Phenelzine

Phenelzine, sold under the brand

name Nardil, among others, is a Phenelzine
nonselective and irreversible
monoamine oxidase inhibitor (MAOI) of
the hydrazine class which is used as an
antidepressant and anxiolytic. Along
with tranylcypromine and
isocarboxazid, phenelzine is one of the
few nonselective and irreversible MAOIs
still in widespread clinical use. It is
available in Australia,[2][3] the United
Kingdom,[4] the United States,[5] and
Canada.[6] It is taken by mouth.

Contents
Indications
Pharmacology Clinical data
Pharmacodynamics Trade names Nardil
Pharmacokinetics AHFS/Drugs.com Monograph (https://www.
Adverse effects drugs.com/monograph/p
Interactions henelzine-sulfate.html)
MedlinePlus a682089 (https://medline
Research
plus.gov/druginfo/meds/
History
a682089.html)
See also License data US DailyMed: Phenelzine
References (https://dailymed.nlm.nih.
External links gov/dailymed/search.cfm
?labeltype=all&query=Ph
enelzine)
Indications Pregnancy AU: B3[1]
category
Phenelzine is used primarily in the Routes of By mouth
treatment of major depressive disorder administration
(MDD). Patients with depressive ATC code N06AF03 (WHO (https://
symptomology characterized as
:
"atypical", "nonendogenous", and/or www.whocc.no/atc_ddd_
"neurotic" respond particularly well to index/?code=N06AF03))
phenelzine.[7] The medication is also
Legal status
useful in patients who do not respond
favorably to first and second-line Legal status AU: S4 (Prescription
treatments for depression, or are only)
"treatment-resistant".[8] In addition to US: ℞-only
being a recognized treatment for major
depressive disorder, phenelzine is In general:
℞ (Prescription only)
effective in treating dysthymia,[9]
bipolar depression (BD),[10] panic Pharmacokinetic data
disorder (PD),[11] social anxiety Metabolism Liver
disorder,[12] bulimia,[13] post-traumatic Elimination 11.6 hours
stress disorder (PTSD),[14] and half-life
obsessive-compulsive disorder Excretion Urine
(OCD). [15][16][17]
Identifiers
IUPAC name
Pharmacology
2-phenylethylhydrazine
CAS Number 51-71-8 (https://common
Pharmacodynamics chemistry.cas.org/detail?
cas_rn=51-71-8) 
Phenelzine is a non-selective and
irreversible inhibitor of the enzyme PubChem CID 3675 (https://pubchem.n
monoamine oxidase (MAO). It inhibits cbi.nlm.nih.gov/compoun
both of the respective isoforms of MAO, d/3675)
MAO-A and MAO-B, and does so almost
equally, with slight preference for the IUPHAR/BPS 7266 (http://www.guideto
former. By inhibiting MAO, phenelzine pharmacology.org/GRAC
prevents the breakdown of the /LigandDisplayForward?l
monoamine neurotransmitters
igandId=7266)
serotonin, melatonin, norepinephrine,
epinephrine, and dopamine, as well as DrugBank DB00780 (https://www.dr
the trace amine neuromodulators such ugbank.ca/drugs/DB007
as phenethylamine, tyramine,
80) 
octopamine, and tryptamine. This leads
to an increase in the extracellular ChemSpider 3547 (https://www.chem
concentrations of these neurochemicals spider.com/Chemical-Str
and therefore an alteration in ucture.3547.html) 
neurochemistry and neurotransmission.
This action is thought to be the primary UNII O408N561GF (https://pr
mediator in phenelzine's therapeutic ecision.fda.gov/uniisearc
benefits. h/srs/unii/O408N561GF)
KEGG D08349 (https://www.keg
:
Phenelzine and its metabolites also g.jp/entry/D08349) 
inhibit at least two other enzymes to a
lesser extent, of which are alanine ChEMBL ChEMBL1089 (https://w
transaminase (ALA-T),[18] and γ- ww.ebi.ac.uk/chembldb/i
aminobutyric acid transaminase (GABA- ndex.php/compound/ins
T),[19] the latter of which is not caused pect/ChEMBL1089) 
by phenelzine itself, but by a phenelzine CompTox
metabolite phenylethylidenehydrazine DTXSID2041094 (https:/
Dashboard (EPA)
(PEH). By inhibiting ALA-T and GABA- /comptox.epa.gov/dashb
T, phenelzine causes an increase in the oard/chemical/details/DT
alanine and GABA levels in the brain XSID2041094)
and body. GABA is the major inhibitory
ECHA InfoCard 100.000.108 (https://ech
neurotransmitter in the mammalian
central nervous system, and is very a.europa.eu/substance-i
important for the normal suppression of nformation/-/substancein
anxiety, stress, and depression. fo/100.000.108)
Phenelzine's action in increasing GABA Chemical and physical data
concentrations may significantly
Formula C8H12N2
contribute to its antidepressant, and
especially, anxiolytic/antipanic Molar mass 136.198 g·mol−1
properties, the latter of which have been 3D model
considered superior to those of other Interactive image (https:/
(JSmol)
antidepressants. As for ALA-T /chemapps.stolaf.edu/jm
inhibition, though the consequences of ol/jmol.php?model=N%2
disabling this enzyme are currently not 8N%29CCc1ccccc1)
well understood, there is some evidence
Boiling point 74 °C (165 °F)
to suggest that it is this action of the
hydrazines (including phenelzine) which SMILES
may be responsible for the occasional N(N)CCc1ccccc1
incidence of hepatitis and liver failure.
InChI
Phenelzine has also been shown to InChI=1S/C8H12N2/c9-10-7-6-8-4-2-1-3-5-8/
metabolize to phenethylamine h1-5,10H,6-7,9H2 
 
