Fluorodopa F 18 (Systemic)

Primary: DX201

Other commonly used names are 18F-dopa, 18F-6- L-fluorodopa, and L-6-[ 18F]fluoro-3, 4-dihydroxyphenylalanine.
Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).

*Not commercially available in the U.S.

Not commercially available in Canada.


Diagnostic aid, radioactive (brain disease)—


Note: Because fluorodopa F 18 ( 18F-dopa) is not commercially available in the U.S. or Canada, the bracketed information and the use of the superscript 1 in this monograph reflect the lack of labeled (approved) indications for this product.


[Brain imaging, positron emission tomographic]1—Fluorodopa F 18 ( 18F-dopa) is used with positron emission tomography (PET) to visualize the regional distribution of the neurotransmitter dopamine in the human brain {01} {07} {08} {09} {42}. 18F-dopa with PET is used to assess presynaptic dopaminergic function in vivo in the human brain {01} {08} {16} {18} and to examine changes in dopamine neurotransmission in clinically dysfunctional patients {01} {16} {39}. Since patients with Parkinson's disease have been demonstrated to have low 18F-dopa uptake throughout the striatum, 18F-dopa with PET may be used to confirm the diagnosis of Parkinson's disease {08} {17} {18} {24} {29} {30} {39} and to follow the rate of disease progression {30} {33} {38}. A decreased 18F-dopa uptake, especially in the putamen, may be indicative of a primary degeneration of the dopaminergic nigrostriatal neurons typical for idiopathic Parkinson's disease {08} {33} {39}. Also, 18F-dopa has been used to investigate the effect of medications in Parkinson's disease, particularly of catechol O-methyltransferase (COMT) inhibitors (e.g., nitecapone and entacapone), on the accumulation of dopamine in the striatum {34} {37}. 18F-dopa may be useful for identifying preclinical or early Parkinson's disease in clinically normal subjects {18} {31}. 18F-dopa with PET may be helpful in confirming clinical suspicions in the rare cases of psychogenic parkinsonism {20}. In addition, in patients with Parkinson's disease who have received intracerebral transplantation of adrenal medulla tissue or fetal mesencephalic tissue, 18F-dopa with PET may help study the integrity and activity of the implant {32} {35} {36}.
18F-dopa scintigraphy may be useful to demonstrate abnormalities due to presynaptic striatal dopamine deficiency in other disorders, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)–induced {21} and cyanide-induced {22} parkinsonism, multiple-system atrophy {23}, progressive supranuclear palsy {23}, amyotrophic lateral sclerosis-parkinsonism-dementia complex of Guam {24}, cortical-basal ganglionic degeneration {25}, autosomal dominant neurodegenerative diseases (e.g., parkinsonism and dementia with pallido-ponto-nigral degeneration) {26}, and the Lesch-Nyhan disease {28}.
18F-dopa may be useful as an amino acid tracer for the detection of brain tumors and their recurrences {27}.

1 Not included in Canadian product labeling.

Physical Properties

Nuclear Data {01} {43}

Mode of
photon emissions
Mean number
of emissions/
F 18
(110 min) 
* The two annihilation photons emitted in opposite directions at the moment of positron annihilation are used for imaging purposes. Detection devices usually used are positron emission tomography (PET) units; however, conventional planar scintillation cameras equipped with coincidence circuitry or high-energy collimators have been used for some studies {42} {43}.


Physicochemical characteristics:
    Fluorine F 18 ( 18F) may be produced by the 20Ne(d, alpha) 18F or by the 18O(p,n) 18F nuclear reaction {01}. 18F-dopa has been reported to be prepared by different methods (e.g., nonregioselective electrophilic fluorination, regioselective fluorodemetallation, nucleophilic substitution, and regioselective fluorination of protected L-dopa) {06} {10} {12} {13}. For example, one method is based on the reaction of [ 18F]acetyl hypofluorite with a partially blocked dopa derivative in acetic acid {10}. Other methods involve the direct radiofluorination of L-dopa with [ 18F]fluorine in liquid hydrogen fluoride as a solvent for the reaction {07} {10} {13} {41}. In one of the most recent methods, gaseous acetyl [ 18F]-hypofluorite is passed through a solution of L-methyl- N-acetyl-[beta-(3-methoxy-4-acetoxy-phenyl)]alaninate in acetic acid at room temperature followed by the hydrolysis of the intermediate products with concentrated hydriodic acid {06}.

