Amineptine

Last updated

Amineptine
Amineptine.svg
Clinical data
Trade names Survector, others
Other namesS-1694
Routes of
administration 		Oral
ATC code
Legal status
Legal status
Pharmacokinetic data
Metabolism Hepatic
Elimination half-life Amineptine: 0.8–1.0 hours [2] [3]
Metabolite: 1.5–2.5 hours [2] [3]
Excretion Renal
Identifiers
  • 7-[(10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5-yl)amino]heptanoic acid
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.055.271 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C22H28NO2
Molar mass 338.471 g·mol−1
3D model (JSmol)
  • O=C(O)CCCCCCNC1c2ccccc2CCc2ccccc21
  • InChI=1S/C22H27NO2/c24-21(25)13-3-1-2-8-16-23-22-19-11-6-4-9-17(19)14-15-18-10-5-7-12-20(18)22/h4-7,9-12,22-23H,1-3,8,13-16H2,(H,24,25) Yes check.svgY
  • Key:ONNOFKFOZAJDHT-UHFFFAOYSA-N Yes check.svgY
   (verify)

Amineptine, formerly sold under the brand name Survector among others, is an atypical antidepressant of the tricyclic antidepressant (TCA) family. [4] [5] It acts as a selective and mixed dopamine reuptake inhibitor and releasing agent, and to a lesser extent as a norepinephrine reuptake inhibitor. [4] [5]

Contents

Amineptine was developed by the French Society of Medical research in the 1960s. [6] Introduced in France in 1978 by the pharmaceutical company Servier, [7] amineptine soon gained a reputation for abuse due to its short-lived, but pleasant, stimulant effect experienced by some patients.

After its release into the European market, cases of hepatotoxicity emerged, some serious. This, along with the potential for abuse, led to the suspension of the French marketing authorization for Survector in 1999. [8]

Amineptine is illegal in both Germany and the United States.

Medical uses

Amineptine was approved in France for severe clinical depression of endogenous origin in 1978. [9]

Contraindications

Precautions for use

Warnings and precautions before taking amineptine: [10]

Effects on the fetus

Side effects

Dermatological

Severe acne due to amineptine was first reported in 1988 by various authors—Grupper, Thioly-Bensoussan, Vexiau, Fiet, Puissant, Gourmel, Teillac, Levigne, to name a few—simultaneously [11] [12] [13] [14] [15] in the same issue of Annales de Dermatologie et de Vénéréologie and in the 12 March 1988 issue of The Lancet. [16] A year later, Dr Martin-Ortega and colleagues in Barcelona, Spain reported a case of "acneiform eruption" in a 54-year-old woman whose intake of amineptine was described as "excessive." [17] One year after that, Vexiau and colleagues reported six women, one of whom never admitted to using amineptine, getting severe acne concentrated in the face, back and thorax, the severity of which varied with the dosage. [18] Most of them were treated unsuccessfully with isotretinoin (Accutane) for about 18 months; two of the three that discontinued amineptine experienced a reduction in cutaneous symptoms, with the least affected patient going into remission. [18]

Psychiatric

Psychomotor excitation can very rarely occur with this drug.

Abuse and dependence

The risk of addiction is low, but exists nonetheless. Between 1978 and 1988, there were 186 cases of amineptine addiction reported to the French Regional Centres of Pharmacovigilance; an analysis of 155 of those cases found that they were predominantly female, and that two-thirds of cases had known risk factors for addiction. [19] However, a 1981 study of known opiate addicts and schizophrenia patients found no drug addiction in any of the subjects. [20] In a 1990 study of eight amineptine dependence cases, the gradual withdrawal of amineptine could be achieved without problems in six people; in two others, anxiety, psychomotor agitation, and/or bulimia appeared. [21]

Withdrawal

Pharmacodependence is very common with amineptine compared to other antidepressants. [22] A variety of psychological symptoms can occur during withdrawal from amineptine, [23] such as anxiety and agitation. [24]

Cardiovascular

Very rarely:

