Clinical data | |
---|---|
Pronunciation | /səˈlɛdʒɪliːn/ sə-LEJ-i-leen |
Trade names | Eldepryl, Jumex, Zelapar, Emsam, others [1] |
Other names | L-Deprenyl; (R)-(–)-N,α-Dimethyl-N-2-propynylphenethylamine; (R)-(–)-N-Methyl-N-2-propynylamphetamine; (R)-(–)-N-2-propynylmethamphetamine |
AHFS/Drugs.com | Monograph |
MedlinePlus | a697046 |
License data |
|
Pregnancy category |
|
Routes of administration | By mouth, transdermal (patch) |
ATC code | |
Legal status | |
Legal status | |
Pharmacokinetic data | |
Bioavailability | 10% (oral), 73% (patch) |
Protein binding | 94% |
Metabolism | Intestines and liver |
Metabolites | N-Desmethylselegiline, levoamphetamine, levomethamphetamine |
Elimination half-life | 1.5–3.5 hours (oral), [3] 18–25 hours (transdermal) [4] |
Excretion | Urine |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
CompTox Dashboard (EPA) | |
ECHA InfoCard | 100.109.269 |
Chemical and physical data | |
Formula | C13H17N |
Molar mass | 187.286 g·mol−1 |
3D model (JSmol) | |
| |
| |
(verify) |
Selegiline, also known as L-deprenyl and sold under the brand names Eldepryl, Emsam, Selgin, among other names, is a medication which is used in the treatment of Parkinson's disease and major depressive disorder. [1] It is provided in the form of a capsule or tablet taken by mouth or orally disintegrating tablets taken on the tongue for Parkinson's disease and as a patch applied to skin for depression.
Selegiline acts as a monoamine oxidase inhibitor, and increases levels of monoamine neurotransmitters in the brain. At typical clinical doses used for Parkinson's disease, selegiline is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B), increasing levels of dopamine in the brain. In larger doses (more than 20 mg/day), it loses its specificity for MAO-B and also inhibits MAO-A, which increases serotonin and norepinephrine levels in the brain.
In its pill form, selegiline is used to treat symptoms of Parkinson's disease. [5] It is most often used as an adjunct to drugs such as levodopa (L-DOPA), although it has been used off-label as a monotherapy. [6] [7] The rationale for adding selegiline to levodopa is to decrease the required dose of levodopa and thus reduce the motor complications of levodopa therapy. [8] Selegiline delays the point when levodopa treatment becomes necessary from about 11 months to about 18 months after diagnosis. [9] There is some evidence that selegiline acts as a neuroprotectant and reduces the rate of disease progression, though this is disputed. [7] [8]
Selegiline has also been used off-label as a palliative treatment for dementia in Alzheimer's disease. [7]
Selegiline is also delivered via a transdermal patch used as a treatment for major depressive disorder. [10] [11] Administration of transdermal selegiline bypasses hepatic first pass metabolism. This avoids inhibition of gastrointestinal and hepatic MAO-A activity, which would result in an increase of food-borne tyramine in the blood and possible related adverse effects, while allowing for a sufficient amount of selegiline to reach the brain for an antidepressant effect. [12]
A quantitative review published in 2015 found that for the pooled results of the pivotal trials, the number needed to treat (a sign of effect size, so a low number is better) for the patch for symptom reduction was 11, and for remission, was 9. [11] The number needed to harm (inverse of the NNT, a high number here is better) ranged from 387 for sexual side effects to 7 for application site reaction. [11] With regard to the likelihood to be helped or harmed (LHH), the analysis showed that the selegiline patch was 3.6 times as likely to lead to a remission vs. a discontinuation due to side effects; the LHH for remission vs. incidence of insomnia was 2.1; the LHH for remission vs. discontinuation due to insomnia was 32.7. The LHH for remission vs. insomnia and sexual dysfunction were both very low. [11]
For all human uses and all forms, selegiline is pregnancy category C: studies in pregnant lab animals have shown adverse effects on the fetus but there are no adequate studies in humans. [5] [10]
Side effects of the tablet form in conjunction with levodopa include, in decreasing order of frequency, nausea, hallucinations, confusion, depression, loss of balance, insomnia, increased involuntary movements, agitation, slow or irregular heart rate, delusions, hypertension, new or increased angina pectoris, and syncope. [5] Most of the side effects are due to a high dopamine signaling, and can be alleviated by reducing the dose of levodopa. [1]
