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fluvoxamine (Favoxil CR / Favoxile CR / fluvoxamine CR)

✓ Approved

Astellas Pharma · SLC6A4 · Small Molecule

What is fluvoxamine?

fluvoxamine is a small molecule developed by Astellas Pharma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesFavoxil CR, Favoxile CR, fluvoxamine CR
CompanyAstellas Pharma
Drug ClassSmall Molecule
Molecular TargetSLC6A4
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Astellas Pharma

Mechanism of Action

Molecular Targets

fluvoxamine 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

fluvoxamine is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersObsessive-compulsive disorder✓ Approved
Psychiatric disordersSocial anxiety disorder✓ Approved

Related Research Articles

PubMedAnimals : an open access journal from MDPI2026-10-16

Chromium Propionate and Zilpaterol Hydrochloride Supplementation in Finishing Lambs: Growth Performance, Body Composition, Carcass Characteristics, and Meat Quality.

Hernández-Tovar Anselmo A, Hernández-García Esaúl E, Lazalde-Cruz Rosalba R, Rodríguez-Cordero Daniel D et al.

The objective of this study was to evaluate the effects of chromium propionate (Cr-Pr) and zilpaterol hydrochloride (ZH) supplementation on growth performance, performance-derived estimates of dietary energy utilization, body composition, carcass traits, wholesale cut distribution, and meat quality of finishing lambs. Forty intact male Dorper × Katahdin lambs were blocked by initial body weight (38.21 ± 1.72 kg) and assigned to a 2 × 2 factorial arrangement (n = 10/treatment): Control (0 Cr-Pr + 0 ZH), ZH (0 Cr-Pr + 7.2 mg ZH/lamb/d), Cr-Pr (1.2 mg elemental Cr/lamb/d + 0 ZH), and Cr-Pr + ZH (1.2 mg elemental Cr/lamb/d + 7.2 mg ZH/lamb/d). The experimental period lasted 45 d; Cr-Pr was supplemented throughout d 1-45, whereas ZH was administered during d 15-42, followed by a 3 d withdrawal period (d 43-45). Under the conditions evaluated, Cr-Pr, ZH, and their interaction did not affect growth performance or performance-derived estimates of dietary energy utilization (p > 0.05); however, both compounds produced specific changes in body composition and carcass traits. Supplementation with Cr-Pr reduced omental, visceral, and perirenal fat by 21.8, 18.6, and 18.7%, respectively (p ≤ 0.044), and increased longissimus muscle area (LMA) by 5.3% (p = 0.013). An interaction between Cr-Pr and ZH was detected for rib fat thickness (FAT) (p = 0.050), with the ZH and Cr-Pr individual treatments showing lower FAT than Control and Cr-Pr + ZH. Supplementation with ZH increased dressing percentage by 7.2% (p = 0.048). Regarding wholesale cuts, classified according to Institutional Meat Purchase Specifications (IMPS), Cr-Pr increased shoulder (IMPS 206) and loin (IMPS 231) proportions by 10.3 and 10.6%, respectively, and reduced shoulder (IMPS 207) by 3.3% (p = 0.043), whereas ZH increased breast (IMPS 209) weight by 15.0% and its proportion of cold carcass weight (CCW) by 9.7% (p ≤ 0.042). Interactions between Cr-Pr and ZH were also detected for ribs (IMPS 209A) and flank (IMPS 232) weights (p ≤ 0.047). Supplementation did not affect meat quality traits (p ≥ 0.217). Overall, Cr-Pr was associated with reduced internal fat deposition and increased LMA and loin (IMPS 231) proportion, whereas ZH modified dressing percentage and breast (IMPS 209) weight and proportion of CCW. These responses occurred without changes in growth performance or performance-derived estimates of dietary energy utilization and without detectable changes in the evaluated meat quality traits. The interactions observed for FAT, ribs (IMPS 209A), and flank (IMPS 232) were trait-specific and did not indicate a consistent benefit of the combination.

PMID 42883037
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PubMedInternational journal of molecular sciences2026-10-16

Mechanisms of Hexavalent Chromium-Induced Lung Carcinogenesis: DNA Double-Strand Breaks and DNA Repair Inhibition in a Guinea Pig Model.

