Pyrvinium (Viprynium) is an anthelmintic effective for pinworms. Pyrvinium is used in the treatment of enterobiasis caused by Enterobius vermicularis (pinworm). Pyrvinium has being shown to be a potent inhibitor of Wnt signaling (EC(50) of ∼10 nM). Pyrvinium binds all casein kinase 1 (CK1) family members in vitro at low nanomolar concentrations and pyrvinium selectively potentiates casein kinase 1α (CK1α) kinase activity. Pyrvinium pamoate (PP) is a potent noncompetitive inhibitor of the androgen receptor (AR). A noncompetitive AR inhibitor pyrvinium has significant potential to treat CRPC, including cancers driven by ligand-independent AR signaling.

Pyrvinium (Viprynium) is an anthelmintic effective for pinworms. Pyrvinium is used in the treatment of enterobiasis caused by Enterobius vermicularis (pinworm). Pyrvinium has being shown to be a potent inhibitor of Wnt signaling (EC(50) of ∼10 nM). Pyrvinium binds all casein kinase 1 (CK1) family members in vitro at low nanomolar concentrations and pyrvinium selectively potentiates casein kinase 1α (CK1α) kinase activity. Pyrvinium pamoate (PP) is a potent noncompetitive inhibitor of the androgen receptor (AR). A noncompetitive AR inhibitor pyrvinium has significant potential to treat CRPC, including cancers driven by ligand-independent AR signaling.

Pyrvinium (Viprynium) is an anthelmintic effective for pinworms. Pyrvinium is used in the treatment of enterobiasis caused by Enterobius vermicularis (pinworm). Pyrvinium has being shown to be a potent inhibitor of Wnt signaling (EC(50) of ∼10 nM). Pyrvinium binds all casein kinase 1 (CK1) family members in vitro at low nanomolar concentrations and pyrvinium selectively potentiates casein kinase 1α (CK1α) kinase activity. Pyrvinium pamoate (PP) is a potent noncompetitive inhibitor of the androgen receptor (AR). A noncompetitive AR inhibitor pyrvinium has significant potential to treat CRPC, including cancers driven by ligand-independent AR signaling.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Piperidolate hydrochloride is an antimuscarinic, inhibits intestinal cramp induced by acetylcholine (rats and dogs. It’s usually used to kill the cramp-like pain of gastric/duodenal ulcer, gastritis, enteritis, gallstones, cholecystitis and biliary tract dyskinesia and to improve some symptoms in threatened miscarriage/premature delivery. Piperidolate blocked the contraction of ACh, Ba ++ and electrical stimulations on the isolated rat, mouse and guinea-pig ileum and trachea. In guinea-pig teania caeci, piperidolate like papaverine blocked specifically the tonic response, however, piperidolate in high doses completely blocked both spike and tonic responses. These results indicate that spasmolytic action of piperidolate like that of papaverine may depend upon inhibition of the release of store Ca++. Moreover piperidolate, given at high doses, may inhibit the contractile elements in the smooth muscle. In the rat uterus pretreated with sex hormones, piperidolate nonspecifically blocked the contraction of ACh, Ba ++ and oxytocin and sex hormones had no influence on the spasmolytic action of piperidolate.

Thiamylal is a barbiturate that is administered intravenously for the production of complete anesthesia of short duration, for the induction of general anesthesia, or for inducing a hypnotic state. Thiamylal, a barbiturate, is used in combination with acetaminophen or aspirin and caffeine for its sedative and relaxant effects in the treatment of tension headaches, migraines, and pain. Barbiturates act as nonselective depressants of the central nervous system (CNS), capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. In sufficiently high therapeutic doses, barbiturates induce anesthesia. Thiamylal binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.