The main side effects of the patch form for depression include application-site reactions, insomnia, diarrhea, and sore throat. [10] The selegiline patch carries a black box warning about a possible increased risk of suicide, especially for young people, [10] as do all antidepressants since 2007. [13]
Both the oral and patch forms come with strong warnings against combining selegiline with drugs that could produce serotonin syndrome, such as SSRIs and the cough medicine dextromethorphan. [5] [10] [14] Selegiline in combination with the opioid analgesic pethidine is not recommended, as it can lead to severe adverse effects. [14] Several other synthetic opioids such as tramadol and methadone, as well as various triptans, are contraindicated due to potential for serotonin syndrome. [15] [16]
Birth control pills containing ethinylestradiol and a progestin increase the bioavailability of selegiline by 10- to 20-fold. [17] High levels can lead to loss of MAO-B selectivity, and selegiline may begin inhibiting MAO-A as well. This increases susceptibility to side effects of non-selective MAOIs, such as tyramine-induced hypertensive crisis and serotonin toxicity when combined with serotonergic medications. [17]
Both forms of the drug carry warnings about food restrictions to avoid hypertensive crisis that are associated with MAO inhibitors. [5] [10] The patch form was created in part to overcome food restrictions; clinical trials showed that it was successful. Additionally, in post-marketing surveillance from April 2006 to October 2010, only 13 self-reports of possible hypertensive events or hypertension were made out of 29,141 exposures to the drug, and none were accompanied by objective clinical data. [11] The lowest dose of the patch method of delivery, 6 mg/24 hours, does not require any dietary restrictions. [18] Higher doses of the patch and oral formulations, whether in combination with the older non-selective MAOIs or in combination with the reversible MAO-A inhibitor moclobemide, require a low-tyramine diet. [14]
Selegiline is a selective inhibitor of MAO-B, irreversibly inhibiting it by binding to it covalently. [1] [19] It is generally believed to exert its effects by blocking the breakdown of dopamine, thus increasing its activity; [20] however, recent evidence suggests that MAO-A is solely or almost entirely responsible for the metabolism of dopamine. [21] Its possible neuroprotective properties may be due to protecting nearby neurons from the free oxygen radicals that are released by MAO-B activity. At higher doses, selegiline loses its selectivity for MAO-B and inhibits MAO-A as well. [1]
Selegiline potentiates the release of catecholamines independent of its MAO-B inhibiting action. As such, it has been called the "first synthetic catecholaminergic activity enhancer substance". [22] [23]
Selegiline also inhibits CYP2A6 and can increase the effects of nicotine as a result. [24] Selegiline also appears to activate σ1 receptors, having a relatively high affinity for these receptors of approximately 400 nM. [25] [26]
Selegiline has an oral bioavailability of about 10%, which increases when ingested together with a fatty meal, as the molecule is fat soluble. [1] [27] Selegiline and its metabolites bind extensively to plasma proteins (at a rate of 94%). They cross the blood–brain barrier and enter the brain, where they most concentrated at the thalamus, basal ganglia, midbrain, and cingulate gyrus. [7] [10]
Selegiline is mostly metabolized in the intestines and liver; it and its metabolites are excreted in the urine. [1]
Buccal administration of selegiline results in 5-fold higher bioavailability, more reproducible blood concentration, and produces fewer amphetamine metabolites than the oral tablet form. [28]
Selegiline is metabolized by cytochrome P450 to L-desmethylselegiline and levomethamphetamine. [29] [30] Desmethylselegiline has some activity against MAO-B, but much less than that of selegiline. [20] [19] It is thought to be further metabolized by CYP2C19. [31] Levomethamphetamine (the less potent of the two enantiomers of methamphetamine) is converted to levoamphetamine (the less potent of the two enantiomers of amphetamine, with regards to psychological effects).
