関: levodopa

関: Levodopa

WordNet

the 12th letter of the Roman alphabet (同)l
amino acid that is formed in the liver and converted into dopamine in the brain (同)dihydroxyphenylalanine

PrepTutorEJDIC

=L-dopa
lira(イタリアの貨幣単位リラ)
liter[s]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/10/19 19:10:12」(JST)

wiki ja

[Wiki ja表示]

レボドパまたはL-ドパ（正式名称：4-ジヒドロキシフェニルアラニン、英語: L-3,4-dihydroxyphenylalanine）は、動物、植物の体内で生成される化学物質である。

概要

自然界に産生され、ある種の食物や薬草、例えばハッショウマメに含まれ^[1]、哺乳類では準必須アミノ酸であるL-チロシン（L-Tyr）から体内や脳内で合成される。チロシンはチロシン水酸化酵素によりレボドパとなる。レボドパはレボドパ脱炭酸酵素によりドーパミンとなる。すなわちレボドパは、総称的にカテコールアミン（カテコラミン）として知られる神経伝達物質である、ドーパミン、ノルアドレナリン、アドレナリンの前駆体である。

その本来の生物学的に必須な役割以外に、レボドパはパーキンソン病（PD）とドパミン反応性デストニア（DSD）の臨床療法に用いられる。医薬品としては、国際一般名を用いてレボドパと呼ばれるのが普通である。これを含む商品名としては、シネメット、パーコーパ、アタメット、スタレボ、マドパー、プロローパ等がある。補助食品（サプリメント）または向精神薬として用いられる。

適応

パーキンソン病・パーキンソン症候群。ドパ反応性ジストニア(en)。

出典

^ 藤井義晴、「未利用植物の有効利用と調理科学への期待」、『日本調理科学会誌』Vol. 41 (2008) No. 3　p. 204-209

Medical use

L-DOPA crosses the protective blood–brain barrier, whereas dopamine itself cannot. Thus, L-DOPA is used to increase dopamine concentrations in the treatment of Parkinson's disease and dopamine-responsive dystonia. This treatment was made practical and proven clinically by George Cotzias and his coworkers, for which they won the 1969 Lasker Prize.^[4]^[5] Once L-DOPA has entered the central nervous system, it is converted into dopamine by the enzyme aromatic L-amino acid decarboxylase, also known as DOPA decarboxylase. Pyridoxal phosphate (vitamin B₆) is a required cofactor in this reaction, and may occasionally be administered along with L-DOPA, usually in the form of pyridoxine.

Besides the central nervous system, L-DOPA is also converted into dopamine from within the peripheral nervous system. Excessive peripheral dopamine signaling causes many of the adverse side effects seen with sole L-DOPA administration. To bypass these effects, it is standard clinical practice to coadminister (with L-DOPA) a peripheral DOPA decarboxylase inhibitor (DDCI) such as carbidopa (medicines containing carbidopa, either alone or in combination with L-DOPA, are branded as Lodosyn^[6] (Aton Pharma)^[7] Sinemet (Merck Sharp & Dohme Limited), Pharmacopa (Jazz Pharmaceuticals), Atamet (UCB), and Stalevo (Orion Corporation) or with a benserazide (combination medicines are branded Madopar or Prolopa), to prevent the peripheral synthesis of dopamine from L-DOPA. Coadministration of pyridoxine without a DDCI accelerates the peripheral decarboxylation of L-DOPA to such an extent that it negates the effects of L-DOPA administration, a phenomenon that historically caused great confusion.

In addition, L-DOPA, co-administered with a peripheral DDCI, has been investigated as a potential treatment for restless leg syndrome. However, studies have demonstrated "no clear picture of reduced symptoms".^[8]

The two types of response seen with administration of L-DOPA are:

The short-duration response is related to the half-life of the drug.
The longer-duration response depends on the accumulation of effects over at least two weeks, during which ΔFosB accumulates in nigrostriatal neurons. In the treatment of Parkinson's disease, this response is evident only in early therapy, as the inability of the brain to store dopamine is not yet a concern.

Dietary supplements

Herbal extracts containing L-DOPA are available; high-yielding sources include Mucuna pruriens (velvet bean),^[9] and Vicia faba (broad bean),^[10] while other sources include the genera Phanera, Piliostigma, Cassia, Canavalia, and Dalbergia.^[11]

Biological role

Biosynthesis pathway for trace amines and catecholamines in the human brain^[12]^[13]^[14]

L-Phenylalanine

L-Tyrosine

L-Dopa

Epinephrine

Phenethylamine

p-Tyramine

Dopamine

Norepinephrine

N-Methylphenethylamine

N-Methyltyramine

p-Octopamine

Synephrine

3-Methoxytyramine

AADC

PNMT

AAAH

brain
CYP2D6

COMT

DBH

In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid phenylalanine.

L-DOPA is produced from the amino acid L-tyrosine by the enzyme tyrosine hydroxylase. It is also the precursor for the monoamine or catecholamine neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). Dopamine is formed by the decarboxylation of L-DOPA.

L-DOPA can be directly metabolized by catechol-O-methyl transferase to 3-O-methyldopa, and then further to vanillactic acid. This metabolic pathway is nonexistent in the healthy body, but becomes important after peripheral L-DOPA administration in patients with Parkinson's disease or in the rare cases of patients with aromatic L-amino acid decarboxylase enzyme deficiency.^[15]

L-Phenylalanine, L-tyrosine, and L-DOPA are all precursors to the biological pigment melanin. The enzyme tyrosinase catalyzes the oxidation of L-DOPA to the reactive intermediate dopaquinone, which reacts further, eventually leading to melanin oligomers.