Note: The labeled fluorodopa has to be synthesized in the L-form since the transport system at the blood-brain barrier only accepts L-amino acids {07}.

Mechanism of action/Effect:

In vivo, dopamine is synthesized from the amino acid L-tyrosine {07}. L-tyrosine is hydroxylated to L-dopa, which subsequently is decarboxylated to dopamine {07}. Dopamine is stored intraneuronally in vesicles and during neurotransmission some of the content of the vesicles is ejected into the synapse {07}. 18F-dopa resembles natural L-dopa biochemically, with similar kinetics {07}. 18F-dopa is a large, neutral amino acid that is transported into presynaptic neurons, where it is converted by the enzyme dopa decarboxylase (i.e., aromatic- L-amino-acid decarboxylase [AAAD]) into 18F-fluorodopamine, which subsequently enters cathecholamine-storage vesicles {07} {28} {39}. 18F-dopa crosses the blood-brain barrier {07}; therefore, when injected into the blood stream, it reaches the dopaminergic cells in the brain and is used by the brain as a precursor for dopamine {07}. This makes it possible to monitor intracerebral synthesis and uptake of dopamine by means of the gamma-emitting 18F-dopa in conjunction with externally-placed gamma ray detection devices, such as positron emission tomography (PET) units {01} {07} {42}.

For most studies, oral carbidopa is given routinely prior to the administration of 18F-dopa {18}. Carbidopa blocks the AAAD, thus preventing early decarboxylation of 18F-dopa to 18F-dopamine outside the brain {10} {11} {15} {43}. The increased bioavailability of 18F-dopa to the brain improves imaging {03}.

In patients with Parkinson's disease, due to the severe loss of nigrostriatal dopaminergic neurons, the presynaptic uptake of 18F-dopa is impaired, with mean putamen (the region in which 18F-dopa uptake is most severely impaired in patients with Parkinson's disease) values 40% of normal {08} {16} {18} {23} {39}. When 18F-dopa uptake is very much lower into the putamen than into the caudate, this may be an indication of early or preclinical Parkinson's disease {18}. The reduction of 18F-dopa uptake in patients with Parkinson's disease is typically most severe in the striatum contralateral to the clinically most affected limbs {18}.

In addition, since 18F-dopa is a large, neutral amino acid, it possesses the kinetics of this group of amino acids. Its unmetabolized form therefore is actively transported and accumulated into brain tumors at a much higher rate than in normal brain tissue {27}.


Slow uptake of 18F-dopa by brain tissue, preferentially in the striatum {08}. The uptake of 18F radioactivity in the brain is approximately 0.2% of the administered activity {07}.


18F-dopa follows the metabolic pathway of L-dopa both in the brain and in the periphery {10}. Peripherally, 18F-dopa is metabolized to 3- O-methyl-6-[ 18F]fluoro- L-dopa (3-OMFD) by catechol O-methyltransferase (COMT) and to 6-[ 18F]fluorodopamine (FDA) by AAAD {01} {07} {10}. The free amine is rapidly sulphated to give 6-[ 18F]fluorodopamine sulphate or deaminated by monoamine oxidase to give 6-[ 18F]fluorodihydroxyphenyl acetic acid (FDOPAC), which is methylated by COMT to give 6-[ 18F]fluorohomovanillic acid (FHVA), which slowly leaves the brain {01} {07} {10}. In the striatum, 18F-dopa is readily decarboxylated to FDA, but no further metabolism of FDA occurs {10}.

Note: The use of carbidopa inhibits peripheral AAAD activity, thus eliminating FDA formation {10}. Consequently, this may increase 18F-dopa bioavailability to the brain, but also, it may provide more 18F-dopa accessibility to COMT, thereby possibly increasing 3-OMFD levels {10}.

Time to peak concentration

The peak of radioactivity after 18F-dopa administration has been reported to occur at 28.8 ± 5.3 minutes in normal subjects, and at 29.3 ± 0 minutes in patients with Parkinson's disease {08}. The absolute concentration of 18F-dopa in striatum of normal subjects may reach a plateau between 30 and 45 minutes and, thereafter, decrease slightly {08}. 18F-dopa may remain in the human striatum for up to 4 hours after administration {08}.