Due to the presence of these metabolites, people taking selegiline may test positive for "amphetamine" or "methamphetamine" on drug screening tests. [32] While the amphetamine metabolites may contribute to selegiline's ability to inhibit reuptake of the neurotransmitters dopamine and norepinephrine, they have also been associated with orthostatic hypotension and hallucinations. [30] [33] [34] The recovery of selegiline from urine is high at 87%, which has caused some researchers to question the clinical relevance of its amphetamine metabolites. [35] The amphetamine metabolites are hydroxylated and, in phase II, conjugated by glucuronyltransferase.
A newer anti-Parkinson MAO-B inhibitor, rasagiline, metabolizes into 1(R)-aminoindan, which has no amphetamine-like characteristics. [36]
Following application of the patch to humans, an average of 25% to 30% of the selegiline content is delivered systemically over 24 hours. Transdermal dosing results in significantly higher exposure to selegiline and lower exposure to all metabolites when compared to oral dosing; this is due to the extensive first-pass metabolism of the pill form and low first-pass metabolism of the patch form. The site of application is not a significant factor in how the drug is distributed. In humans, selegiline does not accumulate in the skin, nor is it metabolized there. [10]
Selegiline belongs to the phenethylamine and amphetamine chemical families. It is also known as L-deprenyl, as well as (R)-(–)-N,α-dimethyl-N-(2-propynyl)phenethylamine or (R)-(–)-N-methyl-N-2-propynylamphetamine. The compound is a derivative of levomethamphetamine (L-methamphetamine) with a propargyl group attached to the nitrogen atom. This detail is borrowed from pargyline, an older MAO-B inhibitor of the phenylalkylamine group. [22] Selegiline is the levorotatory enantiomer of the racemic mixture deprenyl.
Selegiline is synthesized by the alkylation of (–)-methamphetamine using propargyl bromide. [37] [38] [39] [40]
Another clinically used MAOI of the amphetamine class is tranylcypromine.
Following the discovery in 1952 that the tuberculosis drug iproniazid elevated the mood of people taking it, and the subsequent discovery that the effect was likely due to inhibition of MAO, many people and companies started trying to discover MAO inhibitors to use as antidepressants. Selegiline was discovered by Zoltan Ecseri at the Hungarian drug company, Chinoin (part of Sanofi since 1993), [41] which they called E-250. [42] : 66–67 Chinoin received a patent on the drug in 1962 and the compound was first published in the scientific literature in English in 1965. [42] : 67 [43] Work on the biology and effects of E-250 in animals and humans was conducted by a group led by József Knoll at Semmelweis University which was also in Budapest. [42] : 67
Deprenyl is a racemic compound (a mixture of two isomers called enantiomers). Further work determined that the levorotatory enantiomer was a more potent MAO-inhibitor, which was published in 1967, and subsequent work was done with the single enantiomer L-deprenyl. [42] : 67 [44] [45]
In 1971, Knoll showed that selegiline selectively inhibits the B-isoform of monoamine oxidase (MAO-B) and proposed that it is unlikely to cause the infamous "cheese effect" (hypertensive crisis resulting from consuming foods containing tyramine) that occurs with non-selective MAO inhibitors. A few years later, two Parkinson's disease researchers based in Vienna, Peter Riederer and Walther Birkmayer, realized that selegiline could be useful in Parkinson's disease. One of their colleagues, Prof. Moussa B.H. Youdim, visited Knoll in Budapest and took selegiline from him to Vienna. In 1975, Birkmayer's group published the first paper on the effect of selegiline in Parkinson's disease. [45] [46]
In the 1970s there was speculation that it could be useful as an anti-aging drug or aphrodisiac. [47]
In 1987 Somerset Pharmaceuticals in New Jersey, which had acquired the US rights to develop selegiline, filed a new drug application (NDA) with the FDA to market the drug for Parkinson's disease in the US. [48] While the NDA was under review, Somerset was acquired in a joint venture by two generic drug companies, Mylan and Bolan Pharmaceuticals. [48] Selegiline was approved for Parkinson's disease by the FDA in 1989. [48]
In the 1990s, J. Alexander Bodkin at McLean Hospital, an affiliate of Harvard Medical School, began a collaboration with Somerset to develop delivery of selegiline via a transdermal patch in order to avoid the well known dietary restrictions of MAO inhibitors. [47] [49] [50] Somerset obtained FDA approval to market the patch in 2006. [51]
