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			{{Short description|Chemical compound}}
	{{Drugbox
			{{DISPLAYTITLE:α-Methyl-''p''-tyrosine}}
	| verifiedrevid = 435192797
			{{Chembox
	| IUPAC_name = 2-amino-3-(4-hydroxyphenyl)-2-methylpropanoic acid
			| ImageFile = Racemetirosine.svg
	| image = AMPT-2d-skeletal.png
			| Name = α-Methyl-''p''-tyrosine
	| width = 150
			|Section1={{Chembox Identifiers
			| index_label = 2S
			| index1_label = 2R
			| index2_label = 2RS
			| index_comment = Metirosine
			| index1_comment = (Inactive isomer)
			| index2_comment = α-Methyl-''p''-tyrosine
			| CASNo_Ref = {{cascite|correct|CAS}}
			| CASNo = 672-87-7
			| CASNo1_Ref = {{cascite|correct|CAS}}
			| CASNo1 = 672-86-6
			| CASNo2_Ref = {{cascite|correct|CAS}}
			| CASNo2 = 658-48-0
			| ChEBI2 =
			| ChEMBL2 =
			| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID = 390103
			| ChemSpiderID1_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID1 = 12129
			| ChemSpiderID2_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID2 = 3013
			| PubChem = 441350
			| PubChem1 = 12650
			| PubChem2 = 3125
			| EC_number1 =
			| EC_number2 =
			| IUPHAR_ligand = 6956
			| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
			| DrugBank = DB00765
			| RTECS =
			| UNII_Ref = {{fdacite|correct|FDA}}
			| UNII = DOQ0J0TPF7
			| KEGG_Ref = {{keggcite|correct|kegg}}
			| KEGG = D00762
			| ChEMBL_Ref = {{ebicite|correct|EBI}}
			| ChEMBL = 1200862
			| InChI = 1S/C10H13NO3/c1-10(11,9(13)14)6-7-2-4-8(12)5-3-7/h2-5,12H,6,11H2,1H3,(H,13,14)/t10-/m0/s1
			| InChI1 = 1S/C10H13NO3/c1-10(11,9(13)14)6-7-2-4-8(12)5-3-7/h2-5,12H,6,11H2,1H3,(H,13,14)/t10-/m1/s1
			| InChI2 = 1S/C10H13NO3/c1-10(11,9(13)14)6-7-2-4-8(12)5-3-7/h2-5,12H,6,11H2,1H3,(H,13,14)
			| InChIKey = NHTGHBARYWONDQ-JTQLQIEISA-N
			| InChIKey1 = NHTGHBARYWONDQ-SNVBAGLBSA-N
			| InChIKey2 = NHTGHBARYWONDQ-UHFFFAOYSA-N
			| SMILES = C(Cc1ccc(cc1)O)(C(=O)O)N
			<!-- Use only isomeric SMILES for metirosine, so 3D model will show correct 2S sterochemistry -->
			}}
			|Section2={{Chembox Properties
			| Properties_ref =
			| C=10 | H=13 | N=1 | O=3
			| Appearance =
			| Density =
			| MeltingPtC =
			| BoilingPt =
			| Solubility =
			| LogP=
			| pKa =
			}}
			}}
			'''α-Methyl-''p''-tyrosine''' ('''AMPT'''), or simply '''α-methyltyrosine''', also known in its ] 2-(''S'') form as '''metirosine''', is a ] enzyme inhibitor and is therefore a drug involved in inhibiting the ].<ref name="nestler">{{Cite book|url=https://books.google.com/books?id=YYUMZDeQNV4C&q=Molecular+Neuropharmacology%3A+A+Foundation+for+Clinical+Neuroscience|title=Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | edition = Second | vauthors = Nestler EJ, Hyman SE, Malenka RC |date=2008|publisher=McGraw Hill Professional|isbn=9780071641197|language=en}}</ref> AMPT inhibits tyrosine hydroxylase whose enzymatic activity is normally regulated through the ] of different ] residues in regulatory domain sites.