Note: In one study with normal subjects who received 18F-dopa, the radioactivity in the striatum was reported to decrease only slightly (from 8.7% of arterial peak plasma value at 70 minutes to 8% at 180 minutes) {08}. In patients with Parkinson's disease, striatal activity decreased more rapidly (from 5.7 to 4.1% between 70 and 170 minutes) {08}.
In the same study, the average ratio of striatum to surrounding brain radioactivity at 20-minute intervals in the normal subjects progressively increased throughout the time of the PET study (0 to 4 hours after injection), while in the patient groups the average ratio reached a plateau about 100 minutes following 18F-dopa administration {08}.
The ratio of radioactivity in striatum compared to that in surrounding brain was reported to increase steadily over time in the normal subjects for at least 120 minutes after injection of 18F-dopa, but by that time the overall absolute count rates are extremely low because of physical decay of the radioisotope {08} {42}.

Radiation dosimetry:

Estimated absorbed radiation dose (mean)* 
Organ  mGy/MBq  rad/mCi 
Urinary bladder wall  0.15  0.56 
Kidneys  0.027  0.1 
Pancreas  0.02  0.073 
Uterus  0.019  0.069 
Large intestine wall, lower  0.016  0.059 
Liver  0.015  0.057 
Adrenals  0.015  0.056 
Testes  0.015  0.055 
Ovaries  0.014  0.052 
Small intestine wall  0.014  0.052 
Large intestine wall, upper  0.014  0.052 
Lungs  0.013  0.048 
Stomach wall  0.012  0.045 
Spleen  0.012  0.043 
Bone (total)  0.01  0.04 
Red marrow  0.01  0.039 
Thyroid  0.01  0.038 
Other tissues (muscle)  0.0089  0.033 
Skin  0.0085  0.031 
Total body  0.01  0.039 
Effective dose: 0.02 mSv/MBq (0.074 rem/mCi) 
* Based on data collected during studies with healthy human subjects and parkinsonian patients following pretreatment with carbidopa {03}.

    Renal (following carbidopa pretreatment, about 23% of the administered activity eliminated in 2 hours and about 31% at 3 hours) {03}.

Precautions to Consider


Studies to assess transplacental transfer of 18F-dopa have not been done in humans. The possibility of pregnancy should be assessed in women of childbearing potential. Clinical situations exist where the benefit to the patient and fetus, based on information derived from radiopharmaceutical use, outweighs the risks from fetal exposure to radiation. In these situations, the physician should use discretion and reduce the administered activity to the lowest practical amount. {04}


It is not known whether 18F-dopa is distributed into breast milk. However, due to the short physical half-life of 18F-dopa {01}, any excretion of this agent during lactation is unlikely to result in significant radiation exposure to the breast-feeding infant. The absorbed radiation dose to the breast-feeding infant will be negligible after waiting at least 8 hours {43}.


Appropriate studies on the relationship of age to the effects of 18F-dopa have not been performed in children. However, diagnostic studies performed in children have not demonstrated pediatrics-specific problems that would limit the usefulness of 18F-dopa in children {09} {28}.


Appropriate studies on the relationship of age to the effects of 18F-dopa have not been performed in the geriatric population. However, studies that included older patients were conducted, and geriatrics-specific problems that would limit the usefulness of this agent in the elderly are not expected {08} {18} {25}. In one of these studies, the rate of peripheral metabolism of 18F-dopa to 3- O-methyl-6-[ 18F]fluoro- L-dopa (3-OMFD) was shown to increase as a function of age {11}.

Drug interactions and/or related problems
See Diagnostic interference .

