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fluoxetine (EDG005)

✓ Approved

Edgemont Pharmaceuticals, LLC · SLC6A4 · 小分子

什么是 fluoxetine？

fluoxetine 是一种小分子，由Edgemont Pharmaceuticals, LLC研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名EDG005
公司Edgemont Pharmaceuticals, LLC
药物类别小分子
分子靶点SLC6A4
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Edgemont Pharmaceuticals, LLC

作用机制

分子靶点

fluoxetine 作用于 1 个分子靶点：

SLC6A4solute carrier family 6 member 4 (5HTT, 5-HTT)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

fluoxetine 针对 4 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Psychiatric disordersBulimia nervosa✓ Approved
Psychiatric disordersObsessive-compulsive disorder✓ Approved
Psychiatric disordersPanic disorder✓ Approved
Psychiatric disordersMajor depression✓ Approved

相关研究文献

PubMedLife (Basel, Switzerland)2026-10-27

Fluoxetine Is Associated with Reduced Cell Viability and Decreased pERK1/2 Immunoreactivity in Ishikawa Endometrial Cancer Cells In Vitro: An Exploratory Study.

Arı Neziha Senem NS, Çakır Gündoğdu Ayşe A, Meriç Neslihan N, Özatik Orhan O

Selective serotonin reuptake inhibitors are widely prescribed in oncology, yet their direct effects on endometrial cancer cell fate remain unclear. This study examined whether fluoxetine, at concentrations referenced to reported plasma exposure ranges, alters viability, cell death phenotype, DNA integrity and extracellular signal-regulated kinase 1/2 (ERK1/2) signalling. Ishikawa endometrial cancer cells and normal human dermal fibroblasts (HDFs) were exposed to fluoxetine (100-300 ng/mL) for a single exposure period of 48 h. Metabolic viability was assessed by MTT assay, cell death phenotypes by annexin V/propidium iodide (PI) flow cytometry, DNA fragmentation by TUNEL, and total and phosphorylated ERK1/2 (pERK1/2) by immunofluorescence; all experiments were performed in three independent experiments (n = 3), and per-experiment means were used as the unit of analysis. Fluoxetine reduced metabolic viability in Ishikawa cells, with significant reductions detected at 100 and 300 ng/mL, whereas HDF viability remained largely preserved. Flow cytometry showed predominantly viable populations in both cell types, with low early apoptotic, late apoptotic and annexin V-/PI+ fractions; no statistically significant treatment-related differences were detected in these cell death-associated populations, although analysis at a single 48 h endpoint cannot exclude earlier transient changes. TUNEL positivity showed a concentration-related numerical increase in Ishikawa cells, reaching statistical significance at 300 ng/mL, while remaining low in HDF cells. pERK1/2 immunoreactivity was significantly decreased at 300 ng/mL in both Ishikawa and HDF cells without a comparable change in total ERK1/2 immunoreactivity; because this readout was obtained by immunofluorescence only and was not validated by Western blotting, it is reported as a change in immunoreactivity rather than as confirmed pathway inhibition. These exploratory in vitro findings indicate that fluoxetine exposure is associated with reduced viability, DNA fragmentation and decreased pERK1/2 immunoreactivity in Ishikawa cells; the limited injury in HDF cells reflects a general non-malignant comparator response rather than cancer-specific selectivity. The findings are hypothesis-generating and require confirmation by protein- and transcript-level validation, pathway modulation experiments and additional malignant and non-malignant cell models.

PMID 42942215
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PubMedPharmaceutics2026-10-27

Microbiota-Gut-Brain Axis Interactions with CNS Drugs: A Critical Mechanistic Review of Biopharmaceutical, Pharmacokinetic, and Pharmacodynamic Evidence.