Hepatic

Amineptine can rarely cause hepatitis, of the cytolytic, cholestatic varieties. [25] Amineptine-induced hepatitis, which is sometimes preceded by a rash, is believed to be due to an immunoallergic reaction. [26] It resolves upon discontinuation of the offending drug. [25] The risk of getting this may or may not be genetically determined. [27]

Additionally, amineptine is known to rarely elevate transaminases, alkaline phosphatase, and bilirubin. [28]

Mixed hepatitis, which is very rare, generally occurs between the 15th and 30th day of treatment of amineptine. Often preceded by sometimes intense abdominal pains, nausea, vomiting or a rash, the jaundice is variable. Hepatitis is either of mixed type or with cholestatic prevalence. The evolution was, in all the cases, favorable to the discontinuation of the drug. The mechanism is discussed (immunoallergic and/or toxic). [29]

In circa 1994 Spain, there was a case associating acute pancreatitis and mixed hepatitis, after three weeks of treatment. [30]

Lazaros and colleagues at the Western Attica General Hospital in Athens, Greece reported two cases of drug induced hepatitis 18 and 15 days of treatment. [31]

One case of cytolytic hepatitis occurred after ingestion of only one tablet. [32]

Gastrointestinal

Immunological

A case of anaphylactic shock in a woman who had been taking amineptine has been reported. [33]

Pharmacology

Pharmacodynamics

Amineptine [34]
SiteKi (nM)SpeciesRef
SERT Tooltip Serotonin transporter>100,000 (IC50)Rat [35]
NET Tooltip Norepinephrine transporter10,000 (IC50)
3,560		Rat
Canine		 [35] [36]
[37]
DAT Tooltip Dopamine transporter1,000–1,400 (IC50)
3,330		Rat
Canine		 [35] [38] [36]
[37]
5-HT1A >100,000Rat [39]
5-HT2A 74,000Rat [39]
α1 >100,000Rat [39]
α2 >100,000Rat [39]
β >100,000Rat [39]
D1 >100,000Canine [35]
D2 >100,000Rat/canine [35] [39]
H1 >100,000
13,000		Rat
Guinea pig		 [39]
[40]
mACh Tooltip Muscarinic acetylcholine receptor>100,000Rat [39]
Values are Ki (nM), unless otherwise noted. The smaller the value, the more strongly the drug binds to the site.

Amineptine inhibits the reuptake of dopamine and, to a much lesser extent, of norepinephrine. [36] [35] [41] In addition, it has been found to induce the release of dopamine. [36] [35] [41] However, amineptine is much less efficacious as a dopamine releasing agent relative to D-amphetamine, and the drug appears to act predominantly as a dopamine reuptake inhibitor. [36] [35] [41] In contrast to the case for dopamine, amineptine does not induce the release of norepinephrine, and hence acts purely as a norepinephrine reuptake inhibitor. [36] [35] [41] Unlike other TCAs, amineptine interacts very weakly or not at all with the serotonin, adrenergic, dopamine, histamine, and muscarinic acetylcholine receptors. [39] [40] [41] The major metabolites of amineptine have similar activity to that of the parent compound, albeit with lower potency. [41]

No human data appear to be available for binding or inhibition of the monoamine transporters by amineptine. [42]

Pharmacokinetics

Peak plasma levels of amineptine following a single 100 mg oral dose have been found to range between 277 and 2,215 ng/mL (818–6,544 nM), with a mean of 772 ng/mL (2,281 nM), whereas maximal plasma concentrations of its major metabolite ranged between 144 and 1,068 ng/mL (465–3,452 nM), with a mean of 471 ng/mL (1,522 nM). [2] After a single 200 mg oral dose of amineptine, mean peak plasma levels of amineptine were around 750 to 940 ng/mL (2,216–2,777 nM), while those of its major metabolite were about 750 to 970 ng/mL (2,216–3,135 nM). [3] The time to peak concentrations is about 1 hour for amineptine and 1.5 hours for its major metabolite. [2] [3] The elimination half-life of amineptine is about 0.80 to 1.0 hours and that of its major metabolite is about 1.5 to 2.5 hours. [2] [3] Due to their very short elimination half-lives, amineptine and its major metabolite do not accumulate significantly with repeated administration. [2]

Society and culture

Brand names

Amineptine has been sold under a variety of brand names including Survector, Maneon, Directim, Neolior, Provector, and Viaspera.