(PEA).[20] PEA acts as a releasing agent Key:RMUCZJUITONUFY-UHFFFAOYSA-N
of norepinephrine and dopamine, and   (verify)
this occurs in the same manner as
amphetamine (very similar in structure) by being taken up into vesicles, and displacing,
and causing the release of those monoamines (though with markedly different
pharmacokinetics such as a far shorter duration of action). Although this is indeed the
same mechanism to which some (but not all) of amphetamine's effects are attributable to,
this is not all that uncommon a property among phenethylamines in general, many of
which do not have psychoactive properties comparable to amphetamine. Amphetamine is
different in that it binds with high affinity to the reuptake pumps of dopamine,
norepinephrine, and serotonin, which phenethylamine and related molecules may as well
to some extent, but with far less potency, such that it is basically insignificant in
comparison. And, often being metabolized too quickly or not having the solubility to
enable it to have a psychostimulant effect in humans. Claims that phenethylamine has
:
comparable or roughly similar effects to psychostimulants such as amphetamine when
administered are misconstrued. Phenethylamine does not have any obvious, easily
discernible, reliably induced effects when administered to humans. Phenelzine's
enhancement of PEA levels may contribute further to its overall antidepressant effects to
some degree. In addition, phenethylamine is a substrate for MAO-B, and treatment with
MAOIs that inhibit MAO-B such as phenelzine have been shown to consistently and
significantly elevate its concentrations.

Phenelzine usually requires six to eight weeks of treatment, and a minimum dose of
60 mg/day, to achieve therapeutic effects. The reason for the delay in therapeutic effect is
not fully understood, but it is believed to be due to many factors, including achieving
steady-state levels of MAO inhibition and the resulting adaptations in mean
neurotransmitter levels, the possibility of necessary desensitization of autoreceptors
which normally inhibit the release of neurotransmitters like serotonin and dopamine, and
also the upregulation of enzymes such as serotonin N-acetyltransferase. Typically, a
therapeutic response to MAOIs is associated with an inhibition of at least 80-85% of
monoamine oxidase activity.[21]

Pharmacokinetics

Phenelzine is administered orally in the form of

phenelzine sulfate and is rapidly absorbed from the
gastrointestinal tract. Time to peak plasma
concentration is 43 minutes and half-life is 11.6 hours.
Unlike most other drugs, phenelzine irreversibly
disables MAO, and as a result, it does not necessarily
need to be present in the blood at all times for its
effects to be sustained. Because of this, upon
phenelzine treatment being ceased, its effects typically
do not actually wear off until the body replenishes its Phenelzine 15 mg tablets.
enzyme stores, a process which can take as long as 2–
3 weeks.