<ref name="nestler" /> Catecholamine biosynthesis starts with dietary ], which is hydroxylated by tyrosine hydroxylase and it is hypothesized that AMPT competes with tyrosine at the tyrosine-binding site, causing inhibition of tyrosine hydroxylase.<ref name="Ankenman_2007">{{cite journal | vauthors = Ankenman R, Salvatore MF | title = Low dose alpha-methyl-para-tyrosine (AMPT) in the treatment of dystonia and dyskinesia | journal = The Journal of Neuropsychiatry and Clinical Neurosciences | volume = 19 | issue = 1 | pages = 65–69 | date = 2007 | pmid = 17308229 | doi = 10.1176/jnp.2007.19.1.65 }}</ref>
			It has been used in the treatment of ].<ref name="Ankenman_2007" /> It has been demonstrated to inhibit the production of melanin.<ref>{{cite patent | country = US | number = 6359001 | inventor = Drago F | assign1 = Pfizer Health AB |title=Use of α-methyl-''p''-tyrosine to inhibit melanin production in iris melanocytes | gdate= 19 March 2002 |url=http://www.google.com/patents/US6359001 | postscript = . }}</ref> It is available as a generic medication.<ref>{{cite web | title=Metyrosine: FDA-Approved Drugs | website=U.S. Food and Drug Administration | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=213734 | access-date=15 August 2020}}</ref>
	<!--Clinical data-->
	| tradename =
	| pregnancy_AU =
	| pregnancy_US =
	| pregnancy_category =
	| legal_status =
	| routes_of_administration =
			==Structure and stereochemistry==
	<!--Pharmacokinetic data-->
			AMPT is related to ], an ] component of ]. It contains an extra ] group in the α-position where tyrosine would have a ] atom.<ref>{{cite web |url=https://pubchem.ncbi.nlm.nih.gov/compound/441350 | work = PubChem | publisher = U.S. National Library of Medicine |title=Metyrosine |access-date=2023-10-30}}</ref><ref>{{cite book |url = https://iupac.qmul.ac.uk/BlueBook/P10.html#103 |title=Nomenclature of Organic Chemistry. IUPAC Recommendations and Preferred Names 2013 |chapter = Amino Acids and Peptides |year=2013 | publisher = IUPAC-IUB Joint Commission on Biochemical Nomenclature |isbn = 978-0-85404-182-4 }}</ref> This position is a ] and in natural amino-acids takes the ''S'' ]. However, the alternative ''R'' form of AMPT is also known,<ref>{{cite web |url=https://pubchem.ncbi.nlm.nih.gov/compound/12650 |title=(R)-2-Amino-3-(4-hydroxyphenyl)-2-methylpropanoic acid | work = PubChem | publisher = U.S. National Library of Medicine |access-date=2023-10-30}}</ref> as is the ] material which contains equal amounts of the ''R'' and ''S'' isomers.<ref>{{cite web |url=https://pubchem.ncbi.nlm.nih.gov/compound/3125 | work = PubChem | publisher = U.S. National Library of Medicine |title=Racemetirosine |access-date=2023-10-30}}</ref> The ''S'' isomer has been developed as the drug '''metirosine''' and, as with many ], the racemate was also of interest as a potentially cheaper material, known as '''racemetirosine'''.