Side effects

The side effects of L-DOPA may include:

Hypotension, especially if the dosage is too high
Arrhythmias, although these are uncommon
Nausea, which is often reduced by taking the drug with food, although protein interferes with drug absorption
Gastrointestinal bleeding
Disturbed respiration, which is not always harmful, and can actually benefit patients with upper airway obstruction
Hair loss
Disorientation and confusion
Extreme emotional states, particularly anxiety, but also excessive libido
Vivid dreams or insomnia
Auditory or visual hallucinations
Effects on learning; some evidence indicates it improves working memory, while impairing other complex functions
Somnolence and narcolepsy
A condition similar to stimulant psychosis

Although many adverse effects are associated with L-DOPA, in particular psychiatric ones, it has fewer than other antiparkinsonian agents, such as anticholinergics and dopamine receptor agonists.

More serious are the effects of chronic L-DOPA administration in the treatment of Parkinson's disease, which include:

End-of-dose deterioration of function
On/off oscillations
Freezing during movement
Dose failure (drug resistance)
Dyskinesia at peak dose (levodopa-induced dyskinesia)
Possible dopamine dysregulation: The long-term use of L-DOPA in Parkinson's disease has been linked to the so-called dopamine dysregulation syndrome.^[16]

Clinicians try to avoid these side effects by limiting L-DOPA doses as much as possible until absolutely necessary.

Possible overdose symptoms

Some in vitro studies suggest a cytotoxic role in the promotion and occurrence of adverse effects associated with L-DOPA treatment.^[17] Though the drug is generally safe in humans, some researchers have reported an increase in cytotoxicity markers in rat pheochromocytoma PC12 cell lines treated with L-DOPA.^[18]^[19] Other authors have attributed the observed toxic effects of L-DOPA in neural dopamine cell lines to enhanced formation of quinones through increased auto-oxidation and subsequent cell death in mesencephalic cell cultures.^[20]^[21] There is no evidence of neurotoxicity in patients with Parkinson's disease and it is generally considered safe, but some controversy surrounds its use in the treatment of Parkinson's disease, given some test tube data indicate a deleterious effect on intracellular and neuronal tissue involved in the pathogenesis of the disease.^[22]

History

In work that earned him a Nobel Prize in 2000, Swedish scientist Arvid Carlsson first showed in the 1950s that administering L-DOPA to animals with drug-induced (reserpine) Parkinsonian symptoms caused a reduction in the intensity of the animals' symptoms. In 1960/61 Oleh Hornykiewicz, after discovering greatly reduced levels of dopamine in autopsied brains of patients with Parkinson’s disease,^[23] published together with the neurologist Walther Birkmayer dramatic therapeutic antiparkinson effects of intravenously administered L-DOPA in patients.^[24] This treatment was later extended to manganese poisoning and later Parkinsonism by George Cotzias and his coworkers,^[25] who used greatly increased oral doses. The neurologist Oliver Sacks describes this treatment in human patients with encephalitis lethargica in his book Awakenings, upon which the movie of the same name is based.

The 2001 Nobel Prize in Chemistry was also related to L-DOPA: the Nobel Committee awarded one-quarter of the prize to William S. Knowles for his work on chirally catalysed hydrogenation reactions, the most noted example of which was used for the synthesis of L-DOPA.^[26]^[27]^[28]

Marine adhesion

L-DOPA is a key compound in the formation of marine adhesive proteins, such as those found in mussels.^[29]^[30] It is believed to be responsible for the water-resistance and rapid curing abilities of these proteins. L-DOPA may also be used to prevent surfaces from fouling by bonding antifouling polymers to a susceptible substrate.^[31]

As a nootropic

One double-blind, placebo controlled study (n=40) found that L-DOPA enhances learning of pseudowords. The drug group showed better learning in all comparisons. Furthermore, a dose-response relationship was tested and found to be the case: lighter people from the drug group did better than the heavier people.^[32]

As a treatment for age-related macular degeneration

In 2015 a retrospective analysis comparing the incidence of age-related macular degeneration (AMD) between patients taking vs. not taking L-DOPA found that the drug delayed onset of AMD by ~8 years. The authors state that significant effects were obtained for both dry and wet AMD.^[33]

