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fluoxetine (EDG005)

✓ Approved

Edgemont Pharmaceuticals, LLC · SLC6A4 · Small Molecule

What is fluoxetine?

fluoxetine is a small molecule developed by Edgemont Pharmaceuticals, LLC. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesEDG005
CompanyEdgemont Pharmaceuticals, LLC
Drug ClassSmall Molecule
Molecular TargetSLC6A4
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Edgemont Pharmaceuticals, LLC

Mechanism of Action

Molecular Targets

fluoxetine acts on 1 molecular target:

SLC6A4solute carrier family 6 member 4 (5HTT, 5-HTT)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

fluoxetine is developed for 4 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersBulimia nervosa✓ Approved
Psychiatric disordersObsessive-compulsive disorder✓ Approved
Psychiatric disordersPanic disorder✓ Approved
Psychiatric disordersMajor depression✓ Approved

Related Research Articles

PubMedJournal of microbiology and biotechnology2026-08-28

Banhasasim-tang Attenuates Corticosterone-Induced Behavioral Despair-like Responses and Is Associated with Gut Microbiota and Serum Metabolomic Changes in Mice.

Seo Seung-Ho SH, Kang Sang-Mi SM, Kang Siwon S, You Yanghee Y et al.

Banhasasim-tang (BHSST) is a classical East Asian herbal formula traditionally used for gastrointestinal disorders, but its effects on stress-related depressive-like behavior and the associated microbiome-metabolome signatures remain unclear. This study evaluated the antidepressant-like effects of BHSST in a corticosterone (CORT)-induced mouse model and investigated fecal microbiota and serum metabolomic alterations. Male C57BL/6 mice were assigned to Normal, CORT, fluoxetine, low-dose BHSST, or high-dose BHSST groups. CORT was administered for 21 days, and immobility-based behavioral responses were assessed using the forced swimming test and tail suspension test. Fecal microbiota were analyzed by 16S rRNA gene sequencing, and serum metabolites were profiled using untargeted UPLC-QTOF-MS. BHSST reduced CORT-induced immobility time in both behavioral tests. Although alpha diversity was not significantly altered, BHSST treatment was associated with changes in fecal microbial community structure and discriminative bacterial taxa. Serum metabolomics revealed BHSST-H-associated changes in metabolites related to amino acid metabolism, energy metabolism, redox-related metabolism, lipid metabolism, and microbial co-metabolism. Integrated microbiome-metabolome analysis identified association-based multi-omics signatures involving selected bacterial taxa, serum metabolites, and immobility-based behavioral outcomes. These findings suggest that BHSST-induced behavioral improvement is accompanied by changes in the microbiome-metabolome profile in CORT-induced mice.

PMID 42661364
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PubMedInsects2026-08-27

Establishment and Validation of a CUMS Model for Depression-like Behavior in Honeybees: A Tool for Pollinator Stress Research.

Yang Yunqi Y, Dai Shuying S, Zhang Lizhen L

Honeybees (Apis mellifera), as key pollinating insects, are undergoing population decline, which has become a critical environmental challenge affecting ecosystem stability and sustainable agriculture. Moreover, a potential association exists between the physiological and behavioral responses of honeybees induced by environmental stress and the pathological mechanisms of depression. The pathogenesis of depression remains complex and not fully understood, and a stable animal model is a prerequisite for investigating its mechanisms and screening antidepressants. This study aimed to examine the alterations induced by CUMS and to evaluate behavioral changes related to depression-like phenotypes and neurotransmitter levels in the honeybee brain. The results showed that CUMS treatment induced typical depression-like behaviors and downregulated monoamine neurotransmitters in honeybees, consistent with observations in mammalian depression models. Fluoxetine was found to reverse these abnormalities, further supporting the validity of the model. This study provides a novel tool for depression research, antidepressant screening, and stress-related investigations in pollinators.

PMID 42652428
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PubMedThe Journal of general physiology2026-08-27

A hERG blocker facilitates K+ channel current by promoting 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 underpins 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 unblocking of these open-yet-blocked channels results in supranormal hERG current. We developed rate-theory kinetic models to identify features of agonism-while-blocking that produce facilitation. We generated atomistic models that predict that nifekalant blocks the hERG conduction path while modulating the intracellular conduction gate. Voltage-clamp measurements revealed that agonism-while-blocking can result in nifekalant block and facilitation. We speculate that this agonism-while-blocking mechanism contributes to the relative safety of hERG blockers that induce facilitation.

PMID 42658189
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PubMedBiomedicines2026-08-27

In Silico and In Vitro Evaluation of Calm Supplement Constituents on Antidepressant-Related Molecular Targets and Neuroplasticity-Associated Gene Expression.

Batur Lutfiye Karcioglu LK, Pektas Ahsen A, Aslan Buse B, Akcali Nermin N et al.