	| bioavailability =
	| metabolism =
	| elimination_half-life =
	| excretion =
			==Pharmacology==
	<!--Identifiers-->
			{{Infobox drug
	| CASNo_Ref = {{cascite|??|??}}
			| drug_name = Metirosine
	| CAS_number = 658-48-0
	| PubChem = 3125		| INN =
			| type = <!-- empty -->
	| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| image = Metirosine.svg
	| ChemSpiderID = 3013
			| width =
	| UNII_Ref = {{fdacite|correct|FDA}}
			| alt = Skeletal formula
	| UNII = X88TTO174Z
			| caption =
			| USAN = Metyrosine
	<!--Chemical data-->		<!-- Clinical data -->
			| pronounce =
	| C=10 | H=13 | N=1 | O=3
			| tradename = Demser
	| molecular_weight = 195.215 g/mol
			| Drugs.com = {{drugs.com|cons|metyrosine}}
	| smiles = O=C(O)C(N)(Cc1ccc(O)cc1)C
			| MedlinePlus =
	| InChI = 1/C10H13NO3/c1-10(11,9(13)14)6-7-2-4-8(12)5-3-7/h2-5,12H,6,11H2,1H3,(H,13,14)
			| licence_CA = <!-- Health Canada may use generic or brand name (generic name preferred) -->
	| InChIKey = NHTGHBARYWONDQ-UHFFFAOYAH
			| licence_EU = <!-- EMA uses INN (or special INN_EMA) -->
	| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
			| DailyMedID = Metyrosine
	| StdInChI = 1S/C10H13NO3/c1-10(11,9(13)14)6-7-2-4-8(12)5-3-7/h2-5,12H,6,11H2,1H3,(H,13,14)
			| licence_US = <!-- FDA may use generic or brand name (generic name preferred) -->
	| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
			| pregnancy_AU = <!-- A / B1 / B2 / B3 / C / D / X -->
	| StdInChIKey = NHTGHBARYWONDQ-UHFFFAOYSA-N
			| pregnancy_AU_comment =
			| pregnancy_US = <!-- A / B / C / D / X / N -->
			| pregnancy_US_comment =
			| pregnancy_category = C
			| dependency_liability =
			| addiction_liability =
			| routes_of_administration =
			| class =
			| ATC_prefix = C02
			| ATC_suffix = KB01
			| ATC_supplemental =
			<!-- Legal status -->
			| legal_AU = <!-- S2, S3, S4, S5, S6, S7, S8, S9 or Unscheduled -->
			| legal_AU_comment =
			| legal_BR = <!-- OTC, A1, A2, A3, B1, B2, C1, C2, C3, C4, C5, D1, D2, E, F -->
			| legal_BR_comment =
			| legal_CA = <!-- OTC, Rx-only, Schedule I, II, III, IV, V, VI, VII, VIII -->
			| legal_CA_comment =
			| legal_DE = <!-- Anlage I, II, III or Unscheduled -->
			| legal_DE_comment =
			| legal_NZ = <!-- Class A, B, C -->
			| legal_NZ_comment =
			| legal_UK = <!-- GSL, P, POM, CD, CD Lic, CD POM, CD No Reg POM, CD (Benz) POM, CD (Anab) POM or CD Inv POM / Class A, B, C -->
			| legal_UK_comment =
			| legal_US = Rx-only
			| legal_US_comment =
			| legal_EU =
			| legal_EU_comment =
			| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV -->
			| legal_UN_comment =
			| legal_status = <!-- For countries not listed above -->
			<!-- Pharmacokinetic data -->
			| bioavailability =
			| protein_bound =
			| metabolism =
			| metabolites =
			| onset =
			| elimination_half-life = 3.4–3.7 hours
			| duration_of_action =
			| excretion =
			<!-- Identifiers -->
			| CAS_number_Ref = {{cascite|correct|CAS}}
			| CAS_number = 672-87-7
			| CAS_supplemental =
			| PubChem = 441350
			| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
			| DrugBank = DB00765
			| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
			| ChemSpiderID = 390103
			<!-- Chemical and physical data -->
			| IUPAC_name = (2''S'')-2-amino- 3-(4-hydroxyphenyl)- 2-methylpropanoic acid
			| density =
			| density_notes =
			| melting_point =
			| melting_high =
			| melting_notes =
			| boiling_point =
			| boiling_notes =
			| solubility =
			| sol_units =
			| specific_rotation =
	}}		}}
	'''Alpha-methyl-p-tyrosine (AMPT)''' is a ] enzyme inhibitor. It has been used in the treatment of ].<ref name="pmid17308229">{{cite journal |author=Ankenman R, Salvatore MF |title=Low dose alpha-methyl-para-tyrosine (AMPT) in the treatment of dystonia and dyskinesia |journal=J Neuropsychiatry Clin Neurosci |volume=19 |issue=1 |pages=65–69 |year=2007 |pmid=17308229 |doi=10.1176/appi.neuropsych.19.1.65 |url=}}</ref> It has been demonstrated to inhibit the production of melanin.<ref></ref>
