Trifluoperazine Research Articles

Trifluoperazine exerts anti-osteosarcoma effect by inducing mitochondria-dependent apoptosis via AKT/TXNIP signaling pathway

The survival rates for patients with osteosarcoma (OS) have stagnated over the past few decades. It is essential to find new therapies and drugs. A licensed antipsychotic medication called trifluoperazine (TFP) significantly reduces the growth of several cancers. However, the exact molecular pathways of TFP in OS remain to be discovered. Our research revealed that TFP greatly reduced OS cell migration and growth and caused the arrest of G0/G1 cell cycle. Combined with RNA-Seq data and further research, we confirmed that TFP promoted reactive oxygen species (ROS) production by elevating thioredoxin binding protein (TXNIP) expression to induce mitochondria-dependent apoptosis. Interestingly, we first demonstrated that AKT was an upstream regulatory target of TXNIP in OS cells. Dephosphorylation of AKT led to an increase in TXNIP expression, further elucidating the anticancer mechanism of TFP. In vivo, TFP inhibited subcutaneous OS cell proliferation and induced OS cell apoptosis without noticeable side effects. In conclusion, our findings imply that TFP is a potential treatment for OS.

Quantification of the interaction forces between dengue virus and dopamine type-2 receptor using optical tweezers

BackgroundDengue virus (DENV) causes the most significant mosquito-borne viral disease with a wide spectrum of clinical manifestation, including neurological symptoms associated with lethal dengue diseases. Dopamine receptors are expressed in central nervous system, and dopamine antagonists have been reported to exhibit antiviral activity against DENV infection in vivo and in vitro. Although identification of host-cell receptor is critical to understand dengue neuropathogenesis and neurotropism, the involvement of dopamine receptors in DENV infection remains unclear.ResultsWe exploited the sensitivity and precision of force spectroscopy to address whether dopamine type-2 receptors (D2R) directly interact with DENV particles at the first step of infection. Using optical tweezers, we quantified and characterized DENV binding to D2R expressed on Chinese hamster ovary (CHO) cells. Our finding suggested that the binding was D2R- and DENV-dependent, and that the binding force was in the range of 50–60 pN. We showed that dopamine antagonists prochlorperazine (PCZ) and trifluoperazine (TFP), previously reported to inhibit dengue infection, interrupt the DENV-D2R specific binding.ConclusionsThis study demonstrates that D2R could specifically recognize DENV particles and function as an attachment factor on cell surfaces for DENV. We propose D2R as a host receptor for DENV and as a potential therapeutic target for anti-DENV drugs.Graphical abstract

Fluorometric Detection of Five Nitrogen-Based Pharmaceuticals Based on Ion-Pairing Association with EY: DFT Calculations

Fluorometric method for detecting of five nitrogen-based drugs concentration based on inhibition of emission Eosin Y (EY). The selection of N-drugs comprised indapamide (INDP), clomipramine hydrochloride (CMI), promethazine hydrochloride (PMH), lisinopril (LSP), and trifluoperazine hydrochloride (TFPH). The Stern–Volmer style was plotted between relative emissions of EY vs. N-drugs concentration. The standard curves were linear over the concentration range of 5–50 µg mL−1 with R2 > 0.9, and the LOD for INDP, CMI, PMH, LSP, and TFPH were 2.07, 1.36, 3.02, 3.52, and 2.09 µmol·L−1, respectively. The binding constant Kapp for LSP was greater than other N-drugs. Furthermore, the suggested method was hence applied for the routine detection of the concentration of N-drugs in bulk and tablet or syrup dosage forms. FTIR analysis and the electron-mapping density provided the chemical affinity of N-drugs towards EY.

