Hydromorphone (oral)

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Hydromorphone (oral)
Clinical data
  • C
Routes of
oral, intramuscular, intravenous, intranasal, rectal
ATC code
Legal status
Legal status
Pharmacokinetic data
BioavailabilityOral: 30–35%, Intranasal: 52–58%[1]
Protein binding20%
Elimination half-life2–3 hours[2]
CAS Number
PubChem CID
E number{{#property:P628}}
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Chemical and physical data
Molar mass285.338 g/mol

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Hydromorphone is a drug which was researched and developed in Germany in 1924, and introduced to the mass market beginning in 1926. It is used to relieve moderate to severe pain and severe, painful dry coughing. Hydromorphone is known by the trade names Hydal, Sophidone, Hydrostat, Hydromorfan, Hydromorphan, Laudicon, and most famously, Dilaudid. An extended-release version called Palladone SR was available for a short time in the United States before being voluntarily withdrawn from the market after an FDA advisory released in July 2005 warned of a high overdose potential when taken with alcohol; it is still available in the United Kingdom as of March 2007. Another extended-release version called Hydromorph Contin, manufactured as controlled release capsules, continues to be produced and distributed in Canada by Purdue Pharma Inc. in Pickering, Ontario.

Hydromorphone is becoming more popular in the treatment of chronic pain in many countries, and it is used as a substitute for heroin and morphine where one or both of these drugs are not marketed. Hydromorphone is preferred even over morphine in many cases on account of hydromorphone's superior solubility and speed of onset and less troublesome side effect profile and lower dependence liability as compared to morphine and heroin. Many chronic pain patients find that hydromorphone has a spectrum of actions which suit them just as well as morphine, and better than synthetics like methadone or levorphanol in alleviating suffering, as contrasted with simple pain of equal objective intensity. Hydromorphone's side effect profile is closer to that of dihydromorphine than that of morphine and resultantly produces less nausea and vomiting and fewer histamine-related side effects than morphine.

Available Forms

  • Tablets - 0.5mg, 1mg, 2mg, 3mg, 4mg, 8mg
  • Capsules (Palladone) - 1.3mg, 2.6mg
  • Modified Release capsules (Palladone SR) - 2mg, 4mg, 8mg, 16mg, 24mg, 30mg, 32mg
  • Controlled Release capsules (Hydromorph Contin) - 3mg, 6mg, 12mg, 18mg, 24mg, 30mg
  • Suppository - 3mg
  • Powder for injection - 250 mg (hydromorphone HCl)
  • Oral liquid (HCl) - 1 mg/mL (480 mL)
  • Injection (HCl) - 1 mg/mL (1 mL), 2 mg/mL (1 mL, 20 mL), 4 mg/mL (1 mL),
  • Dilaudid-HP - 10 mg/ml (1 mL, 5mL, 50mL)


Hydromorphone, a semi-synthetic μ-opioid agonist, is a hydrogenated ketone of morphine and shares the pharmacologic properties typical of opioid analgesics. Hydromorphone and related opioids produce their major effects on the central nervous system and gastrointestinal tract. These include analgesia, drowsiness, mental clouding, changes in mood, euphoria or dysphoria, respiratory depression, cough suppression, decreased gastrointestinal motility, nausea, vomiting, increased cerebrospinal fluid pressure, increased biliary pressure, pinpoint constriction of the pupils, increased parasympathetic activity and transient hyperglycemia.

CNS depressants, such as other opioids, anesthetics, sedatives, hypnotics, barbiturates, phenothiazines, chloral hydrate and glutethimide may enhance the depressant effects of hydromorphone. MAO inhibitors (including procarbazine), first-generation antihistamines (brompheniramine, promethazine, diphenhydramine, chlorpheniramine), beta-blockers and alcohol may also enhance the depressant effect of hydromorphone. When combined therapy is contemplated, the dose of one or both agents should be reduced.


Patients with kidney problems must exercise caution when dosing hydromorphone. In those with renal impairment, the half-life of hydromorphone can increase to as much as 40 hours. This could cause an excess buildup of the drug in the body, and result in fatality. The typical half-life of intravenous hydromorphone is 2.3 hours.[3] Peak plasma levels usually occur between 30 and 60 minutes after oral dosing.[4]

Side effects

Adverse effects of hydromorphone are similar to those of other opioid analgesics, and represent an extension of pharmacological effects of the drug class. The major hazards of hydromorphone include respiratory and CNS depression. To a lesser degree, circulatory depression, respiratory arrest, shock and cardiac arrest have occurred. The most frequently observed adverse effects are sedation, nausea, vomiting, constipation, lightheadedness, dizziness and sweating.


Commercially, hydromorphone is made from morphine either by direct re-arrangement (made by reflux heating of alcoholic or acidic aqueous solution of morphine in the presence of platinum or palladium catalyst), or reduction to dihydromorphine (usually via catalytic hydrogenation), followed by oxidation with benzophenone in presence of potassium tert butoxide or aluminium tert butoxide (Oppenauer oxidation). The 6 ketone group can be replaced with a methylene group via the Wittig reaction to produce 6 methylene desomorphine which is 80x stronger than morphine.[5]

The human liver produces hydromorphone when processing hydrocodone using the cytochrome p450 II-D-6 enzyme pathway (CYP2D6). This is the same route that is used to convert many different opiate prodrugs into the active form. The proportion of drug that is converted into the stronger form is around 10% on average although this varies markedly between individuals. Drugs that are bioactivated in this way include codeine into morphine, nicocodeine to nicomorphine, oxycodone to oxymorphone and dihydrocodeine to dihydromorphine.

Some bacteria have been shown to be able to turn morphine into hydromorphone. As reported in the July 1993 issue of Applied Enviromental Bacteriology, the bacterium Pseudomonas putida, serotype M10 a naturally occurring NADH-dependent morphinone reductase which can work on unsaturated 7,8 bonds -- with result that when these bacteria are living in an aqueous solution containing morphine, sigificant amounts of hydromophone form as it is an intermediary metabolite in this process; the same goes for codeine being turned into hydrocodone. At this time no information on whether or not this process can change dihydromorphine into metopon or acetylated morphine derivatives into the respective ketones of the acetylmorphone series.

See also



  1. Coda BA, Rudy AC, Archer SM, Wermeling DP. "Pharmacokinetics and Bioavailability of Single-Dose Intranasal Hydromorphone Hydrochloride in Healthy Volunteers." Anesthesia Analgesia. 2003 Jul;97(1):117-23. PMID 12818953 Fulltext
  2. Vallner JJ, Stewart JT, Kotzan JA, Kirsten EB, Honigberg IL. "Pharmacokinetics and bioavailability of hydromorphone following intravenous and oral administration to human subjects." Journal of Clinical Pharmacology. 1981 Apr;21(4):152-6. PMID 6165742 Fulltext
  3. That's Poppycock - Hydromorphone
  4. Dilaudid Clinical Pharmacology
  5. http://www.acsmedchem.org/module/opioid.html

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