References

^ Citation; Lopez, VM; Decatur, CL; Stamer, WD; Lynch, RM; McKay, BS (2008). "L-DOPA is an endogenous ligand for OA1". PLoS Biol. 6 (9): e236. doi:10.1371/journal.pbio.0060236. PMC 2553842. PMID 18828673.
^ Hiroshima Y1, Miyamoto H; Nakamura, F; et al. (Jan 2014). "The protein Ocular albinism 1 is the orphan GPCR GPR143 and mediates depressor and bradycardic responses to DOPA in the nucleus tractus solitarii". Br J Pharmacol. 171 (2): 403–14. doi:10.1111/bph.12459.
^ Jürgen Martens, Kurt Günther, Maren Schickedanz: "Resolution of Optical Isomers by Thin-Layer Chromatography: Enantiomeric Purity of Methyldopa", Arch. Pharm. (Weinheim) 1986, 319, S. 572−574. (DOI:10.1002/ardp.19863190618)
^ Lasker Award 1969 Description, accessed April 1, 2013
^ Tanya Simuni and Howard Hurtig. "Levadopa: A Pharmacologic Miracle Four Decades Later", in Parkinson's Disease: Diagnosis and Clinical Management (Google eBook). Eds. Stewart A Factor and William J Weiner. Demos Medical Publishing, 2008
^ "Medicare D". Medicare. 2014. Retrieved 12 November 2015.
^ "Lodosyn", Drugs, nd, retrieved 12 November 2012
^ "L-dopa for RLS". Bandolier. 1 April 2007. Retrieved 2008-10-16.
^ Pankaj Oudhia. "Kapikachu or Cowhage". Retrieved Nov 3, 2013.
^ Singh, AK; Bharati, RC; Manibhushan, NC; Pedpati, A (December 2013). "An assessment of faba bean (Vicia faba L.) current status and future prospect" (PDF). African Journal of Agricultural Research. 8 (50): 6634–6641. doi:10.5897/AJAR2013.7335.
^ Ingle, PK (May–June 2003). "L-DOPA bearing plants". Natural Product Radiance. 2 (3): 126–133. |access-date= requires |url= (help)
^ Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacol. Ther. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
^ Lindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends Pharmacol. Sci. 26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID 15860375.
^ Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". Eur. J. Pharmacol. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199. The highest level of brain CYP2D activity was found in the substantia nigra (Bromek et al., 2010). The in vitro and in vivo studies have shown the contribution of the alternative CYP2D-mediated dopamine synthesis to the concentration of this neurotransmitter although the classic biosynthetic route to dopamine from tyrosine is active. CYP2D6 protein level is approximately 40% lower in the frontal cortex, cerebellum, and hippocampus in PD patients, even when controlling for CYP2D6 genotype (Mann et al., 2012). ... Tyramine levels are especially high in the basal ganglia and limbic system, which are thought to be related to individual behavior and emotion (Yu et al., 2003c). Studies have demonstrated that dopamine is formed from p-tyramine as well as m-tyramine via tyramine 3-hydroxylation or 4-hydroxylation by rat CYP2D2, 2D4, and 2D18 as well as human CYP2D6. ... Both rat CYP2D and human CYP2D6 have a higher affinity for m-tyramine compared with p-tyramine for the generation of dopamine. Rat CYP2D isoforms (2D2/2D4/2D18) are less efficient than human CYP2D6 for the generation of dopamine from p-tyramine. The K_m values of the CYP2D isoforms are as follows: CYP2D6 (87–121 μm) ≈ CYP2D2 ≈ CYP2D18 > CYP2D4 (256 μm) for m-tyramine and CYP2D4 (433 μm) > CYP2D2 ≈ CYP2D6 > CYP2D18 (688 μm) for p-tyramine (Bromek et al., 2010; Thompson et al., 2000).
^ Hyland K, Clayton PT (December 1992). "Aromatic L-amino acid decarboxylase deficiency: diagnostic methodology" (PDF). Clinical Chemistry. 38 (12): 2405–10. PMID 1281049.
^ Merims D, Giladi N (2008). "Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson's disease". Parkinsonism Relat Disord. 14 (4): 273–280. doi:10.1016/j.parkreldis.2007.09.007. PMID 17988927.
^ Cheng N, Maeda T, Kume T, et al. (December 1996). "Differential neurotoxicity induced by L-DOPA and dopamine in cultured striatal neurons". Brain Research. 743 (1–2): 278–83. doi:10.1016/S0006-8993(96)01056-6. PMID 9017256.
^ Sadigh-Eteghad, Saeed; Talebi, Mahnaz; Farhoudi, Mehdi; Mahmoudi, Javad; Reyhani, Bahram (2013). "Effects of Levodopa loaded chitosan nanoparticles on cell viability and caspase-3 expression in PC12 neural like cells". Neurosciences (Riyadh). 18 (3): 281–283. PMID 23887222.
^ Basma AN, Morris EJ, Nicklas WJ, Geller HM (February 1995). "L-dopa cytotoxicity to PC12 cells in culture is via its autoxidation". Journal of Neurochemistry. 64 (2): 825–32. doi:10.1046/j.1471-4159.1995.64020825.x. PMID 7830076.
^ Pardo B, Mena MA, Casarejos MJ, Paíno CL, De Yébenes JG (June 1995). "Toxic effects of L-DOPA on mesencephalic cell cultures: protection with antioxidants". Brain Research. 682 (1–2): 133–43. doi:10.1016/0006-8993(95)00341-M. PMID 7552304.
^ Mytilineou C, Han SK, Cohen G (October 1993). "Toxic and protective effects of L-dopa on mesencephalic cell cultures". Journal of Neurochemistry. 61 (4): 1470–8. doi:10.1111/j.1471-4159.1993.tb13642.x. PMID 8376999.
^ Simuni T, Stern MB (June 1999). "Does levodopa accelerate Parkinson's disease?". Drugs & aging. 14 (6): 399–408. doi:10.2165/00002512-199914060-00001. PMID 10408739.
^ EHRINGER H, HORNYKIEWICZ O (1960). "Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system.". Klin Wochenschr. 38: 1236–9. PMID 13726012.
^ BIRKMAYER W, HORNYKIEWICZ O (1961). "The L-3,4-dioxyphenylalanine (DOPA)-effect in Parkinson-akinesia.". Wien Klin Wochenschr. 73: 787–8. PMID 13869404.
^ Cotzias GC, Papavasiliou PS, Gellene R (1969). "L-dopa in parkinson's syndrome". The New England Journal of Medicine. 281 (5): 272–273. doi:10.1056/NEJM196907312810518. PMID 5791298.
^ Knowles, William S. (1983). "Asymmetric hydrogenation". Accounts of Chemical Research. 16 (3): 106–112. doi:10.1021/ar00087a006.
^ "Synthetic scheme for total synthesis of DOPA, L- (Monsanto)". UW Madison, Department of Chemistry. Retrieved Sep 30, 2013.
^ Knowles, W. S. (March 1986). "Application of organometallic catalysis to the commercial production of L-DOPA". Journal of Chemical Education. 63 (3): 222. doi:10.1021/ed063p222.
^ Waite, J. Herbert; Andersen, Niels Holten; et al. (2005). "Mussel Adhesion: Finding the Tricks Worth Mimicking". J Adhesion. 81 (3–4): 1–21. doi:10.1080/00218460590944602.
^ "Study Reveals Details Of Mussels' Tenacious Bonds". Science Daily. Aug 16, 2006. Retrieved Sep 30, 2013.
^ Mussel Adhesive Protein Mimetics
^ Knecht, S; Breitenstein, C; Bushuven, S; Wailke, S; Kamping, S; Flöel, A; Zwitserlood, P; Ringelstein, EB (July 2004). "Levodopa: faster and better word learning in normal humans". Annals of Neurology. 56 (1): 20–6. doi:10.1002/ana.20125. PMID 15236398.
^ Brilliant, Murray H.; Vaziri, Kamyar; Connor, Thomas B.; Schwartz, Stephen G.; Carroll, Joseph J.; McCarty, Catherine A.; Schrodi, Steven J.; Hebbring, Scott J.; Kishor, Krishna S.; Flynn, Harry W.; Moshfeghi, Andrew A.; Moshfeghi, Darius M.; Fini, M Elizabeth; McKay, Brian S. (October 2015). "Mining Retrospective Data for Virtual Prospective Drug Repurposing: L-DOPA and Age-related Macular Degeneration". The American Journal of Medicine. doi:10.1016/j.amjmed.2015.10.015.