			===Effect on catecholamine biosynthesis===
	==Side effects==
			AMPT inhibits catecholamine biosynthesis at the first step—the hydroxylation of tyrosine.<ref name="brogden">{{cite journal | vauthors = Brogden RN, Heel RC, Speight TM, Avery GS | title = alpha-Methyl-p-tyrosine: a review of its pharmacology and clinical use | journal = Drugs | volume = 21 | issue = 2 | pages = 81–89 | date = February 1981 | pmid = 7009139 | doi = 10.2165/00003495-198121020-00001 | s2cid = 46982584 }}</ref> Reduction in catecholamines and their metabolites (normetanephrine, metanephrine, and 4-hydroxy-3-methoxymandelic acid) result from the inhibition of tyrosine using AMPT.<ref name="brogden" /> AMPT doses of 600 to 4,000&nbsp;mg per day cause a 20 to 79 percent reduction in total catecholamines in Pheochromocytoma patients.<ref name="brogden" /> Increase in dosage increases the magnitude of catecholamine synthesis inhibition.<ref name="brogden" /> This increasing inhibitory effect is seen in dosages up to 1500&nbsp;mg per day; at higher doses, the inhibitory effect of AMPT decreases.<ref name="brogden" /> The maximum effect of orally administered AMPT occurs 48 to 72&nbsp;hours after administration of the drug.<ref name="engelman 1968">{{cite journal | vauthors = Engelman K, Horwitz D, Jéquier E, Sjoerdsma A | title = Biochemical and pharmacologic effects of alpha-methyltyrosine in man | journal = The Journal of Clinical Investigation | volume = 47 | issue = 3 | pages = 577–594 | date = March 1968 | pmid = 5637145 | pmc = 297204 | doi = 10.1172/JCI105754 }}</ref> Catecholamine production levels return to normal 72 to 96 hours after administration of the drug ceases.<ref name="engelman">{{Cite journal| vauthors = Engelman K, Sjoerdsma A |date=1966|title=Inhibition of Catecholamine Biosynthesis in Man|journal=Circulation Research|language=en|volume=18|issue=S6|pages=I–104–I–109|doi=10.1161/01.RES.18.S6.I-104|s2cid=83701035|issn=0009-7330}}</ref> Dosages as low as 300&nbsp;mg per day have been found to have an effect on catecholamine production, which can be measured through urinary excretion analysis and cerebral spinal fluid assays.<ref name="brogden" />
	AMPT administration leads to a transient exacerbation of depressive symptoms in patients that have responded to catecholaminergic ]. The ] changes induced by AMPT may be mediated by decreases in ], while changes in selective attention and motivation may be mediated by ].
			AMPT is successful at inhibiting catecholamine production in humans whether the rate of synthesis is high, as in pheochromocytoma, or normal as in patients with hypertension.<ref name="engelman 1968" />
			===Effect on blood pressure===
	Prolonged administration can have an impact upon the ].<ref name="pmid11390253">{{cite journal |author=Zimmermann RC, Krahn LE, Klee GG, Ditkoff EC, Ory SJ, Sauer MV |title=Prolonged inhibition of presynaptic catecholamine synthesis with alpha-methyl-para-tyrosine attenuates the circadian rhythm of human TSH secretion |journal=J. Soc. Gynecol. Investig. |volume=8 |issue=3 |pages=174–178 |year=2001 |pmid=11390253 |doi= 10.1016/S1071-5576(01)00104-6|url=http://linkinghub.elsevier.com/retrieve/pii/S1071557601001046}}</ref>
			Pheochromocytoma patients exhibited a drop in blood pressure when taking AMPT.<ref name=engelman /> AMPT had no effect in patients with hypertension (high blood pressure).<ref name=engelman />
			==Pharmacokinetics==
			===Absorption===
			AMPT is minimally metabolized by the body and absorbed well after oral ingestion making its bioavailability high.<ref name=brogden /> Single-dose studies have shown that a 1,000&nbsp;mg dose results in AMPT levels in the plasma of 12-14&nbsp;μg/mL after 1 to 3 hours of ingestion.<ref name=engelman /> Maintenance-dose studies have shown that absorption of AMPT is overall the same in all individuals taking doses in the range of 300-4,000&nbsp;mg per day.<ref name=engelman />
			===Half-life===
			The half-life of AMPT in normal patients is 3.4 to 3.7 hours.<ref name=brogden /> In amphetamine addicts the half-life is 7.2 hours.<ref name=brogden />
			===Elimination===
			Small amounts of metabolites (alpha-methyldopa and alpha-methyldopamine) were found after the administration of both single-doses and maintenance-doses of AMPT.<ref name="engelman 1968" /> Small amounts of methyltyramine and alpha-methylnoradrenaline were found in patients undergoing AMPT therapy.<ref name="engelman 1968" /> Urine analysis also recovered 45 to 88 percent of unchanged AMPT after drug ingestion.<ref name=brogden /> Of the total AMPT excreted, 50 to 60 percent appeared in urine within the first 8 hours and 80 to 90 percent appeared within 24 hours of oral administration.<ref name=brogden />
			==Clinical use==
			Metirosine has been shown to suppress catecholamine synthesis and alleviate symptoms related to catecholamine excess, including ], ], ], constipation, and ].<ref>{{cite journal | vauthors = Naruse M, Satoh F, Tanabe A, Okamoto T, Ichihara A, Tsuiki M, Katabami T, Nomura M, Tanaka T, Matsuda T, Imai T, Yamada M, Harada T, Kawata N, Takekoshi K | display-authors = 6 | title = Efficacy and safety of metyrosine in pheochromocytoma/paraganglioma: a multi-center trial in Japan | journal = Endocrine Journal | volume = 65 | issue = 3 | pages = 359–371 | date = March 2018 | pmid = 29353821 | doi = 10.1507/endocrj.EJ17-0276 | doi-access = free }}</ref> Metirosine is primarily used to reduce these symptoms in patients with ].<ref name="pmid7179194">{{cite journal | vauthors = Green KN, Larsson SK, Beevers DG, Bevan PG, Hayes B | title = Alpha-methyltyrosine in the management of phaeochromocytoma | journal = Thorax | volume = 37 | issue = 8 | pages = 632–633 | date = August 1982 | pmid = 7179194 | pmc = 459390 | doi = 10.1136/thx.37.8.632 }}</ref> It is contraindicated for the treatment of ]. Pheochromocytoma is a rare neuroendocrine tumor that results in the release of too much epinephrine and norepinephrine, hormones that control heart rate, metabolism, and blood pressure.<ref name="Gupta_2023">{{cite book | vauthors = Gupta PK, Marwaha B | chapter = Pheochromocytoma | date = March 2023 | title = StatPearls . | location = Treasure Island (FL) | publisher = StatPearls Publishing | pmid = 36944004 | chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK589700/ }}</ref> AMPT was used in the 1960s for preoperative pharmacological control of catecholamine overexpression that causes hypertension and other arterial and cardiac abnormalities.<ref name="Prys-Roberts_2000">{{cite journal | vauthors = Prys-Roberts C | title = Phaeochromocytoma--recent progress in its management | journal = British Journal of Anaesthesia | volume = 85 | issue = 1 | pages = 44–57 | date = July 2000 | pmid = 10927994 | doi = 10.1093/bja/85.1.44 | doi-access = free }}</ref> The use of AMPT to treat Pheochromocytoma prior to surgery was discontinued due to its extensive side effects.<ref name="Prys-Roberts_2000" />
			Phosphorylation of tyrosine hydroxylase at Ser31 or Ser40 can increase dopamine biosynthesis; therefore an increase in pSer31 or pSer40 elevates dopamine synthesis in DA neurons.<ref name="Ankenman_2007" /> Excessive dopamine in the mesolimbic pathways of the brain produces psychotic symptoms.<ref name=nestler /> Antipsychotic medications block dopamine D2 receptors in the caudate and putamen as well as in limbic target areas, they can also block or partially block serotonin.<ref name=nestler /> Therapy with AMPT could prove to be more specific to dopamine and therefore eliminate some of the negative side effects of antipsychotic drugs. Metirosine is used as an off-label treatment for ].<ref>{{cite news | vauthors = Talan J |newspaper=The Washington Post |date= 30 April 2021 |title= Doctors said the boy was suffering from teenage psychosis. What he really had was a rare genetic condition. |url=https://www.washingtonpost.com/health/teenage-psychosis-genetic-condition/2021/04/30/65133794-6be5-11eb-9ead-673168d5b874_story.html}}</ref>