It had been proposed that Amineptine become a Schedule I controlled substance in the United States in July 2021. [43] This announcement was followed by the placement of Amineptine into Schedule I. [44]

Research

Wakefulness

Amineptine shows wakefulness-promoting effects in animals and might be useful in the treatment of narcolepsy. [45] [46] [47] [48]

Related Research Articles

<span class="mw-page-title-main">Tricyclic antidepressant</span> Class of medications

Tricyclic antidepressants (TCAs) are a class of medications that are used primarily as antidepressants. TCAs were discovered in the early 1950s and were marketed later in the decade. They are named after their chemical structure, which contains three rings of atoms. Tetracyclic antidepressants (TeCAs), which contain four rings of atoms, are a closely related group of antidepressant compounds.

<span class="mw-page-title-main">Bupropion</span> Medication mainly used for depression and smoking cessation

Bupropion, formerly called amfebutamone, and sold under the brand name Wellbutrin among others, is an atypical antidepressant primarily used to treat major depressive disorder and to support smoking cessation. It is also popular as an add-on medication in the cases of "incomplete response" to the first-line selective serotonin reuptake inhibitor (SSRI) antidepressant. Bupropion has several features that distinguish it from other antidepressants: it does not usually cause sexual dysfunction, it is not associated with weight gain and sleepiness, and it is more effective than SSRIs at improving symptoms of hypersomnia and fatigue. Bupropion, particularly the immediate release formulation, carries a higher risk of seizure than many other antidepressants, hence caution is recommended in patients with a history of seizure disorder. The medication is taken by mouth.

<span class="mw-page-title-main">Serotonin–norepinephrine reuptake inhibitor</span> Class of antidepressant medication

Serotonin–norepinephrine reuptake inhibitors (SNRIs) are a class of antidepressant medications used to treat major depressive disorder (MDD), anxiety disorders, social phobia, chronic neuropathic pain, fibromyalgia syndrome (FMS), and menopausal symptoms. Off-label uses include treatments for attention-deficit hyperactivity disorder (ADHD), obsessive–compulsive disorder (OCD), and migraine prevention. SNRIs are monoamine reuptake inhibitors; specifically, they inhibit the reuptake of serotonin and norepinephrine. These neurotransmitters are thought to play an important role in mood regulation. SNRIs can be contrasted with the selective serotonin reuptake inhibitors (SSRIs) and norepinephrine reuptake inhibitors (NRIs), which act upon single neurotransmitters.

A dopamine reuptake inhibitor (DRI) is a class of drug which acts as a reuptake inhibitor of the monoamine neurotransmitter dopamine by blocking the action of the dopamine transporter (DAT). Reuptake inhibition is achieved when extracellular dopamine not absorbed by the postsynaptic neuron is blocked from re-entering the presynaptic neuron. This results in increased extracellular concentrations of dopamine and increase in dopaminergic neurotransmission.

<span class="mw-page-title-main">Amoxapine</span> Tricyclic antidepressant medication

Amoxapine, sold under the brand name Asendin among others, is a tricyclic antidepressant (TCA). It is the N-demethylated metabolite of loxapine. Amoxapine first received marketing approval in the United States in 1980, approximately 10 to 20 years after most of the other TCAs were introduced in the United States.

<span class="mw-page-title-main">Imipramine</span> Antidepressant

Imipramine, sold under the brand name Tofranil, among others, is a tricyclic antidepressant (TCA) mainly used in the treatment of depression. It is also effective in treating anxiety and panic disorder. Imipramine is taken by mouth.

<span class="mw-page-title-main">Cocaethylene</span> Chemical compound

Cocaethylene (ethylbenzoylecgonine) is the ethyl ester of benzoylecgonine. It is structurally similar to cocaine, which is the methyl ester of benzoylecgonine. Cocaethylene is formed by the liver when cocaine and ethanol coexist in the blood. In 1885, cocaethylene was first synthesized, and in 1979, cocaethylene's side effects were discovered.

