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Trifluoperazine - Crossref

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Last Updated: 10 September 2022

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Indications for the use of Tranylcypromine and Trifluoperazine: (Parstelin)

The combination of tranylcypromine and trifluoperazine was used by thirty-two patients. In ten of the 15 patients with phobic symptoms, a satisfactory response was recorded in ten out of ten out of the 15 patients with phobic symptoms. In the neurotic depressive reaction group, side effects were troubling. In the phobic group, the signs of the patients who responded were likely to recur as a result of therapy were stopped.

Source link: https://doi.org/10.1177/003693307802300410


Effects of trifluoperazine on rat prolactin, growth hormone, thyroid stimulating hormone and adrenocorticotrophin secretion in vitro

A significant reversible dose-related decrease in basal Prl secrecy that was linked to dipocalcination and hypothesis was achieved by trifluoperazine in 10 u22126 m and 10 m, but it was less effective on basal GH signalion, with significant reversible inhibition observed only with 10 u22125 m. Trifluoperazine did not consistently alter basal ACTH or TSH secretion, but did delay 10-12212 m theophylline stimulation of ACTH, Prl, and TSH secretion, which culminated in TSH and Prl secretion stimulation, which culminated in TSH and Prl secretion stimulation.

Source link: https://doi.org/10.1530/acta.0.1030492


Effects of trifluoperazine on prolactin release and cyclic AMP formation and degradation in GH4C1 pituitary cells

TFP was reduced by 30 bcmol/l TFP because of the increase in basal hormone release triggered by TRH and a high extracellular concentration of K +. The Ca 2+ antagonists Co 2+ and Verapamil, as well as the Ca 2+ chelator EgTA, also stopped the PRL release of TRH and K + 50 mmol/l, although only Co 2+ blocked the TFP-induced stimulation induced by 100 u03bcmol/l TFP stimulation caused by 100 u03bcmol/l TFP stimulation caused by 100 0/l TFP. The incubation of intact GH 4 C 1 cells with TFP had an inhibitory effect on both the low and the high affinity forms of cAMP phosphodiesterase.

Source link: https://doi.org/10.1530/acta.0.1160027


Abstract 96: Conformational and thermodynamics analyses of the regulation of trifluoperazine on camodulin binding to Fas: Implications for cancer chemotherapy

calmodulin binds to Fas and controls Fas-mediated DISC formation, according to latest experimental results, and the binding of CaM to Fas is hampered by the CaM antagonist, trifluoperazine. We investigated the effects of various number of TFP with CaM's CaM conformational changes on CaM/Fas binding. The binding affinity of one TFP to CaM was influenced by sequential binding of other TFP to CaM, which was consistent with near-UC circular dichroism results. The number of TFP bound to CaM was shown to influence CaM's conformational and motion changes, and therefore directly affect CaM binding to Fas. One TFP bound to CaM inhibited CaM-Fas binding, indicating that TFP concentrations influenced CaM-Fas binding, which was inconsistent with previous experimental findings that TFP concentrations interfered with CaM-Fas binding, although the subsequent two TFPs or four TFPs bound to CaM resulted in CaM-Fas binding returning to CaM. The number of TFPs bound to CaM was also correlated to Fas' conformational and movemental changes, which may have a direct correlation to the number of TFPs bound to CaM, which may also influence Fas recruitment of FADD to the DISC. Table 1. The change of CaM-Fas binding affinity by the CaM antagonist, TFP, in regulating CaM-Fas binding and Fas-mediated DISC formation and apoptosis is revealed by this research.

Source link: https://doi.org/10.1158/1538-7445.am10-96


Abstract 684: Trifluoperazine modulates DNA damage-induced cell death in human lung cancer cells through inhibition of DNA repair, cell cycle delays, and augmentation of pro-apoptotic signaling

Abstract Trifluoperazine modifies DNA damage-induced cell death in human lung cancer cells by inhibition of DNA repair, cell cycle arrest, and increase of pro-apoptotic signaling resistance of human lung cancer cells is a major obstacle to current treatment's success. We exposed human non-small cell lung cancer cell line cells to the DNA damaging drug bleomycin in the presence or absence of TFP, and we investigated potential differences in terms of DNA repair and cell death signaling. In conclusion, we show here that the chemosensitizing effect of TFP in NSCLC cells is linked to interference with DNA DSB repair, resulting in second G-M checkpoint arrest after initial checkpoint conversion, and concomitant rises in pro-apoptotic signaling.

