Anti-prostate Cancer Drug Research Articles

Electrocatalytic degradation of flutamide an anti-prostate cancer drug and its metabolite 4-nitro-3-(trifluoromethyl) aniline using a simple graphite/β-PbO2 electrode

Flutamide is an anti-androgen drug used to treat prostate cancer. It has been determined that this drug exists in aqueous environments at ng/L levels. On the other hand, the environmental impacts of flutamide (FLU) have not yet been determined. This paper reports a simple electrocatalytic convergent-paired strategy for the degradation of FLU and its metabolite 4-nitro-3-(trifluoromethyl) aniline (NTA) using a simple graphite/β-PbO2 anode. The prepared electrode has good electrochemical stability and lifetime (more than 60 h). The results showed that the degradation efficiency of FLU and NTA under optimal conditions (pH 5.0, pollutant concentration 138 ppm and applied current density 4.9 mA/cm2) is 86 and 99 %, respectively. Also, in the solution containing both FLU and NTA with a concentration of 138 ppm of each compound, the degradation efficiency of FLU and NTA is 82 % and 92 %, respectively. Furthermore, we have comprehensively investigated the electrochemical behavior of FLU and NTA and we compared the electrochemical similarities and differences of the drug with its metabolite, and also reported important data such as electrochemical reaction mechanism, pH-potential relationship, and drug absorption/diffusion activity.

Enzalutamide inhibits PEX10 function and sensitizes prostate cancer cells to ROS activators

Sharply increased reactive oxygen species (ROS) are thought to induce oxidative stress, damage cell structure and cause cell death; however, its role in prostate cancer remains unclear. Enzalutamide is a widely used anti-prostate cancer drug that antagonizes androgen binding with its receptor. Further exploration of the mechanism and potential application strategies of enzalutamide is crucial for the treatment of prostate cancer. Here, we confirmed PEX10 can be induced by ROS activators while reduce ROS level in prostate cancer cells, which weakened the anti-tumor effect of ROS activators. The androgen receptor (AR) can promote the expression of PEX10 by acting as an enhancer in cooperation with FOXA1. The anti-tumor drug enzalutamide inhibits PEX10 by inhibiting the function of AR, and synergize with ROS activators ML210 or RSL3 to produce a stronger anti-tumor effect, thereby sensitizing cells to ROS activators. This study reveals a previously unrecognized function of enzalutamide and AR by regulating PEX10 and suggests a new strategy of enzalutamide application in prostate cancer treatment.

Microtubule depolymerization induces ferroptosis in neuroblastoma cells.

Estramustine (EM), a clinically successful hormone-refractory anti-prostate cancer drug, exhibited potent anti-proliferative activity, depolymerized microtubules, blocked cells at mitosis, and induced cell death in different cancer cells. Altered iron metabolism is a feature of cancer cells. Using EM, we examined the plausible relationship between microtubule depolymerization and induction of ferroptosis in human neuroblastoma (SH-SY5Y and IMR-32) cells. EM reduced glutathione (GSH) levels and induced reactive oxygen species (ROS) generation. The pre-treatment of neuroblastoma cells with ROS scavengers (N-acetyl cysteine and dithiothreitol) reduced the anti-proliferative effects of EM. EM treatment increased labile iron pool (LIP), depleted glutathione peroxidase 4 (GPX4) levels, and lipid peroxidation, hallmark features of ferroptosis, highlighting ferroptosis induction. Ferroptosis inhibitors (deferoxamine mesylate and liproxstatin-1) abrogated the cytotoxic effects of EM, further confirming ferroptosis induction. Vinblastine and nocodazole also increased LIP and induced lipid peroxidation in neuroblastoma cells. This study provides evidence for the coupling of microtubule integrity to ferroptosis. The results also suggest that microtubule-depolymerizing agents may be considered for developing pro-ferroptosis chemotherapeutics.

Ilicicolin C suppresses the progression of prostate cancer by inhibiting PI3K/AKT/mTOR pathway.

