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Metaphit acts as an acylator of NMDARAn, sigma and DAT binding sites. This drug is used in the prevention of d-amphetamine induced hyperactivity, while remarkably diminishing dopamine content in the nucleus accumbens.
During the pre-treatment of Metaphit, the cataleptic effects get increases that are generated by cumulative doses of PCP-type drugs such as PCP, ketamine and m-amino PCP. The other cumulative doses that increase the effects are Dexoxadrol, LY 154716 and Cyclazocine.
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Metaphit is a chemical for research which acts as an acylator at cns-binding sites nmdaran, sigma and dat. This is the pcp m-isothiocyanate analog, which is irreversiblely bound to the binding site of the pcp at the nmda receptor complex (pcp).
However, subsequent experiments indicate that metaphit is controlled by sites not associated with passive prevention deficits due to pcp and that are not connected to the nmda receptor complex.
Their application is focused on the nmda receptor complex. Metaphit was also shown to inhibit hyperactivity caused by d-amphetamine and substantially deplete the dopamine production of the nucleus accumbens.
The first acylating ligand to study the cocaine receptor was metaphite. It is a structural isomer of the like study compound, fourphit, because both metaphit and isothiocyanate replaced by an equivalent scaffold are widely shared with pcp.
Phencyclidine derived (pcp) metaphit is known to be a highly specific pcp antagonist, irreversibly connected to populations of pcp receptor sites in the cerebral rat. However, metaphit was seen in whole animal experiments to have antagonistic or pcp behavior, which are dependent on the animal species being used
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