<span class="mw-page-title-main">Viloxazine</span> Medication used to treat ADHD

Viloxazine, sold under the brand name Qelbree among others, is a selective norepinephrine reuptake inhibitor medication which is used in the treatment of attention deficit hyperactivity disorder (ADHD) in children and adults. It was marketed for almost 30 years as an antidepressant for the treatment of depression before being discontinued and subsequently repurposed as a treatment for ADHD. Viloxazine is taken orally. It was used as an antidepressant in an immediate-release form and is used in ADHD in an extended-release form, latterly with comparable effectiveness to atomoxetine and methylphenidate.

<span class="mw-page-title-main">Trimipramine</span> Antidepressant

Trimipramine, sold under the brand name Surmontil among others, is a tricyclic antidepressant (TCA) which is used to treat depression. It has also been used for its sedative, anxiolytic, and weak antipsychotic effects in the treatment of insomnia, anxiety disorders, and psychosis, respectively. The drug is described as an atypical or "second-generation" TCA because, unlike other TCAs, it seems to be a fairly weak monoamine reuptake inhibitor. Similarly to other TCAs, however, trimipramine does have antihistamine, antiserotonergic, antiadrenergic, antidopaminergic, and anticholinergic activities.

<span class="mw-page-title-main">Nomifensine</span> Group of stereoisomers

Nomifensine, sold under the brand names Merital and Alival, is a norepinephrine–dopamine reuptake inhibitor (NDRI), i.e. a drug that increases the amount of synaptic norepinephrine and dopamine available to receptors by blocking the dopamine and norepinephrine reuptake transporters. This is a mechanism of action shared by some recreational drugs like cocaine and the medication tametraline (see DRI). Research showed that the (S)-isomer is responsible for activity.

<span class="mw-page-title-main">Radafaxine</span> Chemical compound

Radafaxine (developmental code GW-353,162; also known as (2S,3S)-hydroxybupropion or (S,S)-hydroxybupropion) is a norepinephrine–dopamine reuptake inhibitor (NDRI) which was under development by GlaxoSmithKline in the 2000s for a variety of different indications but was never marketed. These uses included treatment of restless legs syndrome, major depressive disorder, bipolar disorder, neuropathic pain, fibromyalgia, and obesity. Regulatory filing was planned for 2007, but development was discontinued in 2006 due to "poor test results".

A serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), also known as a triple reuptake inhibitor (TRI), is a type of drug that acts as a combined reuptake inhibitor of the monoamine neurotransmitters serotonin, norepinephrine, and dopamine. It does this by concomitantly inhibiting the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT), respectively. Inhibition of the reuptake of these neurotransmitters increases their extracellular concentrations and, therefore, results in an increase in serotonergic, adrenergic, and dopaminergic neurotransmission. The naturally-occurring and potent SNDRI cocaine is widely used recreationally and often illegally for the euphoric effects it produces.

<span class="mw-page-title-main">Desmetramadol</span> Opioid painkiller medication

Desmetramadol, also known as O-desmethyltramadol (O-DSMT), is an opioid analgesic and the main active metabolite of tramadol. Tramadol is demethylated by the liver enzyme CYP2D6 to desmetramadol in the same way as codeine, and so similarly to the variation in effects seen with codeine, individuals who have a less active form of CYP2D6 will tend to have reduced analgesic effects from tramadol. Because desmetramadol itself does not need to be metabolized to induce an analgesic effect, it can be used in individuals with low CYP2D6 activity unlike tramadol.

<span class="mw-page-title-main">Nisoxetine</span> Chemical compound

Nisoxetine, originally synthesized in the Lilly research laboratories during the early 1970s, is a potent and selective inhibitor for the reuptake of norepinephrine (noradrenaline) into synapses. It currently has no clinical applications in humans, although it was originally researched as an antidepressant. Nisoxetine is now widely used in scientific research as a standard selective norepinephrine reuptake inhibitor. It has been used to research obesity and energy balance, and exerts some local analgesia effects.