Phenelzine is metabolized primarily in the liver and its metabolites are excreted in the
urine. Oxidation is the primary routine of metabolism, and the major metabolites are
phenylacetic acid and parahydroxyphenylacetic acid, recovered as about 73% of the
excreted dose of phenelzine in the urine over the course of 96 hours after single doses.
Acetylation to N2-acetylphenelzine is a minor pathway. Phenelzine may also interact with
cytochrome P450 enzymes, inactivating these enzymes through formation of a heme
adduct. Two other minor metabolites of phenelzine, as mentioned above, include
phenylethylidenehydrazine and phenethylamine.

Adverse effects
:
Common side effects of phenelzine may include dizziness, blurry vision, dry mouth,
headache, lethargy, sedation, somnolence, insomnia, anorexia, weight gain or loss,
nausea and vomiting, diarrhea, constipation, urinary retention, mydriasis, muscle
tremors, hyperthermia, sweating, hypertension or hypotension, orthostatic hypotension,
paresthesia, hepatitis, and sexual dysfunction (consisting of loss of libido and
anorgasmia). Rare side effects usually only seen in susceptible individuals may include
hypomania or mania, psychosis and acute liver failure, the last of which is usually only
seen in people with pre-existing liver damage, old age, long-term effects of alcohol
consumption, or viral infection.[22]

Interactions
The MAOIs have certain dietary restrictions and drug interactions. The amount of such
restrictions and interactions is far less than previously thought, and MAOIs are generally
safe medications when administered correctly.[23][24] Hypertensive crisis is generally a
rare occurrence while taking MAOIs,[25] yet may result from the overconsumption of
tyramine-containing foods. As a result, patients on phenelzine and other MAOIs must
avoid excess quantities of certain foods that contain tyramine such as aged cheeses and
cured meats, among others. Serotonin syndrome may result from an interaction with
certain drugs which increase serotonin activity such as selective serotonin reuptake
inhibitors, serotonin releasing agents, and serotonin agonists.

As is the case with other MAOIs, there is a concern regarding phenelzine and the use of
both local and general anesthetics. Anyone taking phenelzine should inform their dentist
before proceeding with dental surgery, and surgeon in any other contexts.

Phenelzine has also been linked to vitamin B6 deficiency.[26] Transaminases such as

GABA-transaminase have been shown to be dependent upon vitamin B6[27] and may be
involved in a potentially related process, since the phenelzine metabolite
phenylethylidenehydrazine (PEH) is a GABA transaminase inhibitor. Both phenelzine
and vitamin B6 are rendered inactive upon these reactions occurring. For this reason, it
may be recommended to supplement with vitamin B6 while taking phenelzine. The
pyridoxine form of B6 is recommended for supplementation, since this form has been
shown to reduce hydrazine toxicity from phenelzine and, in contrast, the pyridoxal form
has been shown to increase the toxicity of hydrazines.[28]

Research
Phenelzine showed promise in a phase II clinical trial from March 2020 in treating
prostate cancer. [29] Phenelzine has also been shown to have neuroprotective effects in
animal models.[30][31][32]

History
:
Synthesis of phenelzine was first described by Emil Votoček and Otakar Leminger in
1932.[33][34]

See also
Phenylethylidenehydrazine
Hydrazine (antidepressant)
Isocarboxazid
Libby Zion Law (a case involving phenelzine and pethidine)
Monoamine oxidase inhibitor
Tranylcypromine