Joseph Knoll and his team are credited with having developed selegiline. Although selegeline's development as a potential treatment for Parkinson's, Alzheimer's, and major depressive disorder was headed by other teams, Knoll remained at the forefront of research into the potential longevity enhancing effects of selegiline up until his death in 2018. [52] [53] [54] Knoll published How Selegiline ((-)-Deprenyl) Slows Brain Aging (2018) wherein he claims that:
"In humans, maintenance from sexual maturity on (-)-deprenyl (1mg daily) is, for the time being, the most promising prophylactic treatment to fight against the age related decay of behavioral performances, prolonging life, and preventing or delaying the onset of age-related neurodegenerative diseases such as Parkinson's and Alzheimer's". [55]
The mechanism of selegiline's longevity-promoting effect has been researched by several groups, including Joseph Knoll and his associates at Semmelweis University, Budapest. [56] The drug has been determined to be a catecholaminergic activity enhancer when present in minuscule concentrations far below those at which monoamine oxidase inhibitory activity can be observed, thereby potentiating the release of catecholamine neurotransmitters in response to stimuli. Knoll maintains that micro-doses of selegiline act as a synthetic analogue to a known or unknown trace amine in order to preserve the brain catecholaminergic system, which he perceives as integral to the organism's ability to function in an adaptive, goal-directed and motivated manner during advancing physical age:
" ... enhancer regulation in the catecholaminergic brain stem neurons play[s] a key role in controlling the uphill period of life and the transition from adolescence to adulthood. The results of our longevity studies support the hypothesis that quality and duration of life rests upon the inborn efficiency of the catcholaminergic brain machinery, i.e. a high performing, long-living individual has a more active, more slowly deteriorating catecholaminergic system than its low performing, shorter living peer. Thus, a better brain engine allows for a better performance and a longer lifespan.
...
Since the catecholaminergic and serotonergic neurons in the brain stem are of key importance in ensuring that the mammalian organism works as a purposeful, motivated, goal-directed entity, it is hard to overestimate the significance of finding safe and efficient means to slow the decay of these systems with passing time. The conclusion that the maintenance on (-)-deprenyl that keeps the catecholaminergic neurnsn a higher activity level is a safe and efficient anti- aging therapy follows from the discovery of the enhancer regulation in the catecholaminergic neurons of the brain stem. From the finding that this regulation starts working on a high activity level after weaning and the enhanced activity subsists during the uphill period of life, until sexual hormones dampen the enhancer regulation in the catecholaminergic and serotonergic neurons in the brain stem, and this event signifies the transition from developmental longevity into postdevelopmental longevity, the downhill period of life." [55]
Selegiline is considered by some to be a nootropic, [57] both at clinical and sub-clinical dosages, and has been used off-label to improve cognitive performance. It has been shown to have protective activity against a range of neurotoxins and to increase the production of several brain growth factors, such as nerve growth factor, brain-derived neurotrophic factor, and glial cell-derived neurotrophic factor. [56] It has been demonstrated in numerous animal models to improve learning ability and preserve it during both ischemia and aging. [58] [59] [60] [61]
In E for Ecstasy (a book examining the uses of the street drug ecstasy in the UK) the writer, activist and ecstasy advocate Nicholas Saunders highlighted test results showing that certain consignments of the drug also contained selegiline. [62] Consignments of ecstasy known as "Strawberry" contained what Saunders described as a "potentially dangerous combination of ketamine, ephedrine and selegiline," as did a consignment of "Sitting Duck" Ecstasy tablets. [63]
David Pearce wrote The Hedonistic Imperative [64] six weeks after starting taking selegiline. [65]
In Gregg Hurwitz's novel Out of the Dark, [66] selegiline (Emsam) and tyramine-containing food were used to assassinate the president of the United States.