Diagnostic interference
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With results of this test
Foods, especially high-protein{10}{14}    (previous ingestion of food may decrease the uptake of 18F-dopa; proteins in food may be degraded into amino acids that compete with 18F-dopa for transport to the brain)

Due to other medications
Carbidopa{10}{11}{15}{29}    (prior to 18F-dopa administration, use of carbidopa may increase 18F-dopa bioavailability to the brain by eliminating peripheral decarboxylase activity and restricting peripheral 18F-dopa metabolism to 3- O-methyl-6-[ 18F]fluoro- L-dopa formation; most researchers advocate routine use of carbidopa as a normalization factor for PET studies using 18F-dopa)

Haloperidol{07}    (increased intracerebral dopamine turnover caused by haloperidol may result in increased accumulation of 18F-dopa)

Monoamine oxidase (MAO) inhibitors{07}    (concurrent use with MAO inhibitors may result in increased accumulation of 18F-dopa in the brain)

Reserpine{07}{19}{43}    (reserpine-induced depletion of the contents of intraneuronal vesicles may prevent retention of 18F-dopa in the brain)

Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).

Risk-benefit should be considered when the following medical problem exists
Sensitivity to the radiopharmaceutical preparation

Side/Adverse Effects
There are no known side/adverse effects associated with the use of 18F-dopa {07}.

Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Radiopharmaceuticals (Diagnostic) .
In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Description of use
Action in the body: Uptake of 18 F-dopa in dopaminergic cells of the brain; used by the brain as a precursor for dopamine

Small amounts of radioactivity used in diagnosis; radiation received is low and considered safe

Before having this test
»   Conditions affecting use, especially:
Sensitivity to the radiopharmaceutical preparation

Pregnancy—Risk to fetus from radiation exposure as opposed to benefit derived from use should be considered

Preparation for this test
Nuclear medicine department should advise patient on any preparatory instructions

Fasting recommended prior to 18F-dopa administration

Precautions after having this test
No special precautions needed

General Dosing Information
Radiopharmaceuticals are to be administered only by or under the supervision of physicians who have had extensive training in the safe use and handling of radioactive materials and who are authorized by the appropriate federal or state regulatory agency, if required, or, outside the U.S., the appropriate authority {05}.

Fasting (e.g., overnight fasting with standard low-protein breakfast on the morning of the PET study) is recommended prior to 18F-dopa administration since a significant reduction of tracer uptake into the brain may occur due to the interference by dietary amino acids {10} {14} {27} {29}.

Use of carbidopa (100 to 150 mg orally) given 1 hour prior to 18F-dopa administration may increase 18F-dopa bioavailability to the brain by eliminating peripheral decarboxylase activity and restricting peripheral 18F-dopa metabolism to 3- O-methyl-6-[ 18F]fluoro- L-dopa formation {10} {11} {15} {27} {29}. The increased 18F-dopa bioavailability results in improved images.

Safety considerations for handling this radiopharmaceutical
Guidelines for the receipt, storage, handling, dispensing, and disposal of radioactive materials are available from scientific, professional, state, federal, and international bodies. Handling of this radiopharmaceutical should be limited to those individuals who are appropriately qualified and authorized. {02}

Parenteral Dosage Forms

Note: Because 18F-dopa is not commercially available in the U.S. or Canada, the bracketed information and the use of the superscript 1 in this monograph reflect the lack of labeled (approved) indications for this product.


Usual adult administered activity
[Brain imaging]1
Intravenous infusion, 74 to 370 megabecquerels (2 to 10 millicuries), with a specific activity of 20 to 40 megabecquerels (740 to 1480 millicuries) per micromole {08} {27} {28} {39}.

Usual pediatric administered activity
Children up to 18 years of age—Intravenous infusion, 37 megabecquerels (1 millicurie) {28}.

Usual geriatric administered activity
See Usual adult administered activity.

Strength(s) usually available
Prepared on-site at various clinical facilities.

Prepared on-site at various clinical facilities.

Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F) {01}. Unless otherwise specified by the supplier, it is prudent to avoid extreme temperatures {43}.

Stability of formulated 18F-dopa may depend on local production conditions {10}. Instability may be related to factors involved in the oxidation of levodopa, such as the degree of metal contamination, oxygen concentration, and pH {10}. Preparations of 18F-dopa have been shown to be stable at pH levels between 4 and 5 {10}.

Radioactive material.

