Amfonelic acid powder (15180-02-6)

Amfonelic acid (AFA) is a dopamine reuptake inhibitor. Experiments on rats have shown that AFA treatment completely prevented the effects of methamphetamine on the dopaminergic system, both morphologically and biochemically.

Amfonelic acid (AFA) is a nootropic drug of the racetam family and stimulant.Several animal studies suggest that the substance is safe even when high doses are consumed for a long period of time. However, the mechanism of action of the racetam drug family is still a matter of research.

The stimulant properties of AFA were discovered serendipitously at Sterling-Winthrop in the midst of research on the antibiotic nalidixic acid. In addition to behaving as antibiotics, it was found that many derivatives of nalidixic acid have either stimulant or depressant effects on the central nervous system. Researchers at Sterling-Winthrop found that AFA had a higher potency and therapeutic index than cocaine or amphetamine and so it was singled out for further study. A small number of clinical trials were held in the 1970s, but when it was found that AFA exacerbated psychotic symptoms in schizophrenic patients and produced undesirable stimulant properties in geriatric depressives clinical evaluation of AFA was discontinued. AFA remains a widely used pharmacological tool for study of the brain’s reward system, dopamine pathways, and the dopamine transporter. Since 2013 AFA has been sold on the gray market and there are numerous anecdotal reports detailing its non-medical use.

In studies it proved to be a potent and highly selective dopamine reuptake inhibitor (DRI) in rat brain preparations. A study found a moderately long half-life of approximately 12 hours and a dopaminergic potency approximately 50 fold that of methylphenidate in rat brain preparations.Despite lack of direct serotonin activity, rats treated with subchronic doses of amfonelic acid display subsequent decreases in 5HT and 5HIAA. Amfonelic acid displays no activity in the norepinephrine system.

Despite its different mechanism of action, amfonelic acid displays discriminatory substitution with 150% the stimulant potency of dextroamphetamine. Amfonelic acid has been shown to be neuroprotective against methamphetamine damage to dopamine neurons. It also increases the effects of the antipsychotic drugs haloperidol, trifluoperazine and spiperone. Rats are shown to self-administer amfonelic acid in a dose-dependent manner.

Improved Memory

• Increased Learning Ability
• Improved Cognitive Processing
• Heightened Reflexes
• Heightened Perception
• Reduced Anxiety

The main ingredient of NEUPRAMIR is pramiracetam, a pharmaceutical product with nootropic effects. Experimental studies have proved it to be effective in improving memory and learning capacity.

This medicine has a sedative effect, which does not influence the activity of the autonomous nervous system. Its action is mildly disinhibitory and antidepressant.Pramiracetam is a nootropic drug derived from piracetam, and is more potent (i.e. lower dosage is used). It belongs to the racetam family of nootropics.Pramiracetam was developed by Parke-Davis based on Piracetam, and is 8-30 times stronger than Piracetam. It goes by the trade name Neupramir or Pramistar

Though AFA was discovered in the course of antibiotic research, there is very little data available on the drug’s antimicrobial activity. In 1988 the biologist G.C. Crumplin wrote, “[AFA] is less active against bacteria than are many other 4-quinolones, but studies in our laboratory on selected mammalian cell lines have shown it to be markedly more toxic to these cells than are the 4-quinolones that are more active antibacterial agents. Furthermore, it can be shown that sublethal doses induced marked changes in the pattern of proteins produced by the cell, thus suggesting a possible effect of 4-quinolones on gene transcription in mammalian cells.” When evaluated via broth microdilution the MIC of AFA for Escherichia coli is 125 μg/mL, a concentration thirty times higher than the MIC for nalidixic acid in the same E. coli strain.

COA

• Cox ET, Jarrett TM, McMurray MS, Greenhill K, Hofler VE, Williams SK, Joyner PW, Middleton CL, Walker CH, Johns JM. Combined norepinephrine/serotonergic reuptake inhibition: effects on maternal behavior, aggression, and oxytocin in the rat. Front Psychiatry. 2011 Jun 8;2:34. doi: 10.3389/fpsyt.2011.00034. eCollection 2011. PubMed PMID: 21713063; PubMed Central PMCID: PMC3114092.
• Bongiovanni R, Young D, Newbould E, Jaskiw GE. Increased striatal dopamine synthesis is associated with decreased tissue levels of tyrosine. Brain Res. 2006 Oct 18;1115(1):26-36. Epub 2006 Aug 24. PubMed PMID: 16934236.
• Johns JM, Joyner PW, McMurray MS, Elliott DL, Hofler VE, Middleton CL, Knupp K, Greenhill KW, Lomas LM, Walker CH. The effects of dopaminergic/serotonergic reuptake inhibition on maternal behavior, maternal aggression, and oxytocin in the rat. Pharmacol Biochem Behav. 2005 Aug;81(4):769-85. PubMed PMID: 15996723; PubMed Central PMCID: PMC3110079.
• Johns JM, Lubin DA, Walker CH, Joyner P, Middleton C, Hofler V, McMurray M. Gestational treatment with cocaine and fluoxetine alters oxytocin receptor number and binding affinity in lactating rat dams. Int J Dev Neurosci. 2004 Aug-Oct;22(5-6):321-8. PubMed PMID: 15380831; PubMed Central PMCID: PMC3109071.