Stepensky David D

Background/Objectives: The microbiota-gut-brain axis (MGBA) modifies central nervous system (CNS) pharmacotherapy by influencing the biopharmaceutics, pharmacokinetics (PK), and pharmacodynamics (PD) of drugs, while CNS drugs reciprocally reshape the MGBA. This review examines these interactions and their clinical relevance, explicitly grading the strength of the evidence. Methods: This narrative, mechanistically oriented review focuses on four oral drugs representing distinct mechanistic archetypes: levodopa/carbidopa (biopharmaceutical-dominant), olanzapine (PK-dominant), sertraline (PD-dominant), and amitriptyline (mixed). PubMed/MEDLINE, Google Scholar, and Google were searched up to 1 September 2026; of approximately 260 records screened, 64 were cited. No PRISMA reporting or dual screening was performed. Findings were assigned to five evidence tiers (L1-L5) and classified as associative or causal. Results: For levodopa/carbidopa, fecal tyrosine decarboxylase (tdc) gene abundance correlates with daily dose requirement (human observational), and Helicobacter pylori eradication or treatment of small intestinal bacterial overgrowth improves levodopa exposure or motor outcomes (human interventional). For olanzapine, microbiota depletion increased bioavailability ~1.8-fold in rats (single study), and microbiome-dependent weight gain is causal in rodents, whereas human data are phenomenological only. For sertraline, antimicrobial activity and fecal depletion are demonstrated in vitro; the pharmacodynamic blockade derives from fluoxetine models. For amitriptyline, antimicrobial and anticholinergic effects are preclinical, and the ATLANTIS trial demonstrates efficacy in irritable bowel syndrome without measuring the microbiome. Conclusions: The microbiome is a measurable modifier of CNS drug fate, but few interactions are clinically actionable. Progress requires prospective trials with standardized MGBA biomarkers, microbiome-informed PK/PD models, and independent replication.

PMID 42942808
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PubMedBehavioural pharmacology2026-10-25

Modulation of social preference and avoidance of zebrafish conspecifics treated with selected neuroactive compounds.

Yang Longen L, Yu Zhili Z, Zhou Meitong M, Xie Xuesong X et al.

Social interaction and preference are essential parts of human and animal behavior. Zebrafish are rapidly emerging as a major model organism in neurobehavioral research and, as highly social animals, enable probing of their social preference and its pharmacological modulation. Neuroactive drug effects, however, can also be socially transmittable, thereby indirectly affecting drug-free animal behavior as well. Here, we examine this possibility in adult zebrafish by assessing their social preference for conspecifics treated using a wide range of neuroactive drugs with well established effects in zebrafish. Zebrafish were treated with acute or chronic neuroactive drugs (GBR-12909, fluoxetine, reserpine, caffeine, arecoline, nicotine, cuprizone, ethanol, and atropine), and exposed to target fish in the three-chamber social preference test, scoring time the latter spent in each zone. Overall, we found their overt social preference for conspecifics treated with acute nicotine and GBR-12909, and social avoidance of fish exposed to all other drugs used, except cuprizone and ethanol. These findings confirm altered social preference for central nervous system (CNS) drug-treated zebrafish, but suggest that this preference is nonlinear and does not correlate with anxiolytic or anxiogenic drug profiles. Further research is needed to explore why some CNS drug-evoked behavioral effects render conspecifics socially attractive or aversive to observer zebrafish, and to determine potential practical and translational implications of these findings for neuropharmacology and biological psychiatry.

PMID 42924866
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PubMedJournal of cellular and molecular medicine2026-10-25

Prophylactic Inhalation of Bergamot Essential Oil Ameliorates Hormone-Simulated Pseudopregnancy Withdrawal-Induced Postpartum Depression by Modulating Hippocampal Synaptic Plasticity.

Xu Huan H, Zhang Shike S, He Hui H, Zhao Xue X et al.

