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A new promising drug for treatment of opioid addiction, Buprinorphine

Buprenorphine is a drug having good safety index and also very good pharmacological profile, due to these features this drug helps patients as well addiction physician to remain with this drug for the treatment of opioid addiction. Pharmacologically buprenorphine is a partial agonist at the mu opioid receptor and an antagonist at the kappa receptor (both of are receptors at opioids acts). Although buprinorphine has a strong affinity but low intrinsic activity at the mu receptor. Once buprinorphine acts on these receptors, it displaces other full agonists opioids (like morphine, methadone) from the receptor. Due to its partial activity at mu receptors it

is clinically very useful pharmacological properties. It has lower abuse potential, lower level of physical dependence, a ceiling effect at higher doses, and greater safety in overdose compared with opioid full agonists.

With regards to buprenorphine, there are 3 phases in treating the patient. They are induction, stabilization, and maintenance.During the induction phase, patients must be experiencing mild withdrawal symptoms and to have avoided opiates for at least 6 hours. Clinicians can use the Clinical Opiate Withdrawal Scale (COWS) or the Adjective Rating Scale for Withdrawal (ARSW) to determine withdrawal status.9 The goal of this phase is to determine the minimum dose of buprenorphine required to prevent further withdrawal symptoms, reduce cravings, and provide minimal adverse effects.18 When patients are no longer experiencing withdrawal symptoms, they have entered the stabilization phase of treatment. At this time, patients should be following up frequently with their physicians, and dose adjustments may beneeded to obtain levels adequate to reduce cravings, yet minimize adverse drug effects.18,19 This phase typically lasts one to two months.
The maintenance phase is the longest phase of treatment. Medication-assisted buprenorphine treatment usually lasts at least 6 months and can continue for 2 years or more. Similar to methadone treatment, the length of buprenophine treatment usually depends on individual patient needs considering past instability (past dysfunction related to work, relationships, and behavior) and chronicity (length of opioid misuse/abuse and
previous response to treatment).20 If the patient regularly has negative urine toxicology screens and receives a stable dose of buprenorphine, the doctor may extend the intervals between visits to up to 30 days.18 During the maintenance stage, psychosocial and family issues must be addressed

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to help the patient be successful in avoiding opioids and managing dependence.

Although buprinorphine has a good pharmacological index but dose and duration of buprinorphine use should be individualized according to patients status. Because of its low intrinsic activity at the mu receptor, however, at increasing doses, unlike a full opioid agonist, the agonist effects of buprenorphine reach a maximum and do not continue to increase linearly with increasing doses of the drug—the ceiling effect. As a result of this ceiling effect, an overdose of buprenorphine is less likely to cause fatal respiratory depression than is an

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overdose of a full mu opioid agonist.

In the pharmacotherapy of opioid addiction, buprenorphine, as a partial opioid agonist, can be thought of as occupying a midpoint between opioid full agonists (e.g., methadone, LAAM) and opioid antagonists (e.g., naltrexone, nalmefene). It has sufficient agonist properties such that individuals addicted to opioids perceive a reinforcing subjective effect from the medication, often described in terms of “feeling normal.” In higher doses, and under certain circumstances, its antagonist properties can cause the precipitation of acute withdrawal if administered to an individual who is physically dependent on opioids and maintained on a sufficient dose of a full agonist. In this scenario, buprenorphine can displace the full agonist from the mu receptors, yet not provide the equivalent degree of receptor activation, thereby leading to a net decrease in agonist effect and the onset of withdrawal. Furthermore, because of the high affinity of buprenorphine for the opioid receptor, this precipitated abstinence syndrome may be difficult to reverse. Buprenorphine produces a blockade to subsequently administered opioid agonists in a dose‐responsive manner. This effect makes the drug particularly appealing to well‐motivated patients, as it provides an additional disincentive

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to continued opioid use.

Buprenorphine can sometime produce euphoria, if it is injected. Buprenorphine does produce physical dependence, although it appears to do so to a lesser degree than do full opioid agonists, and it appears to be easier to discontinue at the end of medication treatment.

A ceiling effect is where the analgesic effect plateaus and no additional benefit is seen by increasing the dose, but an increase in the adverse opioid effects is anticipated. The activity expressed at the kappa-receptor provides analgesicactivity, and also provides benefits for use in opioid deterrence, maintenance, and detoxification. Also, because of the partial activation of the mu-receptor, patients are less likely to abuse buprenorphine.

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