In veterinary medicine, selegiline is sold under the brand name Anipryl (manufactured by Zoetis). It is used in dogs to treat canine cognitive dysfunction and, at higher doses, pituitary-dependent hyperadrenocorticism (PDH). [67] [68] Canine cognitive dysfunction is a form of dementia that mimics Alzheimer's disease in humans. Geriatric dogs treated with selegiline show improvements in sleeping pattern, reduced incontinence, and increased activity level; most show improvements by one month. [69] [70] Though it is labeled for dog use only, selegiline has been used off-label for geriatric cats with cognitive dysfunction. [71]
Selegiline's efficacy in treating pituitary-dependent hyperadrenocorticism has been disputed. [67] Theoretically, it works by increasing dopamine levels, which downregulates the release of ACTH, eventually leading to reduced levels of cortisol. [71] Some claim that selegiline is only effective at treating PDH caused by lesions in the anterior pituitary (which comprise most canine cases). [72] The greatest sign of improvement is lessening of abdominal distention. [69]
Side effects in dogs are uncommon, but they include vomiting, diarrhea, diminished hearing, salivation, decreased weight and behavioral changes such as hyperactivity, listlessness, disorientation, and repetitive motions. [68] [72]
Selegiline does not appear to have a clinical effect on horses. [72]
Selegiline has been limitedly studied in the treatment of attention deficit hyperactivity disorder (ADHD) in both children/adolescents and adults. [73] [74] In a small randomized trial of selegiline for treatment of ADHD in children, there were improvements in attention, hyperactivity, and learning/memory performance but not in impulsivity. [75] A small clinical randomized trial compared selegiline to methylphenidate, a first line treatment for ADHD, and reported equivalent efficacy as assessed by parent and teacher ratings. [76] In another small randomized controlled trial of selegiline for the treatment of adult ADHD, a high dose of the medication for 6 weeks was not significantly more effective than placebo in improving symptoms. [74] [77] [78]
Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit the activity of one or both monoamine oxidase enzymes: monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). They are best known as effective antidepressants, especially for treatment-resistant depression and atypical depression. They are also used to treat panic disorder, social anxiety disorder, Parkinson's disease, and several other disorders.
Phenelzine, sold under the brand name Nardil, among others, is a non-selective and irreversible monoamine oxidase inhibitor (MAOI) of the hydrazine class which is primarily used as an antidepressant and anxiolytic. Along with tranylcypromine and isocarboxazid, phenelzine is one of the few non-selective and irreversible MAOIs still in widespread clinical use.
Phenethylamine (PEA) is an organic compound, natural monoamine alkaloid, and trace amine, which acts as a central nervous system stimulant in humans. In the brain, phenethylamine regulates monoamine neurotransmission by binding to trace amine-associated receptor 1 (TAAR1) and inhibiting vesicular monoamine transporter 2 (VMAT2) in monoamine neurons. To a lesser extent, it also acts as a neurotransmitter in the human central nervous system. In mammals, phenethylamine is produced from the amino acid L-phenylalanine by the enzyme aromatic L-amino acid decarboxylase via enzymatic decarboxylation. In addition to its presence in mammals, phenethylamine is found in many other organisms and foods, such as chocolate, especially after microbial fermentation.
Tranylcypromine, sold under the brand name Parnate among others, is a monoamine oxidase inhibitor (MAOI). More specifically, tranylcypromine acts as nonselective and irreversible inhibitor of the enzyme monoamine oxidase (MAO). It is used as an antidepressant and anxiolytic agent in the clinical treatment of mood and anxiety disorders, respectively.
Dopaminergic means "related to dopamine" (literally, "working on dopamine"), dopamine being a common neurotransmitter. Dopaminergic substances or actions increase dopamine-related activity in the brain. Dopaminergic brain pathways facilitate dopamine-related activity. For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT2), and dopamine receptors can be classified as dopaminergic, and neurons that synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes that regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase or DOPA decarboxylase, monoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Also, any endogenous or exogenous chemical substance that acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids, which enhance dopamine release indirectly in the reward pathways, and some substituted amphetamines, which enhance dopamine release directly by binding to and inhibiting VMAT2.
