Half-life: 21 hours
> IR: 100mg PO BID
> SR: 150mg PO QAM
> ER: 150mg PO QAM
target dosing range: 150mg-450mg
best time to dose: Morning
how to dose:
> IR: Initial 100mg PO BID for 5-7 days then increase to 100mg PO TID.
Max daily dose is 450mg. Each dose should be administered at least 6
hours apart with no more than 150mg per dose.
> SR: Initial 150mg PO QAM for 5-7 days then increase to 150mg PO BID.
Max daily dose is 400mg. Each dose should be administered at least 8
hours apart with no more than 200mg per dose.
> ER: Initial 150mg PO QAM for 5-7 days then increase to 300mg PO
QAM. Max daily dose is 450mg PO QAM.
PREGNANCY: Minimal data on safety. Not a contraindication.
breastfeeding: Minimal data on safety. Not a contraindication.
1) Major Depressive Disorder
2) Seasonal Affective Disorder
3) Smoking Cessation
- Bupropion is a weak dopamine transporter (DAT) inhibitor (reuptake inhibitor) and a weak norepinephrine transporter (NET) inhibitor (reuptake inhibitor)
- Bupropion is metabolized to a number of active metabolites
- Some of these metabolites are more potent NET inhibitors than bupropion itself but equally potent DAT inhibitors and are more concentrated in the brain
- Bupropion is an active drug and prodrug
- The most potent of bupropion’s metabolites is an enantiomer of the 6-hydroxy metabolite of bupropion, also known as radafaxine
- Human PET scans suggest that no more than 20–30% of striatal DATs may be occupied at therapeutic doses of bupropion
- NET occupancy would be expected to be in this same range.
- 90% DAT and NET occupancy are not required for antidepressant effects (90% SERT occupancy required for antidepressant effects of SSRIs)
- Bupropion is metabolized primarily through CYP2B6 but is also an inhibitor of CYP2D6.
- Rare risk of seizures at high doses and/or rapid increases in doses
- Elevated seizure risk in
- Patients who snort high doses of crushed bupropion
- Patients with preexisting seizure disorders
- Patients with eating disorders
- Patients withdrawing from alcohol or benzodiazepines
- Bupropion has no sexual side effects and is often used to minimize psychotropic induced sexual dysfunction
- Bupropion has actions at nicotine receptors which may explain its use as a smoking cessation agent
- There are few dopamine transporters (DAT) in the prefrontal cortex
- Norepinephrine transporter (NET) blockade increases dopamine’s diffusion radius in the prefrontal cortex (PFC)
- Cooper, J. R., Bloom, F. E., & Roth, R. H. (2003). The biochemical basis of neuropharmacology (8th ed.). New York, NY, US: Oxford University Press.
- Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Introduction to neuropsychopharmacology. Oxford: Oxford University Press.
- Puzantian, T., & Carlat, D. J. (2016). Medication fact book: for psychiatric practice. Newburyport, MA: Carlat Publishing, LLC.
- J. Ferrando, J. L. Levenson, & J. A. Owen (Eds.), Clinical manual of psychopharmacology in the medically ill(pp. 3-38). Arlington, VA, US: American Psychiatric Publishing, Inc.
- Schatzberg, A. F., & DeBattista, C. (2015). Manual of clinical psychopharmacology. Washington, DC: American Psychiatric Publishing.
- Schatzberg, A. F., & Nemeroff, C. B. (2017). The American Psychiatric Association Publishing textbook of psychopharmacology. Arlington, VA: American Psychiatric Association Publishing.
- Stahl, S. M. (2014). Stahl’s essential psychopharmacology: Prescriber’s guide (5th ed.). New York, NY, US: Cambridge University Press.
- Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY, US: Cambridge University Press.
- Whalen, K., Finkel, R., & Panavelil, T. A. (2015). Lippincotts illustrated reviews: pharmacology. Philadelphia, PA: Wolters Kluwer.
(Note: the diagrams were created by me, but the theories behind them were taken from numerous textbooks and articles. For more information, I recommend Dr. Stephen Stahl’s Textbook “Stahl’s Essential Psychopharmacology” 4th edition).