Buprenorphine, is an opioid used to treat opioid use disorder, acute pain, and chronic pain. It can be used under the tongue (sublingual), in the cheek (buccal), by injection (intravenous and subcutaneous), as a skin patch (transdermal), or as an implant.
In the United States, the combination formulation of buprenorphine/naloxone (Suboxone) is usually prescribed to discourage misuse by injection. Maximum pain relief is generally within an hour with effects up to 24 hours. Buprenorphine affects different types of opioid receptors in different ways. Depending on the type of opioid receptor, it may be an agonist, partial agonist, or antagonist. Buprenorphine's activity as an agonist/antagonist is important in the treatment of opioid use disorder: it relieves withdrawal symptoms from other opioids and induces some euphoria (primarily when first starting treatment if one is not already opioid tolerant/dependent), but also blocks the ability for many other opioids, including heroin, to cause an effect. Unlike full agonists like heroin or methadone, buprenorphine has a ceiling effect, such that taking more medicine past a certain point will not increase the effects of the drug.
Being a partial MOR agonist, buprenorphine offers flexibility to prescribers treating opioid use disorder as the dosage can be easily adjusted.
Side effects may include respiratory depression (decreased breathing), sleepiness, adrenal insufficiency, changes in heart electrophysiology (QT prolongation), low blood pressure, allergic reactions, constipation, and opioid addiction. Among those with a history of seizures, a risk exists of further seizures. Opioid withdrawal following stopping buprenorphine is generally less severe than with other opioids. Whether use during pregnancy is safe is unclear, but use while breastfeeding is probably safe, since the dose the infant receives is 1–2% that of the maternal dose, on a weight basis.
Buprenorphine was patented in 1965, FDA approved for medical use as an analgesic in 1981, and FDA approved for treating opioid use disorder in 2002. It is on the World Health Organization's List of Essential Medicines. Despite originally being marketed as an analgesic it is far more commonly prescribed and used to treat opioid use disorders, such as addiction to heroin. In 2020, it was the 186th most commonly prescribed medication in the United States, with more than 2.8million prescriptions.
Buprenorphine does not produce the same kind of euphoria and sense of well-being in most patients. Users do report a far milder effect, and the compound can be misused. It is generally used as a medication for treating opioid use disorder. Buprenorphine has significantly reduced euphoric potential compared with full opioid agonists due to its partial-agonist ceiling effect. In opioid-naïve individuals it may still produce mild euphoria, so the abuse risk is not zero. In the United States, buprenorphine, alone and as a combination drug, is a schedule III controlled substance.
Harm Reduction
It is strongly recommended that one use harm reduction practices when using this drug. As with other opioids,moderately addictive with a high potential for abuse and is capable of causing psychologica...
Buprenorphine arrives quietly. Unlike full agonistopioids that sweep through the body in a dramatic wave, buprenorphine's onset is measured, restrained -- a slow tide rather than a crashing surf. Thirty to sixty minutes after sublingual administration, the first signs emerge: a subtle loosening of tension in the shoulders, a faint warmth that settles in the lower back and spreads outward with deliberate patience. The world does not transform; it simply becomes slightly more tolerable.
As the compound reaches its plateau, a ceiling becomes apparent -- an invisible boundary that the experience cannot exceed no matter the dose. The warmth is present but contained, like sunlight filtered through frosted glass. There is a gentle euphoria, but it lacks the overwhelming quality of morphine or hydromorphone. Instead, it manifests as a quiet contentment, an absence of distress rather than a presence of bliss. Pain recedes to a manageable hum. The body relaxes without becoming leaden, and consciousness remains relatively clear. You can hold conversations, follow thoughts to their conclusions, move through the world with a steadiness that stronger opioids do not permit.
