Trade names Buprenex, Subutex, Suboxone, Butrans
US: Schedule III drug.
Routes of administration are sublingual, IM, IV, transdermal, intranasal, rectally, and orally.
Bioavailabilityis 30% sublingually. and approx 50% intranasally.
Protein binding is 96% with hepatic metabolism via CYP3A4, and CYP2C8
Biological half-life 20–70 hours with a mean of 37 hours
Excreted by renal and biliary mechanisms.
A semisynthetic opioid derivative of thebaine.
A mixed partial agonist opioid receptor modulator.
Used to treat opioid addiction, to control moderate acute pain in non-opioid-tolerant individuals and to control moderate chronic pain.
Sometimes used to treaty nausea in antiemetic intolerant individuals, most often in transdermal patch form.
It is available in a variety of formulations.
While both buprenorphine and methadone are medications used for detoxification for short- and long-term opioid replacement therapy. the former has the advantage of being a partial agonist, and negating the potential for life-threatening respiratory depression in cases of abuse.
The effectiveness of buprenorphine and methadone are essentially identical, and have similar adverse-effect profiles apart from more sedation among methadone users.
Detoxification consists of withdrawal from the drug of dependency on to buprenorphine, sometimes aided by the use of medications such as benzodiazepines that assist with anxiety, sleep, and muscle relaxation, clonidine and anti-inflammatory drugs such as ibuprofen and aspirin.
Suboxone contains buprenorphine as well as the opioid antagonist naloxone to deter the use of tablets by intravenous injection.
Buprenorphine and naloxone at a 4:1 ratio will produce unpleasant withdrawal symptoms if taken intravenously by people who are addicted to opioids.
The Suboxone formulation has potential to produce an opioid agonist high if injected by non-dependent persons.
Naloxone is ineffective in preventing suboxone abuse, as well as the overdosing on buprenorphine, as naloxone is not strong enough to reverse its effects.
Butrans Transdermal Patch System is available in 5 mcg/hour, 7.5 mcg/hour, 10 mcg/hour, 15 mcg/hour, and 20 mcg/hour doses and are applied for 7 days.
Butrans Transdermal Patches are for moderate to severe chronic pain.
Butrans Transdermal Patch is not indicated for use in acute pain, pain that is expected to last only for a short period of time, or post-operative pain.
Butrans Transdermal Patch is not indicated or recommended for use in the treatment of opioid addiction.
Majority of unipolar non-psychotic persons with major depression refractory to conventional antidepressants and electroconvulsive therapy can be successfully treated with buprenorphine.
Used in the treatment of the neonatal abstinence syndrome.
Binds with high affinity and antagonize the putative ε-opioid receptor.
Buprenorphine blocks voltage-gated sodium channels via the local anesthetic binding site as well, and this underlies its potent local anesthetic properties.
Full analgesic efficacy of buprenorphine requires both exon 11-and exon 1-associated μ-opioid receptor splice variants.
Metabolized by the liver, via CYP3A4 isozymes of the cytochrome P450 enzyme system.
Glucuronidation is primarily carried out by UGT1A1 and UGT2B7, and that of norbuprenorphine by UGT1A1 and UGT1A3.
Glucuronides are then eliminated mainly through excretion into the bile.
The elimination half-life of buprenorphine is 20–73 hours.
There is no risk of accumulation in people with renal impairment.
One of the major active metabolites of buprenorphine is norbuprenorphine.
Relative to buprenorphine, norbuprenorphine has extremely little antinociceptive potency which is 1/50th that of buprenorphine.
Norbuprenorphine markedly depresses respiration, 10-fold more than buprenorphine.
Very poor brain penetration of norbuprenorphine due to a high affinity of the compound for P-glycoprotein.
In contrast to norbuprenorphine, buprenorphine and its glucuronide metabolites are negligibly transported by P-glycoprotein.
Glucuronides of buprenorphine and norbuprenorphine are biologically active, and represent major active metabolites of buprenorphine.
Buprenorphine and norbuprenorphine may be detected in blood or urine to monitor use, abuse, or confirm a diagnosis of poisoning.
Common adverse drug reactions include: nausea and vomiting, drowsiness, dizziness, headache, memory loss, cognitive and neural inhibition, perspiration, itchiness, dry mouth, miosis, orthostatic hypotension, male ejaculatory difficulty, decreased libido, and urinary retention.
Constipation and CNS effects are seen less frequently than with morphine.
Hepatic necrosis and hepatitis with jaundice have been reported.
Has the risk of causing psychological and or physical dependence.
Has a slow onset, mild effect, and is very long acting with a half-life of 24 to 60 hours.
Long term use does not significantly suppress plasma testosterone levels in men.
Shows a ceiling effect for respiratory depression.
Concurrent use with CNS depressants is contraindicated as it may lead to fatal respiratory depression.
It binds tightly to opioid receptors in the central nervous system, so that it takes extremely large dose of potent opioid pain medication to displace the buprenorphine from those receptors and provide pain relief in the acute setting.
Patients on high-dose buprenorphine therapy are unaffected by even very large doses of potent opioids such as fentanyl, morphine, or dilaudid.