Aberrant activation of the PI3K/AKT pathway is a driving factor in the development of prostate cancer. Therefore, inhibiting the function of the PI3K/AKT signaling pathway is a strategy for the treatment of prostate cancer. Ilicicolin C is an ascochlorin derivative isolated from the coral-derived fungus Acremonium sclerotigenum GXIMD 02501. Which has anti-inflammatory activity, but its activity against prostate cancer has not yet been elucidated. MTT assay, plate clone-formation assay, flow cytometry and real-time cell analysis technology were used to detect the effects of ilicicolin C on cell viability, proliferation, apoptosis and migration of prostate cancer cells. Molecular docking software and surface plasmon resonance technology were used to analyze the interaction between ilicicolin C and PI3K/AKT proteins. Western blot assay was performed to examine the changes in protein expression. Finally, QikProp software was used to simulate the process of ilicicolin C in vivo, and a zebrafish xenograft model was used to further verify the anti-prostate cancer activity of ilicicolin C in vivo. Ilicicolin C showed cytotoxic effects on prostate cancer cells, with the most significant effect on PC-3 cells. Ilicicolin C inhibited proliferation and migration of PC-3 cells. It could also block the cell cycle and induce apoptosis in PC-3 cells. In addition, ilicicolin C could bind to PI3K/AKT proteins. Furthermore, ilicicolin C inhibited the expression of PI3K, AKT and mTOR proteins and could also regulate the expression of downstream proteins in the PI3K/AKT/mTOR signaling pathway. Moreover, the calculations speculated that ilicicolin C was well absorbed orally, and the zebrafish xenograft model confirmed the in vivo anti-prostate cancer effect of ilicicolin C. Ilicicolin C emerges as a promising marine compound capable of inducing apoptosis of prostate cancer cells by counteracting the aberrant activation of PI3K/AKT/mTOR, suggesting that ilicicolin C may be a viable candidate for anti-prostate cancer drug development. These findings highlight the potential of ilicicolin C against prostate cancer and shed light on its mechanism of action.

High Quality Au-carbon Nitride Catalyst for Monitoring of Anti-prostate Cancer Drug (Flutamide)

High Quality Au-carbon Nitride Catalyst for Monitoring of Anti-prostate Cancer Drug (Flutamide)

Recent advances in flavonoid compounds for the treatment of prostate cancer.

Prostate cancer is a malignant epithelial tumor of the prostate gland and is the most common malignant tumor of the male genitourinary system. Pharmacological therapies, including chemotherapy and androgen deprivation therapy, play a key role in the treatment of prostate cancer. However, drug resistance and side effects limit the use of these drugs and so there is a need for new drug therapies for prostate cancer patients. Flavonoids, with their wide range of sources and diverse biological activities, have attracted much attention in the field of anti-tumor drug screening. In 2016, at least 58 flavonoids were reported to have anti-prostate cancer activity. In recent years, six additional flavonoid compounds have been found to have anti-prostate cancer potential. In this review, we have collected a large amount of evidence on the anti-prostate cancer effects of these six flavonoids, including a large number of cellular experiments and a small number of preclinical animal experiments. In addition, we predicted their drug-forming properties using Schrödinger's QikProp software and ADMETlab due to the lack of in vivo pharmacokinetic data for the six compounds. In conclusion, this review has fully confirmed the anti-prostate cancer effects of these six flavonoids, summarized their mechanisms of action and predicted their druggability. It provides a reference for the further development of these compounds into anti-prostate cancer drugs.

A Linear and Nonlinear QSAR Analysis of Benzimidazole Derivative XY123 in Prostate Cancer Treatment

Background: Metastatic Castration-Resistant Prostate Cancer (mCRPC) represents a critical challenge in current prostate cancer treatment. Benzimidazole Derivative XY123 has emerged as a novel inhibitor for its treatment. Objective: This study aims to establish a robust Quantitative Structure-Activity Relationship (QSAR) model for predicting the activity of Benzimidazole Derivative XY123 derivatives, aiding the development of novel anti-prostate cancer drugs. Methods: Utilizing CODESSA software, descriptors were computed based on various moieties of Benzimidazole Derivative XY123 derivatives. Multiple linear regression models were constructed, and both linear and nonlinear QSAR models were developed using heuristics and gene expression programming. Results: The linear model with two descriptors demonstrated the best predictive capacity for inhibitor activity, while the nonlinear model generated through Gene Expression Programming (GEP) exhibited correlation coefficients of 0.83 and 0.82 for the training and test sets, respectively. The average errors were 0.03 and 0.05, indicating the stability and the improved predictive ability of the nonlinear model. Conclusion: The QSAR linear model has an advantage over the nonlinear model in optimizing Benzimidazole Derivative XY123, providing a direction for the development of effective drugs for mCRPC treatment.

