{{위키데이터 속성 추적}}
{{Infobox drug
| Watchedfields =
| Verifiedfields =
| verifiedrevid = 612854585
| IUPAC_name = 2-Phenylethan-1-amine
| image = Phenethylamine2DCSD.svg
| alt = Image of the phenethylamine skeleton
| width = 300
| image2 = Phenethylamine-3D-balls.png
| alt2 = Ball-and-stick model of phenethylamine
| width2 = 250
<!--Clinical data-->
| pronounce = {{IPAc-en|f|ɛ|n|'|ɛ|θ|ə|l|ə|m|i:|n}}
| routes_of_administration = [[Oral administration|Oral]] (taken by mouth)
| dependency_liability = [[Psychological dependence|Psychological]]: low–moderate<br/>[[Physical dependence|Physical]]: none
| addiction_liability = None–Low (w/o an [[Monoamine oxidase inhibitor#List of MAO inhibiting drugs|MAO-B inhibitor]])<ref name="TAAR1 and TA pharmacology 2016 review">{{저널 인용|vauthors= Pei Y, Asif-Malik A, Canales JJ |title= Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications |journal= Front. Neurosci. |volume= 10 |issue= |pages= 148 |date= April 2016 |pmid= 27092049 |pmc= 4820462 |doi= 10.3389/fnins.2016.00148 |quote= Furthermore, evidence has accrued on the ability of TAs to modulate brain reward (i.e., the subjective experience of pleasure) and reinforcement (i.e., the strengthening of a conditioned response by a given stimulus; Greenshaw, 1984), suggesting the involvement of the TAs in the neurological adaptations underlying drug addiction, a chronic relapsing syndrome characterized by compulsive drug taking, inability to control drug intake and dysphoria when access to the drug is prevented (Koob, 2009). Consistent with its hypothesized role as “endogenous amphetamine,” β-PEA was shown to possess reinforcing properties, a defining feature that underlies the abuse liability of amphetamine and other psychomotor stimulants. β-PEA was also as effective as amphetamine in its ability to produce conditioned place preference (i.e., the process by which an organism learns an association between drug effects and a particular place or context) in rats (Gilbert and Cooper, 1983) and was readily self-administered by dogs that had a stable history (i.e., consisting of early acquisition and later maintenance) of amphetamine or cocaine self-administration (Risner and Jones, 1977; Shannon and Thompson, 1984). In another study, high concentrations of β-PEA dose-dependently maintained responding in monkeys that were previously trained to self-administer cocaine, and pretreatment with a MAO-B inhibitor, which delayed β-PEA deactivation, further increased response rates (Bergman et al., 2001).}}</ref><br/>Moderate (with an MAO-B inhibitor)<ref name="TAAR1 and TA pharmacology 2016 review"/>
<!--Pharmacokinetic data-->
| metabolism = Primarily: [[Monoamine oxidase B|MAO-B]]<ref name="Renaissance">{{저널 인용|vauthors= Lindemann L, Hoener MC |title= A renaissance in trace amines inspired by a novel GPCR family |journal= Trends Pharmacol. Sci. |volume= 26 |issue= 5 |pages= 274–281 |year= 2005 |pmid= 15860375 |doi= 10.1016/j.tips.2005.03.007 |quote= The pharmacology of TAs might also contribute to a molecular understanding of the well-recognized antidepressant effect of physical exercise [51]. In addition to the various beneficial effects for brain function mainly attributed to an upregulation of peptide growth factors [52,53], exercise induces a rapidly enhanced excretion of the main β-PEA metabolite β-phenylacetic acid (b-PAA) by on average 77%, compared with resting control subjects [54], which mirrors increased β-PEA synthesis in view of its limited endogenous pool half-life of ~30 s [18,55].}}</ref><ref name="Vascular">{{저널 인용|author= Broadley KJ |title= The vascular effects of trace amines and amphetamines |journal= Pharmacol. Ther. |volume= 125 |issue= 3 |pages= 363–375 |date=March 2010 |pmid= 19948186 |doi= 10.1016/j.pharmthera.2009.11.005 |quote= Trace amines are metabolized in the mammalian body via monoamine oxidase}}</ref><ref name="HMDB PEA">{{백과사전 인용|title=Phenylethylamine |url=http://www.hmdb.ca/metabolites/hmdb12275 |work=HMDB Version&nbsp;3.6 |publisher=Human Metabolome Database |accessdate=20 September 2016 |date=11 February 2016}}</ref><br/>Other enzymes: [[Monoamine oxidase A|MAO-A]],<ref name="HMDB PEA"/><ref name="PEA_MAO-A_and_B_Substrate-Suzuki">{{저널 인용|vauthors= Suzuki O, Katsumata Y, Oya M |title= Oxidation of beta-phenylethylamine by both types of monoamine oxidase: examination of enzymes in brain and liver mitochondria of eight species |journal= J. Neurochem. |volume= 36 |issue= 3 |pages= 1298–301 |year= 1981 |pmid= 7205271 |doi= 10.1111/j.1471-4159.1981.tb01734.x |url=}}</ref> [[semicarbazide-sensitive amine oxidase|SSAOs]] ([[AOC2]] & [[AOC3]]),<ref name="HMDB PEA"/><ref name="SSAO">{{저널 인용|title= The unique substrate specificity of human AOC2, a semicarbazide-sensitive amine oxidase |journal= Cell. Mol. Life Sci. |volume= 66 |issue= 16 |pages= 2743–57 |year= 2009 |pmid= 19588076 |doi= 10.1007/s00018-009-0076-5 |quote= The preferred in vitro substrates of AOC2 were found to be 2-phenylethylamine, tryptamine and p-tyramine instead of methylamine and benzylamine, the favored substrates of AOC3. |author1= Kaitaniemi |first1= S |last2= Elovaara |first2= H |last3= Grön |first3= K |last4= Kidron |first4= H |last5= Liukkonen |first5= J |last6= Salminen |first6= T |last7= Salmi |first7= M |last8= Jalkanen |first8= S |last9= Elima |first9= K}}</ref> [[Phenylethanolamine N-methyltransferase|PNMT]],<ref name="Renaissance"/><ref name="Vascular"/><ref name="HMDB PEA"/> [[Aralkylamine N-acetyltransferase|AANAT]],<ref name="HMDB PEA"/> [[flavin-containing monooxygenase 3|FMO3]],<ref name="FMO">{{저널 인용|author= Krueger SK, Williams DE |title= Mammalian flavin-containing monooxygenases: structure/function, genetic polymorphisms and role in drug metabolism |journal= Pharmacol. Ther. |volume= 106 |issue= 3 |pages= 357–387 |date=June 2005 |pmid= 15922018 |pmc= 1828602 |doi= 10.1016/j.pharmthera.2005.01.001 |quote= The biogenic amines, phenethylamine and tyramine, are N-oxygenated by FMO to produce the N-hydroxy metabolite, followed by a rapid second oxygenation to produce the trans-oximes (Lin & Cashman, 1997a, 1997b). This stereoselective N-oxygenation to the trans-oxime is also seen in the FMO-dependent N-oxygenation of amphetamine (Cashman et al., 1999)&nbsp;... Interestingly, FMO2, which very efficiently N-oxygenates N-dodecylamine, is a poor catalyst of phenethylamine N-oxygenation. The most efficient human FMO in phenethylamine N-oxygenation is FMO3, the major FMO present in adult human liver; the Km is between 90 and 200 μM (Lin & Cashman, 1997b). |last2= Williams}}</ref><ref name="FMO3 catecholamines">{{저널 인용|vauthors= Robinson-Cohen C, Newitt R, Shen DD, Rettie AE, Kestenbaum BR, Himmelfarb J, Yeung CK |title= Association of FMO3 Variants and Trimethylamine N-Oxide Concentration, Disease Progression, and Mortality in CKD Patients |journal= PLoS ONE |volume= 11 |issue= 8 |pages= e0161074 |date= August 2016 |pmid= 27513517 |pmc= 4981377 |doi= 10.1371/journal.pone.0161074 |quote= TMAO is generated from trimethylamine (TMA) via metabolism by hepatic flavin-containing monooxygenase isoform 3 (FMO3).&nbsp;... FMO3 catalyzes the oxidation of catecholamine or catecholamine-releasing vasopressors, including tyramine, phenylethylamine, adrenaline, and noradrenaline [32, 33].}}</ref> and others
| class = {{abbr|CNS|central nervous system}} [[stimulant]]
<!--Physiological data-->
| source_tissues = [[Substantia nigra pars compacta]];<br/>[[Ventral tegmental area]];<br/>[[Locus coeruleus]];<br/>many others
| target_tissues = System-wide
| receptors = Varies greatly across species;<br/>Human receptors: [[hTAAR1]]<ref name="Human trace amines and hTAARs October 2016 review"/> and [[hTAAR2]]<ref name="Human trace amines and hTAARs October 2016 review"/>
| precursor = [[L-Phenylalanine]]<ref name="Renaissance"/><ref name="Vascular"/>
| biosynthesis = [[Aromatic L-amino acid decarboxylase]] (AADC)<ref name="Renaissance"/><ref name="Vascular"/>
| synonyms = PEA; phenylethylamine
<!--Legal status-->
| legal_AU = Unscheduled
| legal_CA = Unscheduled
| legal_NZ =
| legal_UK = Unscheduled
| legal_UN = Unscheduled
| legal_US = Unscheduled
<!--Pharmacokinetic data-->
| elimination_half-life = {{ubl |Exogenous: 5–10 minutes<ref name="Pubchem exogenous half-life">{{백과사전 인용|title=Phenethylamine |section-url=https://pubchem.ncbi.nlm.nih.gov/compound/1001?from=summary#section=Pharmacology-and-Biochemistry |section=Pharmacology and Biochemistry |work=PubChem Compound |publisher= United States National Library of Medicine&nbsp;– National Center for Biotechnology Information |quote= Plasma Pharmacokinetics of PEA Could Be Described By 1st-Order Kinetics With Estimated T/2 of Approx 5-10 Min.}}</ref> |Endogenous: ~30 seconds<ref name="Renaissance"/>}}
| excretion = [[Renal]] (kidneys)
<!--Identifiers-->
| CAS_number_Ref = {{cascite|correct|CAS}}
| CAS_number = 64-04-0
| PubChem = 1001
| IUPHAR_ligand = 2144
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB04325
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = C05332
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 13856352
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 327C7L2BXQ
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 18397
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 610
| NIAID_ChemDB = 018561
| ATC_prefix = none
| ATC_suffix =
<!--Chemical data-->
| C=8 | H=11 | N=1
| molecular_weight = 121.18 g/mol
| smiles = c1ccc(cc1)CCN
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C8H11N/c9-7-6-8-4-2-1-3-5-8/h1-5H,6-7,9H2
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = BHHGXPLMPWCGHP-UHFFFAOYSA-N
<!--Physical data-->
| boiling_point     = 195
| boiling_notes     =<ref name="Pubchem">{{백과사전 인용|title=Phenethylamine|section-url=https://pubchem.ncbi.nlm.nih.gov/compound/1001?from=summary#section=Chemical-and-Physical-Properties|section=Chemical and Physical Properties |work=PubChem Compound |publisher = United States National Library of Medicine&nbsp;– National Center for Biotechnology Information}}</ref>
| melting_point     = -60
| melting_notes     =<ref name="Pubchem"/>
| density           = 0.9640 <!--Pubchem-->
}}
'''펜에틸아민'''(Phenethylamine,PEA) 또는 페네틸아민은 실온에서 무색 액체인 방향성 아민족 물질이다.
페네틸아민 또는 더 적절하게는 [[치환된 페네틸아민]](Substituted phenethylamines)은 페네틸아민을 백본(backbone)으로 포함하는 페네틸아민 유도체 그룹이다. 다시 말해서, 이 화학 부류는 페네틸아민 코어(core) 구조에서 하나 이상의 수소 원자를 치환기로 대체하여 형성된 유도체 화합물을 포함한다. 치환된 페네틸아민 부류에는 모든 치환된 [[암페타민]] 및 치환된 [[메틸렌디옥시펜에틸아민]](MDxx,methylenedioxyphenethylamines 또는 Substituted methylenedioxy- phenethylamines)이 포함되며, 특히 공감, 각성, 환각, 식욕 부진, 기관지 확장, 충혈 완화 및 또는 항우울에 관여하여 작용하는 많은 메커니즘에서의 생화학 반응을  포함한다.