			The dopamine transporter (DAT) is a principal site of action for cocaine. Cocaine inhibits DAT function and vesicular dopamine transport (VMAT).<ref name="brown">{{cite journal | vauthors = Brown JM, Hanson GR, Fleckenstein AE | title = Regulation of the vesicular monoamine transporter-2: a novel mechanism for cocaine and other psychostimulants | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 296 | issue = 3 | pages = 762–767 | date = March 2001 | pmid = 11181904 | url = http://jpet.aspetjournals.org/content/296/3/762 }}</ref> Cocaine administration abruptly and reversibly increases both the Vmax of dopamine uptake and the Bmax of ] (VMAT-2) ligand (dihydrotetrabenazine) binding.<ref name=brown /> Dopamine depletion resulting from administration of AMPT had similar neuropharmacological effects as cocaine.<ref name=brown /> Administration of methamphetamine, a dopamine-releasing agent, rapidly decreased vesicular uptake.<ref name=brown /> A relationship between cytoplasmic dopamine concentration and VMAT activity was established using cocaine, methamphetamines, and AMPT. Although it is not well understood, this relationship allows for AMPT’s inhibitory property, which blocks tyrosine hydroxylase, to increase dopamine transport by the vesicle monoamine transporter-2.<ref name=brown /> This leads to a reduction in the newly synthesized pool of dopamine from replenished tyrosine.<ref name="thomas">{{cite journal | vauthors = Thomas DM, Francescutti-Verbeem DM, Kuhn DM | title = The newly synthesized pool of dopamine determines the severity of methamphetamine-induced neurotoxicity | journal = Journal of Neurochemistry | volume = 105 | issue = 3 | pages = 605–616 | date = May 2008 | pmid = 18088364 | pmc = 2668123 | doi = 10.1111/j.1471-4159.2007.05155.x }}</ref> AMPT’s effect on dopamine concentration and transport is reversible and short-lived. If methamphetamine is administered while cytoplasmic dopamine is depleted to about 50% of the control levels, its neurotoxic effects are averted (Thomas et al., 2008). The recovery of dopamine to normal levels after AMPT administration takes about 2 to 7 days, and this repletion of dopamine is not changed by methamphetamine.<ref name=thomas /> For these reasons AMPT seems to be a better treatment drug in methamphetamine addicts than reserpine, which is also being researched as a possible methamphetamine treatment drug. Reserpine causes almost full loss of dopamine from the striatum by disrupting vesicle storage. The repletion of dopamine after reserpine administration is slower than AMPT.<ref name=thomas /> Additionally, administration of reserpine when dopamine is maximally depleted causes neurotoxic effects, which does not occur with AMPT treatment.<ref name=thomas /> AMPT’s role in addiction has also been studied via changes in dopamine binding to D2 and D3 receptors in the striatum (caudate, putamen, and ventral striatum) after the administration of AMPT.<ref name="martinez">{{cite journal | vauthors = Martinez D, Greene K, Broft A, Kumar D, Liu F, Narendran R, Slifstein M, Van Heertum R, Kleber HD | display-authors = 6 | title = Lower level of endogenous dopamine in patients with cocaine dependence: findings from PET imaging of D(2)/D(3) receptors following acute dopamine depletion | journal = The American Journal of Psychiatry | volume = 166 | issue = 10 | pages = 1170–1177 | date = October 2009 | pmid = 19723785 | pmc = 2875882 | doi = 10.1176/appi.ajp.2009.08121801 }}</ref> Findings revealed that cocaine-dependent subjects exhibited lower levels of endogenous dopamine relative to healthy subjects after AMPT administration. Similar positive effects were found in the role of AMPT in methamphetamine-addicted subjects. Dystonias and dyskinesias onset seems to derive from inconsistent regulation of dopamine in dopamine pathways.<ref name="Ankenman_2007" /> AMPT’s ability to deplete dopamine in the CNS makes it a promising target for treatment of dopamine related disorders.