Photocatalytic Sulfonyl Peroxidation of Alkenes via Deamination of N-Sulfonyl Ketimines.

A photocatalytic three-component sulfonyl peroxidation of alkenes with N-sulfonyl ketimines and tert-butyl hydroperoxide is reported. The reaction takes place via the photoinduced EnT process, which allows the efficient synthesis of a variety of β-peroxyl sulfones under mild reaction conditions in the absence of a transition metal catalyst. The downstream derivatizations of the peroxides were also performed. Furthermore, the utility of this protocol was manifested by the synthesis of 11β-HSD1 inhibitor and the antiprostate cancer drug bicalutamide.

Exploring substituted 3,4-dihydropyrimidinone and thione derivatives as anti-prostate cancer agents: Computational screening, synthesis, characterization, and in vitro efficacy assessment

Despite decades of research, anticancer medication therapy is still largely constrained to prevent growth and limit the spread of tumour cells. To speed up the process of finding anticancer drugs, exploring novel therapeutic macromolecules and identifying the right small molecules using an integration of computational and experimental approaches is a recent tactic adopted by investigators. In the present study, we designed and created a library of 200 ligands with 3,4-dihydropyrimidinones or their thiones linked with imidazolidinones through amide linkage and explored the extent of their in vitro anticancer activity towards human topoisomerase IIalpha (TOP2α or TOP2A) using DU-145 and PC-3 prostate cancer cell lines using the SRB assay method. This was accomplished by the molecular docking and synthesis of the titled compounds using a series of organic nucleophilic addition reactions, including the Biginelli one-pot condensation reaction. The preliminary physical character evaluation was employed for the synthesized compounds, and the structural parameters were analyzed using FTIR, proton NMR, 13C NMR, and LC-MS/MS. The anti-prostate cancer activity of the prepared Biginelli analogues was evaluated against cancer cell lines and mild-to-moderate reduction in the viability of cell lines was observed with compounds 5, 6, 9, 14, 15, 16, 17, and 19. Among them, compounds 5, 14, 15, and 16 exhibited significant potent activity against TOP2α or TOP2A. This result indicated that the derivatives of Biginelli (3,4-dihydropyrimidinones/thiones) could be promising anti-prostate cancer drug candidates.

Alpha Satellite DNA in Targeted Drug Therapy for Prostate Cancer.

Prostate cancer is the most common solid cancer in men and, despite the development of many new therapies, metastatic castration-resistant prostate cancer still remains a deadly disease. Therefore, novel concepts for the treatment of metastatic prostate cancer are needed. In our opinion, the role of the non-coding part of the genome, satellite DNA in particular, has been underestimated in relation to diseases such as cancer. Here, we hypothesise that this part of the genome should be considered as a potential target for the development of new drugs. Specifically, we propose a novel concept directed at the possible treatment of metastatic prostate cancer that is mostly based on epigenetics. Namely, metastatic prostate cancer is characterized by the strongly induced transcription of alpha satellite DNA located in pericentromeric heterochromatin and, according to our hypothesis, the stable controlled transcription of satellite DNA might be important in terms of the control of disease development. This can be primarily achieved through the epigenetic regulation of pericentromeric heterochromatin by using specific enzymes as well as their activators/inhibitors that could act as potential anti-prostate cancer drugs. We believe that our concept is innovative and should be considered in the potential treatment of prostate cancer in combination with other more conventional therapies.

YIV-818-A: a novel therapeutic agent in prostate cancer management through androgen receptor downregulation, glucocorticoid receptor inhibition, epigenetic regulation, and enhancement of apalutamide, darolutamide, and enzalutamide efficacy.