Developed: 06/09/1999

  1. Stöcklin G, Pike VW, editors. Radiopharmaceuticals for positron emission tomography: methodological aspects. Boston: Kluwer Academic Publishers; 1993. p. 2, 138, 159, 160.
  1. Radiopharmaceuticals Advisory Panel Meeting, 4/96.
  1. Brown WD, Oakes TR, DeJesus OT, et al. Dosimetry for 18F-fluoro- L-DOPA with carbidopa pretreatment using the MIRD pamphlet 14 bladder model. In press.
  1. Radiopharmaceuticals Advisory Panel Meeting, 5/8/91.
  1. Radiopharmaceuticals Advisory Panel Meeting, 8/4/92.
  1. Adam MJ, Ruth TJ, Grierson JR, et al. Routine synthesis of L-[ 18F]6-fluorodopa with fluorine-18 acetyl hypofluorite. J Nucl Med 1986; 27: 1462-6.
  1. Firnau G, Garnett ES, Chirakal R, et al. [ 18F]Fluoro- L-DOPA for the in vivo study of intracerebral dopamine. Appl Radiat Isot 1986; 37: 669-75
  1. Leenders KL, Palmer AJ, Quinn N, et al. Brain dopamine metabolism in patients with Parkinson's disease measured with positron emission tomography. J Neurol Neurosurg Psychiatry 1986; 49: 853-60.
  1. Grant DB, Dunger DB, Smith I, et al. Familial glucocorticoid deficiency with achalasia of the cardia associated with mixed neuropathy, long-tract degeneration and mild dementia. Eur J Pediatr 1992 Feb; 151(2): 85-9.
  1. Luxen A, Guillaume M, Melega WP, et al. Production of 6-[ 18F]Fluoro- L-DOPA and its metabolism in vivo: a critical review. Nucl Med Biol 1992; 19(2): 149-58.
  1. Boyes BE, Cumming P, Martin WR, et al. Determination of plasma [ 18F]-6-fluorodopa during positron emission tomography: elimination and metabolism in carbidopa treated subjects. Life Sci 1986 Dec; 39(23): 2243-52.
  1. Chaly T, Diksic M. High yield synthesis of 6-[ 18F]fluoro- L-dopa by regioselective fluorination of protected L-dopa with [ 18F]acetylhypofluorite. J Nucl Med 1986 Dec; 27(12): 1896-1901.
  1. Chirakal R, Firnau G, Garnett ES. High yield synthesis of 6-[ 18F]fluoro- L-dopa. J Nucl Med 1986 Mar; 27(3): 417-21.
  1. Leenders KL, Poewe WH, Palmer AJ, et al. Inhibition of L-[ 18F]fluorodopa uptake into human brain by amino acids demonstrated by positron emission tomography. Ann Neurol 1986 Aug; 20(2): 258-62.
  1. Melega WP, Hoffman JM, Luxen A, et al. The effects of carbidopa on the metabolism of 6-[ 18F]fluoro-L-dopa in rats, monkeys and humans. Life Sci 1990; 47(2): 149-57.
  1. Leenders KL, Salmon EP, Tyrrell P, et al. The nigrostratial dopaminergic system assessed in vivo by positron emission tomography in healthy volunteer subjects and patients with Parkinson's disease. Arch Neurol 1990 Dec; 47(12): 1290-8.
  1. Sawle GV, Leenders KL, Brooks DJ, et al. Dopa-responsive dystonia: [ 18F]-dopa positron emission tomography. Ann Neurol 1991 Jul; 30(1): 24-30.
  1. Sawle GV, Playford ED, Burn DJ, et al. Separating Parkinson's disease from normality. Arch Neurol 1994 Mar; 51: 237-43.
  1. Garnett S, Firnau G, Nahmias C, et al. Striatal dopamine metabolism in living monkeys examined by positron emission tomography. Brain Res 1983 Nov; 280(1): 169-71.
  1. Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch Neurol 1995 Aug; 52(8): 802-10.
  1. Calne DB, Langston JW, Martin WR, et al. Positron emission tomography after MPTP: observations relating to the cause of Parkinson's disease. Nature 1985 Sep; 317(6034): 246-8.
  1. Rosenberg NL, Myers JA, Martin WR. Cyanide-induced parkinsonism: clinical, MRI, and 6-fluorodopa PET studies. Neurology 1989 Jan; 39(1): 142-4.