			Metirosine is used in scientific research to investigate the effects of catecholamine depletion on behavior.<ref>{{cite journal | vauthors = O'Leary OF, Bechtholt AJ, Crowley JJ, Hill TE, Page ME, Lucki I | title = Depletion of serotonin and catecholamines block the acute behavioral response to different classes of antidepressant drugs in the mouse tail suspension test | journal = Psychopharmacology | volume = 192 | issue = 3 | pages = 357–371 | date = June 2007 | pmid = 17318507 | doi = 10.1007/s00213-007-0728-9 | s2cid = 24850438 }}</ref> There is evidence that catecholamine depletion causes an increase in sleepiness that is more pronounced than sleep deprivation, and that the fatigue lingers after the drug is discontinued. Catecholamine depletion has also been linked to a negative mood, though this is reported less often than sleepiness.<ref>{{cite journal | vauthors = McCann UD, Penetar DM, Shaham Y, Thorne DR, Sing HC, Thomas ML, Gillin JC, Belenky G | display-authors = 6 | title = Effects of catecholamine depletion on alertness and mood in rested and sleep deprived normal volunteers | journal = Neuropsychopharmacology | volume = 8 | issue = 4 | pages = 345–356 | date = June 1993 | pmid = 8099791 | doi = 10.1038/npp.1993.34 | authorlink1 = Una D. McCann | doi-access = free }}</ref>
			==Side-effects==
			AMPT administration in healthy subjects has shown to cause increased sleepiness, decreased calmness, increased tension and anger, and a trend for increased depression.<ref name=brogden /> Sedation was also reported as a side effect of AMPT ingestion. However, sedation was not seen in AMPT doses of less than 2g per day.<ref name=engelman /> Patients have reported insomnia as a withdrawal symptom post AMPT exposure.<ref name="engelman 1968" /> When L-dopa is administered following AMPT administration, the effects of AMPT are reversed.<ref name="mccann">{{cite journal | vauthors = McCann UD, Thorne D, Hall M, Popp K, Avery W, Sing H, Thomas M, Belenky G | display-authors = 6 | title = The effects of L-dihydroxyphenylalanine on alertness and mood in alpha-methyl-para-tyrosine-treated healthy humans. Further evidence for the role of catecholamines in arousal and anxiety | journal = Neuropsychopharmacology | volume = 13 | issue = 1 | pages = 41–52 | date = August 1995 | pmid = 8526970 | doi = 10.1016/0893-133X(94)00134-L | doi-access = free | authorlink1 = Una D. McCann }}</ref> These findings suggest that AMPT's effect on alertness and anxiety is catecholamine-specific and further supports that catecholamines are involved in the regulation of normal states of arousal and pathological anxiety symptoms.<ref name="mccann" /> Patients have reported hand, leg, and trunk tremors as well as tightening of the jaw post AMPT drug therapy. These Parkinson like side effects are supported by the lack of dopamine in the brain as in Parkinson’s patients.<ref name=brogden /> Tourette syndrome patients treated with AMPT developed akinesia, akathisia, and oculogyric crisis.<ref name="sweet">{{cite journal | vauthors = Sweet RD, Bruun R, Shapiro E, Shapiro AK | title = Presynaptic catecholamine antagonists as treatment for Tourette syndrome. Effects of alpha methyl para tyrosine and tetrabenazine | journal = Archives of General Psychiatry | volume = 31 | issue = 6 | pages = 857–861 | date = December 1974 | pmid = 4613321 | doi = 10.1001/archpsyc.1974.01760180095012 }}</ref> Most severe of all, patients developed crystalluria (crystals in the urine) after undergoing AMPT drug treatments.<ref name="sweet" />
			Prolonged administration can have an impact upon the ].<ref name="pmid11390253">{{cite journal | vauthors = Zimmermann RC, Krahn LE, Klee GG, Ditkoff EC, Ory SJ, Sauer MV | title = Prolonged inhibition of presynaptic catecholamine synthesis with alpha-methyl-para-tyrosine attenuates the circadian rhythm of human TSH secretion | journal = Journal of the Society for Gynecologic Investigation | volume = 8 | issue = 3 | pages = 174–178 | year = 2001 | pmid = 11390253 | doi = 10.1016/S1071-5576(01)00104-6 }}</ref>
	==Mechanism==		==Mechanism==
			]
	As a ] of ], it prevents the conversion of ] to ], the precursor to ]. This results in lowered systematic ] (], ] and ]) levels.		As a ] of ], it prevents the conversion of ] to ], the precursor to ]. This results in lowered systematic ] (], ] and ]) levels.
	==References==		== References ==
	{{reflist}}		{{reflist|2}}
	==External links==		== External links ==
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