Introduction: Prostate cancer is the second leading cause of cancer death among men in the United States. Castration-Resistant Prostate Cancer (CRPC) often develops resistance to androgen deprivation therapy. Resistance in CRPC is often driven by AR variants and glucocorticoid receptor (GR). Thus, drugs that target both could be vital in overcoming resistance. Methods: Utilizing the STAR Drug Discovery Platform, three hundred medicinal plant extracts were examined across 25 signaling pathways to identify potential drug candidates. Effects of the botanical drug YIV-818-A, derived from optimized water extracts of Rubia cordifolia (R.C.), on Dihydrotestosterone (DHT) or Dexamethasone (DEX) induced luciferase activity were assessed in 22RV1 cells harboring the ARE luciferase reporter. Furthermore, the key active compounds in YIV-818-A were identified through activity guided purification. The inhibitory effects of YIV-818-A, RA-V, and RA-VII on AR and GR activities, their impact on AR target genes, and their roles in modifying epigenetic status were investigated. Finally, the synergistic effects of these compounds with established CRPC drugs were evaluated both in vitro and in vivo. Results: YIV-818-A was found to effectively inhibit DHT or DEX induced luciferase activity in 22RV1 cells. Deoxybouvardin (RA-V) was identified as the key active compound responsible for inhibiting AR and GR activities. Both YIV-818-A and RA-V, along with RA-VII, effectively downregulated AR and AR-V proteins through inhibiting protein synthesis, impacted the expression of AR target genes, and modified the epigenetic status by reducing levels of Bromodomain and Extra-Terminal proteins (Brd2/Brd4) and H3K27Ac. Furthermore, these compounds exhibited synergistic effects with apalutamide, darolutamide, or enzalutamide, and suppressed AR mediated luciferase activity of 22RV1 cells. Co-administration of YIV-818-A and enzalutamide led to a significant reduction of 22RV1 tumor growth in vivo. Different sources of R.C. had variable levels of RA-V, correlating with their potency in AR inhibition. Discussion: YIV-818-A, RA-V, and RA-VII show considerable promise in addressing drug resistance in CRPC by targeting both AR protein and GR function, along with modulation of vital epigenetic markers. Given the established safety profile of YIV-818-A, these findings suggest its potential as a chemopreventive agent and a robust anti-prostate cancer drug.

Follow up of the prostate cancer treatment based on a novel sensing method for anti-prostate cancer drug (flutamide)

In this work, novel modified electrode (MXene/MIL-101(Cr)/GCE) are manufactured through simple layer-by-layer immobilization procedure. The fabricated electrochemical sensor was utilized for electrochemical sensing of flutamide in biological fluids. The immobilization of both MXene and metal-organic framework (MOF) materials on the electrode surface could improve the electrochemical performance of the modified glassy carbon electrode (GCE) towards flutamide due to the synergic effects. The established sensor illustrated the significant sensing ability for the determination of flutamide. The influence of solution pH and volume ratio of MXene/MIL-101(Cr) on electrochemical performance of the modified GCE was researched and optimized. The sensor demonstrated a favorable detection limit of 0.009 μM and a linear range of 0.025–100 μM using differential pulse voltammetry (DPV) technique. The suggested assay illustrated an excellent sensing efficiency towards flutamide in body fluids with recoveries ranging from 97.7% to 102.5%, which indicates its potential in real matrices. In addition, the MXene/MIL-101(Cr)/GCE was illustrated some advantages including simple preparation, good selectivity and reproducibility, and rapid flutamide detection.

Pharmacokinetics and pharmacodynamics of Rh2 and aPPD ginsenosides in prostate cancer: a drug interaction perspective.

Ginsenoside Rh2 and its aglycon (aPPD) are one of the major metabolites from Panax ginseng. Preclinical studies suggest that Rh2 and aPPD have antitumor effects in prostate cancer (PCa). Our aims in this review are (1) to describe the pharmacokinetic (PK) properties of Rh2 and aPPD ginsenosides; 2) to provide an overview of the preclinical findings on the use of Rh2 and aPPD in the treatment of PCa; and (3) to highlight the mechanisms of its PK and pharmacodynamic (PD) drug interactions. Increasing evidence points to the potential efficacy of Rh2 or aPPD for PCa treatment. Based on the laboratory studies, Rh2 or aPPD combinations revealed an additive or synergistic interaction or enhanced sensitivity of anticancer drugs toward PCa. This review reveals that enhanced anticancer activities were demonstrated in preclinical studies through interactions of Rh2 and/or aPPD with the proteins related to PK (e.g., cytochrome P450 enzymes, transporters) or PD of the other anticancer drugs or PCa signaling pathways. In conclusion, combining Rh2 or aPPD with anti-prostate cancer drugs leads to PK or PD interactions which could facilitate either therapeutically beneficial or toxic effects.