  1. Brooks DJ, Ibañez V, Sawle GV, et al. Differing patterns of striatal [ 18F]-dopa uptake in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy. Ann Neurol 1990 Oct; 28(4): 547-55.
  1. Snow BJ, Peppard RF, Guttman M, et al. Positron emission tomographic scanning demonstrates a presynaptic dopaminergic lesion in Lytico-Bodig. The amyotrophic lateral sclerosis-parkinsonism-dementia complex of Guam. Arch Neurol 1990 Aug; 47(8): 870-4.
  1. Sawle GV, Brooks DJ, Marsden CD, et al. Corticobasal degeneration. A unique pattern of regional cortical oxygen hypometabolism and striatal fluorodopa uptake demonstrated by positron emission tomography. Brain 1991 Feb; 114(Pt 1B): 541-56.
  1. Wszolek ZK, Pfeiffer RF, Bhatt MH, et al. Rapidly progressive autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration. Ann Neurol 1992 Sep; 32(3): 312-20.
  1. Heiss WD, Wienhard K, Wagner R, et al. F-Dopa as an amino acid tracer to detect brain tumors. J Nucl Med 1996 Jul; 37(7): 1180-2.
  1. Ernst M, Zametkin AJ, Matochik JA, et al. Presynaptic dopaminergic deficits in Lesch-Nyhan disease. N Engl J Med 1996 Jun 13; 334(24): 1568-72.
  1. Vingerhoets FJG, Schulzer M, Ruth TJ, et al. Reproducibility and discriminating ability of fluorine-18-6-fluoro-L-Dopa PET in Parkinson's disease. J Nucl Med 1996 Mar; 37(3): 421-6.
  1. Brooks DJ. Motor disturbance and brain functional imaging in Parkinson's disease. Eur Neurol 1997; 38(Suppl 2): 26-32.
  1. Brooks DJ. Advances in imaging Parkinson's disease. Curr Opin Neurol 1997 Aug; 10(4): 327-31.
  1. Guttman M, Burns RS, Martin WR, et al. PET studies of parkinsonian patients treated with autologous adrenal implants. Can J Neurol Sci 1989 Aug; 16(3): 305-9.
  1. Bhatt MH, Snow BJ, Martin WR, et al. Positron emission tomography suggests that the rate of progression of idiopathic parkinsonism is slow. Ann Neurol 1991 Jun; 29(6): 673-7.
  1. Laihinen A, Rinne JO, Rinne UK, et al. [ 18F]-6-fluorodopa PET scanning in Parkinson's disease after selective COMT inhibition with nitecapone (OR-462). Neurology 1992 Jan; 42(1): 199-203.
  1. Sawle GV, Bloomfield PM, Bjorklund A, et al. Transplantation of fetal dopamine neurons in Parkinson's disease: PET [ 18F]-6- L-fluorodopa studies in two patients with putaminal implants. Ann Neurol 1992 Feb; 31(2): 166-73.
  1. Widner H, Tetrud J, Rehncrona S, et al. Bilateral fetal mesencephalic grafting in two patients with parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. N Engl J Med 1992 Nov; 327(22): 1556-63.
  1. Sawle GV, Burn DJ, Morrish PK, et al. The effect of entacapone (OR-611) on brain [ 18F]-6- L-fluorodopa metabolism: implications for levodopa therapy of Parkinson's disease. Neurology 1994 Jul; 44(7): 1292-7.
  1. Vingerhoets FJ, Snow BJ, Lee CS, et al. Longitudinal fluorodopa positron emission tomographic studies of the evolution of idiopathic parkinsonism. Ann Neurol 1994 Nov; 36(5): 759-64.
  1. Holthoff-Detto VA, Kessler J, Herholz K, et al. Functional effects of striatal dysfunction in Parkinson disease. Arch Neurol 1997 Feb; 54(2): 145-50.
  1. Chirakal R, Firnau G, Couse J, et al. Radiofluorination with 18F-labelled acetyl hypofluorite: [ 18F]L-6-fluorodopa. Int J Appl Radiat Isot 1984; 35: 651-3.
  1. Firnau G, Chirakal R, Garnett ES. Aromatic radiofluorination with [ 18F] fluorine gas: 6-[ 18F]fluoro- L-dopa. J Nucl Med 1984; 25: 1228-33.
  1. Reviewers' comments per monograph revision of 9/15/98.
  1. Advisory Panel consensus per 10/28/98 meeting.