References
1. "Phenelzine (Nardil) Use During Pregnancy" (https://www.drugs.com/pregnancy/phen
elzine.html). Drugs.com. 3 March 2020. Retrieved 11 July 2020.
2. "Shortage of Nardil phenelzine 15mg (as sulfate) tablet bottle (AUST R 93600) and
alternative supply arrangement under Section 19A of the Therapeutic Goods Act
1989" (https://www.shpa.org.au/sites/default/files/uploaded-content/website-content/M
anufacturers_alerts/shortage_of_nardil_phenelzine_15mg_as_sulfate_tablet_bottle_a
ust_r_93600_and_aas_10feb2021.pdf) (PDF). Generic Health Pty Ltd. Lupin Group
Company. 10 February 2021.
3. "Schedule of Pharmaceutical Benefits" (https://www.pbs.gov.au/publication/schedule/
2021/02/2021-02-01-general-soc.pdf) (PDF). Department of Health. The Australian
Government. 1 February 2021.
4. "Phenelzine" (https://www.sps.nhs.uk/medicines/phenelzine/). Specialist Pharmacy
Service. 9 April 2015.
5. "Phenelzine Sulfate Tablets USP" (https://www.lupin.com/US/product/phenelzine-sulfa
te-tablets-usp/). Lupin Pharmaceuticals, Inc.
6. "Nardil (Phenelzine Sulfate) Antidepressant" (https://web.archive.org/web/201604030
84524/https://eci2012.net/product/nardil/). ERFA Canada 2012. Archived from the
original (https://eci2012.net/product/nardil/) on 3 April 2016.
7. Parke-Davis Division of Pfizer Inc. (2007). "Nardil(R) (Phenelzine sulfate tablets,
USP), labeling information" (http://www.accessdata.fda.gov/drugsatfda_docs/label/20
07/011909s038lbl.pdf) (PDF). U.S. Food and Drug Administration's. Archived (https://
web.archive.org/web/20091127225136/http://www.accessdata.fda.gov/drugsatfda_do
cs/label/2007/011909s038lbl.pdf) (PDF) from the original on 2009-11-27. Retrieved
14 December 2009.
8. Fiedorowicz JG, Swartz KL (July 2004). "The role of monoamine oxidase inhibitors in
current psychiatric practice"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2075358). Journal of Psychiatric
Practice. 10 (4): 239–248. doi:10.1097/00131746-200407000-00005 (https://doi.org/1
0.1097%2F00131746-200407000-00005). PMC 2075358 (https://www.ncbi.nlm.nih.g
ov/pmc/articles/PMC2075358). PMID 15552546 (https://pubmed.ncbi.nlm.nih.gov/155
52546).
9. Vallejo J, Gasto C, Catalan R, Salamero M (November 1987). "Double-blind study of
:
 9. Vallejo J, Gasto C, Catalan R, Salamero M (November 1987). "Double-blind study of
imipramine versus phenelzine in Melancholias and Dysthymic Disorders". The British
Journal of Psychiatry. 151 (5): 639–642. doi:10.1192/bjp.151.5.639 (https://doi.org/10.
1192%2Fbjp.151.5.639). PMID 3446308 (https://pubmed.ncbi.nlm.nih.gov/3446308).
S2CID 145651628 (https://api.semanticscholar.org/CorpusID:145651628).
10. Quitkin FM, McGrath P, Liebowitz MR, Stewart J, Howard A (March 1981).
"Monoamine oxidase inhibitors in bipolar endogenous depressives". Journal of
Clinical Psychopharmacology. 1 (2): 70–74. doi:10.1097/00004714-198103000-00005
(https://doi.org/10.1097%2F00004714-198103000-00005). PMID 7028797 (https://pu
bmed.ncbi.nlm.nih.gov/7028797). S2CID 32909169 (https://api.semanticscholar.org/C
orpusID:32909169).
11. Buigues J, Vallejo J (February 1987). "Therapeutic response to phenelzine in patients
with panic disorder and agoraphobia with panic attacks". The Journal of Clinical
