fluphenazine

Fluphenazine dihydrochloride (Prolixin) is an inhibitor of phenothiazine-class D1DR and D2DR; In studies, Fluphenazine can be used to probe the effects and metabolic process of this commonly used dopamine antagonist.

Flufenazine is an antipsychotic drug. It is used to treat chronic mental illnesses such as schizophrenia. Flufenazine works by blocking postsynaptic dopamine D2 receptors in the limbic system, cortical system, and basal ganglia. This prevents the effects

Fluphenazine enanthate is a novel long-acting injectable (LAI) antipsychotic compound specifically designed for the treatment of schizophrenia.

Fluphenazine Decanoate Dihydrochloride is an antipsychotic agent, it could block postsynaptic dopamine D2 receptors in the limbic, cortical system and basal ganglia.

Fluphenazine-d8 Dihydrochloride is a deuterated compound of Fluphenazine Dihydrochloride. Fluphenazine Dihydrochloride has a CAS number of 146-56-5. Fluphenazine dihydrochloride is an inhibitor of phenothiazine-class D1DR and D2DR; In studies, Fluphenazine can be used to probe the effects and metabolic process of this commonly used dopamine antagonist.

Fluphenazine is a traditional antipsychotic compound that tightly binds the dopamine D2 receptor (Ki = 0.55 nM) and also reversibly inhibits calmodulin at micromolar concentrations. Fluphenazine-N-2-chloroethane is a derivative of fluphenazine that contains an alkylating chlorethylamine chain, which produces irreversible protein binding. It is a relatively selective, irreversible antagonist of D2 receptors both in vitro (IC50 = 100 nM) and in vivo, inactivating approximately 90% of D2 receptors in mice within 4 hours of treatment. Through this action, fluphenazine-B-2-chloroethane can be used to induce catalepsy in mice. It irreversibly inhibits calmodulin at higher doses (IC50 = 10 μM), which can sensitize cancer cells to TRAIL-induced apoptosis.

Fluphenazine decanoate is dopamine D2 receptor blocke,and is a long-acting phenothiazine neuroleptic that used to treat schizophrenia.

ADTN hydrobromide (6,7-ADTN) is a dopamine receptor agonist (EC50s = 3.5 and 0.65 μM in rat striatal and nucleus accumbens homogenates, respectively). ADTN hydrobromide stimulates production of cAMP in rat striatal homogenates, a process that is reduced by 70% in the presence of the dopamine antagonist fluphenazine at a concentration of 1 μM.

Gonadorelin, a gonadotropin-releasing hormone receptor (GNRHR; Ki= 13 nM in CHO cells expressing the human receptor) agonist and tropic hormone, effectively stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from rat anterior pituitary cultures at 0.1 μg doses. Additionally, it triggers LH release from bovine anterior pituitary cultures at a 1 μM concentration. In vivo, gonadorelin induces ovulation in rats pretreated with fluphenazine (ED50= 610.3 ng/kg). Gonadorelin-based formulations are utilized as diagnostic tools to evaluate pituitary gland function.

TPC2-A1-N is a novel, lipophilic, membrane permeable isoform-selective small molecule agonist of two-pore channel 2 (TPC2). TPC2-A1-N plays its role by mimicking the physiological actions of NAADP and PI(3,5)P2 through independent binding sites. TPC2-A1-N has inverse effects on key lysosomal activities and increases the pH in the lysosomal lumen in a TPC2-dependent manner[1]. Two-pore channels (TPC1-3) are ancient members of the voltage-gated ion channel superfamily. TPCs are expressed throughout the endo-lysosomal system and regulates the trafficking of various cargoes.TPC2 can mediate different physiological and possibly pathophysiological effects depending on how it is activated. The ion selectivity of TPC2 is not fixed but rather agonist-dependent. TPC2 is a unique example of an ion channel that conducts different ions in response to different activating ligands.TPC2-A1-N (10 μM) reproducibly evokes Ca2+ signals, and TPC2-A1-N response reachs its plateau faster than TPC2-A1-P. The EC50 in full concentration-effect relationships for the plateau response is 7.8 μM for TPC2-A1-N in a cell line stably expressing TPC2L11A/L12A.TPC2-A1-N (10 μM) evokes Ca2+ influx through the TPC2 pore evokes Ca2+ signals in cells expressing TPC2L11A/L12A but not TPC2L11A/L12A/L265P. Additionally, the responses to TPC2-A1-N can be selectively blocked by the identified TPC2 blockers Tetrandrine , Raloxifene , and Fluphenazine by removal of extracellular Ca2+[1].In endo-lysosomal patch-clamp experiments, TPC2-A1-N (30 μM) elicits currents using Na+ as the major permeant ion, in vacuolin-enlarged endo-lysosomes isolated from isolated from HEK293 cells transiently expressing human TPC2 (hTPC2) but not in cells expressing TPC1[1].In endo-lysosomal patch-clamp experiments, TPC2-A1-N (30 μM) induces larger currents in endo-lysosomes isolated from cells expressing a gain-of-function variant of TPC2 (TPC2M484L) compared to the wild-type isoform, and exhibits an EC50 value of 0.6 μM for TPC2-A1-N[1]. [1]. Susanne Gerndt, et al. Agonist-mediated switching of ion selectivity in TPC2 differentially promotes lysosomal function. Elife