External links

PBS NOVA episode 5, season 13, February 1986, "The Case Of The Frozen Addict," WGBH Educational Foundation, YouTube.

UpToDate Contents

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1. パーキンソン病の薬理学的治療 pharmacologic treatment of parkinson disease
2. 成人におけるレストレスレッグ症候群の治療 treatment of restless legs syndrome in adults
3. 進行性核上性麻痺（PSP） progressive supranuclear palsy psp
4. 大脳皮質基底核変性症 corticobasal degeneration
5. パーキンソン病における症状の変動およびジスキネジア motor fluctuations and dyskinesia in parkinson disease

English Journal

Combined delusional misidentification syndrome in a patient with Parkinson's disease.

Cercy SP, Marasia JC.
The Journal of neuropsychiatry and clinical neurosciences.J Neuropsychiatry Clin Neurosci.2012 Dec 1;24(1):E3-4.
PMID 22450637

Key factors determining the efficacy of gene therapy for continuous DOPA delivery in the Parkinsonian brain.

Cederfjäll E, Sahin G, Kirik D.Abstractl-DOPA is currently the standard treatment for alleviating the motor symptoms in Parkinson's disease. The therapeutic efficacy, however, diminishes as the disease progresses. It has been suggested that the beneficial effect of l-DOPA could be reestablished by changing the mode of administration. Indeed, continuous delivery of l-DOPA has been shown to be an effective way to circumvent many of the side effects seen with traditional oral administration, which results in an intermittent supply of the dopamine precursor to the brain. However, all currently tested continuous dopaminergic stimulation approaches rely on peripheral administration. This is not ideal since it gives rise to off target effects and is difficult to maintain long-term. Thus, there is an unmet need for an effective continuous administration method with an acceptable side effect profile. Viral-mediated gene therapy is a promising alternative paradigm that can meet this demand. Encouraging preclinical studies in animal models of Parkinson's disease showed therapeutic efficacy after expression of the genes encoding the enzymes required for biosynthesis of dopamine. Although the first phase I clinical trials using these approaches have been conducted, clear positive data in placebo controlled efficacy studies is still lacking. We are now at a critical junction and need to carefully review the preclinical data from the clinical translation perspective and identify the key factors that will determine the potential for success in gene therapy for Parkinson's disease.
Neurobiology of disease.Neurobiol Dis.2012 Nov;48(2):222-7. Epub 2011 Oct 25.
l-DOPA is currently the standard treatment for alleviating the motor symptoms in Parkinson's disease. The therapeutic efficacy, however, diminishes as the disease progresses. It has been suggested that the beneficial effect of l-DOPA could be reestablished by changing the mode of administration. Ind
PMID 22048069

Japanese Journal

Yokukansan, a Traditional Japanese Medicine, Enhances the L-DOPA-Induced Rotational Response in 6-Hydroxydopamine-Lesioned Rats: Possible Inhibition of COMT

Biological and Pharmaceutical Bulletin 39(1), 104-113, 2016
NAID 130005116498

Parkinson病患者における脊椎手術後のParkinsonism増悪 : 周術期のL-dopa投与方法について (日本脊椎・脊髄神経手術手技学会特集号) -- (術前術後)

Journal of spine research : official journal of the Japanese Society for Spine Surgery and Related Research 6(7), 1190-1194, 2015-07
NAID 40020546198

Phenotypic changes of AADC-only-immunoreactive cells in the alimentary canal of the laboratory shrew, Suncus murinus, induced by systemic administration of monoamine precursors

Okajimas Folia Anatomica Japonica 92(2), 43-47, 2015
NAID 130005112017

Related Pictures

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★リンクテーブル★

リンク元	「レボドパ」「L-dihydroxyphenylalanine」「levodopa」
関連記事	「L」「DOPA」「DO」「dopa」

「レボドパ」

L-DOPA
Systematic (IUPAC) name
	(S)-2-Amino-3-(3,4-dihydroxyphenyl)propanoic acid
Clinical data
Pregnancy; category	AU: B3; US: C (Risk not ruled out); ;
Routes of; administration	oral, intravenous
Legal status
Legal status	AU: S4 (Prescription only); UK: POM (Prescription only); US: ℞-only Oral tablets, OTC Mucuna pruriens extract;
Pharmacokinetic data
Bioavailability	30%
Metabolism	Aromatic-L-amino-acid decarboxylase
Biological half-life	0.75–1.5 hours
Excretion	renal 70–80%
Identifiers
CAS Number	59-92-7
ATC code	N04BA01 (WHO)
PubChem	CID 6047
IUPHAR/BPS	3639
DrugBank	DB01235
ChemSpider	5824
UNII	46627O600J
KEGG	D00059
ChEBI	CHEBI:15765
ChEMBL	CHEMBL1009
Chemical data
Formula	C9H11NO4
Molar mass	197.19 g/mol
	SMILES O=C(O)[C@@H](N)Cc1cc(O)c(O)cc1 ;
	InChI InChI=1S/C9H11NO4/c10-6(9(13)14)3-5-1-2-7(11)8(12)4-5/h1-2,4,6,11-12H,3,10H2,(H,13,14)/t6-/m0/s1 ; Key:WTDRDQBEARUVNC-LURJTMIESA-N ;
(verify)