Moclobemide, sold under the brand names Amira, Aurorix, Clobemix, Depnil and Manerix among others, is a reversible inhibitor of monoamine oxidase A (RIMA) drug primarily used to treat depression and social anxiety. It is not approved for use in the United States, but is approved in other Western countries such as Canada, the UK and Australia. It is produced by affiliates of the Hoffmann–La Roche pharmaceutical company. Initially, Aurorix was also marketed by Roche in South Africa, but was withdrawn after its patent rights expired and Cipla Medpro's Depnil and Pharma Dynamic's Clorix became available at half the cost.
Levomethamphetamine is the levorotatory (L-enantiomer) form of methamphetamine. Levomethamphetamine is a sympathomimetic vasoconstrictor that is the active ingredient in some over-the-counter (OTC) nasal decongestant inhalers in the United States.
Omigapil is a drug that was developed by Novartis and tested in clinical trials for its ability to help treat Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). The development for PD and ALS have been terminated due to lack of benefit, but Santhera Pharmaceuticals bought the compound for development for the treatment of congenital muscular dystrophy (CMD).
Trace amines are an endogenous group of trace amine-associated receptor 1 (TAAR1) agonists – and hence, monoaminergic neuromodulators – that are structurally and metabolically related to classical monoamine neurotransmitters. Compared to the classical monoamines, they are present in trace concentrations. They are distributed heterogeneously throughout the mammalian brain and peripheral nervous tissues and exhibit high rates of metabolism. Although they can be synthesized within parent monoamine neurotransmitter systems, there is evidence that suggests that some of them may comprise their own independent neurotransmitter systems.
Rasagiline is an irreversible inhibitor of monoamine oxidase-B used as a monotherapy to treat symptoms in early Parkinson's disease or as an adjunct therapy in more advanced cases.
Benzofuranylpropylaminopentane is a drug with an unusual monoamine-release potentiating mechanism of action. It can loosely be grouped with the stimulant or antidepressant drug families, but its mechanism of action is quite different.
(-)-1-Phenyl-2-propylaminopentane is a stimulant of the substituted phenethylamine class that has been derived from selegiline. When compared with selegiline and other substituted phenethylamines (-)-PPAP has a notably different mechanism of action and pharmacological effect.
Monoamine oxidase B, also known as MAO-B, is an enzyme that in humans is encoded by the MAOB gene.
Safinamide is a drug used as an add-on treatment for Parkinson's disease with "off" episodes; it has multiple modes of action, including the inhibition of monoamine oxidase B.
d-Deprenyl, also known as or dextro-N-propargyl-N-methylamphetamine, is an MAO-B inhibitor that metabolizes into d-amphetamine and d-methamphetamine and is therefore also a norepinephrine–dopamine releasing agent. It is the opposite enantiomer of l-deprenyl (selegiline).
Mofegiline (MDL-72,974) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) and semicarbazide-sensitive amine oxidase (SSAO) which was under investigation for the treatment of Parkinson's disease and Alzheimer's disease, but was never marketed.
Moussa B. H. Youdim is an internationally renowned Israeli neuroscientist specializing in neurochemistry and neuropharmacology. He is the discoverer of both monoamine oxidase (MAO) B inhibitors l-deprenyl (Selegiline) and rasagiline (Azilect) as anti-Parkinson drugs which possess neuroprotective activities. He is currently professor emeritus at Technion - Faculty of Medicine and President of Youdim Pharmaceuticals.
Opicapone, sold under the brand name Ongentys, is a medication which is administered together with levodopa in people with Parkinson's disease. Opicapone is a catechol-O-methyltransferase (COMT) inhibitor.
Monoamine activity enhancers (MAE), also known as catecholaminergic/serotoninergic activity enhancers, are a class neuro-biologically active compounds that enhance the release of monoamines in the nervous system. Monoamine activity enhancers are distinct from monoamine releasing agents in that they do not cause the release of monoamines from synaptic vesicles but rather potentiate impulse-evoked monoamine-release. Monoamine activity enhancers increase the number of monoamines released per electrical impulse received.
4-Fluoroselegiline or p-fluoro-L-deprenyl is a substituted amphetamine designer drug. Much like its parent compount, selegiline, it is a selective and irreversible inhibitor of monoamine oxidase B.
{{cite journal}}
: CS1 maint: DOI inactive as of April 2024 (link){{cite book}}
: |journal=
ignored (help)