Dankasterone A induces prostate cancer cell death by inducing oxidative stress

Oxidative stress plays a dual role in tumor survival, either promoting tumor development or killing tumor cells under different conditions. Dankasterone A is a secondary metabolite derived from the fungus Talaromyces purpurogenu. It showed good potential in a screen for anti-prostate cancer compounds. In this study, MTT results showed dankasterone A was cytotoxic to prostate cancer cells, with an IC50 of 5.10 μM for PC-3 cells and 3.41 μM for 22Rv1 cells. Further studies, plate cloning assays and real-time cell analysis monitoring showed that dankasterone A significantly inhibited clonal colony formation and cell migration in 22Rv1 and PC-3 cells. In addition, flow cytometry results showed that dankasterone A induced apoptosis in prostate cancer cells while having no impact on cell cycle distribution. At the molecular level, Protein microarray experiments and western blot assays revealed that dankasterone A specifically and dramatically upregulated HO-1 protein expression; and the results of cell fluorescence staining showed that dankasterone A induced overexpression of reactive oxygen species in 22Rv1 and PC-3 cells. Taken together, dankasterone A induced prostate cancer cells to undergo intense oxidative stress, which resulted in the production of large amounts of HO-1 and the release of large amounts of reactive oxygen species, leading to apoptosis of prostate cancer cells, ultimately resulting in the inhibition of both cell proliferation and migration. We also validated the anti-prostate cancer effects of dankasterone A in vivo in a zebrafish xenograft tumor model. In conclusion, dankasterone A has the potential to be developed as an anti-prostate cancer drug.

Synthesis, biological evaluation, and molecular docking of novel hydroxyzine derivatives as potential AR antagonists.

Prostate cancer (PCa) is a malignant tumor with a higher mortality rate in the male reproductive system. In this study, the hydroxyazine derivatives were synthesized with different structure from traditional anti-prostate cancer drugs. In the evaluation of in vitro cytotoxicity and antagonistic activity of PC-3, LNCaP, DU145 and androgen receptor, it was found that the mono-substituted derivatives on the phenyl group (4, 6, 7, and 9) displayed strong cytotoxic activities, and compounds 11-16 showed relatively strong antagonistic potency against AR (Inhibition% >55). Docking analysis showed that compounds 11 and 12 mainly bind to AR receptor through hydrogen bonds and hydrophobic bonds, and the structure-activity relationship was discussed based on activity data. These results suggested that these compounds may have instructive implications for drug structural modification in prostate cancer.

Gadolinium vanadate nanosheets entrapped with 1D-halloysite nanotubes-based nanocomposite for the determination of prostate anticancer drug nilutamide

High-performance, low-cost electrode materials with distinct structural characteristics are still needed for electrochemical sensors. In this paper, 1D-halloysite nanotubes are embedded over 2D nanosheets of gadolinium vanadate nanosheets (GdV/HNT), which are hydrothermally constructed for the first time. Structural and physicochemical evaluations reveal the essential properties of the produced composite material. Because of the 3D flower-like morphology, it was simpler to establish contact with the HNT with GdV NS, which had developed. The anti-prostate cancer drug nilutamide (NLT) was then examined utilizing voltammetric methods on a GdV/HNT nanocomposite modified glassy carbon electrode (GdV/HNT/GCE). For NLT detection, the nanocomposite material GdV/HNT/GCE demonstrates high electrochemical efficiency because of its synergy, many active sites, and quick electron transfer. Under ideal conditions, the GdV/HNT nanocomposite-based electrochemical sensor can achieve a wide linear range (0.5–478 µM), low detection limit (1.8 nM), strong sensitivity (1.33 µA µM−1 cm−2), high repeatability, and significant recovery results in actual sample analysis are all possible with the GdV/HNT nanocomposite-based electrochemical sensor under optimal circumstances. Electrochemical sensors for NLT trace-level detection with simple manufacturing and high activity are shown in this study.