レボドパ
IUPAC命名法による物質名
	IUPAC名 (S)-2-amino-3-(3,4-dihydroxyphenyl); propanoic acid
臨床データ
投与方法	経口
薬物動態データ
生物学的利用能	30%
代謝	芳香族-L-アミノ酸脱炭酸酵素
半減期	0.75–1.5 時間
排泄	腎から 70–80%
識別
CAS番号; (MeSH)	59-92-7
ATCコード	N04BA01
PubChem	CID: 6047
DrugBank	APRD00309
KEGG	D00059
化学的データ
化学式	C9H11NO4
分子量	197.19 g/mol

　　[★]

英: levodopa
同: L-dopa、L-DOPA、LD、Lドーパ、L-ドーパ、L-ドパ、ドパ、ドーパ、3,4-ジヒドロキシフェニルアラニン 3,4-dihydroxyphenylalanine、ジヒドロキシフェニルアラニン dihydroxyphenylalanine
商: ドパストン、ドパゾール、ドパール、イーシー・ドパール配合、カルコーパ配合、スタレボ配合、デュオドーパ配合、ドパコール配合、ドパゾール、ネオドパストン配合、ネオドパゾール配合、パーキストン配合、マドパー配合、メネシット配合、レプリントン配合

[show details]

Lドパ ドパミン : 約 10,800 件
Lドーパ ドパミン : 約 3,130 件
ドパ ドパミン : 約 5,160 件
ドーパ ドパミン : 約 6,590 件

ドパミンの前駆体

相互作用

薬剤名等	臨床症状・措置方法	機序・危険因子
レセルピン製剤	脳内ドパミンが減少し本剤の作用が減弱するおそれ	脳内のドパミンを減少させてパーキンソン症状を悪化させる。
テトラベナジン	脳内ドパミンが減少し本剤の作用が減弱するおそれ	脳内のドパミンを減少させてパーキンソン症状を悪化させる。
血圧降下剤（メチルドパ水和物、レセルピン、節遮断剤等）	血圧降下剤の作用を増強することがある	機序は不明であるが、レボドパに血圧降下作用があるためと考えられている。
抗精神病薬（フェノチアジン系薬剤 (クロルプロマジン等) 、ブチロフェノン系薬剤 (ハロペリドール等)、ペロスピロン等	本剤の作用が減弱することがある	これらの薬剤によりドパミン受容体が遮断される。
全身麻酔剤（ハロタン等）	不整脈を起こすことがある	ハロタン等は交感神経のα、βレセプターの感受性を高める。一方、レボドパとの併用ではレボドパから転換したドパミンがα、βレセプターに作用して、不整脈を起こす可能性がある。
ピリドキシン	末梢での本剤の脱炭酸化を促進するため、本剤の作用が減弱することがある	ピリドキシンはレボドパ脱炭酸酵素の補酵素であり、併用によりレボドパの末梢での脱炭酸化を促進し、レボドパの脳内作用部位への到達量を減少させると考えられる。
抗コリン剤、アマンタジン塩酸塩、ブロモクリプチンメシル酸塩	精神神経系の副作用が増強することがある	併用によりレボドパの効果増加につながるが、同時に精神神経系の副作用が増強される可能性もある。
NMDA受容体拮抗剤（メマンチン塩酸塩等）	本剤の作用を増強するおそれ	これらの薬剤により、ドパミン遊離が促進する可能性がある。
パパベリン塩酸塩	本剤の作用が減弱するおそれ	パパベリン塩酸塩が線条体にあるドパミンレセプターをブロックする可能性がある。
鉄剤	本剤の作用が減弱するおそれ	キレートを形成し、本剤の吸収が減少するとの報告がある。
イソニアジド	本剤の作用が減弱するおそれ	機序は不明であるが、イソニアジドによりドパ脱炭酸酵素が阻害されると考えられている。

「L-dihydroxyphenylalanine」

　　[★]

関: Levodopa

同: L-DOPA

「levodopa」

　　[★] レボドパ L-DOPA 　

「L」

　　[★]

「DOPA」

　　[★] レボドパ。ドパ 3,4-dihydroxyphenylalanine

「DO」

　　[★]

溶存酸素 dissolved O2 dissolved oxygen

「dopa」

　　[★] レボドパ。ドパ　

[fujii-1] 藤井義晴、「未利用植物の有効利用と調理科学への期待」、『日本調理科学会誌』Vol. 41 (2008) No. 3　p. 204-209

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[Trace_amine_template_1-12] Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacol. Ther. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.

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[CYP2D6_tyramine-dopamine_metabolism-14] Wang X, Li J, Dong G, Yue J (February 2014). "The endogenous substrates of brain CYP2D". Eur. J. Pharmacol. 724: 211–218. doi:10.1016/j.ejphar.2013.12.025. PMID 24374199. The highest level of brain CYP2D activity was found in the substantia nigra (Bromek et al., 2010). The in vitro and in vivo studies have shown the contribution of the alternative CYP2D-mediated dopamine synthesis to the concentration of this neurotransmitter although the classic biosynthetic route to dopamine from tyrosine is active. CYP2D6 protein level is approximately 40% lower in the frontal cortex, cerebellum, and hippocampus in PD patients, even when controlling for CYP2D6 genotype (Mann et al., 2012). ... Tyramine levels are especially high in the basal ganglia and limbic system, which are thought to be related to individual behavior and emotion (Yu et al., 2003c). Studies have demonstrated that dopamine is formed from p-tyramine as well as m-tyramine via tyramine 3-hydroxylation or 4-hydroxylation by rat CYP2D2, 2D4, and 2D18 as well as human CYP2D6. ... Both rat CYP2D and human CYP2D6 have a higher affinity for m-tyramine compared with p-tyramine for the generation of dopamine. Rat CYP2D isoforms (2D2/2D4/2D18) are less efficient than human CYP2D6 for the generation of dopamine from p-tyramine. The K_m values of the CYP2D isoforms are as follows: CYP2D6 (87–121 μm) ≈ CYP2D2 ≈ CYP2D18 > CYP2D4 (256 μm) for m-tyramine and CYP2D4 (433 μm) > CYP2D2 ≈ CYP2D6 > CYP2D18 (688 μm) for p-tyramine (Bromek et al., 2010; Thompson et al., 2000).