Background: Depression-related mechanisms involve not only monoaminergic neurotransmission but also neurotrophic signaling, synaptic plasticity and intracellular survival pathways. Materials and Methods: In this study, the potential neuropharmacological properties of Calm, a multi-component supplement product, were evaluated using in silico and in vitro approaches. Molecular docking analyses were performed to estimate the binding profiles of Calm-derived constituents and reference antidepressants, sertraline and fluoxetine, against SLC6A4, MAOA, AKT1 and NTRK2. In parallel, SH-SY5Y human neuroblastoma cells were treated with Calm, and MTT-based metabolic activity and the relative expression levels of BDNF, NTRK2 and SYN1 were assessed after 24 h. Results: Docking results showed that several Calm constituents, particularly apigenin, rosmarinic acid, xanthohumol and valerenic acid, exhibited favorable predicted interactions with SLC6A4 and NTRK2. Calm treatment increased MTT signal at low concentrations, with significant increases observed at 10, 30, and 60 µg/mL. However, 24 h exposure to 10 µg/mL Calm significantly reduced BDNF, NTRK2 and SYN1 expression levels. Conclusions: These findings suggest that Calm constituents may interact with antidepressant-related molecular targets and modulate neuroplasticity-associated transcriptional markers. However, the results should be considered preliminary and require protein-level and functional validation.

PMID 42652132
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PubMedBrain sciences2026-08-27

Neuromodulation to Promote Recovery Following Traumatic Brain Injury: A Narrative Review of Current Pharmacologic and Non-Pharmacologic Approaches.

Wong Cindy K CK, Khurana Nilsha N, Aliakbar Raya T RT, Poblete Roy A RA

Traumatic brain injury (TBI) is a leading cause of long-term neurological disability worldwide and is frequently associated with persistent impairments in consciousness, cognition, mood, and functional independence. Despite advances in acute neurocritical care, effective therapies that enhance neurological recovery remain limited. Neuromodulation has emerged as a promising strategy to augment neuroplasticity and improve recovery through both pharmacologic and non-pharmacologic approaches. This narrative review summarizes current evidence supporting pharmacologic neuromodulatory therapies, including central nervous system stimulants (methylphenidate and modafinil), dopaminergic agents (amantadine and bromocriptine), acetylcholinesterase inhibitors (donepezil and rivastigmine), and selective serotonin reuptake inhibitors (sertraline and fluoxetine). Mechanisms of action, clinical efficacy, adverse effects, and practical considerations across the acute, subacute, and chronic phases of TBI recovery are discussed. Emerging non-pharmacologic neuromodulation techniques, including repetitive transcranial magnetic stimulation, transcranial direct current stimulation, electroconvulsive therapy, vagus nerve stimulation, and deep brain stimulation, are also reviewed. Although amantadine remains the only neuromodulator supported by moderate-quality guideline recommendations for accelerating recovery in disorders of consciousness, accumulating evidence suggests that several additional pharmacologic and non-pharmacologic neuromodulation interventions may improve attention, executive function, fatigue, mood, and rehabilitation participation in carefully selected patients. However, current evidence is limited by heterogeneous study populations, small sample sizes, inconsistent outcome measures, and a paucity of long-term randomized controlled trials. Future research should prioritize adequately powered comparative studies, standardized outcome measures, biomarker-guided patient selection, and multimodal treatment strategies to optimize neurological recovery following TBI.

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PubMedAutism research : official journal of the International Society for Autism Research2026-08-27

Antidepressant Prescribing Trends for Adults With and Without Autism in the United Kingdom From 1997 to 2023: A Population-Based Cohort Study Using Clinical Practice Research Datalink Aurum.

Sadik Aws A, Khandaker Golam M GM, Pardiñas Antonio F AF, Lundberg Michael M et al.

Antidepressant prescribing and autism diagnoses have increased in recent years. We aimed to describe and compare trends in antidepressant prescribing, indications, doses and durations in autistic and non-autistic males and females in the United Kingdom (UK) from 1997 to 2023. Using population-representative UK primary care records, we defined three autistic groups-autistic adults with intellectual disability (ID), autistic adults without ID and all autistic adults-and four non-autistic groups. In each calendar year we calculated: annual, lifetime and new antidepressant prescribing; indications for serotonin-selective reuptake inhibitor initiation; average doses prescribed for citalopram, fluoxetine, and sertraline; and the proportion of courses that lasted over 1, 2, and 3 years. We also repeated analyses with sex-stratification. In all, 34,173,295 non-autistic adults and 172,242 autistic adults were included (47,011 with ID and 125,231 without ID). 30% of autistic adults and 14.7% of non-autistic adults were prescribed an antidepressant in 2023. Prescriptions, doses and course durations increased over time for all groups. Prescriptions were highest in autistic adults without ID and females, whereas course durations were highest in autistic adults with ID. Recording of depression and anxiety as indications was lower for those with ID. Antidepressant prescribing has increased more for autistic adults than non-autistic adults since 1997, with more new starters, higher doses and longer course durations. This potentially increases the risk of adverse medication effects for autistic adults and emphasizes the need for stronger evidence around the effectiveness and tolerability of mental health interventions and the reasons for systematic differences in prescribing.

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