Postpartum depression (PPD) affects approximately 17.2% of women giving birth globally, but current pharmacotherapies face significant limitations including invasive intravenous delivery (brexanolone) and high costs Bergamot essential oil (BEO) has demonstrated efficacy in aromatherapy for depression, yet its role in PPD remains unexplored. This study investigated whether prophylactic or therapeutic inhalation of nebulized BEO ameliorates PPD-like phenotypes in a rat model of hormone-simulated pseudopregnancy (HSP) with abrupt withdrawal, and explored potential mechanisms involving hippocampal synaptic plasticity and neuroinflammation. The main components of BEO were characterized using gas chromatography-mass spectrometry (GC-MS). A rat model of PPD was constructed using the HSP post-withdrawal method, and animals were randomly divided into control group (Ctrl), sham surgery group (Sham), model group (PPD), fluoxetine group (Flu; 10 mg/kg, i.p., post-modelling) as a positive control representing first-line SSRI therapy (brexanolone, though FDA-approved for PPD, requires costly intravenous administration and specialized medical supervision, and was therefore not used as a comparator), therapeutic BEO group (BEO; 2.5% v/v inhalation post-modelling) and prophylactic BEO group (P-BEO; 2.5% v/v inhalation during HSP modelling). The sucrose preference test (SPT), open field test (OFT) and elevated plus maze (EPM) were used to evaluate the depressive-like behaviours, and HE staining was used to observe the effects of BEO on the thymus and spleen of immune organs. Nissl staining was utilized to quantify the Nissl bodies in the hippocampus (HIPP) of PPD model rats. Additionally, immunohistochemistry and Western blotting were conducted to detect alterations in postsynaptic density protein-95 (PSD-95) and synaptophysin (SYP) within the hippocampus of the rats. Enzyme-linked immunosorbent assay (ELISA) was employed to further analyse the levels of insulin-like growth factor-1 (IGF-1, a neurotrophic factor linked to synaptic plasticity), interleukin-1β (IL-1β, a pro-inflammatory cytokine implicated in PPD pathogenesis) and interleukin-10 (IL-10, an anti-inflammatory cytokine implicated in PPD pathogenesis) in serum, cerebrospinal fluid (CSF) and HIPP. Molecular docking was performed to predict interactions between BEO's core constituents (limonene, γ-terpinene, α-pinene, β-pinene, α-phellandrene) and target proteins (PSD-95, SYP, IL-1β, IGF-1, IL-10). Both therapeutic and prophylactic BEO inhalation significantly increased sucrose preference (from 78.78% ± 17.25% to 96.44% ± 2.60% [BEO] and 97.33% ± 0.87% [P-BEO], p < 0.05), total distance travelled in the OFT (from 900.07 ± 523.07 to 1932.64 ± 665.88 cm [BEO] and 1671.51 ± 544.36 cm [P-BEO]; p < 0.05) and open arm time in the EPM (from 16.34 ± 15.44 to 49.91 ± 24.99 s [BEO] and 50.81 ± 16.12 s [P-BEO]; p < 0.05). Both BEO groups exhibited increased Nissl body counts in hippocampal CA1 (from 7.44 ± 1.59 to 18.44 ± 2.60 [BEO] and 19.56 ± 2.07 [P-BEO]; p < 0.05), CA2, CA3 and DG subregions (p < 0.05 vs. PPD), as well as increased PSD-95/SYP protein abundance. Both BEO regimens increased IGF-1 levels in serum and CSF (p < 0.05 vs. PPD), with the P-BEO group showing a significantly higher serum IGF-1 levels compared to the Flu group (p < 0.05). Additionally, both P-BEO and BEO groups decreased IL-1β levels in serum and HIPP, while increasing IL-10 levels in the CSF (p < 0.05 vs. PPD for all). Molecular docking revealed favourable binding affinities (binding energy < -5.0 kcal/mol) between BEO constituents and all five target proteins. No significant histopathological alterations were observed in thymus or spleen following BEO exposure. Collectively, these findings suggest that BEO inhalation may attenuate PPD-like phenotypes in this rat model, potentially through modulation of hippocampal synaptic plasticity and neuroinflammation via regulation of IGF-1, IL-1β and IL-10. While these results are preliminary, the non-invasive delivery and observed dual-phase efficacy suggest that BEO inhalation may represent a more accessible approach worthy of further investigation for PPD management, particularly in resource-limited settings where current FDA-approved treatments are unavailable.