[pmid1281049-15] Hyland K, Clayton PT (December 1992). "Aromatic L-amino acid decarboxylase deficiency: diagnostic methodology" (PDF). Clinical Chemistry. 38 (12): 2405–10. PMID 1281049.

[pmid17988927-16] Merims D, Giladi N (2008). "Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson's disease". Parkinsonism Relat Disord. 14 (4): 273–280. doi:10.1016/j.parkreldis.2007.09.007. PMID 17988927.

[pmid9017256-17] Cheng N, Maeda T, Kume T, et al. (December 1996). "Differential neurotoxicity induced by L-DOPA and dopamine in cultured striatal neurons". Brain Research. 743 (1–2): 278–83. doi:10.1016/S0006-8993(96)01056-6. PMID 9017256.

[18] Sadigh-Eteghad, Saeed; Talebi, Mahnaz; Farhoudi, Mehdi; Mahmoudi, Javad; Reyhani, Bahram (2013). "Effects of Levodopa loaded chitosan nanoparticles on cell viability and caspase-3 expression in PC12 neural like cells". Neurosciences (Riyadh). 18 (3): 281–283. PMID 23887222.

[pmid7830076-19] Basma AN, Morris EJ, Nicklas WJ, Geller HM (February 1995). "L-dopa cytotoxicity to PC12 cells in culture is via its autoxidation". Journal of Neurochemistry. 64 (2): 825–32. doi:10.1046/j.1471-4159.1995.64020825.x. PMID 7830076.

[pmid7552304-20] Pardo B, Mena MA, Casarejos MJ, Paíno CL, De Yébenes JG (June 1995). "Toxic effects of L-DOPA on mesencephalic cell cultures: protection with antioxidants". Brain Research. 682 (1–2): 133–43. doi:10.1016/0006-8993(95)00341-M. PMID 7552304.

[pmid8376999-21] Mytilineou C, Han SK, Cohen G (October 1993). "Toxic and protective effects of L-dopa on mesencephalic cell cultures". Journal of Neurochemistry. 61 (4): 1470–8. doi:10.1111/j.1471-4159.1993.tb13642.x. PMID 8376999.

[pmid10408739-22] Simuni T, Stern MB (June 1999). "Does levodopa accelerate Parkinson's disease?". Drugs & aging. 14 (6): 399–408. doi:10.2165/00002512-199914060-00001. PMID 10408739.

[pmid13726012-23] EHRINGER H, HORNYKIEWICZ O (1960). "Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system.". Klin Wochenschr. 38: 1236–9. PMID 13726012.

[pmid13869404-24] BIRKMAYER W, HORNYKIEWICZ O (1961). "The L-3,4-dioxyphenylalanine (DOPA)-effect in Parkinson-akinesia.". Wien Klin Wochenschr. 73: 787–8. PMID 13869404.

[25] Cotzias GC, Papavasiliou PS, Gellene R (1969). "L-dopa in parkinson's syndrome". The New England Journal of Medicine. 281 (5): 272–273. doi:10.1056/NEJM196907312810518. PMID 5791298.

[26] Knowles, William S. (1983). "Asymmetric hydrogenation". Accounts of Chemical Research. 16 (3): 106–112. doi:10.1021/ar00087a006.

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[33] Brilliant, Murray H.; Vaziri, Kamyar; Connor, Thomas B.; Schwartz, Stephen G.; Carroll, Joseph J.; McCarty, Catherine A.; Schrodi, Steven J.; Hebbring, Scott J.; Kishor, Krishna S.; Flynn, Harry W.; Moshfeghi, Andrew A.; Moshfeghi, Darius M.; Fini, M Elizabeth; McKay, Brian S. (October 2015). "Mining Retrospective Data for Virtual Prospective Drug Repurposing: L-DOPA and Age-related Macular Degeneration". The American Journal of Medicine. doi:10.1016/j.amjmed.2015.10.015.

v t e Stimulants (category)

Adamantanes	Adaphenoxate Adapromine Amantadine Bromantane Chlodantane Gludantane Memantine Rimantadine

Adenosine antagonists	8-Chlorotheophylline 8-Cyclopentyltheophylline 8-Phenyltheophylline Aminophylline Caffeine CGS-15943 Dimethazan Paraxanthine SCH-58261 Theobromine Theophylline

Alkylamines	Cyclopentamine Cypenamine Cyprodenate Heptaminol Isometheptene Levopropylhexedrine Methylhexaneamine Octodrine Propylhexedrine Tuaminoheptane

Ampakines	CX-516 CX-546 CX-614 CX-691 CX-717 IDRA-21 LY-404,187 LY-503,430 Nooglutyl Org 26576 PEPA S-18986 Sunifiram Unifiram

Arylcyclohexylamines	Benocyclidine Dieticyclidine Esketamine Eticyclidine Gacyclidine Ketamine Phencyclamine Phencyclidine Rolicyclidine Tenocyclidine Tiletamine

Benzazepines	6-Br-APB SKF-77434 SKF-81297 SKF-82958

Cholinergics	A-84,543 A-366,833 ABT-202 ABT-418 AR-R17779 Altinicline Anabasine Arecoline Bradanicline Cotinine Cytisine Dianicline Epibatidine Epiboxidine GTS-21 Ispronicline Nicotine PHA-543,613 PNU-120,596 PNU-282,987 Pozanicline Rivanicline Sazetidine A SIB-1553A SSR-180,711 TC-1698 TC-1827 TC-2216 Tebanicline UB-165 Varenicline WAY-317,538

Convulsants	Anatoxin-a Bicuculline DMCM Flurothyl Gabazine Pentetrazol Picrotoxin Strychnine Thujone

Eugeroics	Adrafinil Armodafinil CRL-40,940 CRL-40,941 Fluorenol JZ-IV-10 Modafinil

Oxazolines	4-Methylaminorex Aminorex Clominorex Cyclazodone Fenozolone Fluminorex Pemoline Thozalinone

