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Ethylmorphine

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3 sources

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Collated from PsychonautWiki, TripSit, Pharmacology. Where sources differ (e.g. dosing), Compare shows them side by side.

Sections
OpioidSubstituted morphinansHabit-formingDepressantPW

Also known as Ethylmorphine, Codethyline, DioninePW

Fatal overdose may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.[1] It is strongly discouraged to combine these substances, particularly in common to heavy doses.PW

Addiction potentialPW
very addictive with a high potential for abuse
ToxicityPW
low toxicity; potentially lethal when mixed with depressants like alcohol or benzodiazepines
TolerancePW
full tolerance develops with prolonged and repeated use; half after 3 - 7 days; baseline after 1 - 2 weeks
Cross-tolerancePW
opioids

Oral

Route dataPsychonautWiki

Dose
WeakerStronger
ThresholdLightCommonStrongHeavy
20 mg40–50 mg50–100 mg100–200 mg200 mg+
0250 mg
LightCommonStrongHeavy
Duration
ShorterLonger
Total4–5 hours

Caution / uncertainPW

MAOIsNitrousPCPStimulants

Mechanism of actionPH

Ethylmorphine is metabolized by the liver enzyme cytochrome P450 2D6 to morphine. 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.

PharmacodynamicsPH

Ethylmorphine is metabolized by the enzyme cytochrome P450 2D6 to morphine. 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.

Pharmacokinetics

MetabolismPH

After ingestion, ethylmorphine is converted to morphine in the human liver by the CYP450-isozyme CYP2D6, similarly to codeine.
Ethylmorphine has known human metabolites that include Norethylmorphine and Morphine.

Plan when to take Ethylmorphine — see where onset, peak and comedown land on the clock

Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.