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Adrafinil

$24.99

SKU: TN-N-0006

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Adrafinil is a synthetically (man-made and not naturally occurring or found in foods) developed Nootropic compound and it is a peripheral member to the eugeroic family of nootropic agents. Adrafinil is a prodrug to Modafinil i.e. Adrafinil is believed to increase concentration of modafinil within the body. Once ingested, it is broken down in the liver to produce modafinil. Adrafinil and Modafinil are both enhancers of wakefulness. Adrafinil acts as a cognitive enhancer and as a stimulant just like other eugeroics. Adrafinil is believed to be very effective in increasing daytime alertness and wakefulness and has shown positive effects on motivation, mood, energy levels, and reaction time. Adrafinil is also referred to as Olmifon, Adrafinil, CRL-40028, and Benzhydrylsulfinyl Acetohydroxamic acid. In terms of structure, Adrafinil has a similar structure to its close chemical relative and bioactive metabolite Modafinil. However, they differ due to the terminal amide hydroxyl group that is found in adrafinil. In other words, ((diphenylmethyl)sulfinyl-2 acetohydroxamic acid)) is not found in modafinil (Diphenyl Methyl)sulfinyl-2 acetamide). Adrafinil should be carefully administered because of its anti-sleep and long half-life., preferably to be taken in the morning after waking up.

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HISTORY

Adrafinil was discovered by scientists at Group Lafon, a French Pharmaceutical Company during the late 1970s. Adrafinil was later offered in France as a trial treatment for narcolepsy in 1986. In the initial stages, it was researched under the name CRL-40028 and was available to users under the name Olmifon. The company later went forward and developed modafinil. Modafinil is the primary metabolite of adrafinil. The mechanism of action for Adrafinil is not very well known. In 2001, Group Lafon was acquired by Cephalon. Cephalon went ahead and terminated the production of Olmifon in 2011 after its marketing license was withdrawn by the French. Currently its array of adrafinil products comprised of Rafini and Modafinil are used as α1-adrenergic receptor agonists. Within the United States, Adrafinil is not regulated, and the U.S. Food and Drug Administration (FDA) has not approved its use in a clinical capacity. Adrafinil is not classified as a regulated or controlled substance like Modafinil. You can possess Adrafinil without prescription within the U.S. and in Europe. It was at first prescribed for individuals with sleeping disorders like narcolepsy. Adrafinil in most cases is used off-label to ease the symptoms of excessive daytime sleepiness and fatigue. It has been used by athletes as a stimulatory agent at times. In 2014, Adrafinil was identified as a nonspecific stimulant and featured as a banned substance by WADA (World Anti-Doping Agency) under section 6 of the banned substances list.

CLINICAL STUDIES

In a rat study, when rats were orally administered with 20mg/kg adrafinil, the substance was observed to peak after 4 hours post-administration. Adrafinil’s half-life based on this dosage was observed to be 4.95 hours although traces of the substance still detectable in serum 7 hours post ingestion. In the case of human, a dosage of 900mg of adrafinil was seen to climax in the blood within an hour’s time. However, the neurological effects of the substance were only detectable within the next one hour as Adrafinil was seen to be converted into Modafinil.

A canine based dose-response study revealed that after 10 hours, a high dose of 50mg/kg had a lower concentration of adrafinil in serum compared to a lower dose of 10mg/kg but a modest dose of 30mg/kg was noted to have the highest levels of concentration. It was observed that adrafinil had a dose dependent increases in serum concentration after 2 hours. The researchers concluded that when adrafinil is taken in high doses it can stimulate the body to metabolize or eliminate it more than lower doses.