Biotransformation of Abiraterone Into Five Characteristic Metabolites by the Rat Gut Microbiota and Liver Microsomes

It is well known that the role of gut microbiota in drug metabolism, especially in oral difficult absorbable drugs. Understanding the gut microbiota could enable us to understand drugs in new ways. The purpose of the study was to investigate explore the metabolites of the anti-prostate cancer drug Abiraterone by examining gut microbiota metabolism and hepatic metabolism in vitro. In this study, five metabolites (M1, M2, M3, M4 and M5) of Abiraterone were discovered using LC/MSn-IT-TOF. Four isomeric metabolites M1-M4 were found in liver microsome. M5 was found in the intestinal contents of Sprague-Dawley rats with a molecular weight of 388.31. Among them, M4 was found to be Abiraterone N-Oxide by comparison with the standard sample. After further comparing the metabolic behavior of Abiraterone in rat gut microbiota and liver microsomes, we delineated the possible metabolic pathways of Abiraterone. In conclusion, Abiraterone is metabolized specifically in liver microsomes and gut microbiota. This study can provide a theoretical basis for elucidating the metabolic mechanism of Abiraterone and guide its rational application in clinic.

Insights into Aptamer-Drug Delivery Systems against Prostate Cancer.

Prostate cancer is a common cancer in elderly males. Significant progress has been made in the drug therapies for prostate cancer in recent years. However, side effects are still problems that have not been overcome by the currently used anti-prostate cancer drugs. Novel technologies can be applied to reduce or even eliminate the side effects of drugs. An aptamer may be a sequence of nucleic acids or peptides that can specifically recognize proteins or cells. Taking advantage of this feature, scientists have designed aptamer–drug delivery systems for the development of anti-prostate cancer agents. Theoretically, these aptamer–drug delivery systems can specifically recognize prostate cancer cells and then induce cell death without attacking normal cells. We collected the relevant literature in this field and found that at least nine compounds have been prepared as aptamer–drug delivery systems to evaluate their precise anti-prostate cancer effects. However, the currently studied aptamer–drug delivery systems have not yet entered the market due to defects. Here, we analyze the published data, summarize the characteristics of these delivery systems, and propose ways to promote their application, thus promoting the development of the aptamer–drug delivery systems against prostate cancer.

Novel indazole skeleton derivatives containing 1,2,3-triazole as potential anti-prostate cancer drugs

In this study, a novel batch of indazole containing 1,2,3-triazole agents were designed and synthesized. The antiproliferative activity of target compounds in four human cancer cells, PC-3 (human prostate cancer cell), MCF-7 (human breast cancer cell), HepG-2 (human hepatoma cell) and MGC-803 (human gastric cancer cell), was evaluated by thiazole blue (MTT). In the antiproliferative activity screening, we were surprised to find that most compounds have specific cytotoxicity to PC-3 cancer cells. In particular, 9a has an IC50 value of 4.42 ± 0.06 μmol/L against PC-3 cell. Cloning experiments showed that 9a could inhibit the formation of PC-3 cancer cell clone in a dose-dependent manner. Through cell cycle arrest experiment, we found that compound 9a can block the cell cycle in G2/M phase and inhibit cell proliferation. Finally, by evaluating the safety of compound 9a, we noticed that it showed fairly good safety both in vivo and in vitro. Overall, based on the biological activity evaluation and safety, analogue 9a can be viewed as a potential lead compound for further development of novel anti-prostate cancer drug.

Synthesis and characterization of iron-cobalt oxide/polypyrrole nanocomposite: An electrochemical sensing platform of anti-prostate cancer drug flutamide in human urine and serum samples

The invention of easy, selective, and responsive anti-cancer drug analysis platforms of high significance in biomedical research with accuracy. Fortunately, creating an innovative electrode material with a low detection limit, high sensitivity, and stability remains a challenging task. Herein, we describe a simple approach to synthesize iron-cobalt oxide anchored with polypyrrole (FCO/PPy) nanocomposite through a sonochemical approach. XRD, FTIR, and XPS analysis have confirmed the construction of FCO/PPy nanocomposite. FESEM and TEM have been used to demonstrate the nanocomposite morphological and structural properties. The electrochemical characterization has been monitored by EIS, CV, and DPV methods. The results of the nanocomposite revealed higher electrochemical performance for flutamide (FLT) reduction than the single electrodes. Under optimized experimental conditions, the sensor exhibits broad linearity from 0.4 µM to 376 µM, with a low detection limit of 0.086 µM and excellent sensitivity of 1.45 µA µM–1 cm–2. Further, FCO/PPy electrode shows outstanding repeatability, stability, reproducibility, and good selectivity of FLT in the presence of nitrofurantoin (NFT), and 4-nitroaniline (4-NA). The practical applicability of the developed sensor is applied for FLT detection in human serum and urine samples with satisfactory recovery values.