Phenethylamines	1-(4-Methylphenyl)-2-aminobutane 1-Phenyl-2-(piperidin-1-yl)pentan-3-one 1-Methylamino-1-(3,4-methylenedioxyphenyl)propane 2-Fuoroamphetamine 2-Fuoromethamphetamine 2-OH-PEA 2-Phenyl-3-aminobutane 2-Phenyl-3-methylaminobutane 2,3-MDA 3-Fuoroamphetamine 3-Fluoroethamphetamine 3-Fluoromethcathinone 3-Methoxyamphetamine 3-Methylamphetamine 3,4-DMMC 4-BMC 4-CMC 4-Ethylamphetamine 4-Fluoroamphetamine 4-Fluoromethamphetamine 4-MA 4-Methylbuphedrone 4-Methylcathinone 4-MMA 4-Methylpentedrone 4-MTA 6-FNE AL-1095 Alfetamine a-Ethylphenethylamine Amfecloral Amfepentorex Amfepramone Amidephrine 2-Amino-1,2-dihydronaphthalene 2-Aminoindane 5-(2-Aminopropyl)indole 2-Aminotetralin Acridorex Amphetamine (Dextroamphetamine, Levoamphetamine) Amphetaminil Arbutamine β-Methylphenethylamine β-Phenylmethamphetamine Benfluorex Benzedrone Benzphetamine BDB BOH 3-Benzhydrylmorpholine BPAP Buphedrone Bupropion Butylone Camfetamine Cathine Cathinone Chlorphentermine Cilobamine Cinnamedrine Clenbuterol Clobenzorex Cloforex Clortermine Cypenamine D-Deprenyl Denopamine Dimethoxyamphetamine Dimethylamphetamine Dimethylcathinone Dobutamine DOPA (Dextrodopa, Levodopa) Dopamine Dopexamine Droxidopa EBDB Ephedrine Epinephrine Epinine Etafedrine Ethcathinone Ethylnorepinephrine Ethylone Etilamfetamine Etilefrine Famprofazone Fencamfamine Fencamine Fenethylline Fenfluramine (Dexfenfluramine, Levofenfluramine) Fenproporex Feprosidnine Flephedrone Fludorex Formetorex Furfenorex Gepefrine Hexapradol Hexedrone HMMA Hordenine 4-Hydroxyamphetamine 5-Iodo-2-aminoindane Ibopamine IMP Indanylamphetamine Iofetamine Isoetarine Isoethcathinone Isoprenaline L-Deprenyl (Selegiline) Lefetamine Lisdexamfetamine Lophophine MBDB MDA MDBU MDEA MDMA MDMPEA MDOH MDPR MDPEA Mefenorex Mephedrone Mephentermine Metanephrine Metaraminol Mesocarb Methamphetamine (Dextromethamphetamine, Levomethamphetamine) Methoxamine Methoxyphenamine MMA Methcathinone Methedrone Methoxyphenamine Methylenedioxycathinone Methylone Mexedrone MMDA MMDMA MMMA Morforex N,alpha-Diethylphenylethylamine N-Benzyl-1-phenethylamine N-Ethylbuphedrone N-Ethylhexedrone N,N-Dimethylphenethylamine Naphthylamphetamine Nisoxetine Norepinephrine Norfenefrine Norfenfluramine Normetanephrine L-Norpseudoephedrine Octopamine (drug) Orciprenaline Ortetamine Oxifentorex Oxilofrine PBA PCA PCMA PHA Pentorex Pentedrone Pentylone Phenatine Phenpromethamine Phentermine Phenylalanine Phenylephrine Phenylpropanolamine Pholedrine PIA PMA PMEA PMMA PPAP Phthalimidopropiophenone Prenylamine Propylamphetamine Pseudoephedrine Ropinirole Salbutamol (Levosalbutamol) Sibutramine Synephrine Theodrenaline Tiflorex Tranylcypromine Tyramine Tyrosine Xylopropamine Zylofuramine

Phenylmorpholines	3-Fluorophenmetrazine Fenbutrazate Fenmetramide G-130 Manifaxine Morazone Morforex Oxaflozane PD-128,907 Phendimetrazine Phenmetrazine 2-Phenyl-3,6-dimethylmorpholine Pseudophenmetrazine Radafaxine

Piperazines	2C-B-BZP 3C-PEP BZP CM156 DBL-583 GBR-12783 GBR-12935 GBR-13069 GBR-13098 GBR-13119 MeOPP MBZP Vanoxerine

Piperidines	1-Benzyl-4-(2-(diphenylmethoxy)ethyl)piperidine 1-(3,4-Dichlorophenyl)-1-(piperidin-2-yl)butane 2-Benzylpiperidine 2-Methyl-3-phenylpiperidine 3-Chloromethylphenidate 3,4-Dichloromethylphenidate 4-Benzylpiperidine 4-Fluoromethylphenidate 4-Methylmethylphenidate Desoxypipradrol Difemetorex Diphenylpyraline Ethylnaphthidate Ethylphenidate Methylnaphthidate Isopropylphenidate Methylphenidate (Dexmethylphenidate) N-Methyl-3β-propyl-4β-(4-chlorophenyl)piperidine Nocaine Phacetoperane Pipradrol Propylphenidate SCH-5472

Pyrrolidines	2-Diphenylmethylpyrrolidine 5-DBFPV α-PPP α-PBP α-PHP α-PVP α-PVT Diphenylprolinol DMPVP FPOP FPVP MDPPP MDPBP MPBP MPHP MPPP MOPVP MOPPP Indapyrophenidone MDPV Naphyrone PEP Picilorex Prolintane Pyrovalerone

