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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

PubMedBMC psychiatry2026-06-13

Cost-benefit analysis of interpersonal therapy and fluoxetine for treating depression and PTSD in primary care settings in Kenya.

Olwanda Easter E, Mwai Daniel D, Mathai Muthoni A MA, Burger Rachel L RL et al.

Kenya faces a significant mental health crisis, with 1.9 million reported cases of depression and 10.6% prevalence of post-traumatic stress disorder (PTSD). The economic burden of mental health conditions was 62.2 billion Kenyan shillings in 2021, accounting for 0.6% of GDP. This study performed a cost-benefit analysis (CBA) of Interpersonal Psychotherapy (IPT) and fluoxetine (FLX) for treating depression and PTSD in a primary care setting. The SMART-DAPPER project in western Kenya (Kisumu County Referral Hospital) employed a Sequential, Multiple Assignment Randomized Trial design to train non-specialist providers in administering IPT and FLX for adult depression and PTSD. No standard-of-care arm was used. A cost-benefit analysis (CBA) compared intervention costs with income gains from increased productivity, using micro-costing for treatment expenses and the World Bank's Living Standards Measurement Study to assess productivity. The benefit-cost ratio was calculated over one and ten years with annual relapse rates of 10%, 25%, and 50%. All currency measurements were in KES, converted to USD rate of 118.02 KES per USD. The study enrolled 1,918 participants: 986 received IPT and 932 received FLX. Remission was achieved after the first round of therapy by 782 (79.3%) and 798 (85.6%), respectively. IPT averaged 11.5 sessions of 60 min, costing in total 5,050 KES (USD42.79); FLX averaged 5.3 sessions of 20 min, costing 2,511 KES (USD 21.28), including the medication. Both treatments increased income, with IPT participants gaining 16,242 KES (137.62 USD) and FLX participants 13,239 KES (112.18 USD) in the first year. Benefit-cost ratios were 3.2:1 for IPT and 5.3:1 for FLX. Over ten years, FLX showed higher CBA ratios (10 to 31:1) than IPT (6 to 18:1). This study found productivity gains greater than primary care-based treatment costs for IPT and FLX for depression and PTSD in Kenya. FLX demonstrated a more favorable benefit-to-cost ratio. Future research should address the capacity of government health care to sustain delivery of psychological and pharmacological therapy.

PMID 42286483
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PubMedbioRxiv : the preprint server for biology2026-06-12

A hERG Blocker Facilitates K + Channel Current by Agonizing Pore Opening while Blocking.

Docken Steffen S SS, Marquis Matthew J MJ, Ngo Khoa K, Wada Yuumu Y et al.

Many drugs that block voltage-gated K + channels encoded by the human Ether-à-go-go-Related Gene (hERG) can cause long QT syndrome and life-threatening cardiac arrhythmias, yet the molecular mechanisms that determine this risk remain unclear. A process that may counteract arrhythmogenic hERG block, termed facilitation, is common to many clinically-approved hERG blockers including nifekalant, amiodarone, promethazine, imipramine, nortriptyline, haloperidol, verapamil, carvedilol, metoprolol, propranolol, quinidine, fluoxetine, and chlorpheniramine. Facilitation is an increase in hERG current, under certain conditions, due to these blockers. Here, we propose that an agonism-while-blocking mechanism undergirds facilitation. We focus on nifekalant, a Class III antiarrhythmic drug and exemplar hERG blocker that induces facilitation. We tested the hypothesis that nifekalant opens hERG channel gates while blocking, and that unblock of these open-yet-blocked channels results in supranormal hERG current. We develop rate-theory kinetic models to identify features of agonism-while-blocking that produce facilitation. We generate atomistic models that predict that nifekalant blocks the hERG conduction path while modulating the intracellular conduction gate. Voltage-clamp measurements reveal that agonism-while-blocking undergirds nifekalant block and facilitation. We speculate that this agonism-while-blocking mechanism contributes to the relative safety of hERG blockers that induce facilitation.

PMID 42282827
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-06-12

Clinical evaluation of adjunctive magnesium therapy in patients receiving antidepressants for depression-open label, nonrandomized clinical trial.

Siddique Afifa A, Naeem Uzma U, Khokhar Muhammad Masood MM, Irshad Mushayada M et al.

Depression causes distress, dysfunction, and disability in terms of physical, mental, and social wellbeing. The challenges of late presentation, no-compliance of patients, and time-lag of antidepressants persist, despite advances. The objective was to determine the efficacy of antidepressants in combination with magnesium, compared to antidepressant monotherapy for treating depression. Forty-four patients with depression (6A70, 6A71, and 6A72 according to ICD-11) were divided into two equal groups, in an open label nonrandomized clinical trial. All patients received evidence-based antidepressants (either escitalopram, sertraline, duloxetine, amitriptyline, or fluoxetine). The experimental group additionally received 800 mg of magnesium glycinate (112 mg elemental magnesium). The psychometric testing was done by Patient Health Questionnaire (PHQ-9) at days 0, 14, and 28. Primary outcome was to see improvement at day 28, while secondary outcomes included time lag and remission (PHQ-9 scores < 4) at day 14 and 28, respectively. Paired sample t-test and Student t-test were applied for within-group and between-group differences using SPSSv27.0. The p-value ≤ 0.05 was considered statistically significant. The improvement in the PHQ-9 scores in groups A and B was 26.42% and 72.17%, respectively, by day 28, and effect size (Cohen's d = 1.76) was in the favor of adjunct therapy. Group B showed 41.34% improvemnet and large effect size (d = 1.29) on day 14 as well. All these values were statistically significant (p ≤ 0.05). The remission rate (44 patients) was higher with adjunt therpay (10.23%), versus 2.27% with monotherapy. Adjunct antidepressant therapy with magnesium is a preliminary effective strategy for patients with depression, potentially augmenting treatment response and decreasing time lag of antidepressants. ClinicalTrials.gov ID: NCT05931965 ( https://clinicaltrials.gov/study/NCT05931965?cond=Depression&intr=magnesium,%20methylfolate,%20B12&rank=1 ), 14-06-2023 (retrospectively registered).