Psychiatry. 48 (2): 55–59. PMID 3542985 (https://pubmed.ncbi.nlm.nih.gov/3542985).
12. Blanco C, Schneier FR, Schmidt A, Blanco-Jerez CR, Marshall RD, Sánchez-Lacay
A, Liebowitz MR (2003). "Pharmacological treatment of social anxiety disorder: a
meta-analysis". Depression and Anxiety. 18 (1): 29–40. doi:10.1002/da.10096 (https://
doi.org/10.1002%2Fda.10096). PMID 12900950 (https://pubmed.ncbi.nlm.nih.gov/129
00950). S2CID 12296484 (https://api.semanticscholar.org/CorpusID:12296484).
13. Walsh BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH (May 1988).
"Phenelzine vs placebo in 50 patients with bulimia". Archives of General Psychiatry.
45 (5): 471–475. doi:10.1001/archpsyc.1988.01800290091011 (https://doi.org/10.100
1%2Farchpsyc.1988.01800290091011). PMID 3282482 (https://pubmed.ncbi.nlm.nih.
gov/3282482).
14. Frank JB, Kosten TR, Giller EL, Dan E (October 1988). "A randomized clinical trial of
phenelzine and imipramine for posttraumatic stress disorder". The American Journal
of Psychiatry. 145 (10): 1289–1291. doi:10.1176/ajp.145.10.1289 (https://doi.org/10.1
176%2Fajp.145.10.1289). PMID 3048121 (https://pubmed.ncbi.nlm.nih.gov/3048121).
15. Vallejo J, Olivares J, Marcos T, Bulbena A, Menchón JM (November 1992).
"Clomipramine versus phenelzine in obsessive-compulsive disorder. A controlled
clinical trial". The British Journal of Psychiatry. 161 (5): 665–670.
doi:10.1192/bjp.161.5.665 (https://doi.org/10.1192%2Fbjp.161.5.665). PMID 1422616
(https://pubmed.ncbi.nlm.nih.gov/1422616). S2CID 36232956 (https://api.semanticsch
olar.org/CorpusID:36232956).
16. Annesley PT (June 1969). "Nardil response in a chronic obsessive compulsive". The
British Journal of Psychiatry. 115 (523): 748. doi:10.1192/bjp.115.523.748 (https://doi.
org/10.1192%2Fbjp.115.523.748). PMID 5806868 (https://pubmed.ncbi.nlm.nih.gov/5
806868). S2CID 31997372 (https://api.semanticscholar.org/CorpusID:31997372).
17. Grant JE, Baldwin DS, Chamberlain SR (July 2021). "Time to Reconsider Monoamine
Oxidase Inhibitors for Obsessive Compulsive Disorder?: A Case Series Using
Phenelzine" (https://eprints.soton.ac.uk/450147/1/OCD_phenelzine_3_27_21.docx).
Journal of Clinical Psychopharmacology. 41 (4): 461–464.
doi:10.1097/JCP.0000000000001418 (https://doi.org/10.1097%2FJCP.000000000000
1418). PMID 34108430 (https://pubmed.ncbi.nlm.nih.gov/34108430).
S2CID 235395484 (https://api.semanticscholar.org/CorpusID:235395484).
18. Tanay VA, Parent MB, Wong JT, Paslawski T, Martin IL, Baker GB (August 2001).
"Effects of the antidepressant/antipanic drug phenelzine on alanine and alanine
transaminase in rat brain". Cellular and Molecular Neurobiology. 21 (4): 325–339.
doi:10.1023/A:1012697904299 (https://doi.org/10.1023%2FA%3A1012697904299).
:
 doi:10.1023/A:1012697904299 (https://doi.org/10.1023%2FA%3A1012697904299).
PMID 11775064 (https://pubmed.ncbi.nlm.nih.gov/11775064). S2CID 20655821 (https
://api.semanticscholar.org/CorpusID:20655821).
19. McKenna KF, McManus DJ, Baker GB, Coutts RT (1994). "Chronic administration of
the antidepressant phenelzine and its N-acetyl analogue: effects on GABAergic
function". Journal of Neural Transmission. Supplementum. 41: 115–122.