PMID 42922098
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PubMedEnvironmental science & technology2026-10-23

Digging into Understudied Sediments: What Lumbriculus variegatus Reveals about Fluoxetine Exposure from the Cellular to the Individual Level.

Hilgendorf Jacqueline J, Calisto Vânia V, Campos Diana D, Cardoso Diogo N DN et al.

Sediments accumulate persistent and toxic compounds, yet assessing their effects on benthic species remains challenging. Especially antidepressants, such as fluoxetine, are of concern due to their sediment affinity and potential to disrupt neuroendocrine functions at low concentrations. This study investigated the chronic effects of fluoxetine in the sediment-dwelling worm Lumbriculus variegatus through two 28-day sediment exposures (0.00025-25 mg/kg) conducted in accordance with OECD 225, with modifications. Endpoints encompassed multiple biological levels, including biochemical markers of neurotoxicity (cholinesterase), oxidative stress (catalase, glutathione-S-transferase, total glutathione), damage (lipid peroxidation), energy metabolism (lipids, sugars, proteins, electron transport system), physiological responses (oxygen consumption), three novel behavioral assays (chemical avoidance, feeding, phototaxis), and conventional apical endpoints (mortality, growth, reproduction). Effects on the non-conventional endpoints occurred at environmentally relevant sediment concentrations. Additionally, oxidative stress and behavioral responses were substantially more sensitive endpoints of fluoxetine exposure than the conventional endpoints growth, reproduction, and mortality. Integrating responses across biological levels, we propose a qualitative Adverse Outcome Pathway linking molecular and cellular events to individual-level effects. Our findings demonstrate that environmentally relevant fluoxetine concentrations elicit ecologically meaningful effects in L. variegatus that current regulatory frameworks would likely overlook, emphasizing the need for standardized behavioral assays in sediment risk assessment.

PMID 42915449
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PubMedEuropean journal of pharmacology2026-10-23

Ineupatorolide B alleviates postpartum depression-like behaviors via the gut microbiota-butyrate-brain axis.

Duan Xiaoyan X, Tian Fei F, Liu Weilan W, Yang Yanyan Y et al.

Postpartum depression (PPD) is a common mood disorder after childbirth and is associated with abrupt hormonal withdrawal, systemic inflammation, and neurobiological dysfunction. Increasing evidence implicates dysregulation of the microbiota-gut-brain axis in PPD pathophysiology, but safe and effective treatments remain limited. Here, we investigated the antidepressant-like effects and mechanisms of ineupatorolide B (InB), a bioactive compound isolated from Inula species, using a hormone-simulated withdrawal mouse model of PPD. InB significantly alleviated depressive- and anhedonia-like behaviors, as shown by reduced immobility in the tail suspension and forced swim tests and restored sucrose preference, with efficacy comparable to fluoxetine. InB also reduced serum interleukin-6 and tumor necrosis factor-α levels and restored the expression of postsynaptic density protein 95 and brain-derived neurotrophic factor in the prefrontal cortex. Gut microbiota analysis revealed marked alterations in microbial diversity and composition in hormone-withdrawal mice, accompanied by reduced fecal butyrate levels, which were largely normalized by InB treatment. Correlation analyses suggested associations among specific bacterial phyla, short-chain fatty acid metabolism, and behavioral outcomes. Notably, oral administration of butyric acid also alleviated depressive-like behaviors, suppressed systemic inflammation, and restored PSD-95, BDNF, and occludin expression in the prefrontal cortex of hormone-withdrawal mice. Together, these findings suggest that InB ameliorates PPD-like phenotypes, possibly through modulation of the gut microbiota, butyrate metabolism, systemic inflammation, and synaptic plasticity. However, the causal relationships among these changes remain to be established.

PMID 42913991
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