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RTI-4793-14 (HBMP), a ligand with high affinity for the PCP site 2 and high selectivity for this site over the PCP site 1, has been developed. [2] [3] Similarly to PCP, RTI-4793-1 inhibits monoamine reuptake with moderate potency, but unlike PCP, has very low potency as an NMDA receptor antagonist. [2]
Phencyclidine or phenylcyclohexyl piperidine (PCP), also known in its use as a street drug as angel dust among other names, is a dissociative anesthetic mainly used recreationally for its significant mind-altering effects. [1] [4] PCP may cause hallucinations, distorted perceptions of sounds, and violent behavior.
Phencyclidine (PCP) is believed to be the first arylcyclohexylamine with recognized anesthetic properties, but several arylcyclohexylamines were described before PCP in the scientific literature, beginning with PCA (1-phenylcyclohexan-1-amine) the synthesis of which was first published in 1907. PCP itself was discovered in 1926 but not ...
Phencyclidine, a hallucinogenic and dissociative recreational drug, also known as angel dust 3-HO-PCP, a designer drug related to phencyclidine; 3-MeO-PCP, a designer drug related to phencyclidine; 4-MeO-PCP, a research chemical related to phencyclidine; Pneumocystis pneumonia, a form of pneumonia caused by the yeast-like fungus Pneumocystis ...
The high affinity of 3-HO-PCP for opioid receptors is unique among arylcyclohexylamines and is in contrast to PCP, which has only very low affinity for the MOR (K i = 11,000–26,000 nM; 282- to 433-fold difference) and the other opioid receptors (K i = 4,100 nM for the KOR and 73,000 nM for the DOR).
3-MeO-PCP was first synthesized in 1979 to investigate the structure–activity relationships of phencyclidine (PCP) derivatives.The effects of 3-MeO-PCP in humans were not described until 1999 when a chemist using the pseudonym John Q. Beagle wrote that 3-MeO-PCP was qualitatively similar to PCP with comparable potency. [1]
Phencyclidine (also known as PCP or "Angel Dust") and ketamine, both of which block glutamate receptors, are known to cause psychosis at least somewhat resembling schizophrenia, further suggesting that psychosis and perhaps schizophrenia cannot fully be explained in terms of dopamine function, but may also involve other neurotransmitters. [57]
The ED 50 (effective dose 50) for neuroprotection was 0.3 mg/kg and the majority of the animals were protected against the ischemia-induced damage at doses greater than or equal to 3 mg/kg, when dizocilpine was given one hour prior to the occlusion of the carotid arteries, although other studies have shown protection up to 24 hours post-insult.