Amineptine

[Jean]

I remember in Europa the name of Survector. The molelecule is Amineptine, it’s is the best dopamine anti-depressant never made with minaprine.
It’s very pity because it’s impossible to find anywhere this good medication. Minaprine is a molecule for “inhibition of action”, it’s improve catecholamine level by IMAOa and IMAOb, DARI, NARI effect with low serotonine and acetylcholine release. But after the death of Henri Laborit in France, the molecule doens’t exist in the pharmacist

I’ve tried Zyban (150 mg bupoprion SR) but after few day many people like me have headache and insomnia.

[DrMariano2]

@Jean 4708 wrote:

I remember in Europa the name of Survector. The molelecule is Amineptine, it’s is the best dopamine anti-depressant never made with minaprine.
It’s very pity because it’s impossible to find anywhere this good medication. Minaprine is a molecule for “inhibition of action”, it’s improve catecholamine level by IMAOa and IMAOb, DARI, NARI effect with low serotonine and acetylcholine release. But after the death of Henri Laborit in France, the molecule doens’t exist in the pharmacist

I’ve tried Zyban (150 mg bupoprion SR) but after few day many people like me have headache and insomnia.

Amineptine is probably the best antidepressant ever.

It is a tricyclic antidepressant developed in the 1960s which blocks dopamine reuptake strongly, blocks norepinephrine reuptake, and blocks serotonine reuptake.

Every antidepressant essentially works like some version of cocaine – which blocks dopamine, serotonin, and norepinephrine equally strongly. The problem of cocaine is that it lasts only a very short time.

Amineptine comes closes of all the antidepressants to long-acting cocaine.

Of course and unfortunately, some people started abusing it.

The Food and Drug Administration of the US denied approval of it because of its potential for abuse and other countries, including France, followed.

There have been no significant antidepressant developed since then which works as a dopamine reuptake blocker. And all antidepressants since then have been much weaker.

This was a huge loss because it actually worked. It was a political loss. Obviously, the FDA has approved other highly abusable medications including methaphetamine (Desoxyn) and other stimulants and numerous version of heroin which we call our opiate pain medications (including Oxycontin).

Amineptine could have been approved as a controlled substance to allow its prescription while being monitored by the DEA like other abusable medications. Then it would have been available to those who are seriously depressed.

Dopamine reuptake blockade is one target in treating depression that actually is effective and can overpower the effects of pro-inflammatory signaling. The stimulants to do not work similarly.

[Jean]

@DrMariano 4714 wrote:

Amineptine is probably the best antidepressant ever.

It is a tricyclic antidepressant developed in the 1960s which blocks dopamine reuptake strongly, blocks norepinephrine reuptake, and blocks serotonine reuptake.

Every antidepressant essentially works like some version of cocaine – which blocks dopamine, serotonin, and norepinephrine equally strongly. The problem of cocaine is that it lasts only a very short time.

Amineptine comes closes of all the antidepressants to long-acting cocaine.

Of course and unfortunately, some people started abusing it.

The Food and Drug Administration of the US denied approval of it because of its potential for abuse and other countries, including France, followed.

There have been no significant antidepressant developed since then which works as a dopamine reuptake blocker. And all antidepressants since then have been much weaker.

This was a huge loss because it actually worked. It was a political loss. Obviously, the FDA has approved other highly abusable medications including methaphetamine (Desoxyn) and other stimulants and numerous version of heroin which we call our opiate pain medications (including Oxycontin).

Amineptine could have been approved as a controlled substance to allow its prescription while being monitored by the DEA like other abusable medications. Then it would have been available to those who are seriously depressed.

Dopamine reuptake blockade is one target in treating depression that actually is effective and can overpower the effects of pro-inflammatory signaling. The stimulants to do not work similarly.

Why a good drug like amineptine disappear !. A Switzerland psychiatry Claude Rifat write some atypical articles : (some of this thinking)

Dopamine is one of the MOST IMPORTANT molecule in our brain because it serves
the purpose to stimulate:

Action
Motivations
Our desire of Freedom

Without dopamine, we could never maintain our structure because we would lose
motivation. We would stop acting in exoreality and become zombies.

Attacking dopamine is like trying to lobotomise people because dopamine is the
ESSENCE of an animal WILL to fight for SURVIVAL.

Dopamine IS the molecule of survival.