Can be put on site Buprephenone
Trade names Buprenex, Subutex, Suboxone, Butrans
US: Schedule III drug.
Routes of administration are sublingual, IM, IV, transdermal, intranasal, rectally, and orally.
Bioavailabilityis 30% sublingually. and approx 50% intranasally.
Protein binding is 96% with hepatic metabolism via CYP3A4, and CYP2C8
Biological half-life 20–70 hours with a mean of 37 hours
Excreted by renal and biliary mechanisms.
A semisynthetic opioid derivative of thebaine.
A mixed partial agonist opioid receptor modulator.
Used to treat opioid addiction, to control moderate acute pain in non-opioid-tolerant individuals and to control moderate chronic pain.
Sometimes used to treaty nausea in antiemetic intolerant individuals, most often in transdermal patch form.
It is available in a variety of formulations.
While both buprenorphine and methadone are medications used for detoxification for short- and long-term opioid replacement therapy. the former has the advantage of being a partial agonist, and negating the potential for life-threatening respiratory depression in cases of abuse.
The effectiveness of buprenorphine and methadone are essentially identical, and have similar adverse-effect profiles apart from more sedation among methadone users.
Detoxification consists of withdrawal from the drug of dependency on to buprenorphine, sometimes aided by the use of medications such as benzodiazepines that assist with anxiety, sleep, and muscle relaxation, clonidine and anti-inflammatory drugs such as ibuprofen and aspirin.
Suboxone contains buprenorphine as well as the opioid antagonist naloxone to deter the use of tablets by intravenous injection.
Buprenorphine and naloxone at a 4:1 ratio will produce unpleasant withdrawal symptoms if taken intravenously by people who are addicted to opioids.
The Suboxone formulation has potential to produce an opioid agonist high if injected by non-dependent persons.
Naloxone is ineffective in preventing suboxone abuse, as well as the overdosing on buprenorphine, as naloxone is not strong enough to reverse its effects.
Butrans Transdermal Patch System is available in 5 mcg/hour, 7.5 mcg/hour, 10 mcg/hour, 15 mcg/hour, and 20 mcg/hour doses and are applied for 7 days.
Butrans Transdermal Patches are for moderate to severe chronic pain.
Butrans Transdermal Patch is not indicated for use in acute pain, pain that is expected to last only for a short period of time, or post-operative pain.
Butrans Transdermal Patch is not indicated or recommended for use in the treatment of opioid addiction.
Majority of unipolar non-psychotic persons with major depression refractory to conventional antidepressants and electroconvulsive therapy can be successfully treated with buprenorphine.
Used in the treatment of the neonatal abstinence syndrome.
Binds with high affinity and antagonize the putative ε-opioid receptor.
Buprenorphine blocks voltage-gated sodium channels via the local anesthetic binding site as well, and this underlies its potent local anesthetic properties.
Full analgesic efficacy of buprenorphine requires both exon 11-and exon 1-associated μ-opioid receptor splice variants.
Metabolized by the liver, via CYP3A4 isozymes of the cytochrome P450 enzyme system.
Glucuronidation is primarily carried out by UGT1A1 and UGT2B7, and that of norbuprenorphine by UGT1A1 and UGT1A3.
Glucuronides are then eliminated mainly through excretion into the bile.
The elimination half-life of buprenorphine is 20–73 hours.
There is no risk of accumulation in people with renal impairment.
One of the major active metabolites of buprenorphine is norbuprenorphine.
Relative to buprenorphine, norbuprenorphine has extremely little antinociceptive potency which is 1/50th that of buprenorphine.
Norbuprenorphine markedly depresses respiration, 10-fold more than buprenorphine.
Very poor brain penetration of norbuprenorphine due to a high affinity of the compound for P-glycoprotein.
In contrast to norbuprenorphine, buprenorphine and its glucuronide metabolites are negligibly transported by P-glycoprotein.
Glucuronides of buprenorphine and norbuprenorphine are biologically active, and represent major active metabolites of buprenorphine.
Buprenorphine and norbuprenorphine may be detected in blood or urine to monitor use, abuse, or confirm a diagnosis of poisoning.
Common adverse drug reactions include: nausea and vomiting, drowsiness, dizziness, headache, memory loss, cognitive and neural inhibition, perspiration, itchiness, dry mouth, miosis, orthostatic hypotension, male ejaculatory difficulty, decreased libido, and urinary retention.
Constipation and CNS effects are seen less frequently than with morphine.
Hepatic necrosis and hepatitis with jaundice have been reported.
Has the risk of causing psychological and or physical dependence.
Has a slow onset, mild effect, and is very long acting with a half-life of 24 to 60 hours.
Long term use does not significantly suppress plasma testosterone levels in men.
Shows a ceiling effect for respiratory depression.
Concurrent use with CNS depressants is contraindicated as it may lead to fatal respiratory depression.
It binds tightly to opioid receptors in the central nervous system, so that it takes extremely large dose of potent opioid pain medication to displace the buprenorphine from those receptors and provide pain relief in the acute setting.
Patients on high-dose buprenorphine therapy are unaffected by even very large doses of potent opioids such as fentanyl, morphine, or dilaudid.