fluoxetine

P=N/A, N=220, Completed, Zunyi Medical University Zhuhai Campus; The Fifth Affiliated (Zhuhai) Hospital of Zunyi Medical University

We verify the structure using mutagenesis and confirm that the conformation corresponds to the active state of the receptor. Subsequent study of TrkB interaction with the antidepressant drug fluoxetine, and the antipsychotic drug chlorpromazine, provides a clear self-consistent model, describing the mechanism by which fluoxetine activates the receptor by binding to its transmembrane domain.

P3, N=316, Active, not recruiting, Children's Hospital Los Angeles | Trial completion date: Dec 2025 --> Jul 2026

P2, N=150, Active, not recruiting, University of Florida | Trial completion date: Sep 2024 --> Jan 2025 | Trial primary completion date: Sep 2024 --> Jan 2025

One hour before CUMS, rats were given a treatment with acupuncture, electroacupuncture, sham-acupuncture, or fluoxetine (2.1 mg/kg)...Additionally, our findings indicate that acupuncture also modulates the ERK and Caspase-3 apoptotic pathways in the hippocampus of CUMS rats. This study suggests that acupuncture may play a potential preventive role by regulating hippocampal neuroinflammatory response, levels of oxidative stress, apoptotic processes, and enhancing synaptic plasticity.

Fluoxetine and CUR-N373 can inhibit CVB4 replication in macrophage cultures...The cytolytic activity of activated GM-CSF macrophages was higher towards CVB4-persistently infected 1.1B4 cells than mock-infected 1.1B4 cells. In conclusion, macrophages may play a role in CVB4 infection of pancreatic cells, and are capable of inducing lysis of infected pancreatic cells.

P1, N=30, Recruiting, Duke University | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

P1/2, N=100, Recruiting, Yale University | Trial completion date: Jul 2024 --> Dec 2025 | Trial primary completion date: Jul 2024 --> Jun 2025

Gps improved the antioxidative stress capacity of the hippocampus and promoted mitophagy in CUMS rats through SIRT1, thus protecting hippocampal neurons and improving depression-like behavior.

The rats were randomly divided into normal group, model group, CD300f blocker(CLM1, 2 μg·kg~(-1)) group, CD300f agonist(Fcγ, 5 μg·kg~(-1)) group, positive drug(0.18 g·kg~(-1) metformin+1.8 mg·kg~(-1) fluoxetine) group, and high-dose and low-dose(20.52 and 10.26 g·kg~(-1)) Zuogui Jiangtang Jieyu Formula groups. They could up-regulate the protein expression of presyna-ptic membrane SYN and postsynaptic membrane PSD-95 in hippocampal neurons and finally improve the damage to the hippocampal synaptic microenvironment. In conclusion, this research confirmed that Zuogui Jiangtang Jieyu Formula effectively alleviated the depression-like behavior and inhibited inflammatory activation of microglial cells in the hippocampus of rats with DD, and the mechanism might be related to the regulation of CD300f/TLR4 signal to alleviate the damage to hippocampal synaptic microenvironment.

P1, N=60, Recruiting, University of Maryland, Baltimore | Trial primary completion date: Feb 2025 --> Sep 2025

Age, antidepressant type, duration of antidepressant use, and comorbidities could be risk factors for NAFLD in patients with depression. Furthermore, mirtazapine can cause steatosis in both AML-12 and MIHA cell lines and may promote the development of NAFLD through the TLR4/MyD88/NF-κB signaling pathway. This study lays a solid foundation for further research on depression and NAFLD and can contribute to the prevention and treatment of these two diseases.

P1, N=64, Recruiting, University of Maryland, Baltimore | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Sep 2025

From 15 th to the 22 nd day, the animals received RIP I or RIP II (50 mg/kg) or fluoxetine (FLU, 10 mg/kg) or vehicle, by gavage...RIP I and RIP II reversed these alterations. These results contribute to the understanding the mechanisms underlying the antidepressant effect of RIP I and RIP II, which may be related to neuroinflammatory suppression.

P2, N=150, Active, not recruiting, University of Florida | Recruiting --> Active, not recruiting | Phase classification: P1 --> P2 | Trial completion date: Jun 2024 --> Sep 2024 | Trial primary completion date: Jun 2024 --> Sep 2024

From 15th to the 22nd day, the animals received RIP I or RIP II (50 mg/kg) or fluoxetine (FLU, 10 mg/kg) or vehicle, by gavage...RIP I and RIP II reversed these alterations. These results contribute to the understanding the mechanisms underlying the antidepressant effect of RIP I and RIP II, which may be related to neuroinflammatory suppression.

P4, N=6, Completed, Massachusetts General Hospital | Recruiting --> Completed | N=25 --> 6 | Trial completion date: Oct 2024 --> Feb 2024 | Trial primary completion date: Oct 2024 --> Feb 2024

P=N/A, N=128, Completed, Capital Medical University | Recruiting --> Completed | Trial completion date: Jan 2024 --> Aug 2023

In Part 1, the rats were divided into the control group, the model group, the model + Jingqianshu group, and the model + fluoxetine group...However, the current study is still preliminary and the pathogenesis of PMDD is complex. Therefore, more in-depth exploration is needed.