== 치환된 페네틸아민 ==
{{본문|치환된 페네틸아민 }}
주요한 치환된 페네틸아민들로는 [[도파민]](3,4-dihydroxyphenethylamine), [[에피네프린]](β,3,4-trihydroxy-N-methylphenethylamine), [[노르에피네프린]](β,3,4-trihydroxyphenethylamine), [[N,N-디메틸페네필아민]](N,N-Dimethylphenethylamine 또는 N,N-DMPEA), [[메스암페타민]](methamphetamine, methylamphetamine, desoxyephedrine), [[MDMA]](3,4-Methylenedioxymethamphetamine)등 다수가 있다.

== 같이 보기 ==
* [[도파민]]

== 각주 ==
{{각주}}

== 참고 문헌 ==
*[참고] (페네틸아민 유도체의 구조적 특성에 관한 이론적 연구 Theoretical Study on Structural Properties of Phenthylamine Derivatives ,국제문화기술진흥원 , The Journal of the Convergence on Culture Technology (JCCT) KCI 등재 Vol.6 No.4 (2020.11)  pp.761-766 이철재 URL) https://www.earticle.net/Article/A386414

== 외부 링크 ==
* [http://gmd.mpimp-golm.mpg.de/Spectrums/af2a22f3-4aa9-4e5c-9e61-bf278b87a7c4.aspx Phenethylamine MS Spectrum]

{{신경전달물질}}

[[분류:펜에틸아민| ]]
[[분류:TAAR1 작용제]]
[[분류:펜에틸아민 알칼로이드]]
[[분류:미량 아민]]
[[분류:VMAT 억제제]]