Suppression of NUPR1 in fibroblast-like synoviocytes reduces synovial fibrosis via the Smad3 pathway

BackgroundSynovial fibrosis is a common complication of knee osteoarthritis (KOA), a pathological process characterized by myofibroblast activation and excessive extracellular matrix (ECM) deposition. Fibroblast-like synoviocytes (FLSs) are implicated in KOA pathogenesis, contributing to synovial fibrosis through diverse mechanisms. Nuclear protein 1 (NUPR1) is a recently identified transcription factor with crucial roles in various fibrotic diseases. However, its molecular determinants in KOA synovial fibrosis remain unknown. This study aims to investigate the role of NUPR1 in KOA synovial fibrosis through in vivo and in vitro experiments.MethodsWe examined NUPR1 expression in the murine synovium and determined the impact of NUPR1 on synovial fibrosis by knockdown models in the destabilization of the medial meniscus (DMM)-induced KOA mouse model. TGF-β was employed to induce fibrotic response and myofibroblast activation in mouse FLSs, and the role and molecular mechanisms in synovial fibrosis were evaluated under conditions of NUPR1 downexpression. Additionally, the pharmacological effect of NUPR1 inhibitor in synovial fibrosis was assessed using a surgically induced mouse KOA model.ResultsWe found that NUPR1 expression increased in the murine synovium after DMM surgical operation. The adeno-associated virus (AAV)-NUPR1 shRNA promoted NUPR1 deficiency, attenuating synovial fibrosis, inhibiting synovial hyperplasia, and significantly reducing the expression of pro-fibrotic molecules. Moreover, the lentivirus-mediated NUPR1 deficiency alleviated synoviocyte proliferation and inhibited fibroblast to myofibroblast transition. It also decreased the expression of fibrosis markers α-SMA, COL1A1, CTGF, Vimentin and promoted the activation of the SMAD family member 3 (SMAD3) pathway. Importantly, trifluoperazine (TFP), a NUPR1 inhibitor, attenuated synovial fibrosis in DMM mice.ConclusionsThese findings indicate that NUPR1 is an antifibrotic modulator in KOA, and its effect on anti-synovial fibrosis is partially mediated by SMAD3 signaling. This study reveals a promising target for developing novel antifibrotic treatment.

Synthesis and Structure of Novel Phenothiazine Derivatives, and Compound Prioritization via In Silico Target Search and Screening for Cytotoxic and Cholinesterase Modulatory Activities in Liver Cancer Cells and In Vivo in Zebrafish.

Phenothiazines (PTZ) are antipsychotics known to modulate a variety of neurotransmitter activities that include dopaminergic and cholinergic signaling and have been identified as potential anticancer agents in vitro. However, it is important to also test whether a highly cytotoxic, repurposed, or novel PTZ has low toxicity and neuromodulatory activity in vivo using vertebrate model organisms, such as zebrafish. In this study, we synthesized novel phenothiazines and screened them in vitro in liver cancer and in vivo in zebrafish embryos/larvae. The syntheses of several intermediate PTZ 10-yl acyl chlorides were followed by elemental analysis and determination of 1H NMR and 13C NMR mass (ESI+) spectra of a large number of novel PTZ 10-carboxamides. Cytotoxicities of 28 PTZ derivatives (1-28) screened against Hep3B and SkHep1 liver cancer cell lines revealed five intermediate and five novel leads along with trifluoperazine (TFP), prochlorperazine (PCP), and perphenazine, which are relatively more cytotoxic than the basic PTZ core. Overall, the derivatives were more cytotoxic to Hep3B than SkHep1 cells. Moreover, in silico target screening identified cholinesterases as some of the commonest targets of the screened phenothiazines. Interestingly, molecular docking studies with acetylcholinesterase (AChE) and butyrylcholinesterase proteins showed that the most cytotoxic compounds 1, 3, PCP, and TFP behaved similar to Huprin W in their amino acid interactions with the AChE protein. The highly cytotoxic intermediate PTZ derivative 1 exhibited a relatively lower toxicity profile than those of 2 and 3 during the zebrafish development. It also modulated in vivo the cholinesterase activity in a dose-dependent manner while significantly increasing the total cholinesterase activity and/or ACHE mRNA levels, independent of the liver cancer cell type. Our screen also identified novel phenothiazines, i.e., 8 and 10, with significant cytotoxic and cholinesterase modulatory effects in liver cancer cells; yet both compounds had low levels of toxicity in zebrafish. Moreover, they modulated the cholinesterase activity or expression of ACHE in a cancer cell line-specific manner, and compound 10 significantly inhibited the cholinesterase activity in zebrafish. Accordingly, using a successful combination of in silico, in vitro, and in vivo approaches, we identified several lead anticancer and cholinesterase modulatory PTZ derivatives for future research.