Meaza Idoia I, Lu Haiyan H, Wise Jamie L JL, Diven Sandra S et al.

Hexavalent chromium [Cr(VI)] is an environmental and occupational pollutant and a known lung carcinogen. Despite the exposure risks, it is unclear how Cr(VI) causes lung cancer. Prolonged Cr(VI) exposure induces DNA double-strand breaks and inhibits their repair in exposed cells, leading to chromosome instability, a hallmark of lung cancer. Specifically, Cr(VI) inhibits RAD51, a key effector protein in the homologous recombination repair pathway. The goal of this study was to translate this molecular mechanism of Cr(VI)-induced lung carcinogenesis to a guinea pig model. Hartley guinea pigs 10 to 11-week-old were exposed to zinc chromate via oropharyngeal aspiration for acute (24 h) or subchronic (90-day) exposure. Lungs were dissected and formalin-fixed paraffin-embedded. DNA double-strand breaks were measured using gamma-H2AX foci, and homologous recombination repair was assessed using RAD51 foci. Acute Cr(VI) exposure induced gamma-H2AX foci and RAD51 foci, whereas subchronic exposure also caused gamma-H2AX foci but inhibited RAD51 foci. These effects of Cr(VI)-induced DNA damage and repair inhibition were largely observed in bronchiolar regions but not in alveolar regions. This study establishes a new human-relevant model to study Cr(VI)-induced carcinogenesis and translates the mechanism of Cr(VI)-induced DNA double-strand break formation and repair inhibition to guinea pig lungs.

PMID 42883778
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PubMedMaterials (Basel, Switzerland)2026-10-16

Structure-Barrier-Release Relationships of Low-Temperature ALD ZrO2 Thin Films on Co-Cr Alloys: Reducing Long-Term Co and Cr Ion Release in Artificial Saliva.

Ziębowicz Anna A, Groelich Wiktoria W, Kajzer Anita A, Kajzer Wojciech W et al.

Co-Cr alloys are widely used in biomedical devices owing to their excellent mechanical properties and corrosion resistance; however, sustained metal-ion release in physiological environments remains an important materials concern. Low-temperature atomic layer deposition (ALD) enables the formation of conformal ceramic barriers that can restrict long-term metal-ion transport. In this study, nominally ~50 nm ALD-derived ZrO2 coatings were deposited on Co-Cr substrates manufactured by investment casting (CAST), CAD/CAM milling (MILLED), and laser powder bed fusion (PRINTED). The coatings were characterized using scanning electron microscopy (SEM), atomic force microscopy (AFM), Raman spectroscopy, transmission electron microscopy with selected-area electron diffraction (TEM/SAED), and X-ray photoelectron spectroscopy (XPS), while the electrochemical response was evaluated by open-circuit potential (OCP) and electrochemical impedance spectroscopy (EIS). Long-term barrier performance was quantified by inductively coupled plasma atomic emission spectroscopy (ICP-AES) as cumulative Co and Cr release for all manufacturing routes and Mo release for the Mo-containing CAST and PRINTED alloys after 28 days in artificial saliva at 37 °C. ZrO2 deposition reduced cumulative Co and Cr release for all manufacturing routes. Mo release was also reduced in the Mo-containing alloys, with Mo remaining below the analytical detection limit (<0.005 µg cm-2) for the PRINTED + ZrO2 system. Electrochemical measurements further demonstrated manufacturing-route-dependent differences in barrier response between the initial and 28-day exposure states. Overall, the findings establish a structure-barrier-release framework linking coating formation and electrochemical response with cumulative ion release, and identify 28-day cumulative ion release as a practical functional descriptor for comparing the long-term performance of ALD-derived ceramic barriers on Co-Cr alloys.

PMID 42882672
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PubMedToxicology mechanisms and methods2026-10-16

NRF2-KEAP1 Signaling in Chromium-Induced Lung Carcinogenesis: Mechanistic Insights and Evidence Gaps.