A dopamine releasing agent (DRA) is a type of drug which induces the release of dopamine in the body and/or brain. No selective and robust DRAs are currently known. On the other hand, many releasing agents of both dopamine and norepinephrine and of serotonin, norepinephrine, and dopamine are known. Serotonin–dopamine releasing agents (SDRAs), for instance 5-chloro-αMT, are much more rare and are not selective for dopamine release but have also been developed. Examples of major NDRAs include the psychostimulants amphetamine and methamphetamine, while an example of an SNDRA is the entactogen methylenedioxymethamphetamine (MDMA). These drugs are frequently used for recreational purposes and encountered as drugs of abuse. Selective DRAs, as well as NDRAs, have medical applications in the treatment of attention deficit hyperactivity disorder (ADHD).

<span class="mw-page-title-main">Norepinephrine–dopamine reuptake inhibitor</span> Drug that inhibits the reuptake of norepinephrine and dopamine

A norepinephrine–dopamine reuptake inhibitor (NDRI) is a drug used for the treatment of clinical depression, attention deficit hyperactivity disorder (ADHD), narcolepsy, and the management of Parkinson's disease. The drug acts as a reuptake inhibitor for the neurotransmitters norepinephrine and dopamine by blocking the action of the norepinephrine transporter (NET) and the dopamine transporter (DAT), respectively. This in turn leads to increased extracellular concentrations of both norepinephrine and dopamine and, therefore, an increase in adrenergic and dopaminergic neurotransmission.

<span class="mw-page-title-main">Serotonin antagonist and reuptake inhibitor</span> Class of drug

Serotonin antagonist and reuptake inhibitors (SARIs) are a class of drugs used mainly as antidepressants, but also as anxiolytics and hypnotics. They act by antagonizing serotonin receptors such as 5-HT2A and inhibiting the reuptake of serotonin, norepinephrine, and/or dopamine. Additionally, most also antagonize α1-adrenergic receptors. The majority of the currently marketed SARIs belong to the phenylpiperazine class of compounds.

A monoamine reuptake inhibitor (MRI) is a drug that acts as a reuptake inhibitor of one or more of the three major monoamine neurotransmitters serotonin, norepinephrine, and dopamine by blocking the action of one or more of the respective monoamine transporters (MATs), which include the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT). This in turn results in an increase in the synaptic concentrations of one or more of these neurotransmitters and therefore an increase in monoaminergic neurotransmission.

<span class="mw-page-title-main">Threohydrobupropion</span> Type of substituted amphetamine derivative

Threohydrobupropion is a substituted amphetamine derivative—specifically a β-hydroxyamphetamine—and a major active metabolite of the antidepressant drug bupropion (Wellbutrin). Bupropion is a norepinephrine–dopamine reuptake inhibitor and nicotinic acetylcholine receptor negative allosteric modulator, with its metabolites contributing substantially to its activities.

