain relief. However, the magnitude of this effect and the optimal dose remain unknown. The objective of this study is to clarify these uncertainties. DESIGN Systematic review and meta-analysis with trial sequential analysis. SETTING Postoperative recovery area and ward, up to 24 h. PATIENTS Any patient undergoing any type of surgery or being in labor. INTERVENTIONS Neuraxial hydromorphone versus control. MEASUREMENTS Our primary outcome was rest pain score (analogue scale, 0-10) at 24 h according to route of administration (epidural versus spinal) and type of surgery (orthopedic versus other). Secondary outcomes included rest pain score at 0-4 and 8-12 h; rates of postoperative nausea and vomiting, and pruritus at 24 h. MAIN RESULTS Six trials, including 436 patients, were identified. Rest pain score at 24 postoperative hours was significantly reduced in the hydromorphone group, with a mean difference (95 %CI) of -0.4 (-0.8 to -0.1), I2 = 74 %, p = 0.01. Neuraxial hydromorphone did not increase postoperative nausea and vomiting (risk ratio [95 %CI]: 1.2 [0.8-1.8], I2 = 27 %, p = 0.47), but increases pruritus (risk ratio [95 %CI]: 3.1 [1.6-5.9], I2 = 0 %, p = 0.0005). The quality of evidence was very low for our primary and secondary outcomes. In conclusion, there is very low level of evidence that neuraxial hydromorphone provides effective analgesia after surgery or labor, at the expense of an increased rate of pruritus. The improvement in pain scores appears to be clinically insignificant. With only six trials published over a period of 30 years, we were unable to perform a meta-regression. CONCLUSIONS If neuraxial hydromorphone is to be used regularly, trials focusing on the optimal dose and side-effects should be performed before widely administering this medication into the neuraxial space. More trials focusing on the optimal dose and side-effects should be performed before widely administering this medication into the neuraxial space.
Abstract licence: CC BY
Mohammadreza Alinejadfard, Shahryar Rajai Firouzabadi, Ida Mohammadi, et al.
BMC Anesthesiology, 2024
Background Cancer pain significantly impacts individuals’ quality of life, with opioids being employed as the primary means for pain relief. Nevertheless, concerns persist regarding the adverse reactions and effectiveness of opioids such as morphine. Hydromorphone, recognized as a potent opioid, is a viable alternative for managing cancer-related pain. The goal of this systematic review and meta-analysis was to determine the effectiveness and safety characteristics of hydromorphone in comparison to other opioids, as well as different methods of administering this medication within the scope of cancer pain treatment. Methods The PubMed, Embase, Cochrane Library, Scopus, and Web of Science databases were searched on December 25th, 2023. Following the PRISMA guidelines, a systematic investigation of databases was carried out, and suitable studies were chosen according to predetermined criteria (PICO framework). The meta-analyses were performed using a random-effects model. Results This review included 18 RCTs with 2271 patients who compared hydromorphone with morphine, oxycodone, or fentanyl, as well as other types of hydromorphone. Hydromorphone demonstrated efficacy similar to that of morphine and oxycodone in reducing cancer pain intensity, decreasing additional analgesic consumption, and improving quality of life. However, morphine showed slight superiority over hydromorphone in reducing breakthrough pain. Adverse events were comparable between hydromorphone and morphine or oxycodone. Patient-controlled and clinician-controlled hydromorphone administration routes yielded similar outcomes. Conclusions The outcomes of this study substantiate the efficacy of hydromorphone in the management of cancer-related pain, demonstrating similar levels of effectiveness and safety as morphine and oxycodone. These findings are consistent with prior comprehensive analyses, suggesting that hydromorphone is a feasible choice for alleviating cancer-associated pain. Additional investigations are warranted to determine its efficacy in distinct patient cohorts and for different modes of administration. Trial registration Prospero registration ID: CRD42024517513. Link: https://www.crd.york.ac.uk/PROSPERO/#recordDetails .
Abstract licence: CC BY
Rongrong Li, Hao Yin, Weijun Luo, et al.
BMC Anesthesiology, 2025
- Hydromorphone
- Analgesics, Opioid
- Cholecystectomy, Laparoscopic
Kathleen A. Lee, Niharika Ganta, J. Horton, et al.
Journal of Palliative Medicine, 2016
S. Spénard, Charles Gélinas, E. D. Trottier, et al.
Archives of Disease in Childhood, 2021
Alessandra Pigni, Cinzia Brunelli, Augusto Caraceni
Palliative Medicine, 2011
- Analgesics, Opioid
- Hydromorphone
- Neoplasms
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
56 found
Half-life
2-3 hour
Mechanism
Hydromorphone is an opioid agonist that can bind to different types of opioid receptors.
