Source of information: Drugbank (External Link). Last updated on: 3rd July 18
*Trade Name used in the content below may not be the same as the HSA-registered product.
Active Ingredient / Synonyms
(−)-morphine | (5alpha,6alpha)-17-methyl-7,8-didehydro-4,5-epoxymorphinan-3,6-diol | (5alpha,6alpha)-didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol | (5R,6S,9R,13S,14R)-4,5-epoxy-N-methyl-7-morphinen-3,6-diol | (5α,6α)-17-methyl-7,8-didehydro-4,5-epoxymorphinan-3,6-diol | (5α,6α)-didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol | (7R,7AS,12bs)-3-methyl-2,3,4,4a,7,7a-hexahydro-1H-4,12-methanobenzofuro[3,2-e]isoquinoline-7,9-diol | anhydrous morphine | morfina | Morphia | Morphin | Morphinum | Morphium | Morphine |
The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. In January, 2017, morphine was approved for the treatment of chronic pain.
For the relief and treatment of severe pain.
Mechanism of Action
The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. Morphine first acts on the mu-opioid receptors. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. It has been shown that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream.
Morphine is a narcotic pain management agent indicated for the relief of pain in patients who require opioid analgesics for more than a few days. Morphine interacts predominantly with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. They are also found on the terminal axons of primary afferents within laminae I and II (substantia gelatinosa) of the spinal cord and in the spinal nucleus of the trigeminal nerve. In clinical settings, morphine exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Its primary actions of therapeutic value are analgesia and sedation. Morphine appears to increase the patient's tolerance for pain and to decrease discomfort, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Opioids also produce respiratory depression by direct action on brain stem respiratory centers.
Bioavailability is approximately 30%.
* 1 to 6 L/kg
Primarily hepatic (90%), converted to dihydromorphinone and normorphine. Also converted to morphine-3-glucuronide (M3G) and morphine-6-glucuronide. Virtually all morphine is converted to glucuronide metabolites; only a small fraction (less than 5%) of absorbed morphine is demethylated.
A small amount of glucuronide conjugates are excreted in bile, with minor enterohepatic recycling. Seven to 10% of administered morphine sulfate is excreted in the feces.
* 20 – 30 mL/min/kg [Adult] * 1852 +/- 116 mL/min [Chinese] * 1495 +/- 80 mL/min [Caucasian]
LD50 = 461 mg/kg (rat, oral), 600 mg/kg (mouse, oral). Human lethal dose by ingestion is 120-250 mg of morphine sulfate. Symptoms of overdose include cold, clammy skin, flaccid muscles, fluid in the lungs, lowered blood pressure, "pinpoint" or dilated pupils, sleepiness leading to stupor and coma, slowed breathing, and slow pulse rate.
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