DIPG-62. REPURPOSING OF ANTIPSYCHOTIC TRIFLUOPERAZINE FOR INHIBITING MITOCHONDRIAL FUNCTION IN DIFFUSE MIDLINE GLIOMA

Abstract BACKGROUND Diffuse Midline Gliomas (DMGs) present formidable challenges in neuro-oncology, prompting the exploration of innovative therapeutic strategies. Repurposing approved drugs, particularly those exhibiting multifaceted effects, holds promise for addressing these challenges efficiently. In this study, we investigate the potential of trifluoperazine (TFP), an antipsychotic medication, with a specific focus on its mitochondrial-targeted actions in DMGs. METHODS TFP, a phenothiazine derivative, displayed robust in vitro anticancer activity against DMGs. Our investigation explored the molecular mechanisms underlying TFP’s interaction with mitochondria, emphasizing its influence on mitochondrial function, membrane potential, and reactive oxygen species (ROS) production. TFP is well known to induce irreversible Ca2+ release from intracellular stores by directly interacting with calmodulin 2 (CaM2) at the inositol triphosphate receptor (IP3R), leading to IP3R opening. In DMGs, intracellular Ca2+ plays a pivotal role in gene expression, cell motility, differentiation, and survival. TFP disrupts calcium homeostasis by elevating intracellular Ca2+ concentration, thereby inhibiting DMG invasion and growth. DMG cell lines, exhibiting heightened CaM2 expression compared to control healthy astrocyte cells, display increased sensitivity to TFP. RESULTS Remarkably, mitochondrial homeostasis was seriously affected by TFP, and a loss of mitochondrial membrane potential, ROS overproduction and fragmentation of mitochondrial network was observed. This mitochondrial stress, coupled with ER stress, activated the integrated stress response. We demonstrated that TFP induces cell death triggered by a poor ATP content, observed in TFP-treated cells as a consequence of a dramatic decrease in OXPHOS metabolism due to mitochondrial stress. CONCLUSIONS Our findings underscore TFP’s potential as a targeted therapeutic agent against DMGs, offering a better understanding of its impact on mitochondrial and intracellular signaling pathways. As the mitochondrial landscape remains critical in DMG biology, the observed mitochondrial damage-induced oxidative stress provides valuable insights for future investigations into the clinical application of TFP in neuro-oncology.

PpCaM7 and PpCAMTA5 synergistically mitigate chilling-induced browning by suppressing reactive oxygen species synthesis in peach fruit

This study investigated the potential regulatory mechanisms influencing chilling injury in peach fruit under various storage temperatures (0 ℃ and 5 ℃) and calcium treatments (calcium chloride (CaCl2) and trifluoperazine (TFP)). The results showed that 0 ℃ storage and CaCl2 treatment activated the expression of PpCAMTA5, while repressed the expression of PpNAC25, PpPAO, PpRBOHA, PpRBOHC, and PpRBOHD, and reduced hydrogen peroxide (H2O2) content. This concerted regulation effectively suppressed chilling-induced browning in peach fruit during cold storage. However, the opposite effects were presented in TFP-treated fruit. Additionally, the interaction between PpCaM7 and PpCAMTA5 inhibited PpNAC25-mediated transcriptional activation of PpPAO, PpRBOHA, PpRBOHC, and PpRBOHD. Thus, these results suggested that the PpCaM7-PpCAMTA5 complex mitigates chilling injury in peach fruit via inhibiting reactive oxygen species (ROS) production.

Amphiphilic Compounds as Antihemolytic Agents: Problems and Prospects

In this research the effect of surface-active substances belonging to different classes of amphiphilic compounds (cationic trifluoperazine (TFP), anionic sodium decyl sulfate (C10) and nonionic decyl-β,D-glucopyranoside (DGP)) on the level of damage of human erythrocytes during posthypertonic shock (PHS) and glycerol removal from cells frozen to –196°C was study. All amphiphilic compounds in low concentrations (at which the antihemolytic activity is approximately 45% under the conditions of PHS cells) show the same efficiency when removing glycerol from thawed cells. It was established that among amphiphilic compounds in effective concentrations the maximum antihemolytic (AHmax) activity was shown by DGP (74%) during the removal of glycerol from thawed cells and C10 (74%) under conditions of PHS of erythrocytes, while the AHmax activity indicators of TFP were comparable in both cases. A feature of the effectiveness of C10 under the conditions of deglycerolization of cryopreserved erythrocytes is almost the same AH when used in both concentrations. The method of flow cytometry showed that the amount of annexin-labeled cells depended on the concentration of C10 both in physiological solution and under PHS conditions.

Trifluoperazine mitigates cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in mice by modulating the AKT/mTOR-driven autophagy and Nrf2/HO-1 signaling cascades

AimThis study aims to investigate the hepatoprotective effect of the antipsychotic drug trifluoperazine (TFP) against cyclophosphamide (CPA)-induced hepatic injury by exploring its effect on autophagy and the Nrf2/HO-1 signaling pathway. Main methodsThe hepatotoxicity of CPA was assessed by biochemical analysis of the serum hepatotoxicity markers (ALT, AST, and direct bilirubin), histopathological examination, and ultrastructure analysis by transmission electron microscopy (TEM). The ELISA technique was used to assess the hepatic content of oxidative stress (MDA and SOD) and inflammatory markers (IL-1β and TNF-α). Immunohistochemical assessment was used to investigate the hepatic expression of NF-κB, Nrf2, caspase-3, as well as autophagy flux markers (p62 and LC3B). The mRNA expression of HO-1 was assessed using RT-qPCR. Western blot assay was used to determine the expression of p-AKT and p-mTOR. Key findingsTFP improved CPA-induced hepatotoxicity by reducing the elevated hepatotoxicity markers, and alleviating the histopathological changes with improving ultrastructure alterations. It also reduced oxidative stress by reducing MDA content and upregulating SOD activity. In addition, it exhibited anti-inflammatory and anti-apoptotic effects by decreasing NF-κB expression, IL-1β, TNF-α levels, and caspase-3 expression. Furthermore, TFP-induced hepatoprotection was mediated by favoring Nrf2 expression and increasing the mRNA level of HO-1. As well, it improved autophagy by increasing LC3B expression concurrently with reducing p62 expression. Moreover, TFP modulated the AKT/mTOR pathway by reducing the expression of p-AKT and p-mTOR. SignificanceTFP significantly protected against CPA-induced hepatotoxicity by upregulating Nrf2/HO-1 signaling along with enhancement of protective autophagy via inhibition of the AKT/mTOR signaling pathway.

High-throughput drug screen identifies calcium and calmodulin inhibitors that reduce JCPyV infection

JC polyomavirus (JCPyV) is a nonenveloped, double-stranded DNA virus that infects the majority of the population. Immunocompetent individuals harbor infection in their kidneys, while severe immunosuppression can result in JCPyV spread to the brain, causing the neurodegenerative disease progressive multifocal leukoencephalopathy (PML). Due to a lack of approved therapies to treat JCPyV and PML, the disease results in rapid deterioration, and is often fatal. In order to identify potential antiviral treatments for JCPyV, a high-throughput, large-scale drug screen was performed using the National Institutes of Health Clinical Collection (NCC). Drugs from the NCC were tested for inhibitory effects on JCPyV infection, and drugs from various classes that reduced JCPyV infection were identified, including receptor agonists and antagonists, calcium signaling modulators, and enzyme inhibitors. Given the role of calcium signaling in viral infection including Merkel cell polyomavirus and simian virus 40 polyomavirus (SV40), calcium signaling inhibitors were further explored for the capacity to impact JCPyV infection. Calcium and calmodulin inhibitors trifluoperazine (TFP), W-7, tetrandrine, and nifedipine reduced JCPyV infection, and TFP specifically reduced viral internalization. Additionally, TFP and W-7 reduced infection by BK polyomavirus, SV40, and SARS-CoV-2. These results highlight specific inhibitors, some FDA-approved, for the possible treatment and prevention of JCPyV and several other viruses, and further illuminate the calcium and calmodulin pathway as a potential target for antiviral drug development.

Development and validation of a stability indicating lc method for the analysis of chlordiazepoxide and trifluoperazine hydrochloride in the presence of their degradation products

Development and validation of a stability indicating lc method for the analysis of chlordiazepoxide and trifluoperazine hydrochloride in the presence of their degradation products

ATP-mediated increase in H+ efflux from retinal Müller cells of the axolotl.

Previous work has shown that activation of tiger salamander retinal radial glial cells by extracellular ATP induces a pronounced extracellular acidification, which has been proposed to be a potent modulator of neurotransmitter release. This study demonstrates that low micromolar concentrations of extracellular ATP similarly induce significant H+ effluxes from Müller cells isolated from the axolotl retina. Müller cells were enzymatically isolated from axolotl retina and H+ fluxes were measured from individual cells using self-referencing H+-selective microelectrodes. The increased H+ efflux from axolotl Müller cells induced by extracellular ATP required activation of metabotropic purinergic receptors and was dependent upon calcium released from internal stores. We further found that the ATP-evoked increase in H+ efflux from Müller cells of both tiger salamander and axolotl were sensitive to pharmacological agents known to interrupt calmodulin and protein kinase C (PKC) activity: chlorpromazine (CLP), trifluoperazine (TFP), and W-7 (all calmodulin inhibitors) and chelerythrine, a PKC inhibitor, all attenuated ATP-elicited increases in H+ efflux. ATP-initiated H+ fluxes of axolotl Müller cells were also significantly reduced by amiloride, suggesting a significant contribution by sodium-hydrogen exchangers (NHEs). In addition, α-cyano-4-hydroxycinnamate (4-cin), a monocarboxylate transport (MCT) inhibitor, also reduced the ATP-induced increase in H+ efflux in both axolotl and tiger salamander Müller cells, and when combined with amiloride, abolished ATP-evoked increase in H+ efflux. These data suggest that axolotl Müller cells are likely to be an excellent model system to understand the cell-signaling pathways regulating H+ release from glia and the role this may play in modulating neuronal signaling.NEW & NOTEWORTHY Glial cells are a key structural part of the tripartite synapse and have been suggested to regulate synaptic transmission, but the regulatory mechanisms remain unclear. We show that extracellular ATP, a potent glial cell activator, induces H+ efflux from axolotl retinal Müller (glial) cells through a calcium-dependent pathway that is likely to involve calmodulin, PKC, Na+/H+ exchange, and monocarboxylate transport, and suggest that such H+ release may play a key role in modulating neuronal transmission.

Combined effect of trifluoperazine and sodium cromoglycate on reducing acute edema and limiting lasting functional impairments after spinal cord injury in rats

Edema formation is one of the very first events to occur after spinal cord injury (SCI) leading to an increase of the intrathecal pressure and consequently to serious spinal tissue and functional impairments. Current edema treatments are still symptomatic and/or non-specific. Since edema formation mechanisms are mainly described as vasogenic and cytotoxic, it becomes crucial to understand the interplay between these two subtypes. Acting on key targets to inhibit edema formation may reduce secondary damage and related functional impairments. In this study, we characterize the edema kinetic after T9–10 spinal contusion. We use trifluoperazine (TFP) to block the expression and the functional subcellular localization of aquaporin-4 supposed to be implicated in the cytotoxic edema formation. We also use sodium cromoglycate (SCG) to deactivate mast cell degranulation known to be implicated in the vasogenic edema formation. Our results show a significant reduction of edema after TFP treatment and after TFP-SCG combined treatment compared to control. This reduction is correlated with limited onset of initial sensorimotor impairments particularly after combined treatment. Our results highlight the importance of potential synergetic targets in early edema therapy after SCI as part of tissue sparing strategies.

Inhibition of Erb-B2 Receptor Tyrosine Kinase 3 and Associated Regulatory Pathways Potently Impairs Malignant Peripheral Nerve Sheath Tumor Proliferation and Survival

Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, currently untreatable Schwann cell-derived neoplasms with hyperactive mitogen-activated protein kinase and mammalian target of rapamycin signaling pathways. To identify potential therapeutic targets, previous studies used genome-scale shRNA screens that implicated the neuregulin-1 receptor erb-B2 receptor tyrosine kinase 3 (erbB3) in MPNST proliferation and/or survival. The current study shows that erbB3 is commonly expressed in MPNSTs and MPNST cell lines and that erbB3 knockdown inhibits MPNST proliferation and survival. Kinomic and microarray analyses of Schwann and MPNST cells implicate Src- and erbB3-mediated calmodulin-regulated signaling as key pathways. Consistent with this, inhibition of upstream (canertinib, sapitinib, saracatinib, and calmodulin) and parallel (AZD1208) signaling pathways involving mitogen-activated protein kinase and mammalian target of rapamycin reduced MPNST proliferation and survival. ErbB inhibitors (canertinib and sapitinib) or erbB3 knockdown in combination with Src (saracatinib), calmodulin [trifluoperazine (TFP)], or proviral integration site of Moloney murine leukemia kinase (AZD1208) inhibition even more effectively reduces proliferation and survival. Drug inhibition enhances an unstudied calmodulin-dependent protein kinase IIα phosphorylation site in an Src-dependent manner. The Src family kinase inhibitor saracatinib reduces both basal and TFP-induced erbB3 and calmodulin-dependent protein kinase IIα phosphorylation. Src inhibition (saracatinib), like erbB3 knockdown, prevents these phosphorylation events; and when combined with TFP, it even more effectively reduces proliferation and survival compared with monotherapy. These findings implicate erbB3, calmodulin, proviral integration site of Moloney murine leukemia kinases, and Src family members as important therapeutic targets in MPNSTs and demonstrate that combinatorial therapies targeting critical MPNST signaling pathways are more effective.

SPRAY-DRIED CHITOSAN MICROSPHERES FOR SUSTAINED DELIVERY OF TRIFLUOPERAZINE HYDROCHLORIDE: FORMULATION AND IN VITRO EVALUATION

Objective: Sustained release systems have the potential to enhance the therapeutic responses in the long-term management of psychiatric disorders. In the present study, cross-linked microspheres of the antipsychotic drug Trifluoperazine (TFP) were prepared using biodegradable polymer-chitosan and various in vitro evaluations were performed on the prepared microspheres. Methods: The spray drying technique was used to prepare TFP-loaded chitosan microspheres. Tripolyphosphate (TPP) was incorporated into the chitosan solutions as a cross-linking agent in varying concentrations. Different evaluations like production yield, encapsulation efficiency, drug-polymer compatibility, Scanning Electron Microscopy (SEM), X-ray diffraction studies (XRD), Differential Scanning Colorimetry (DSC), particle size, zeta potential analysis and in vitro drug release studies were performed on the developed formulations. Results: The formulated microparticles exhibited production yields ranging from 38.51 to 57.21% and had reasonably good encapsulation efficiencies (54.52-78.35%). The drug excipient compatibility was confirmed by Infrared Spectroscopy. All the microspheres showed positive zeta potential with a mean diameter ranging from 1.45-3.61µ. SEM images revealed the formation of spherical particles with indentations on the surface. XRD and DSC studies confirmed the presence of an amorphous form of the drug inside the microspheres. The in vitro release profile of TFP from cross-linked chitosan microspheres was influenced considerably by changing the concentration of polymer and crosslinking agent in the formulation. The drug release from (0.5%) chitosan microspheres reduced from 91% to 79%, when TPP concentration was increased from 10% w/w to 30% w/w. All the formulations clearly showed a burst release of the drug in the initial hours and a subsequent sustained release profile. Conclusion: The results of this study suggest that TPP crosslinked spray-dried chitosan microparticles could be a promising method for developing a long-acting drug delivery system intended to effectively treat schizophrenia.

Determination of trace amount of some drugs as in its pure form and in its Pharmaceutical Preparations by using different spectroscopic methods

The present study includes analytical methods for determination of the drugs Chlorpromazine hydrochloride (CPZ) and trifluoperazine hydrochloride (TFPH) in some pharmaceuticals using molecular absorption, indirect AAS, in addition to investigating complexes obtained throughout. Chlorpromazine hydrochloride and trifluoperazine hydrochloride are widely used for the treatment of schizophrenia. Synthetic formulas for the prepared drug complexes were proposed through the results of the molar ratios of the combination between the drug and each of copper, lead, chrome and iron.

Spectrophotometric determination of Trifluoperazine Hydrochloride by oxidative coupling reaction with 4- amino benzoic acid using potassium iodate

A new sensitive spectrophotometric method for the determination of trifluoperazine hydrochloride (TFPH) is developed. The method is based on an oxidative coupling reaction with 4- amino benzoic acid using potassium iodate as oxidizing agent in acidic midium to produce a violet color, soluble in water, stable product absorbs at 550 nm. Beer's law is in the linear range 10 - 80 μg/ml of TFPH. The molar absorptivity, Sandellʼs and detection limit (LOD) are 0.8032×104 liter. mol-1.cm-1, 0.0598 μg/cm2, 0.3882 μg/ml respectively. The RSD value is 0.177 – 0.295 %. This method is applied successfully for the determination of trifluoperazine hydrochloride in pharmaceutical formulations (tablets of salabid) and injection

Usage of Trifluoperazine Hydrochloride as Colorimetric Reagent for Quantitative Assay of Sulfamethoxazole Drug and Applications on Different Some Infection Treatment Preparations

Usage of Trifluoperazine Hydrochloride as Colorimetric Reagent for Quantitative Assay of Sulfamethoxazole Drug and Applications on Different Some Infection Treatment Preparations

Development of a New Analytical Method for Estimation of Trifluoperazine-HCl in Pharmaceutical Formulation

The estimation of trifluoperazine hydrochloride in pure and dosage forms has been developed using a simple spectrophotometric method. The method is based on using an oxidation-reduction reaction with 4,7diphenyl 1,10-phenanthroline in the presence of Ferric)III( ion solution to produce a red-colored product complex of Fe(II )- 4,7diphenyl 1,10phenanthroline with maximum absorption at 533nm. The molar absorptivity is 0.44x104 L. mole -1.cm-1, Beer's law is followed over a concentration range of 5-100 μg. ml-1.Various parameters that influence the development and stability of the color product were thoroughly researched and optimized, and a reaction pathway proposal was offered. The proposed method was successfully used to determine trifluoperazine hydrochloride in tablet form.

Perovskite lanthanum nickelate nanoparticles: As effective modified screen printed carbon electrode for electrochemical detection of trifluoperazine

Perovskite rare earth nickelates have recently been considered excellent electroanalytical features for sensing a variety of target molecules due to their distinctive properties. In this work, a facile coprecipitation synthesis of perovskite lanthanum nickelate (LaNiO3, LNO) nanoparticles was reported along with its application to the electrochemical sensing of trifluoperazine (TFP). The crystal structure and surface morphology of the LNO was characterized by suitable techniques such as X-ray diffraction (XRD), Fourier transform infrared spectrometry (FTIR), X-ray photoelectron spectroscopy (XPS), field emission scanning electron microscopy (FESEM), and transmission electron microscopy (TEM) with energy-dispersive X-ray (EDX) analysis. The capability of the modified screen printed carbon electrode (LNO/SPCE) to detect TFP in 0.1 M PBS (pH 7) was then examined using cyclic voltammetry (CV) and differential pulse voltammetry (DPV) methods. The electrode modified at 0.759 V vs Ag/AgCl and 30 s exhibited the highest peak current (Ip) for TFP electrooxidation. This optimized electrode showed a broad linear range of 0.165–495.5 µM, a low limit of detection (LOD) of 0.017 µM, and a good sensitivity of 0.704 µA µM–1 cm–2. Moreover, the fabricated sensor revealed promising anti-interfering ability, stability, reproducibility, and repeatability toward TFP detection. Finally, the LNO sensor was able to detect TFP in urine and serum samples, and the recovery rates were satisfactory.