Physically, the experience is characterized by a moderate warmth that settles into the core of the body. There may be mild nausea, particularly in the first hour, and a faint dizziness that passes quickly. The characteristic opioid itch is present but muted. Pupils constrict, but not to the dramatic pinpoints that full agonists produce. Breathing slows slightly but never to the alarming degree associated with more potent compounds. The body feels comfortable -- not euphoric, not numbed, but genuinely comfortable in a way that feels almost medicinal.
The duration is remarkably long. Where other opioids peak and fade within hours, buprenorphine maintains its quiet presence for the better part of a day. The plateau stretches on, flat and steady, without the dramatic peaks and valleys that characterize shorter-acting compounds. This steadiness gives the experience a peculiar quality of normalcy -- after a while, you almost forget you have taken anything at all. The pain relief and emotional stability simply become the backdrop of your day.
The offset is as gradual as the onset. The warmth recedes so slowly that it is difficult to pinpoint the moment it leaves. There is no crash, no sudden return of discomfort. Instead, baseline sensation returns over the course of hours, a slow dimming rather than a switch being thrown. The afterglow is mild -- a faint residual ease that can persist into the following day, a gentleness around the edges of experience that fades so imperceptibly you may only notice its absence in retrospect.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. 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.
Physical Effects
Physical(17)
Appetite suppression— A distinct decrease in hunger and desire to eat, ranging from reduced interest in food to complete d...
Constipation— A slowing or cessation of bowel movements resulting in difficulty passing stool, commonly caused by ...
Cough suppression— A decreased desire and need to cough, medically known as antitussive action, which can also allow in...
Dehydration— A state of insufficient bodily hydration manifesting as persistent thirst, dry mouth, and physical d...
Dizziness— A sensation of spinning, swaying, or lightheadedness that impairs balance and spatial orientation, o...
Headache— A painful sensation of pressure, throbbing, or aching in the head that can range from a dull backgro...
Increased heart rate— A noticeable acceleration of heartbeat that can range from a subtle awareness of one's pulse to a fo...
Itchiness— A persistent, diffuse urge to scratch the skin that arises without any external irritant, most commo...
Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
Pain relief— A suppression of negative physical sensations such as aches and pains, ranging from dulled awareness...
Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
Pupil constriction— A visible narrowing of the pupil diameter (miosis) that reduces the size of the dark center of the e...
Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
Sedation— A state of deep physical and mental calming that manifests as a progressive desire to remain still, ...
Seizure— Uncontrolled brain electrical activity causing convulsions and loss of consciousness -- a life-threa...
Stimulation— A state of heightened physical and mental energy characterized by increased wakefulness, elevated mo...
Cognitive & Perceptual Effects
Visual(2)
Geometry— The experience of perceiving complex, ever-shifting geometric patterns superimposed over the visual ...
Internal hallucination— Vivid, detailed visual experiences perceived within an imagined mental landscape that can only be se...
Cognitive(6)
Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
Buprenorphine acts as a partial agonist of the μ-opioid receptor with a binding affinity of Ki = 1.5 nM in contrast to full agonists like morphine. It also acts as an antagonist of the κ-opioid receptor with a binding affinity of Ki = 2.5 nM and the δ-opioid receptor with a binding affinity of Ki = 6.1 nM. The ratio of these binding affinities is important, if you compare morphine's binding ratio of 1:50:176 to Buprenorphine's ratio of 15:25:61, it is apparent that the side-effect profile will be much higher to Buprenorphine and μ-opioid stimulation for euphoric effects, sequentially the drug will also bind to delta and kappa opioid receptors to a comparatively high degree.
Buprenorphine exerts its effects by binding to and activating the μ-opioid receptor. This occurs because opioids structurally mimic endogenous endorphins which are naturally found within the body and also work upon 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.
low toxicity relative to dose: the ceiling dose for buprenorphine is usually between 16mg and 32mg, and anything above this will not produce an increase in respiratory depression (the primary cause of death in opioid overdose is severe respiratory depression, leading to respiratory collapse). Thus increasing the dose of buprenorphine above this level will not continue to increase risk of death in a fashion similar to other μ-opioid receptor agonists. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss.
Regardless of the ceiling dose, an important distinction has to be made in the dose used in opioid naive individuals and opioid experienced individuals. Even low doses in individuals with no tolerance can cause unpleasant side-effects like dizziness, loss of balance, and vomiting. Because of the long half-life of buprenorphine, these side-effects can last a long while in opioid naive individuals which creates the risk of severe dehydration from uncontrollable vomiting.
Buprenorphine is often sold under the brand name Suboxone, which also contains naloxone. Naloxone is not orally active except at higher doses, so when large amounts of Suboxone are taken, the naloxone takes effect and reverses the effects of the buprenorphine. This is done to deter abuse of Suboxone.
It is strongly recommended that one use harm reduction practices when using this drug.
As with other opioids,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.develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). Buprenorphine presents cross-tolerance with Cross-all other opioids, meaning that after the consumption of buprenorphine all opioids will have a reduced effect.
Precipitated withdrawal syndrome
Buprenorphine has the ability to precipitate withdrawal symptoms in opiate-dependent individuals. This is due to buprenorphine only being a partial agonist, which does not activate the receptor with the appreciable efficacy of a full agonist, as well as having a very high binding affinity for the μ-opioid receptor (Ki = 1.5nM), displacing other agonists that may still be attached when the buprenorphine is ingested.
Note: It is a common misconception that naloxone, in some buprenorphine formulations, is what causes the precipitated withdrawal syndrome to manifest. This is false, as naloxone has a lower binding than Buprenorphine, as well as being inactive through most routes of administration.
In the European Union, buprenorphine can be prescribed either alone or in combination with another substance and is approved for the treatment of opioid addiction.
Austria: Buprenorphine is legal for medical use under the AMG (Arzneimittelgesetz Österreich) and illegal when sold or possessed without a prescription under the SMG (Suchtmittelgesetz Österreich).
Canada: Buprenorphine is a schedule I substance in Canada and is only available with a valid prescription.
Germany: Buprenorphine is controlled under Anlage III BtMG (Narcotics Act, Schedule III) as of September 1, 1984. It can only be prescribed on a narcotic prescription form.
Netherlands: Buprenorphine a List II drug of the Opium Law, although special rules apply to its prescription and dispensation.
Sweden: Buprenorphine is a class IV controlled substance.
Switzerland: Buprenorphine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.
United States: Buprenorphine, either alone or in combination with naloxone (as, for example, Suboxone), is a Schedule III drug.
Prior to the approval of Suboxone in the U.S. for treating opioid addiction, the Drug Addiction Treatment Act of 2000 was passed. This law gives the Secretary of Health and Human Services the authority to grant a waiver to all physicians with appropriate training to prescribe and administer narcotics from Schedules III-V in the treatment of drug addiction. Prior to the passage of this law such authority was restricted solely to physicians working in an outpatient clinic specifically designed for treatment of addiction. The waiver, which requires the physician to undergo an 8-hour training course, initially allowed that physician to treat only 10 patients in this manner; as of 2016, this limit has been increased to 275.
Buprenorphine is a semi-synthetic opioid that requires a dedicated buprenorphine-specific immunoassay for detection. Standard 5-panel opiate screens do NOT detect buprenorphine due to its distinct chemical structure (a thebaine derivative with a C7 side chain). Extended panels used in addiction treatment settings (12-panel or custom) typically include a buprenorphine channel. The standard screening cutoff is 5 to 10 ng/mL.
Urine Detection
Buprenorphine is detectable in urine for approximately 3 to 7 days after a single dose, potentially longer with chronic sublingual dosing (as in Suboxone maintenance). The primary urinary metabolites are norbuprenorphine (via CYP3A4 N-dealkylation) and their glucuronide conjugates. Both buprenorphine-glucuronide and norbuprenorphine-glucuronide are the dominant urinary species. Enzymatic hydrolysis of the sample is often performed before analysis to improve sensitivity.
Blood and Saliva Detection
Blood concentrations of buprenorphine are detectable for approximately 24 to 72 hours. Due to its high binding affinity for opioid receptors, buprenorphine has pharmacological effects that outlast detectable blood concentrations. Oral fluid testing can detect buprenorphine for 24 to 72 hours and is increasingly used in addiction treatment compliance monitoring.
Hair Follicle Detection
Hair testing can detect buprenorphine and norbuprenorphine for up to 90 days. Extended opioid hair panels include buprenorphine. This testing is used in forensic, child protective services, and compliance monitoring applications.
Confirmatory Testing
LC-MS/MS is the preferred confirmatory method for buprenorphine and norbuprenorphine, offering the sensitivity required for the low concentrations encountered (low nanogram-per-milliliter range). Quantification of the buprenorphine-to-norbuprenorphine ratio can help assess compliance versus diversion: sublingual administration produces a higher norbuprenorphine-to-buprenorphine ratio than parenteral abuse.
Reagent Testing
Standard reagent tests are not useful for buprenorphine identification. The compound is typically encountered as sublingual tablets or film (Suboxone, Subutex) with distinctive pharmaceutical markings. Reagent testing has no harm reduction application for buprenorphine.
No significant pharmacological interaction; opioids may slightly dull the psychedelic experience
Showing 62 key interactions out of 82 total.
History
Buprenorphine belongs to the opioid class of substances, which has a history spanning thousands of years from the ancient use of opium poppy to modern synthetic and semi-synthetic analogues.
The isolation of morphine from opium in 1804 by Friedrich Sertürner marked the beginning of modern opioid pharmacology. Subsequent developments included the synthesis of heroin (diacetylmorphine) in 1874, the development of numerous semi-synthetic and fully synthetic opioids throughout the 20th century, and the identification of endogenous opioid receptors and peptides in the 1970s.
The opioid crisis of the early 21st century, driven largely by overprescription of pharmaceutical opioids and the subsequent emergence of illicit fentanyl and its analogues, represents one of the most significant public health challenges in modern history. This crisis has fundamentally reshaped discussions around opioid prescribing, addiction treatment, and harm reduction policy.
Buprenorphine exists within this complex pharmacological and social context, with its history shaped by its development, clinical utility, and the broader dynamics of opioid use and regulation.
Harm Reduction
It is strongly recommended that one use harm reduction practices when using this drug.
As with other opioids,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.develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). Buprenorphine presents cross-tolerance with Cross-all other opioids, meaning that after the consumption of buprenorphine all opioids will have a reduced effect.
Precipitated withdrawal syndrome
Buprenorphine has the ability to precipitate withdrawal symptoms in opiate-dependent individuals. This is due to buprenorphine only being a partial agonist, which does not activate the receptor with the appreciable efficacy of a full agonist, as well as having a very high binding affinity for the μ-opioid receptor (Ki = 1.5nM), displacing other agonists that may still be attached when the buprenorphine is ingested.
Note: It is a common misconception that naloxone, in some buprenorphine formulations, is what causes the precipitated withdrawal syndrome to manifest. This is false, as naloxone has a lower binding than Buprenorphine, as well as being inactive through most routes of administration.
In the Eu
Toxicity & Safety
Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Buprenorphine was found to be the 19th overall most dangerous drug.
A 2007 assessment of harm from recreational drug use (mean physical harm and mean dependence liability): Buprenorphine was ranked 9th in dependence, 8th in physical harm, and 11th in social harm.
Buprenorphine has a low toxicity relative to dose: the ceiling dose for buprenorphine is usually between 16mg and 32mg, and anything above this will not produce an increase in respiratory depression (the primary cause of death in opioid overdose is severe respiratory depression, leading to respiratory collapse). Thus increasing the dose of buprenorphine above this level will not continue to increase risk of death in a fashion similar to other μ-opioid receptor agonists. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss.