Research in animals has noted oral doses of 64-256mg/kg Adrafinil increased activity when measured by locomotion in mice. In dogs, the effects of adrafinil have been found to be affected by time and amount of dose. A study that focused on evaluating nocturnal activity in monkeys showed that 60mg/kg of Adrafinil doubled the levels of activity when two doses were administered while 90-120mg/kg of adrafinil resulted in activity levels that were four times higher with the first dose. This tendency of animals to manifest increased activity in the form of locomotion is thought to be as a result of increased wakefulness (eugeroic) and not related to amphetamine since there is no induced anxiety. The degree of adrafinil’s efficiency was observed to persist when the administration of the substance at 20-40mg/kg was sustained for a period of 33 days. The increase in locomotion in animals is suggested be a secondary effect to the effect of increased wakefulness. Adrafinil was noted to cause more increase in locomotion when administered to monkeys during their nocturnal periods. Tests that used the bioactive metabolite modafinil showed no increases in locomotion during waking periods although some increase in locomotion was observed as the supplement lasted up to nocturnal period.

In another study, researchers gave rats a dose of 400mg/kg adrafinil for one month in one set and in the other set they gave rats 200mg/kg of Adrafinil for three months. These treatments did not show any signs of toxicity. However, LD50 values have been noted to differ from species to species. For example, the peak in rats was detected after dosages of 3,400mg/kg and in the case of mice it was at 1,250mg/kg.

A human-based study was conducted whereby the a patient was given doses of 900mg every day for ten months, and the study results showed the development of orofacial dyskinesia and no signs of Parkinson’s related symptoms. The orafacial dyskinesia did not improve even when adrafinil treatment was halted for about four months, but improved due to tetrabenazine that is a dopamine depleting agent. Modafinil treatment was also noted to have a similar effect that indicates that orofacial dyskinesia initiated by adrafinil may be linked to its conversion into modafinil once ingested. This research was not 100% reliable since the patient who was studied had been diagnosed with various medical conditions that might have been the source of orofacial dyskinesia.

Adrafinil was noted to boost spontaneous motility by acting on the central adrenergic receptors. In other cases, rat based tests have been employed in evaluating the effects of Adrafinil on the external pancreatic secretion that is caused by secretin, acetylcholine, CCK, and electrical vagal stimulation. Adrafinil did not bring about any changes on basal secretion and on secretion activated by agents acting directly on the pancreatic secretory cells although it significantly lowered secretion caused by peripheral or central stimulation on vagus nerves. This substance initiated inhibition of 2DG effect and was minimized by yohimbine. This indicated that alpha 2-adrenergic receptors were involved in the working of Adrafinil on rat’s secretion of exocrine in the pancreas.

Mice studies have shown the following effects of Adrafinil: 64-256 mg/kg enhanced locomotor activity, 16-128mg/kg improved antagonism (caused by hypnotic effects of barbitone), 16-256 mg/kg lowered immobility span during the forced swimming test, 256mg/kg improved slight antagonism caused by electroshock-induced convulsions, no changes in rectal temperature, absence of peripheral sympathetic effects, lack of marginal anti-chlorogenic effects, and absence of effects in provisional tests for antidepressants. When contrasted with no analeptic, antidepressant or anticholinergic drugs, Adrafinil exhibited a distinct behavioral profile in a mice based study. The majority of the effects induced by adrafinil such as increased locomotor activity may be linked to a central alpha 1-adrenergic activation although the unanticipated peripheral sympathetic effects are still a mystery.

In a dog based study, researchers administered daily doses (measurements of 10,20,30, and 40mg/kg) to aged dogs for two weeks in a cross-over design. The researchers then collected data linked to the spontaneous behavior in dogs for 10 minutes in a canine open-field test. The data was collected on day one of treatment and then scheduled for every fourth day. The tests were conducted either in intervals of 2 hours or 10 hours, after oral administration of adrafinil or lactose (the placebo control). Locomotor activity was observed to rise considerably at the three highest doses of the 2 hours or the 10 hours interval. It was also noted to cause a temporary rise in direct sniffing. Urination frequency was changed when Adrafinil was administered at the highest dose levels. During the tests, the enhanced locomotion was noted to indicate stereotypical behavior. Also, the animals seemed to respond differently with sections of the population of animals in the study either showing decreased locomotion or no changes. Most of the scientific research data on Adrafinil is animal based with almost no clinical trials conducted on large samples of human subjects.

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  1. Best Customer Service!

    By Nader G. February 07, 2016

    Thank you for everything. Received my product in FL yesterday!

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