So the new Gestapo against dopamine is a highly politically sensitive subject
because controlling dopamine by law is just, simply stated, CONTROLLING THE
SURVIVAL INSTINCT of us human beings.

The Dopamine Inquisitors are the most dangerous Inquisitors ever because, if
they succeeded in their monstrous quest, it would mean that mankind would be
dispossessed of this very molecule which induces Resistance to Tyranny.

No external self-proclaimed “authority” has the right to manipulate our
dopamine activity.”

From Good drug guide :
“…..Amineptine (Survector) is a clean-ish, (relatively) selective dopamine reuptake blocker. Higher doses promote dopamine release too. Amineptine is pro-sexual and liable occasionally to cause spontaneous orgasms. It is a mild but pleasant psychostimulant and a fast-acting mood-brightener.

The compound was first synthesized by French pharmaceutical giant Servier. Licensed in France from 1978 under the brand name “Survector” and soon widely marketed abroad, amineptine is a clinically useful antidepressant. Unlike most other tricyclics, it doesn’t impair libido or cognitive function.

Amineptine has a small but non-negligible abuse-potential. Its enjoyable but short-lived psychostimulant effect should be distinguished in clinical practice from its sustained antidepressant action. Arguably all too many contemporary “antidepressants” lack abuse-potential not through superior design or clinical efficacy, but because they aren’t any good. The widely prescribed selective serotonin reuptake inhibitors (SSRIs), for instance, don’t reverse the diminished libido and lack of interest in sex characteristic of (many kinds of) depression. Instead, SSRIs exacerbate the problem.

Unlike typical stimulants and other activating agents, amineptine may actually improve sleep architecture. Amineptine can be an especially valuable agent for melancholic, anhedonic and unmotivated people whose mood is sometimes worsened by SSRIs. Amineptine is also a useful agent in treating chronic “low grade” depression or dysthymia. There is little evidence of its value in anxious or agitated depression. Anxious depressives may do better on its chemical cousin, tianeptine (Stablon).

Amineptine isn’t marketed or licensed in Britain and America. In Europe, too, the medication has been driven onto the pharmaceutical grey market. This is because FDA pressure led to the withdrawal of amineptine’s EC product-license early in 1999, causing substantial problems for patients and physicians alike. In early 2005, Servier ceased production of amineptine in Brazil. It is still available in some Uruguayan pharmacies or as a research chemical, but the world-wide famine persists. Amineptine is off-patent, but not cheap. Optimal dosage is variable; but typically 100mg-200mg per day. No exact substitute for amineptine is currently on offer or in prospect….”

[Jean]

The mechanism of amineptine is unique :

Effect of long term amineptine treatment on pre- and postsynaptic mechanisms in rat brain

1
The effect of amineptine and its two metabolites on monoamine uptake, release and receptor binding was studied in vitro.
2
Amineptine and its two metabolities did not displace labelled ligands for known neurotransmitters and drug receptor sites.
3
Amineptine and its two metabolities did not influence [3H]-5-hydroxytryptamine ([3H]-5-HT) uptake or release by rat brain synaptosomes. Amineptine inhibited [3H]-dopamine and [3H]-noradrenaline ([3H]-NA) accumulation, with IC50 values of 1.4 and 10 μM, respectively. The effect was retained, though with lower efficacy, by the two metabolites.
4
Amineptine released [3H]-dopamine from preloaded synaptosomes. Metabolite 1 had no effect on catecholamine release, and metabolite 2 was about half as active as the parent compound on [3H]-dopamine release.
5
The releasing effect of amineptine on [3H]-dopamine was potentiated by reserpine pretreatment, suggesting that the drug acts on the cytoplasmic neurotransmitter pool.
6
Chronic treatment with amineptine (20 mg kg−1, twice daily for 15 days followed by a 3 days drug withdrawal period) resulted in a decrease of [3H]-spiperone binding sites in striatum, and of [3H]-dihyroalprenolol and [3H]-clonidine in cortex.
7
Chronic treatment with amineptine reduced basal [3H]-dopamine accumulation in striatal synaptosomes, without affecting [3H]-NA or [3H]-5-HT accumulation.
8
The adaptive changes in the pre- and postsynaptic dopamine mechanisms observed after long term treatment with amineptine are consistent with the drug acting as an indirect dopamine agonist.
9
The down regulation of β- and α2-noradrenoceptors observed after long term amineptine treatment may play a role in the antidepressant activity of the drug.

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