PMID 42283837
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PubMedScience advances2026-06-11

Mice produce interneurons in the septum as a response to aversive experiences and antidepressant treatment.

Lampada Aikaterini A, Rolando Chiara C, Whittle Nigel N, Engler Anna A et al.

Adult neurogenesis sustains olfactory function, facilitates the acquisition of new memories, and provides resilience against depression in mice. Neural stem cells (NSCs) elicit selective responses to different physiological and pathological stimuli, thereby modulating neuron production. Here, we show that fear conditioning stimulates neurogenesis in the adult mouse brain septum by activating NSCs in the dorsal septum (dsNSCs) situated near a plexus of serotonergic axons originating from raphe nucleus neurons-key regulators of mood, anxiety, and stress responses. Elevation of serotonin (5HT) levels with the antidepressant and anxiolytic drug fluoxetine similarly promoted dsNSC proliferation and neurogenesis. The adult-born GABAergic interneurons integrate into septal nuclei. These findings suggest a potential adaptive response in mice to stress-inducing aversive experiences and elevated 5HT in the adult septum.

PMID 42268980
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PubMedProgress in neuro-psychopharmacology & biological psychiatry2026-06-10

Fluoxetine-associated adverse event signals with a focus on seizure: A study based on the FAERS database, network pharmacology, and molecular docking.

Cheng Cui C, Li Jun J, Zhang Huihui H, Wei Li L et al.

To evaluate fluoxetine-associated adverse event reporting signals in the FDA Adverse Event Reporting System (FAERS), focusing on seizure, and to explore potential biological plausibility using network pharmacology and molecular docking. FAERS reports with fluoxetine as the suspected drug were extracted. Clinical characteristics, adverse event profiles, seriousness, outcomes, and time-to-onset were analyzed. Disproportionality analysis was performed using reporting odds ratio (ROR). Overlapping targets between fluoxetine and seizure were identified, followed by GO/KEGG enrichment, PPI analysis, and molecular docking. Females accounted for 58.11% of fluoxetine-associated reports, and serious adverse events accounted for 86.45%. Psychiatric disorders and nervous system disorders were the main SOC categories, with RORs of 4.24 and 1.71, respectively. Seizure was reported in 496 cases (0.48%). Most adverse events occurred within 0-30 days, with a median onset of 11 days, while 14.34% occurred after 360 days. Mechanistic analysis identified 37 overlapping targets, mainly enriched in ion transport, neurotransmitter receptor activity, serotonergic and dopaminergic synapses, and inflammatory pathways. MAOA, BDNF, IL1B, CRH, IL6, and NTRK2 were identified as core targets. Docking suggested stable binding of fluoxetine with MAOA and NTRK2. Fluoxetine-associated adverse events showed prominent psychiatric and neurological features. Seizure, although infrequent, warrants pharmacovigilance attention. MAOA and NTRK2 may be key candidate targets involved in fluoxetine-associated seizure.

PMID 42264128
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PubMedThe journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG2026-06-10

A Case of Prolonged Serotonin Toxicity After Fluoxetine Ingestion in an Adolescent Patient.

Tuttle Merritt M, Allen Madison M, Cummings Austin A, Theobald Jillian J

Selective serotonin reuptake inhibitors (SSRIs), indicated for many disorders, have nuanced pharmacology. Half-lives of fluoxetine and its active metabolite, norfluoxetine, are 7 days and up to 17.5 days, respectively. Norfluoxetine inhibits CYP2D6, which metabolizes fluoxetine. A single substance ingestion could cause prolonged serotonin toxicity. CYP2D6 genotyping may identify patients at increased risk. In fluoxetine overdose, clinicians can expect prolonged hospitalization requiring aggressive sedation as in this case. A 16-year-old female with anxiety, depression, and headaches on no prescribed medications presented to emergency care after ingesting fluoxetine, benztropine, trimethoprim-sulfamethoxazole (TMP-SMX), gabapentin, omeprazole, and atorvastatin. She was intubated, sedated with propofol and fentanyl, and transported to higher-level care. In the pediatric intensive care unit (PICU), she had examination findings suggestive of serotonin toxicity. She was extubated hospital day (HD) 2 but required sedation for persistent agitation. Her mental status improved 24 hours after receiving cyproheptadine HD8, but she remained hyperthermic until HD10. She was externally cooled for maximum temperature 40.1°C. Peak creatine kinase level was 827 international units/L (reference, 27-140 units/L). Fluoxetine and norfluoxetine concentrations obtained HD8 were 350 ng/mL and 280 ng/mL (therapeutic steady-state range, 72-258 ng/mL for norfluoxetine and 91-302 ng/mL for fluoxetine). CYP2D6 metabolizer phenotype was normal. The patient was discharged home at neurologic baseline HD19.

PMID 42267072
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