doi:10.1007/978-3-7091-9324-2_15 (https://doi.org/10.1007%2F978-3-7091-9324-2_
15). ISBN 978-3-211-82521-1. PMID 7931216 (https://pubmed.ncbi.nlm.nih.gov/7931
216).
20. Dyck LE, Durden DA, Boulton AA (June 1985). "Formation of beta-phenylethylamine
from the antidepressant, beta-phenylethylhydrazine". Biochemical Pharmacology. 34
(11): 1925–1929. doi:10.1016/0006-2952(85)90310-7 (https://doi.org/10.1016%2F000
6-2952%2885%2990310-7). PMID 4004908 (https://pubmed.ncbi.nlm.nih.gov/400490
8).
21. Raft D, Davidson J, Wasik J, Mattox A (1981). "Relationship between response to
phenelzine and MAO inhibition in a clinical trial of phenelzine, amitriptyline and
placebo". Neuropsychobiology. 7 (3): 122–126. doi:10.1159/000117841 (https://doi.or
g/10.1159%2F000117841). PMID 7231652 (https://pubmed.ncbi.nlm.nih.gov/7231652
).
22. Gómez-Gil E, Salmerón JM, Mas A (April 1996). "Phenelzine-induced fulminant
hepatic failure". Annals of Internal Medicine. 124 (7): 692–693. doi:10.7326/0003-
4819-124-7-199604010-00014 (https://doi.org/10.7326%2F0003-4819-124-7-199604
010-00014). PMID 8607601 (https://pubmed.ncbi.nlm.nih.gov/8607601).
S2CID 43020372 (https://api.semanticscholar.org/CorpusID:43020372).
23. Grady MM, Stahl SM (March 2012). "Practical guide for prescribing MAOIs:
debunking myths and removing barriers". CNS Spectrums. 17 (1): 2–10.
doi:10.1017/S109285291200003X
(https://doi.org/10.1017%2FS109285291200003X). PMID 22790112 (https://pubmed.
ncbi.nlm.nih.gov/22790112). S2CID 206312008 (https://api.semanticscholar.org/Corp
usID:206312008).
24. Stahl SM, Felker A (October 2008). "Monoamine oxidase inhibitors: a modern guide
to an unrequited class of antidepressants". CNS Spectrums. 13 (10): 855–870.
doi:10.1017/s1092852900016965 (https://doi.org/10.1017%2Fs1092852900016965).
PMID 18955941 (https://pubmed.ncbi.nlm.nih.gov/18955941). S2CID 6118722 (https:/
/api.semanticscholar.org/CorpusID:6118722).
25. Gillman PK (January 2019). "The risk of harm from acute tyramine-induced
hypertension: how significant?" (https://psychotropical.com/risk_of_harm_from_acute
_tyr_hypertension/). PsychoTropical Commentaries. 5: 1–10.
doi:10.13140/RG.2.2.11909.40165 (https://doi.org/10.13140%2FRG.2.2.11909.40165
).
26. Malcolm DE, Yu PH, Bowen RC, O'Donovan C, Hawkes J, Hussein M (November
1994). "Phenelzine reduces plasma vitamin B6" (https://www.ncbi.nlm.nih.gov/pmc/art
icles/PMC1188621). Journal of Psychiatry & Neuroscience. 19 (5): 332–334.
PMC 1188621 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1188621).
PMID 7803366 (https://pubmed.ncbi.nlm.nih.gov/7803366).
27. PDB: 1OHW (https://www.rcsb.org/structure/1OHW); Storici P, De Biase D, Bossa F,
Bruno S, Mozzarelli A, Peneff C, et al. (January 2004). "Structures of gamma-
aminobutyric acid (GABA) aminotransferase, a pyridoxal 5'-phosphate, and [2Fe-2S]
cluster-containing enzyme, complexed with gamma-ethynyl-GABA and with the
antiepilepsy drug vigabatrin" (https://doi.org/10.1074%2Fjbc.M305884200). The
:
 antiepilepsy drug vigabatrin" (https://doi.org/10.1074%2Fjbc.M305884200). The
Journal of Biological Chemistry. 279 (1): 363–373. doi:10.1074/jbc.M305884200 (http
s://doi.org/10.1074%2Fjbc.M305884200). PMID 14534310 (https://pubmed.ncbi.nlm.n