References

  1. ↑ Anvisa (31 March 2023). "RDC Nº 784 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No. 784 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control] (in Brazilian Portuguese). Diário Oficial da União (published 4 April 2023). Archived from the original on 3 August 2023. Retrieved 16 August 2023.
  2. 1 2 3 4 5 6 Lachatre G, Piva C, Riche C, Dumont D, Defrance R, Mocaer E, et al. (1989). "Single-dose pharmacokinetics of amineptine and of its main metabolite in healthy young adults". Fundamental & Clinical Pharmacology. 3 (1): 19–26. doi:10.1111/j.1472-8206.1989.tb00026.x. PMID   2714729. S2CID   25992333.
  3. 1 2 3 4 5 Sbarra C, Castelli MG, Noseda A, Fanelli R (1981). "Pharmacokinetics of amineptine in man". European Journal of Drug Metabolism and Pharmacokinetics. 6 (2): 123–126. doi:10.1007/bf03189478. PMID   7274306. S2CID   31069503.
  4. 1 2 Vaugeois JM, Corera AT, Deslandes A, Costentin J (June 1999). "Although chemically related to amineptine, the antidepressant tianeptine is not a dopamine uptake inhibitor". Pharmacology, Biochemistry, and Behavior. 63 (2): 285–290. doi:10.1016/S0091-3057(98)00242-1. PMID   10371658. S2CID   32862145.
  5. 1 2 Dunlop BW, Nemeroff CB (March 2007). "The role of dopamine in the pathophysiology of depression". Archives of General Psychiatry. 64 (3): 327–337. doi:10.1001/archpsyc.64.3.327. PMID   17339521. S2CID   26550661.
  6. ↑ DE 2011806,Fresnes C, Malen JS,"New Tricyclic Derivatives and Process for their Manufacture",issued 3 December 1981, assigned to Science Union et Cie. Societe Francaise de Recherche Medical, Suresnes (Frankreich)
  7. ↑ Sittig M (1 April 1988) [1979]. Pharmaceutical Manufacturing Encyclopedia (2nd ed.). Park Ridge, New Jersey, United States American: William Andrew Publishing/Noyes Publications. ISBN   978-0-8155-1144-1. Archived from the original on 23 October 2005. Retrieved 29 October 2005.[ page needed ]
  8. ↑ "Docket No. 02N-0101". U.S. Food and Drug Administration. 9 April 2002. Retrieved 30 January 2014.
  9. ↑ Doctissimo (2005). "SURVECTOR – Amineptine" (in French). Archived from the original on 9 March 2005. Retrieved 27 October 2005.
  10. ↑ Amineptine Medication – Uses, Side Effects and Precautions of Amineptine. Health-care-information.org. Retrieved on 28 September 2013
  11. ↑ Grupper C (1988). "[New iatrogenic acne: acne caused by amineptin (Survector)]". Annales de Dermatologie et de Venereologie (in French). 115 (11): 1174–1176. PMID   2977079.
  12. ↑ Thioly-Bensoussan D, Charpentier A, Triller R, Thioly F, Blanchet P, Tricoire N, et al. (1988). "[Iatrogenic acne caused by amineptin (Survector). Apropos of 8 cases]". Annales de Dermatologie et de Venereologie (in French). 115 (11): 1177–1180. PMID   2977080.
  13. ↑ Vexiau P, Gourmel B, Husson C, Castot A, Rybojad M, Julien R, et al. (1988). "[Severe lesions of acne type induced by chronic amineptin poisoning: apropos of 6 cases]". Annales de Dermatologie et de Venereologie (in French). 115 (11): 1180–1182. PMID   2977081.
  14. ↑ Teillac D, Weber MJ, Lowenstein W, de Prost Y (1988). "[Acne caused by Survector]". Annales de Dermatologie et de Venereologie (in French). 115 (11): 1183–1184. PMID   2977082.
  15. ↑ Lévigne V, Faisant M, Mourier C, Garcier F, Millon-Paitel M, Barthélémy H, et al. (1988). "[Monstrous acne in the adult. Inducer role of Survector?]". Annales de Dermatologie et de Venereologie (in French). 115 (11): 1184–1185. PMID   2977083.
  16. ↑ Vexiau P, Gourmel B, Julien R, Husson C, Fiet J, Puissant A, et al. (March 1988). "Severe acne-like lesions caused by amineptine overdose". Lancet. 1 (8585): 585. doi:10.1016/S0140-6736(88)91373-6. PMID   2894512. S2CID   32936080.