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
30-60 minutes
[A176468]…
Half-life
2-3 hour
[A176468]
Protein binding
8-19%
[A176468]
Volume of distribution
4 L/kg
[A176468]
Metabolism
62%
[A176468]…
Elimination
7%
Clearance
105.7 ml/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The first reported approved product containing hydromorphone in the form of hydromorphone hydrochloride was developed by Fresenius Kabi USA and FDA approved in 1984.[L5795]
[A176468]
The WHO has proposed a three-step ladder for the management of pain in which it is suggested to start with a non-opioid medication followed by addition of weak opioids to the non-opioid treatment for moderate pain and finishing in the use of strong opioids such as hydromorphone along with the existing regimen for cases of severe pain.
[A176471]
Off-label, hydromorphone can be administered for the suppression of refractory cough.
[A176468]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1641 interactions
The management of an overdose might require assisted ventilation, supportive measures, as well as cardiac massage and defibrillation. It can be recommended the use of [naloxone] solely in the cases of respiratory depression. The use of opioid antagonist should be restricted to patients that present respiratory depression as they can produce acute abstinence symptoms.[FDA label]
Hydromorphone was not shown to be mutagenic nor clastogenic and long-term studies of carcinogenicity studies have not been performed.
On the other hand, reduced implantation sites and viable fetuses were noted at a 2X normal concentration.[FDA label]
The onset of action of the immediate release form of hydromorphone is achieved in 15-20 minutes and having a lasting effect for 3-4 hours while the extended-release form onset of action is of 6 hours lasting for about 13 hours.[A176468]
Some of the observed effects of the consumption of hydromorphone for acute pain are complete and longlasting pain relief when compared to other pain relief agents such as [meperidine], [morphine], [diamorphine], [bupivacaine], [indomethacin], and [fentanyl]. On the same trials, hydromorphone was shown to produce respiratory depression, lower cognitive function, miosis, mydriasis, constipation, hypotension, and vertigo but to present a reduced incidence of pruritus (which indicates a lower release of histamine) and nausea.[A176507]
The respiratory depression is known to be caused by the effect on the brain stem respiratory centers as well as to a reduction in the responsiveness of this brain stems to increase carbon dioxide tension.[L5798]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A176468]
When administered orally, hydromorphone is absorbed mainly in the upper small intestine with a bioavailability of 60% due to intensive first-pass metabolism. In the controlled-release version of hydromorphone, the absorption follows a biphasic pharmacokinetic profile. However, even though there are clear distinctions in the absorption pathway of hydromorphone, the AUC of both versions is reported to be of 34 ng.h/ml which indicates an equivalence.
[A176471]
The parenteral administration of hydromorphone, which is the most common pathway, presents an almost immediate absorption as observed by the presence of peak plasma concentration almost immediately.
This peak plasma concentration declines rapidly due to fast redistribution into liver, spleen, kidney and skeletal muscle. In the parenteral route, the pharmacokinetic profile is log-linear and dose-dependent and to present a higher bioavailability of 78%.
[A176471]
Other administration routes such as rectal, nasal, intraspinal and transdermal present lower bioavailability and changes in their pharmacokinetic profile.
[A176471]
[A176468]
[A176468]
[A176468]
[A176468]
This primary metabolic pathway is done by the activity of the UDP-glucuronosyltransferase-2B7.
[A176501]
The first-pass hepatic metabolism is so large that it represents 62% of the initial administered dose.
[A176495]
On the other hand, hydromorphone is also characterized by the presence of minor metabolic pathways such as the CYP3A4- and CYP2C9-driven generation of norhydromorphone.
[A39478]
[A176468]
[A176510]
The systemic clearance is reported to be of 1.96 L/min.
[L5798]
Proteins and enzymes this drug interacts with in the body
PMID:10529478 PMID:12589820 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone .
PMID:10529478 PMID:10836142 PMID:12589820 PMID:19300905 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors .
PMID:7905839
The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 .
PMID:12068084
They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity).
The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity).
The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation (By similarity). Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling (By similarity).
Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity)
Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine
Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain.
Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions
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 N02AA53
ATC N02AA03
ATC N02AG04
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)
Hydromorphone
Additional database identifiers
Drugs Product Database (DPD)
20280
ChemSpider
4447624
BindingDB
50241341
ZINC
ZINC000000402954
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8156
GenAtlas
OPRM1
GeneCards
OPRM1
GenBank Gene Database
L25119
GenBank Protein Database
452073
Guide to Pharmacology
319
UniProt Accession
OPRM_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8153
GenAtlas
OPRD1
GeneCards
OPRD1
GenBank Gene Database
U07882
GenBank Protein Database
27545517
Guide to Pharmacology
317
UniProt Accession
OPRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12535
GeneCards
UGT1A3
GenBank Gene Database
M84127
GenBank Protein Database
340135
UniProt Accession
UD13_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q303646), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.