ih.gov/14534310).
28. Dubnick B, Leeson GA, Scott CC (July 1960). "Effect of forms of vitamin B6 on acute
toxicity of hydrazines". Toxicology and Applied Pharmacology. 2 (4): 403–409.
doi:10.1016/0041-008X(60)90007-7 (https://doi.org/10.1016%2F0041-008X%2860%2
990007-7). PMID 13818307 (https://pubmed.ncbi.nlm.nih.gov/13818307).
29. Stone L (April 2020). "MAOA inhibitor phenelzine efficacious in recurrent prostate
cancer". Nature Reviews. Urology. 17 (4): 192. doi:10.1038/s41585-020-0307-y (https
://doi.org/10.1038%2Fs41585-020-0307-y). PMID 32203303 (https://pubmed.ncbi.nlm
.nih.gov/32203303). S2CID 212681980 (https://api.semanticscholar.org/CorpusID:212
681980).
Lay summary in: McDonald R (March 25, 2020). "Antidepressant Appears Safe,
Effective in Men with Biochemical Recurrent Prostate Cancer" (https://www.cureto
day.com/view/antidepressant-appears-safe-effective-in-men-with-biochemical-recu
rrent-prostate-cancer). Curetoday.com.
30. Baker G, Matveychuk D, MacKenzie EM, Holt A, Wang Y, Kar S (May 2019).
"Attenuation of the effects of oxidative stress by the MAO-inhibiting antidepressant
and carbonyl scavenger phenelzine". Chemico-Biological Interactions. 304: 139–147.
doi:10.1016/j.cbi.2019.03.003 (https://doi.org/10.1016%2Fj.cbi.2019.03.003).
PMID 30857888 (https://pubmed.ncbi.nlm.nih.gov/30857888). S2CID 75140657 (https
://api.semanticscholar.org/CorpusID:75140657).
31. Matveychuk D, MacKenzie EM, Kumpula D, Song MS, Holt A, Kar S, et al. (January
2022). "Overview of the Neuroprotective Effects of the MAO-Inhibiting Antidepressant
Phenelzine" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8732914). Cellular and
Molecular Neurobiology. 42 (1): 225–242. doi:10.1007/s10571-021-01078-3 (https://d
oi.org/10.1007%2Fs10571-021-01078-3). PMC 8732914 (https://www.ncbi.nlm.nih.go
v/pmc/articles/PMC8732914). PMID 33839994 (https://pubmed.ncbi.nlm.nih.gov/3383
9994). S2CID 233211407 (https://api.semanticscholar.org/CorpusID:233211407).
32. Cebak JE, Singh IN, Hill RL, Wang JA, Hall ED (April 2017). "Phenelzine Protects
Brain Mitochondrial Function In Vitro and In Vivo following Traumatic Brain Injury by
Scavenging the Reactive Carbonyls 4-Hydroxynonenal and Acrolein Leading to
Cortical Histological Neuroprotection" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
5385448). Journal of Neurotrauma. 34 (7): 1302–1317. doi:10.1089/neu.2016.4624 (h
ttps://doi.org/10.1089%2Fneu.2016.4624). PMC 5385448 (https://www.ncbi.nlm.nih.g
ov/pmc/articles/PMC5385448). PMID 27750484 (https://pubmed.ncbi.nlm.nih.gov/277
50484).
33. Budavari S, O'Neil, Smith A, Heckelman PE, Kinneary JF (1996). "Phenelzine". The
Merck Index (12th ed.). Whitehouse Station: Merck & Co. 7181.
34. Votoček E, Leminger O (1932). "Sur la β-phenoéthylhydrazine" [On the [preparation
and properties of] β-phenoethylhydrazine]. Collection of Czechoslovak Chemical
Communications (in French). 4: 271–281. doi:10.1135/cccc19320271 (https://doi.org/
10.1135%2Fcccc19320271).

External links
:
 "Phenelzine" (https://druginfo.nlm.nih.gov/drugportal/name/phenelzine). Drug
Information Portal. U.S. National Library of Medicine.

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