  17. ↑ Martín-Ortega E, Zamora E, Herrero C, Palou J (1989). "[Acneiform eruption induced by amineptin (Survector)]". Medicina Cutanea Ibero-Latino-Americana (in Spanish). 17 (6): 414–416. PMID   2534534.
  18. 1 2 Vexiau P, Gourmel B, Castot A, Husson C, Rybojad M, Julien R, et al. (1990). "Severe acne due to chronic amineptine overdose". Archives of Dermatological Research. 282 (2): 103–107. doi:10.1007/BF00493467. PMID   2141246. S2CID   39394890.
  19. ↑ Castot A, Benzaken C, Wagniart F, Efthymiou ML (1990). "[Amineptin abuse. Analysis of 155 cases. An evaluation of the official cooperative survey of the Regional Centers of Pharmacovigilance]". Therapie (in French). 45 (5): 399–405. PMID   2260032.
  20. ↑ Deniker P, Lôo H, Zarifian E, Peron P, Benyacoub A, Roux JM, et al. (1981). "[Amineptine and amotival syndrome (author's transl)]". L'Encephale (in French). 7 (1): 59–64. PMID   7227285.
  21. ↑ Bertschy G, Luxembourger I, Bizouard P, Vandel S, Allers G, Volmat R (1990). "[Amineptin dependence. Detection of patients at risk. Report of 8 cases]". L'Encephale (in French). 16 (5): 405–409. PMID   2265603.
  22. ↑ Blayac JP, Hillaire-Buys D, Peyrière H (1997). "[Pharmacovigilance of new antidepressants: evaluation of neuro-psychobehavioral disorders]". Therapie. 52 (2): 117–122. PMID   9231505.
  23. ↑ Castot A, Benzaken C, Wagniart F, Efthymiou ML (1990). "[Amineptin abuse. Analysis of 155 cases. An evaluation of the official cooperative survey of the Regional Centers of Pharmacovigilance]". Therapie. 45 (5): 399–405. PMID   2260032.
  24. ↑ Bertschy G, Luxembourger I, Bizouard P, Vandel S, Allers G, Volmat R (1990). "[Amineptin dependence. Detection of patients at risk. Report of 8 cases]". L'Encephale. 16 (5): 405–409. PMID   2265603.
  25. 1 2 Bories P, Pomier-Layrargues G, Chotard JP, Citron D, Capron-Chivrac D, Capron JP, et al. (December 1980). "[Amineptine-induced cholestatic hepatitis. 5 cases (author's transl)]". La Nouvelle Presse Médicale (in French). 9 (48): 3689–3692. PMID   7454584.
  26. ↑ Pessayre D, Larrey D (April 1988). "Acute and chronic drug-induced hepatitis". Bailliere's Clinical Gastroenterology. 2 (2): 385–422. doi:10.1016/0950-3528(88)90009-7. PMID   3044468.
  27. ↑ Larrey D, Pageaux GP (1997). "Genetic predisposition to drug-induced hepatotoxicity". Journal of Hepatology. 26 (Suppl 2): 12–21. doi:10.1016/S0168-8278(97)80492-8. PMID   9204405.
  28. ↑ "[Drug-induced liver disorders. Questions for Professor Daniel Dhumeaux]" [Drug-induced liver disorders. Questions for Professor Daniel Dhumeaux]. Gastroenterologie Clinique et Biologique (in French). 23 (8–9): 917–920. 1999. PMID   10533145.
  29. ↑ Concours Med 1982; 104:5733-5734[ verification needed ]
  30. 1 2 Sebastián Domingo JJ, Simón Marco MA, Uribarrena Echebarría R (March 1994). "Hepatic and pancreatic injury associated with amineptine therapy". Journal of Clinical Gastroenterology. 18 (2): 168–169. doi:10.1097/00004836-199403000-00023. PMID   8189020.
  31. ↑ Lazaros GA, Stavrinos C, Papatheodoridis GV, Delladetsima JK, Toliopoulos A, Tassopoulos NC (1996). "Amineptine induced liver injury. Report of two cases and brief review of the literature". Hepato-Gastroenterology. 43 (10): 1015–1019. PMID   8884331.
  32. ↑ Jonville AP, Dutertre JP, Autret E (1992). "[Immediate acute hepatic cytolysis after the administration of a single amineptin tablet]". Gastroenterologie Clinique et Biologique (in French). 16 (4): 368. PMID   1397859.