Varma Bhavani Manoj BM, Gopalakrishnan Abilash Valsala AV

Hexavalent chromium [Cr(VI)] is a recognized environmental and occupational carcinogen associated with an increased risk of lung cancer. The nuclear factor erythroid 2-related factor 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) pathway regulates cellular responses to oxidative and electrophilic stress and may influence cell survival following Cr(VI) exposure. Under basal conditions, KEAP1 promotes NRF2 ubiquitination and proteasomal degradation. Oxidative or electrophilic stress can impair this process, allowing NRF2 to accumulate and activate genes involved in antioxidant defense, detoxification, and cellular redox regulation, including HMOX1, NQO1, and GCLC. Although these responses can protect normal cells from acute stress, persistent NRF2 activity has also been associated with metabolic adaptation, resistance to apoptosis, and tumor-promoting phenotypes in several cancer models.However, the extent to which NRF2-KEAP1 signaling directly contributes to Cr(VI)-induced lung carcinogenesis remains incompletely established. Many studies on Cr(VI) have investigated oxidative stress, inflammation, genotoxicity, and cellular transformation. In contrast, relatively few have directly tested whether NRF2 activation is causally involved in tumor initiation or progression in chromium-exposed lung models. This review examines the relationship among Cr(VI) exposure, redox imbalance, and NRF2-KEAP1 signaling, distinguishing findings from chromium-specific experimental systems from mechanisms inferred from broader lung cancer research. It also discusses downstream processes relevant to carcinogenesis, occupational exposure, and risk assessment, as well as potential preventive or therapeutic strategies. The available evidence supports NRF2-KEAP1 signaling as an important component of the cellular response to Cr(VI)-associated stress, but further mechanistic studies are needed to establish its specific causal contribution to chromium-induced lung carcinogenesis.

PMID 42885242
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PubMedJournal of general internal medicine2026-10-16

The ACEs of Clinical Reasoning: a Formal, Longitudinal, Leadership Role for Medical Students to Augment Clinical Reasoning Education.

Tang Zeyu Z, Swallow Madisen A MA, Bahar Ryan C RC, Gaeta Gazzola Marina M et al.

Clinical reasoning (CR) is integral to undergraduate medical education but requires significant resources to deliver adequate practice and individualized feedback. Peer-assisted learning (PAL) may improve instructional capacity and enhance the learning climate. We describe the development, implementation, and impact of the Associate Course Educator (ACE) role, a structured PAL and leadership position for medical students within a CR longitudinal course. A private, not-for-profit U.S. medical school. Senior medical students who completed core clerkships. ACEs completed a 12-month term with optional term renewal for eligible students. They received close mentorship and instruction in CR pedagogy. ACEs delivered at least 20h of teaching annually, led educational projects, contributed to scholarship, and supported curricular review. Across six recruitment cycles (2020-2026), 84 students applied and 44 were selected (52.4%). Annual CR sessions increased from eight to 22 and shifted from large-group to predominantly small-group and one-on-one formats. ACEs contributed multiple educational innovations and disseminated scholarship at regional and national venues. The ACE role formalizes PAL as a mentored medical education experience that expands instructional capacity, supports instructor-intensive teaching formats, and enhances feedback mechanisms. For students, the role provides structured mentorship in CR, teaching, and scholarship while enabling meaningful contributions to institutional curricula.

PMID 42881336
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PubMedVirulence2026-10-16

Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome.

Gao Zhixin Z, Li Zheng Z, Cui Jianyang J, Zhang Qing Q et al.

The intestinal tract is a key immune organ and microecological system, where colonization resistance (CR) mediated by gut microbiota prevents pathogen invasion. Salmonella disrupts CR via type VI and type III secretion systems (T6SS/T3SS), inducing dysbiosis, inflammasome-driven inflammation, and intestinal barrier damage. This creates a self-reinforcing cycle:dysbiosis alters microbial metabolites, sustains inflammation, and enhances pathogen fitness, favoring chronic infection. This review integrates molecular mechanisms of microbiota disruption, inflammasome activation, and metabolic imbalance to explain how Salmonella overcomes CR. We also highlight microbiota-based countermeasures, including probiotics, natural antimicrobials, and phage therapy, as promising strategies to restore gut homeostasis.

PMID 42885908
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