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| Related FDA Approved Drug |
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| Mechanism of Action |
Buprenorphine¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Buprenorphine's analgesic effect is due to partial agonist activity at mu-opioid receptors. Buprenorphine is also a kappa-opioid receptor antagonist. The partial agonist activity means that opioid receptor antagonists (e.g., an antidote such as naloxone) only partially reverse the effects of buprenorphine. The binding to the mu and kappa receptors results in hyperpolarization and reduced neuronal excitability.
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| Pharmacology |
Buprenorphine¿¡ ´ëÇÑ Pharmacology Á¤º¸ Buprenorphine is a synthetic opioid analgesic and thebaine derivative, with a longer duration of action than morphine. Buprenorphine interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, buprenorphine exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Buprenorphine may increase the patient's tolerance for pain and decrease the perception of suffering, 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. Buprenorphine depresses the respiratory centers, depresses the cough reflex, and constricts the pupils.
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| Metabolism |
Buprenorphine¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)Cytochrome P450 2D6 (CYP2D6)
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| Protein Binding |
Buprenorphine¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 96%
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| Half-life |
Buprenorphine¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 37 hours
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| Absorption |
Buprenorphine¿¡ ´ëÇÑ Absorption Á¤º¸ 31% bioavailability (sublingual)
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| Pharmacokinetics |
Buprenorphine HClÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ÁøÅëÈ¿°ú ¹ßÇö½Ã°£ : 10-30ºÐ À̳»
- Èí¼ö : IM, SC : 30-40%
- ºÐÆ÷ : Vd : 97-187 L/kg
- ´Ü¹é°áÇÕ : ³ôÀ½
- ´ë»ç : ÁÖ·Î °£´ë»ç, ÃÊȸÅë°úÈ¿°ú Å
- ¹Ý°¨±â : 2.2-3 ½Ã°£
- ¼Ò½Ç : ¹Ìº¯Èü·Î 70%°¡ ´ãÁó¹è¼³, 20%´Â ½Å¹è¼³µÊ
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| Biotransformation |
Buprenorphine¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic. Buprenorphine undergoes both N-dealkylation to norbuprenorphine and glucuronidation. The N-dealkylation pathway is mediated by cytochrome P-450 3A4 isozyme. Norbuprenorphine, an active metabolite, can further undergo glucuronidation.
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| Toxicity |
Buprenorphine¿¡ ´ëÇÑ Toxicity Á¤º¸ Manifestations of acute overdose include pinpoint pupils, sedation, hypotension, respiratory depression and death.
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| Drug Interactions |
Buprenorphine¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Buprenorphine¿¡ ´ëÇÑ Food Interaction Á¤º¸ Not Available
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| Drug Target |
[Drug Target]
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| Description |
Buprenorphine¿¡ ´ëÇÑ Description Á¤º¸ A derivative of the opioid alkaloid thebaine that is a more potent and longer lasting analgesic than morphine. It appears to act as a partial agonist at mu and kappa opioid receptors and as an antagonist at delta receptors. The lack of delta-agonist activity has been suggested to account for the observation that buprenorphine tolerance may not develop with chronic use. [PubChem]
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| Dosage Form |
Buprenorphine¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Tablet Sublingual
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| Drug Category |
Buprenorphine¿¡ ´ëÇÑ Drug_Category Á¤º¸ Analgesics, OpioidNarcotic AntagonistsNarcotics
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| Smiles String Canonical |
Buprenorphine¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ COC12CCC3(CC1C(C)(O)C(C)(C)C)C1CC4=C5C(OC2C35CCN1CC1CC1)=C(O)C=C4
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| Smiles String Isomeric |
Buprenorphine¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CO[C@@]12CC[C@@]3(C[C@@H]1C(C)(O)C(C)(C)C)[C@H]1CC4=C5C(OC2[C@@]35CCN1CC1CC1)=C(O)C=C4
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| InChI Identifier |
Buprenorphine¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C29H41NO4/c1-25(2,3)26(4,32)20-15-27-10-11-29(20,33-5)24-28(27)12-13-30(16-17-6-7-17)21(27)14-18-8-9-19(31)23(34-24)22(18)28/h8-9,17,20-21,24,31-32H,6-7,10-16H2,1-5H3/t20-,21-,24?,26?,27-,28+,29+/m1/s1
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. BUPRENORPHINE[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[SGOT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[SGPT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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