  33. ↑ Sgro C, Lacroix S, Waldner A, Lacroix M, Ferrut O, Bureau A (1989). "[Anaphylactic shock caused by amineptine. Report of a case]". La Revue de Medecine Interne (in French). 10 (5): 461–462. doi:10.1016/s0248-8663(89)80054-2. PMID   2488491.
  34. ↑ Roth BL, Driscol, J. "PDSP Ki Database". Psychoactive Drug Screening Program (PDSP). University of North Carolina at Chapel Hill and the United States National Institute of Mental Health. Retrieved 14 August 2017.
  35. 1 2 3 4 5 6 7 8 9 Garattini S, Mennini T (1989). "Pharmacology of amineptine: synthesis and updating". Clinical Neuropharmacology. 12 (Suppl 2): S13–S18. doi:10.1097/00002826-198912002-00003. PMID   2698268. S2CID   10947713.
  36. 1 2 3 4 5 6 Ceci A, Garattini S, Gobbi M, Mennini T (May 1986). "Effect of long term amineptine treatment on pre- and postsynaptic mechanisms in rat brain". British Journal of Pharmacology. 88 (1): 269–275. doi:10.1111/j.1476-5381.1986.tb09495.x. PMC   1917102 . PMID   3708219.
  37. 1 2 Nishino S, Mao J, Sampathkumaran R, Shelton J (1998). "Increased dopaminergic transmission mediates the wake-promoting effects of CNS stimulants". Sleep Research Online. 1 (1): 49–61. PMID   11382857.
  38. ↑ Protais P, Arbaoui J, Bakkali EH, Bermejo A, Cortes D (October 1995). "Effects of various isoquinoline alkaloids on in vitro 3H-dopamine uptake by rat striatal synaptosomes". Journal of Natural Products. 58 (10): 1475–1484. doi:10.1021/np50124a001. PMID   8676127.
  39. 1 2 3 4 5 6 7 8 9 Hall H, Sällemark M, Wedel I (May 1984). "Acute effects of atypical antidepressants on various receptors in the rat brain". Acta Pharmacologica et Toxicologica. 54 (5): 379–384. doi:10.1111/j.1600-0773.1984.tb01945.x. PMID   6464782.
  40. 1 2 Hall H, Ogren SO (February 1984). "Effects of antidepressant drugs on histamine-H1 receptors in the brain". Life Sciences. 34 (6): 597–605. doi:10.1016/0024-3205(84)90494-6. PMID   6141518.
  41. 1 2 3 4 5 6 Garattini S (July 1997). "Pharmacology of amineptine, an antidepressant agent acting on the dopaminergic system: a review". International Clinical Psychopharmacology. 12 (Suppl 3): S15–S19. doi:10.1097/00004850-199707003-00003. PMID   9347388. S2CID   23014661.
  42. ↑ Andersen J, Kristensen AS, Bang-Andersen B, Strømgaard K (July 2009). "Recent advances in the understanding of the interaction of antidepressant drugs with serotonin and norepinephrine transporters". Chemical Communications (25): 3677–3692. doi:10.1039/b903035m. PMID   19557250.
  43. ↑ "2021 - Placement of Amineptine in Schedule I". Archived from the original on 3 December 2021. Retrieved 30 November 2021.
  44. ↑ "Federal Register". Federal Register. National Archives & Drug Enforcement Administration. 17 November 2022.
  45. ↑ Nishino S, Kotorii N (2016). "Modes of Action of Drugs Related to Narcolepsy: Pharmacology of Wake-Promoting Compounds and Anticataplectics". Narcolepsy. Cham: Springer International Publishing. pp. 307–329. doi:10.1007/978-3-319-23739-8_22. ISBN   978-3-319-23738-1.
  46. ↑ Nishino S (2007). "Narcolepsy: pathophysiology and pharmacology". The Journal of Clinical Psychiatry. 68 (13): 9–15. PMID   18078360.
  47. ↑ Mignot EJ (October 2012). "A practical guide to the therapy of narcolepsy and hypersomnia syndromes". Neurotherapeutics. 9 (4): 739–752. doi:10.1007/s13311-012-0150-9. PMC   3480574 . PMID   23065655.
  48. ↑ Nishino S, Mao J, Sampathkumaran R, Shelton J (1998). "Increased dopaminergic transmission mediates the wake-promoting effects of CNS stimulants". Sleep Research Online. 1 (1): 49–61. PMID   11382857.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.