Sunifiram was initially developed in 2000 and as such is more of a newcomer when compared to other nootropic agents. The first studies revealed that Sunifiram is a memory enhancing compound. The substance was availed to the public just recently (has been in the market for around a year or so), but it’s now the most popular nootropic agent in the AMPAkine class among users of nootropic agents. This can be attributed to the exceptional benefits experienced by its users. There are numerous online reviews posted by nootropic users who attest the effectiveness of Sunifiram with minimal or no serious complications arising after consumption. Currently, Sunifiram is being studied to evaluate its effects on Alzheimer’s disease that causes a decline in cognitive abilities. In all animal studies, Sunifiram has been found to be more potent than Piracetam, and it has anti-amnesiac, cognitive, and nootropic effects. At the moment, it is still set aside for scientific research only. Most of the studies carried out on Sunifiram focus mainly on its anti-amnesiac effect and its effects in the treatment of Alzheimer’s disease in comparison with Piracetam. Sunifiram has been found to have a potency of approximately 1000 times that of Piracetam. Research is still underway for clinical use of Sunifiram although no formal clinical trials had been conducted in humans by 2014. Therefore, the safety of Sunifiram is still not clinically known in humans.
Several animal-based studies have been conducted to determine the effects of Sunifiram on amnesia and other mental related conditions. In a scientific study seeking to establish Sunifiram’s anti-amnesiac properties, normal adult rats were administered with 0.1mg/kg of Sunifiram through injection. The results indicated that this dose was able to produce cognitive enhancement effects that were found to be matched by administration of a dose of about 30mg/kg of Piracetam. A study involving Sunifiram and Unifiram showed that both nootropics agents were effective in increasing the output of acetylcholine in the prefrontal cortex in lab rats. Anti-amnesiac effects were also observed. These mice test results have shown that Sunifiram could be effective in the treatment of a number of mental based conditions among the Alzheimer’s disease.
Scientific research carried out on olfactory bulbectomized (OBX) mice that had induced amnesia (hippocampal dependent memory shortages also established that Sunifiram was effective in assisting eliminate these mental deficiencies in the rats. Amnesia was induced by use of scopolamine, baclofen, mecamylamine, and clonidine, and then the mice were tested for their ability to navigate the Morris Water maze while under the amnesia-inducing drugs. Sunifiram was then administered by intraperitoneal or orally in various dosages and the mice were once again tested on their ability to escape the Morris Water maze. The effect of Sunifiram on amnesiac effects was quantified by measurement of the escape latency scores of the mice. Sunifiram treatment was found to lower amnesiac effects from the amnesiac-inducing drugs. Short term memory was also noted but the mice did not exhibit any anti-depressant effects. Additionally, due to the nature of the study, the researchers were not able to assess the effects of Sunifiram in healthy individuals. In another scientific study that sought to evaluate the effects of Sunifiram on the ability of rats (with induced with amnesia) to escape a maze, the results (escape latency scores) indicated a significant reduction in amnesiac effects.
In a study aimed at determining the effects of Sunifiram on memory deficiency and depression, OBX (olfactory bulbectomized) mice were administered with 0.1-1.0mg/kg of Sunifiram on a daily basis for 7-12 days. The mice had been operated with or without gavestinel (a glycine binding site inhibitor of the NMDR receptor). Treatment with this nootropic agent was observed to significantly enhance both spatial memory when the OBX mice were evaluated using a Y-maze, and short term memory when novel recognition task was employed for assessment compared to OBX mice that had not received Sunifiram treatment. The nootropic agent was also seen to restore hippocampal LTP that had been injured in OBX mice previously treated with gavestinel. Tail suspension task, on the other hand, was used to evaluate the effects of Sunifiram on depression; the results showed that Sunifiram did not have effects on depressive behavior in OBX mice. When the OBX mice treated with Sunifiram were compared to the control group, the Tail Suspension task did not show any significant difference involving the two. Researchers involved in the study observed neurochemical changes whereby the phosphorylation of CaMKIIα, PKCα, NR1, and GluR1 returned to control levels in OBX mice under Sunifiram treatment. The study concluded that Sunifiram lowers OBX-induced deficits of impaired LTP and memory-related behaviors in the hippocampal region by activation of the glycine-binding site of the NMDAR. The failure of Sunifiram to have depressive effects in OBX mice is suggested to be as a result of this study focusing on depressive effects that are associated with low levels of ERK activation, and Sunifiram does not affect ERK. Just after its development, mice were used in a test for passive avoidance to assess the nootropic properties of Sunifiram. The results indicated that an N-acylpiperazine group was able to mimic the 2-pyrrolidinone ring (1, 4-diazabycyclo[4.3.0]nonan-9-one) and that it had a high level of nootropic activity. Sunifiram was seen to increase the release of acetylcholine in rat brains. The potency of Sunifiram was also observed to be very high with success noted after administration of doses at 0.001mg/kg.
Researchers have also investigated the involvement of AMPA receptors in Sunifiram’s and Unifiram’s mechanism of action and from their study results they established that both substances were effective in lowering amnesia that had been induced by NBQX (the AMPA receptor antagonist) in mice passive avoidance test. When rota rod test was used, the two compounds did not negatively affect motor coordination at the effective doses. Hole board test also revealed that they did not change spontaneous inspection and motility activity. Additionally, when the kynurenate test was run, the two compounds reversed the antagonism stimulated by the kynurenic acid of the NMDA-mediated release of [(3)H]NA in hippocampal slices of the rat. This alteration was corrected by an increase in NBQX.DM 232 in excitatory synaptic transmission in the rat’s hippocampus. The results suggested that DM 235 and DM232 function as cognition enhancers by stimulation of the AMPA-mediated neurotransmission system.
Another mice based study was conducted in which the researchers were attempting to establish if Sunifiram has effects on NMDAR (N-methyl-D-aspartate receptor) dependent synaptic function in CA1 region of the hippocampal. The researchers evaluated the effects of Sunifiram on NMDAR-dependent LTP (long-term potentiation) using electrophysiology and its effects on phosphorylation of synaptic proteins using immunoblotting analysis. Sunifiram was observed to improve LTP significantly, but the improvement was noted to be inhibited by 7-CIKN (7-chloro-kynurenic acid) which happens to be a great antagonist for glycine -binding sites (within the NMDAR). The enhancement observed in LTP due to Sunifiram was linked to a rise in phosphorylation of AMPAR (α-amino-3-hydroxy-5-methylisozazole-4-propionate receptor) by activation of CaMKII and a boost in the phosphorylation of NMDAR by activation of PKCα (Protein kinase II). The rise in phosphorylation of PKCα and Src(Tyr-416) stimulated by Sunifiram was observed to be inhibited by 7-CIKN therapy. Sunifiram’s enhancement of LTP was considerably inhibited by PP2 (a member of Src family of inhibitors). When mice were treated with a high concentration of glycine prior to Sunifiram treatment, administration of Sunifiram did not have any positive effects on LTP in the CA1 region of the hippocampus. Generally, Sunifiram activates the glycine-binding site of the NMDAR with concomitant PKCα activation via Src kinase. Improvement in the activities of PKCα triggers to potentiate hippocampal LTP via activation of CaMKII.
Due to lack of human trials, these Sunifiram effects observed in animal models have not been tested in humans and, therefore, clinical trials are needed.
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