Racetams	Oxiracetam Phenylpiracetam Phenylpiracetam hydrazide

Tropanes	3-CPMT 3'-Chloro-3a-(diphenylmethoxy)tropane 4-fluorotropacocaine 4'-Fluorococaine AHN-1055 Altropane (IACFT) Brasofensine CFT (WIN 35,428) β-CIT (RTI-55) Cocaethylene Cocaine Dichloropane (RTI-111) Difluoropine FE-β-CPPIT FP-β-CPPIT Ioflupane (¹²³I) Norcocaine PIT PTT RTI-31 RTI-32 RTI-51 RTI-105 RTI-112 RTI-113 RTI-117 RTI-120 RTI-121 (IPCIT) RTI-126 RTI-150 RTI-154 RTI-171 RTI-177 RTI-183 RTI-193 RTI-194 RTI-199 RTI-202 RTI-204 RTI-229 RTI-241 RTI-336 RTI-354 RTI-371 RTI-386 Salicylmethylecgonine Tesofensine Troparil (β-CPT, WIN 35,065-2) Tropoxane WF-23 WF-33 WF-60

Tryptamines	4-HO-αMT 4-Methyl-αET 4-Methyl-αMT 5-Chloro-αMT 5-Fluoro-αMT 5-MeO-αET 5-MeO-αMT 5-MeO-DIPT 6-Fluoro-αMT 7-Methyl-αET αET αMT

Others	2-MDP 2-Phenylcyclohexylamine 3,3-Diphenylcyclobutanamine Amfonelic acid Amineptine Amiphenazole Atipamezole Atomoxetine Bemegride Benzydamine BTQ BTS 74,398 Centanafadine Ciclazindol Clofenciclan Cropropamide Crotetamide D-161 Diclofensine Dimethocaine Efaroxan Etamivan Fenisorex Fenpentadiol Gamfexine Gilutensin GSK1360707F GYKI-52895 Hexacyclonate Idazoxan Indanorex Indatraline JNJ-7925476 Lazabemide Leptacline Lomevactone LR-5182 Mazindol Meclofenoxate Medifoxamine Mefexamide Methamnetamine Methastyridone Methiopropamine Naphthylaminopropane Nefopam Nikethamide Nomifensine O-2172 Oxaprotiline PNU-99,194 PRC200-SS Rasagiline Rauwolscine Rubidium chloride Setazindol Tametraline Tandamine Thiopropamine Thiothinone Trazium UH-232 Yohimbine

ATC code: N06B

v t e Dietary supplements

Types	Amino acids Bodybuilding supplement Energy drink Energy bar Fatty acids Herbal Supplements Minerals Prebiotics Probiotics (Lactobacillus Bifidobacterium) Protein bar Vitamins

Vitamins and chemical elements ("minerals")	Retinol (Vitamin A) B vitamins: Thiamine (B₁) Riboflavin (B₂) Niacin (B₃) Pantothenic acid (B₅) Pyridoxine (B₆) Biotin (B₇) Folic acid (B₉) Cyanocobalamin (B₁₂) Ascorbic acid (Vitamin C) Ergocalciferol and Cholecalciferol (Vitamin D) Tocopherol (Vitamin E) Naphthoquinone (Vitamin K) Calcium Choline Chromium Cobalt Copper Fluorine Iodine Iron Magnesium Manganese Molybdenum Phosphorus Potassium Selenium Sodium Sulfur Zinc

Other common ingredients	AAKG β-hydroxy β-methylbutyrate Carnitine Chondroitin sulfate Cod liver oil Copper gluconate Creatine/Creatine supplements Dietary fiber Echinacea Elemental calcium Ephedra Fish oil Folic acid Ginseng Glucosamine Glutamine Grape seed extract Guarana Iron supplements Japanese Honeysuckle Krill oil Lingzhi Linseed oil Lipoic acid Milk thistle Melatonin Red yeast rice Royal jelly Saw palmetto Spirulina St John's wort Taurine Wheatgrass Wolfberry Yohimbine Zinc gluconate

Related articles	Codex Alimentarius Enzyte Hadacol Herbal tea Nutraceutical Multivitamin Nutrition

IUPAC命名法による物質名


IUPAC名 (S)-2-amino-3-(3,4-dihydroxyphenyl) propanoic acid
臨床データ
投与方法	経口
薬物動態データ
生物学的利用能	30%
代謝	芳香族-L-アミノ酸脱炭酸酵素
半減期	0.75–1.5 時間
排泄	腎から 70–80%
識別
CAS番号 (MeSH)	59-92-7
ATCコード	N04BA01
PubChem	CID: 6047
DrugBank	APRD00309
KEGG	D00059
化学的データ
化学式	C₉H₁₁NO₄
分子量	197.19 g/mol

Systematic (IUPAC) name


(S)-2-Amino-3-(3,4-dihydroxyphenyl)propanoic acid
Clinical data
Pregnancy category	AU: B3 US: C (Risk not ruled out)
Routes of administration	oral, intravenous
Legal status
Legal status	AU: S4 (Prescription only) UK: POM (Prescription only) US: ℞-only Oral tablets, OTC Mucuna pruriens extract
Pharmacokinetic data
Bioavailability	30%
Metabolism	Aromatic-L-amino-acid decarboxylase
Biological half-life	0.75–1.5 hours
Excretion	renal 70–80%
Identifiers
CAS Number	59-92-7^Y
ATC code	N04BA01 (WHO)
PubChem	CID 6047
IUPHAR/BPS	3639
DrugBank	DB01235^Y
ChemSpider	5824^Y
UNII	46627O600J^Y
KEGG	D00059^Y
ChEBI	CHEBI:15765^Y
ChEMBL	CHEMBL1009^Y
Chemical data
Formula	C₉H₁₁NO₄
Molar mass	197.19 g/mol
SMILES O=C(O)[C@@H](N)Cc1cc(O)c(O)cc1
InChI InChI=1S/C9H11NO4/c10-6(9(13)14)3-5-1-2-7(11)8(12)4-5/h1-2,4,6,11-12H,3,10H2,(H,13,14)/t6-/m0/s1^Y Key:WTDRDQBEARUVNC-LURJTMIESA-N^Y
(verify)

匿名

検索

案内

L-DOPA