Source link: https://doi.org/10.1158/1538-7445.am10-684


Abstract 2541: Inhibition of DNA repair by trifluoperazine sensitizes human lung cancer cells to apoptosis associated with lysosomal dysfunction following prolonged G2-M checkpoint arrest

Abstract : The use of DNA damaging chemotherapy in human lung non-small cell lung carcinoma is severely limited by clinical toxicity. Here we demonstrate that chemosensitization can be achieved in NSCLC by combining clinically relevant DNA damaging agents with trifluoperazine. TFP clearly improved the cytotoxicity of bleomycin and cisplatin cell lines in NSCLC cell lines, according to Colony formation assays. NSCLC cells co-treated with TFP, bleomycin or cisplatin at the initial G2-M checkpoint arrest were able to recover the initial G2-M checkpoint arrest at two separate time points, as shown by the reappearance of the mitosis markers and decrease in CFSE fluorescence at later time points. TFP co-treated NSCLC cells underwent little lysosomal membrane permeabilization prior to Bak/Bax activation and mitochondrial depolarization, according to TFP co-treated NSCLC cells. In conclusion, our results point to the conclusion that TFP prolongs NSCLC cells into prolonged checkpoint arrest, which exposes them to apoptosis associated with lysosomal dysfunction.

Source link: https://doi.org/10.1158/1538-7445.am2011-2541


Abstract 109: Effects of trifluoperazine analogue on A549 human lung cancer cells

Abstract Although research in technology, molecular diagnosis, and therapeutics has improved, lung cancer is still the most common cause of cancer-related deaths around the world. The viability of A549 cells following pharmaceutical therapy was determined by a comparison to TFP. TFP and KCFC51 alter cell apoptosis and cell cycle, according to a Western blot review, which revealed that TFP and KCFC51 had an effect on protein expression profiles related to cell apoptosis and cell cycle. KCFC51 caused a sub-G1 population and reduced cell count in S and G2/M phase, according to a flow cytometric report by Flow cytometry. In addition, TFP's two experimental models in vivo, KCFC51 showed greater anticancer activity in skin xenograft tumor formation and orthotropic lung cancer formation than TFP. A synthetic TFP analog has anti-lung cancer activity and is a potential therapeutic candidate for lung cancer, according to the present study. Human lung cancer cells cell lines in A549 are among the A549 human lung cancer cells [abstract].

Source link: https://doi.org/10.1158/1538-7445.am2017-109


The antipsychotic drug trifluoperazine inhibits DNA repair and sensitizes non–small cell lung carcinoma cells to DNA double-strand break–induced cell death

We investigated the effect of trifluoperazine on the survival of bleomycin-treated human non-u2013small cell lung carcinoma U1810 cells, induction and repair of bleomycin-induced DNA fragment breaks, and nonhomologous end-joining, mammalian cells' key DNA double-strand break repair pathway. Moreover, trifluoperazine prolongs strand breaks in U1810 cells, as shown by both comet assay and a portion of activity published, according to assay. We believe that TFP could be capable of blocking one or two aspects of the DNA DSB repair machinery, thereby raising the cytotoxicity of bleomycin in lung cancer cells.

Source link: https://doi.org/10.1158/1535-7163.mct-06-0402


Trifluoperazine, a Well-Known Antipsychotic, Inhibits Glioblastoma Invasion by Binding to Calmodulin and Disinhibiting Calcium Release Channel IP3R

Trifluoperazine, an FDA-approved antipsychotic drug for schizophrenia, is a trifluoperazine. However, the potential anticancer effects of TFP on glioblastoma has yet to be investigated. In an in vitro xenograft mouse model, we find that TFP potently inhibits proliferation, motility, and invasion of glioblastoma cells in vitro, as well as tumor formation. Unlike caffeine, TFP induces dramatic and irreversible release of Ca2+ from intracellular stores by IP3R subtype 1 and 2 by directly visiting a Ca2+-binding protein, calmodulin subtype 2, TFP-binding protein, a Ca2+-binding protein, calmodulin subtype 2. CaM2 is dissociated from IP3R and subsequent opening of IP3R as a result of a TFP binding to CaM2 causing a loss of CaM2 from IP3R and subsequent opening of IP3R. Compared to the control neural stem cells, several glioblastoma cell lines showed elevated expression of CaM2 and therefore elevated sensitivity to TFP. We suggest TFP as a potential therapeutic agent for glioblastoma by aberrantly and irreversibly increasing Ca2+ in glioblastoma cells.

Source link: https://doi.org/10.1158/1535-7163.mct-16-0169-t


The dopamine receptor antagonist trifluoperazine prevents phenotype conversion and improves survival in mouse models of glioblastoma

We're aware that radiation promotes a glioma-initiating cell phenotype, and we've identified trifluoperazine as a drug that interferes with this phenotype conversion. In syngeneic and patient-derived orthotopic xenograft mouse models of GBM, continuous therapy with TFP and a single dose of radiation reduced the number of GICs in vivo and prolonged survival. Our results show that a combination of a dopamine receptor antagonist and radiation enhances the effectiveness of RT in GBM by preventing radiation-induced phenotype conversion of radiosensitive non-GICs into treatment-resistant, induced GICs.

Source link: https://doi.org/10.1073/pnas.1920154117

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions