Sunifiram(DM235) powder video
Sunifiram(DM235) powder basic Characters
|Melt Point:||57-58 °C|
|Storage Temp:||Store at room temperature or cooler|
|Color:||White or off-white powder|
Sunifiram(DM235) powder in brain boost usage
Sunifiram powder,DM235 powder is with trade name as BisfluoroModafinil, Flmodafinil.
DM235 powder Usage
DM235 powder is a novel, highly potent nootropic and AMPAkine-like compound with cognition-enhancing effects in animal models.
Sunifiram powder is a piperazine which has some structural similarities to piracetam. Piracetam was developed for neurodegenerative disorders like Alzheimer’s disease, and Sunifiram powder is known to enhance cognitive function in some behavioral experiments. In receptor binding studies, Sunifiram raw powder does not show affinity for most neurotransmitter receptors or channels (no affinity at 1μM for serotoninergic, dopaminergic, muscarinic, nicotinic, adrenergic, glutamatergic, histaminergic, opioid, or GABAergic receptors), yet promotes the release of acetylcholine from rat cerebral cortex, likely through positive modulation of AMPA receptor response.
Sunifiram powder prevents amnesia induced by scopolamine, after i.p. and p.o. administration, in the mouse passive avoidance test with a minimal effective dose of 0.01 mg/kg p.o. The antiamnesic effect of Sunifiram powder is comparable to that exerted by well known nootropic drugs such as piracetam (30 mg/kg i.p.), aniracetam (100 mg/kg p.o.) and rolipram (30 mg/kg p.o.), but with a potency 1,000 – 10,000 times higher.
Warning on DM235 powder side effects
Sunifiram powder (DM-235) is a piperazine derived research chemical which has anti-amnesiac effects in animal studies with significantly higher potency than piracetam. Sunifiram raw powder is a molecular simplification of unifiram. Based on in vitro and animal studies, it appears that Sunifiram powder acts via AMPA-receptor activation.
Sunifiram raw powder operates by activating AMPA receptors; that is, the receptors that are responsible for the mediation of synaptic transmission in the central nervous system. Its mechanics also increases phosphorylation of AMPAR and NMDAR through protein kinase activation, which in turn enhances long-term potentiation – that is, an enhancement in signal transmission between two neurons resulting from simultaneous stimulation.
The kinase activation that is influenced by Sunifiram powder also improves cognitive defects. Additionally, Sunifiram raw powder works in the cerebral cortex of animal test subjects by assisting in the release of acetylcholine, the organic molecule that acts as a neurotransmitter in a host of various organisms. These operational mechanisms enable Sunifiram powder to exert anti-amnesiac properties.
Sunifiram powder is also able to prevent the amnesia induced by the nicotinic antagonist mecamylamine, the GABAB agonist baclofen, the α2 agonist clonidine and the AMPA receptor antagonist NBQX in the passive avoidance test.
In the rat Morris water maze test, the administration of scopolamine inhibits the reduction of escape latency in both acquisition and retention retraining test. Sunifiram raw powder, administered 20 min before each daily acquisition training, is able to prevent scopolamine-induced memory impairment at 0.1 mg/kg i.p.
Sunifiram powder produces maximal antiamnesic and procognitive effects without any visible modification in gross behavior of mice or rats, and at 0.1 mg/kg i.p., Sunifiram powder reduces the duration of hypnosis induced by pentobarbital in mice without modifying the induction time of hypnosis. Moreover, mice treated with Sunifiram raw powder retain motor coordination in the rotarod test. The spontaneous motility of mice, evaluated by the Animex apparatus, as well as exploratory behavior, evaluated by the hole-board test, remain normal after Sunifiram powder administration.
Sunifiram raw powder modulates cholinergic transmission in the cerebral cortex of freely moving rats. As shown by microdialysis experiments, Sunifiram powder is able to increase the release of ACh at a dose of 0.01 mg/kg, with higher potency than Unifiram.
Exposure of rat hippocampal slices to 100 μM NMDA elicits an increase of [3H]NE (48). The effect of NMDA is largely prevented by 100 μM kynurenic acid (KYNA). Addition of nanomolar concentrations of Sunifiram raw powder significantly reverses KYNA antagonism. The effect of Sunifiram powder is concentration-dependent (EC50 0.1 μM) and almost complete at 1 μM.
The involvement of AMPA receptors can be assessed via application of the selective AMPA receptor antagonist NBQX. When applied at 5 μM, NBQX prevents the [3H]NE release induced by AMPA (100 μM), but not the 100 μM NMDA-mediated tritium release from rat hippocampal slices (48). NBQX, inactive on its own, antagonizes the Sunifiram rwa powder reversal of the KYNA antagonism of the NMDA-evoked tritium release, suggesting involvement of AMPA receptors in the effects of Sunifiram powder.
Interestingly, under basal conditions, Sunifiram raw powder treatments increased PKCa (Ser-657) and Src family (Tyr-416) activities with the same bell-shaped dose-response curve as that of LTP, peaking at 10 nM. The increase in phosphorylation of PKCa (Ser-657) and Src (Tyr-416) induced by Sunifiram powder was inhibited by 7-ClKN treatment. The LTP enhancement by Sunifiram raw powder was significantly inhibited by PP2, a Src family inhibitor.
Finally, when pretreated with a high concentration of glycine (300 lM), Sunifiram powder treatments failed to potentiate LTP in the CA1 region.
Taken together, the above evidence suggests that Sunifiram raw powder stimulates the glycine-binding site of NMDAR with concomitant PKCa activation through Src kinase. Enhancement of PKCa activity triggers potentiation of hippocampal LTP through CaMKII activation.
Sunifiram(DM235) Raw Powder
Min order 10grams.
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DM235 powder Marketing
To be provided in the coming future.
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