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. 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

In 1989, Sgro and colleagues at the Centre de Pharmacovigilance [33] in Dijon reported a case of anaphylactic shock in a woman who had been taking amineptine. [34]

Pharmacology

Pharmacodynamics

Amineptine [35]
SiteKi (nM)SpeciesRef
SERT Tooltip Serotonin transporter>100,000 (IC50)Rat [36]
NET Tooltip Norepinephrine transporter10,000 (IC50)
3,560		Rat
Canine		 [36] [37]
[38]
DAT Tooltip Dopamine transporter1,000–1,400 (IC50)
3,330		Rat
Canine		 [36] [39] [37]
[38]
5-HT1A >100,000Rat [40]
5-HT2A 74,000Rat [40]
α1 >100,000Rat [40]
α2 >100,000Rat [40]
β >100,000Rat [40]
D1 >100,000Canine [36]
D2 >100,000Rat/canine [36] [40]
H1 >100,000
13,000		Rat
Guinea pig		 [40]
[41]
mACh Tooltip Muscarinic acetylcholine receptor>100,000Rat [40]
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. [37] [36] [42] In addition, it has been found to induce the release of dopamine. [37] [36] [42] 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. [37] [36] [42] In contrast to the case for dopamine, amineptine does not induce the release of norepinephrine, and hence acts purely as a norepinephrine reuptake inhibitor. [37] [36] [42] Unlike other TCAs, amineptine interacts very weakly or not at all with the serotonin, adrenergic, dopamine, histamine, and muscarinic acetylcholine receptors. [40] [41] [42] The major metabolites of amineptine have similar activity to that of the parent compound, albeit with lower potency. [42]

No human data appear to be available for binding or inhibition of the monoamine transporters by amineptine. [43]

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. [44] This announcement was followed by the placement of Amineptine into Schedule I. [45]

Related Research Articles

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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">Venlafaxine</span> Antidepressant medication

Venlafaxine, sold under the brand name Effexor among others, is an antidepressant medication of the serotonin–norepinephrine reuptake inhibitor (SNRI) class. It is used to treat major depressive disorder, generalized anxiety disorder, panic disorder, and social anxiety disorder. Studies have shown that venlafaxine improves post-traumatic stress disorder (PTSD). It may also be used for chronic pain. It is taken by mouth. It is also available as the salt venlafaxine besylate in an extended-release formulation.

<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.

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

A norepinephrine reuptake inhibitor or noradrenaline reuptake inhibitor or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a reuptake inhibitor for the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline) by blocking the action of the norepinephrine transporter (NET). This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine and therefore can increase adrenergic neurotransmission.

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

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<span class="mw-page-title-main">Norepinephrine transporter</span> Protein-coding gene in the species Homo sapiens

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References

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  33. ↑ centres-pharmacovigilance.net Archived 8 February 2012 at the Wayback Machine
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