Regardless of the ceiling dose, an important distinction has to be made in the dose used in opioid naive individuals and opioid experienced individuals. Even low doses in individuals with no tolerance can cause unpleasant side-effects like dizziness, loss of balance, and vomiting. Because of the long half-life of buprenorphine, these side-effects can last a long while in opioid naive individuals which creates the risk of severe dehydration from uncontrollable vomiting.
Buprenorphine is often sold under the brand name Suboxone, which also contains naloxone. Naloxone is not orally active except at higher doses, so when large amounts of Suboxone are taken, the naloxone takes effect and reverses the effects of the buprenorphine. This is done to deter abuse of Suboxone.
It is strongly recommended that one use harm reduction practices when using this drug.
Tolerance and addiction potential
As with other opioids, the chronic use of buprenorphine 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.
Tolerance to many of the effects of buprenorphine develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Buprenorphine presents cross-tolerance with all other opioids, meaning that after the consumption of buprenorphine all opioids will have a reduced effect.
Precipitated withdrawal syndrome
Buprenorphine has the ability to precipitate withdrawal symptoms in opiate-dependent individuals. This is due to buprenorphine only being a partial agonist, which does not activate the receptor with the appreciable efficacy of a full agonist, as well as having a very high binding affinity for the μ-opioid receptor (Ki = 1.5nM), displacing other agonists that may still be attached when the buprenorphine is ingested.
Note: It is a common misconception that naloxone, in some buprenorphine formulations, is what causes the precipitated withdrawal syndrome to manifest. This is false, as naloxone has a lower binding than Buprenorphine, as well as being inactive through most routes of administration.
Dangerous interactions
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. Tramadol, oxycodone, and fentanyl are all primarily metabolized by the enzyme CYP3A4, which is potently inhibited by grapefruit juice. 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. Codeine and hydrocodone 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.
Addiction Potential
moderately addictive with a high potential for abuse
Overdose Information
overdose is severe respiratory depression, leading to respiratory collapse). Thus increasing the dose of buprenorphine above this level will not continue to increase risk of death in a fashion similar to other μ-opioid receptor agonists. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss.
Regardless of the ceiling dose, an important distinction has to be made in the dose used in opioid naive individuals and opioid experienced individuals. Even low doses in individuals with no tolerance can cause unpleasant side-effects like dizziness, loss of balance, and vomiting. Because of the long half-life of buprenorphine, these side-effects can last a long while in opioid naive individuals which creates the risk of severe dehydration from uncontrollable vomiting.
Buprenorphine is often sold under the brand name Suboxone, which also contains naloxone. Naloxone is not orally active except at higher doses, so when large amounts of Suboxone are taken, the naloxone takes effect and reverses the effects of the buprenorphine. This is done to deter abuse of Suboxone.
It is strongly recommended that one use harm reduction practices when using this drug.
As with other opioids,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.develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about Ti
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Severe respiratory depression risk; leading cause of polydrug overdose
Tolerance
Full
develops with prolonged and repeated use
Half
3 - 7 days
Zero
1 - 2 weeks
Cross-tolerances
opioids
Legal Status
In the European Union, buprenorphine can be prescribed either alone or in combination with another substance and is approved for the treatment of opioid addiction.
Austria: Buprenorphine is legal for medical use under the AMG (Arzneimittelgesetz Österreich) and illegal when sold or possessed without a prescription under the SMG (Suchtmittelgesetz Österreich).
Canada: Buprenorphine is a schedule I substance in Canada and is only available with a valid prescription.
Germany: Buprenorphine is controlled under Anlage III BtMG (Narcotics Act, Schedule III) as of September 1, 1984. It can only be prescribed on a narcotic prescription form.
Netherlands: Buprenorphine a List II drug of the Opium Law, although special rules apply to its prescription and dispensation.