From the beginning of the third week, rats were treated either with saline daily or with etanercept twice a week (0.3 mg/kg, i.p.) or with fluoxetine daily (10 mg/kg, i.p) as a reference. This could be attributed to abrogation of the p38 mitogen-activated protein kinase (p38 MAPK) and signal transducer and activator of transcription 3 (STAT-3) pathways in the PFC. The findings of the present study contribute to the understanding of the potential of etanercept as an antidepressant and provide insights into the neurobiological mechanisms underlying its therapeutic effects.

P1, N=10, Not yet recruiting, Jonsson Comprehensive Cancer Center | Trial completion date: Jun 2026 --> Dec 2026 | Initiation date: Jun 2024 --> Dec 2024 | Trial primary completion date: Jun 2025 --> Dec 2025

These findings provide a foundation for the potential clinical application of CNS drugs in GBM treatment. Additionally, this work offers critical insights into the mechanisms and determinants of cytotoxicity for drugs currently undergoing clinical trials as repurposing agents for various cancers, including Fluoxetine, Sertraline, Thioridazine, Chlorpromazine, and Fluphenazine.

Altogether, our study represents the first report on the potential antineuroinflammatory and antidepressant properties of OC via modulation of BDNF/TrkB neurotrophic activity. This finding underscores the potential of OC as a natural therapeutic agent for depression- and anxiety-related disorders.

Mice were divided into a control group, vehicle group, fluoxetine group, celecoxib group, and auraptene group. The results showed that auraptene reduced the excessive phagocytosis and ROS production of LPS-induced BV2 cells. In conclusion, auraptene relieved depressive-like behaviors in mice probably via modulating hippocampal neuroinflammation mediated by microglia.

We bring the first evidence of a sequential onset of behavioral changes in T. cruzi-infected mice. Fx therapy improves behavioral and biological changes and parasite control in the brain tissue. Moreover, in the central nervous system, cytokine-driven Ser/5-HT consumption may favor parasite persistence, disrupting neurotransmitter balance and promoting a neurotoxic environment likely contributing to behavioral and cognitive disorders.

P3, N=316, Active, not recruiting, Children's Hospital Los Angeles | Recruiting --> Active, not recruiting | Trial completion date: Aug 2025 --> Dec 2025 | Trial primary completion date: Aug 2024 --> Dec 2024

P=N/A, N=2162, Completed, University of California, San Francisco | Active, not recruiting --> Completed | Trial primary completion date: Jan 2024 --> May 2024

P3, N=6246, Recruiting, Cardresearch | Trial primary completion date: Feb 2024 --> Jun 2024

P2, N=60, Recruiting, Stanford University | Trial completion date: Aug 2025 --> Dec 2025 | Trial primary completion date: Aug 2024 --> Apr 2025

P=N/A, N=296, Not yet recruiting, University of Bern

P4, N=487, Active, not recruiting, RAND | Trial completion date: Oct 2024 --> Jun 2025

Randomized clinical trials are needed to confirm these findings and establish the efficacy of the medications in ototoxicity prevention. Further research is also warranted to investigate the potential mechanisms underlying this protective effect.

P2, N=75, Recruiting, Tanta University | Trial primary completion date: Mar 2024 --> Nov 2024

P3, N=1500, Recruiting, Harvard Medical School (HMS and HSDM) | Not yet recruiting --> Recruiting

P=N/A, N=1, Enrolling by invitation, Holland Bloorview Kids Rehabilitation Hospital

Therefore, this study aimed to evaluate the effect of the treatment with fluoxetine and/or galantamine and/or donepezil on the levels of proinflammatory and anti-inflammatory cytokines in a mixed animal model of depression and dementia. In addition, fluoxetine + donepezil reversed the reduction of IL-10 levels in the hippocampus. The results indicate a pathophysiological interaction between AD and depression, and the association of medications in the future may be a possible therapeutic strategy to reduce inflammation, especially the fluoxetine-associated treatments.

P4, N=200, Recruiting, University of Florida | Not yet recruiting --> Recruiting | Phase classification: P1 --> P4

Therefore, in the current communication, an in-silico drug repurposing approach has been employed to target the function of PTP4A3/PRL-3 protein in HCC using antidepressants: Fluoxetine hydrochloride, Citalopram, Amitriptyline, Imipramine, and Escitalopram oxalate as the desired ligands...Escitalopram oxalate exhibited a comparatively significant docking score (-7.4 kcal/mol) compared to the control JMS-053 (-6.8 kcal/mol) against the PRL-3 protein...The docked complexes were subjected to MD studies (100 ns) showing stable interactions. Considering all the findings, it can be concluded that Escitalopram oxalate and related therapeutics can act as potential pharmacological candidates for targeting the activity of PTP4A3/PRL-3 in HCC.

P1, N=60, Recruiting, University of Maryland, Baltimore | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Feb 2024 --> Feb 2025

P1, N=30, Recruiting, Duke University | Trial completion date: Jun 2024 --> Jun 2026 | Trial primary completion date: Dec 2023 --> Dec 2025

P1, N=200, Not yet recruiting, University of Florida | Initiation date: Nov 2023 --> Mar 2024

P4, N=25, Recruiting, Massachusetts General Hospital | Trial completion date: May 2027 --> Oct 2024 | Trial primary completion date: May 2027 --> Oct 2024