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Brorphine is not under international control.<ref name="UNODC2020"/>
Brorphine is not under international control.<ref name="UNODC2020"/>
'''Turkey:''' Metonitazene is a classed as drug and is illegal to possess, produce, supply, or import.<ref>https://resmigazete.gov.tr/eskiler/2020/10/20201007-8.pdf</ref>
*'''Turkey:''' Metonitazene is a classed as drug and is illegal to possess, produce, supply, or import.<ref>https://resmigazete.gov.tr/eskiler/2020/10/20201007-8.pdf</ref>
*'''United States''': As of August 2020, brorphine is not controlled under the Controlled Substances Act.<ref name="DEA2020"/>
*'''United States''': As of August 2020, brorphine is not controlled under the Controlled Substances Act.<ref name="DEA2020"/>
Latest revision as of 20:46, 18 January 2022
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Very little is known about the toxicity of brorphine and it has very little history of human usage. It is currently available as a gray-area research chemical in many countries. It is strongly advised to use harm reduction practices if choosing to use this substance.
As a result, it may contain incomplete or wrong information. You can help by expanding it.
Brorphine was first described in the scientific literature as a μ-opioid receptor agonist in 2018.[3] It was reported to the UNODC Early Warning Advisory on NPS in 2019.[2] In mid-2019 brorphine
emerged in the United States’ drug market.[3] After the temporarily scheduling of isotonitazene in June 2020 by the Drug Enforcement Administration, detections of brorphine in the U.S. began to increase, appearing as similar gray drug powders and an apparent
replacement for isotonitazene.[4]
Brorphine is an atypical opioid of the piperidine and benzimidazolone class which has some structural similarities with fentanyl.[2][4] It is comprised of three main units: A 4-bromophenethyl group, a piperidine ring, and a 1,3-dihydro-2H-benzoimidzole-2-one group. Brorphine is being trafficked as its hydrochloride salt which would be water-soluble.[3]
Opioids exert their effects by binding to and activating the μ-opioidreceptor. This occurs because opioids structurally mimic endorphins which are naturally found in the body and also work with the μ-opioid receptor set. The way in which opioids structurally mimic these natural endorphins results in their euphoria, pain relief and anxiolytic effects. This is because endorphins are responsible for reducing pain, causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or general excitement.
In vitro pharmacological data show brorphine exhibits potency similar to fentanyl[4] and activation of mu-opioid receptors involves recruitment of beta-arrestin-2, a regulatory protein[3]
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Anecdotal reports which describe the effects of this compound within our experience index include:
Toxicity and harm potential
This toxicity and harm potential section is a stub.
As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it. Note: Always conduct independent research and use harm reduction practices if using this substance.
Brorphine has a high toxicity relative to its dose due to its extreme potency. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss. It is also [[Toxicity::potentially lethal when mixed with depressants like alcohol or benzodiazepines]].
Recent detections in drug related deaths leads to the conclusion that brorphine has the potential to cause widespread harm.[4] There are no published studies on safety for human use as of August 2020.[3]
It is strongly recommended that one use harm reduction practices, and take extreme caution when using this substance.
Tolerance and addiction potential
As with other opioids, the chronic use of brorphine can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal symptoms may occur if a person suddenly stops their usage.
Brorphine presents cross-tolerance with [[Cross-tolerance::all other opioids]], meaning that after the consumption of brorphine all opioids will have a reduced effect.
The risk of fatal opioid overdoses rise sharply after a period of cessation and relapse, largely because of reduced tolerance.[5] To account for this lack of tolerance, it is safer to only dose a fraction of one's usual dosage if relapsing. It has also been found that the environment one is in can play a role in opioid tolerance. In one scientific study, rats with the same history of heroin administration were significantly more likely to die after receiving their dose in an environment not associated with the drug in contrast to a familiar environment.[6]
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely
Stimulants - Stimulants increase respiration rate which allows for a higher dose of opiates than would otherwise be used. If the stimulant wears off first then the opiate may overcome the user and cause respiratory arrest.
Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position blackouts/memory loss likely.
DXM - Generally considered to be toxic. CNS depression, difficulty breathing, heart issues, and liver toxicity have been observed. Additionally if one takes DXM, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
GHB/GBL - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position
Ketamine - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.
MAOIs - Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.
MXE - MXE can potentiate the effects of opioids but also increases the risk of respiratory depression and organ toxicity.
Nitrous - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are common.
PCP - PCP may reduce opioid tolerance, increasing the risk of overdose.
Tramadol - Increased risk of seizures. Tramadol itself is known to induce seizures and it may have additive effects on seizure threshold with other opioids. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
Grapefruit - While grapefruit is not psychoactive, it may affect the metabolism of certain opioids. Certain opioids such as oxycodone and fentanyl primarily metabolized by the enzyme CYP3A4, which is potently inhibited by grapefruit juice[7]. This may cause the drug to take longer to clear from the body. it may increase toxicity with repeated doses. Methadone may also be affected[7]. Codeine, hydrocodone, and Tramadol are metabolized by CYP2D6. People who are on medicines that inhibit CYP2D6, or that lack the enzyme due to a genetic mutation will not respond to codeine as it can not be metabolized into its active product: morphine.