Sweden: Buprenorphine is a class IV controlled substance.
Switzerland: Buprenorphine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.
United States: Buprenorphine, either alone or in combination with naloxone (as, for example, Suboxone), is a Schedule III drug.
Prior to the approval of Suboxone in the U.S. for treating opioid addiction, the Drug Addiction Treatment Act of 2000 was passed. This law gives the Secretary of Health and Human Services the authority to grant a waiver to all physicians with appropriate training to prescribe and administer narcotics from Schedules III-V in the treatment of drug addiction. Prior to the passage of this law such authority was restricted solely to physicians working in an outpatient clinic specifically designed for treatment of addiction. The waiver, which requires the physician to undergo an 8-hour training course, initially allowed that physician to treat only 10 patients in this manner; as of 2016, this limit has been increased to 275.
Starting buprenorphine too early after your last opioid dose will cause precipitated withdrawal, which is far worse than regular withdrawal. Wait at least 12-24 hours after short-acting opioids and 36-72 hours after methadone before your first buprenorphine dose.
OpioidRecovery_Coach · Mar 4
If you are using buprenorphine (Suboxone/Subutex) for opioid use disorder, do not skip doses to get high on other opioids. The buprenorphine occupies your receptors for 24-72 hours, so most opioids will not work, and you risk precipitated withdrawal when you take your next buprenorphine dose.
MAT_Advocate · Mar 4
Buprenorphine has a ceiling effect for respiratory depression, making it much safer than full agonist opioids. However, combining it with benzodiazepines, alcohol, or other CNS depressants can still be fatal. The ceiling effect does not protect against poly-drug combinations.
SuboxonePatient_5yr · Mar 4
Opioid tolerance and cross-tolerance are complex with Buprenorphine. Switching between different opioids requires careful dose conversion. Do not assume equivalent effects at standard conversion ratios; start lower than calculated.
ChemCheck_ · Mar 4
Test every batch of Buprenorphine with fentanyl test strips. Fentanyl contamination is pervasive in the current drug supply. Even a negative test is not 100% reliable due to uneven mixing, but it catches many contaminated batches.
SafeSpaceSam · Mar 4
Constipation from Buprenorphine is universal with regular opioid use. Start a fiber supplement and stool softener proactively. Severe opioid-induced constipation can cause bowel obstruction which is a surgical emergency.
Opioid used to treat pain and opioid use disorder Buprenorphine, is an opioid used to treat opioid use disorder, acute pain, and chronic pain. It can be used under the tongue (sublingual), in the cheek (buccal), by injection (intravenous and subcutaneous), as a skin patch (transdermal), or as an imp
What are the effects of Buprenorphine?
Buprenorphine arrives quietly. Unlike full agonist opioids that sweep through the body in a dramatic wave, buprenorphine's onset is measured, restrained -- a slow tide rather than a crashing surf. Thirty to sixty minutes after sublingual administration, the first signs emerge: a subtle loosening of
Is Buprenorphine addictive?
moderately addictive with a high potential for abuse
What are the risks of Buprenorphine?
Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Buprenorphine was found to be the 19th overall most dangerous drug. A 2007 assessment of harm from recreational drug use (mean physical harm and mean dependence liability): Buprenorphin
How long does Buprenorphine last?
The total duration of Buprenorphine via insufflated is 8 hours to 14 hours. Onset typically occurs within 30 minutes to 1 hour. Peak effects last 4 hours to 8 hours.
— Intense feelings of apprehension, worry, and dread that can range from a subtle background unease to...
Anxiety suppression— A partial to complete suppression of anxiety and general unease, producing a calm, relaxed mental st...
Cognitive euphoria— A cognitive and emotional state of intense well-being, elation, happiness, and joy that manifests as...
Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
Sleepiness— A progressive onset of drowsiness, heaviness, and the desire to sleep that pulls the individual towa...
