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Fluosol-DA (Fluosol)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · Small Molecule · Small Molecule

What is Fluosol-DA?

Fluosol-DA is a small molecule developed by Mitsubishi Tanabe Pharma Corporation. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesFluosol
CompanyMitsubishi Tanabe Pharma Corporation
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Mitsubishi Tanabe Pharma Corporation

Therapeutic Indications

Fluosol-DA is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Blood and lymphatic system disordersAnaemia✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Neoplasm malignant✓ Approved

Related Research Articles

PubMedStructure (London, England : 1993)2026-06-09

Molecular basis for the dopamine reuptake and inhibition mechanism of human dopamine transporter.

Yin Jian J, Liu Chang C, Zhang Sensen S, Xie Min M et al.

Dopamine (DA) is a key neurotransmitter that regulates neuropsychological behaviors, including movement, emotion, motivation, and cognition. Dysregulation of dopaminergic signaling is linked to psychiatric and neurodegenerative disorders, including Parkinson's disease, depression, and schizophrenia. The dopamine transporter (DAT) controls DA levels by facilitating its reuptake from the synaptic cleft, terminating dopaminergic signaling. Here, we report structures of full-length human DAT (hDAT) in its apo state and in complexes with substrates and antidepressant compounds. The antidepressant compounds bupropion and vanoxerine bind to the central site of hDAT and inhibit substrate transport. Integration of structural analysis with functional assays and molecular dynamics simulations further suggests a role for potassium ions in regulating hDAT conformational transitions. Our findings reveal the molecular mechanisms governing DA reuptake and the specific ways in which hDAT interacts with antidepressant compounds. These insights provide a structural basis for the design of therapeutic agents targeting hDAT.

PMID 42259286
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PubMedRheumatology (Oxford, England)2026-06-09

Prospective evaluation of recombinant Herpes zoster vaccine in systemic sclerosis: immunogenicity, safety, and disease outcomes.

Luppino-Assad Ana Paula AP, Mello Renata P RP, Medeiros-Ribeiro Ana Cristina AC, Aikawa Nadia E NE et al.

to evaluate humoral immune response to recombinant zoster vaccine(RZV) in immunosuppressed patients with systemic sclerosis(SSc) compared with healthy controls, to identify factors influencing vaccine response, and to assess RZV safety and impact on patient-reported outcome measures(PROMs) and disease activity(DA). A sub-analysis of a randomized, double-blind, placebo-controlled trial included 76 immunosuppressed SSc patients and 304 healthy controls(CG) receiving two RZV doses. SSc patients were randomized to receive two initial doses of RZV or placebo; after unblinding, the placebo group received two doses of RZV. Anti-glycoprotein-E antibodies were measured at baseline and six-weeks post-second dose. Geometric mean concentrations(GMCs) and factor increase(FI) were calculated. Cell-mediated immunogenicity (CMI) was evaluated. DA and PROMs were assessed using standardized instruments. Body mass index(BMI) defined nutritional status. SSc patients(47.4%diffuse/52.6%limited) were younger(53.0 vs 55.0 years, p= 0.002) and had lower BMI(p= 0.005) than CG. Humoral response were significantly lower in SSc compared with controls(92.6% vs 99.7%,p= 0.001). SSc patients showed significantly lower GMC(5.81 vs 12.6, p< 0.001) and FI(31.0 vs 59.4, p< 0.001) than controls, with comparable CMI(p> 0.05). Disease subtypes, demographic factors, immunosuppressive therapies or nutritional status did not predict impaired vaccine response(p> 0.05). Local adverse events were reduced in SSc patients(73.7% vs 86.5%,p= 0.024), while systemic reactions were comparable overall(59.2% vs 61.5%,p= 0.712). DA and PROMs outcomes remained stable(p> 0.05). RZV was well tolerated. Despite the high seroconversion rate, the immune response was significantly lower in magnitude compared with controls, without triggering DA or worsening PROMs. ∼50% lower antibody concentrations in SS raise concerns about long-term protection, underscoring the need for ongoing monitoring. ClinicalTrials.gov; NCT05879419.

PMID 42261247
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-06-09

PRMT9 Aggravated Dopaminergic Neurodegeneration in Parkinson's Disease Model by Facilitating the Degradation of DUSP26 and Inducing Mitochondrial Dysfunction.

Liu Tengfei T, Song Xiaomeng X, Guo Xin X, Xiao Rui R et al.

Protein arginine methyltransferases (PRMTs) catalyze protein arginine methylation and play a crucial role in the pathogenesis of diseases. Mitochondrial dysfunction is implicated in the neurodegeneration of Parkinson's disease (PD). However, whether protein arginine methyltransferase 9 (PRMT9), which is found in mitochondria, is involved in PD remains unclear. In this study, we found that PRMT9 was markedly increased in the nigrostriatal region of PD mice induced by MPTP and in SH-SY5Y cells stimulated with MPP+. In MPP+-exposed SH-SY5Y cells, PRMT9 translocated to mitochondria and exacerbated mitochondrial injury, manifested as decreased mitochondrial membrane potential, reduced ATP production, elevated ROS levels, and mitochondrial fragmentation. Furthermore, PRMT9 deficiency significantly alleviated dopaminergic (DA) neurodegeneration induced by MPTP, while PRMT9 overexpression aggravated MPTP-induced neurodegeneration. Mechanistically, PRMT9 directly interacted with dual-specificity phosphatase 26 (DUSP26) and catalyzed its arginine methylation at residue R29, which then promoted the polyubiquitination and proteasomal degradation of DUSP26 mediated by Trim32. Therefore, PRMT9 drove DA neurodegeneration in PD by promoting DUSP26 degradation and inducing mitochondrial dysfunction. Our study identified PRMT9 as a novel potential therapeutic target and a pharmaceutical intervention targeting the interaction between PRMT9 and DUSP26 may provide a promising strategy for PD.

PMID 42261762
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PubMedNutrition, metabolism, and cardiovascular diseases : NMCD2026-06-09

Plasma metabolomic signatures of adults at elevated-cardiovascular disease risk show improvements in diet quality in response to medical nutrition therapy.

Clarke Erin D ED, Stanford Jordan J, Gómez-Martín María M, Reay William R WR et al.

Metabolomic signatures representing a "healthy" and "unhealthy" dietary pattern have previously been constructed using data from a randomised controlled crossover feeding study (DQFS). The utility of these metabolomic signatures in other populations has not been evaluated. Here, we mapped changes in diet-derived plasma metabolites in a sample of rural adults screened as at elevated-cardiovascular disease (CVD) risk receiving medical nutrition therapy (MNT), against the DQFS dietary metabolite signature. A sub-sample of MNT participants (n = 11) received personalised MNT from a dietitian over 6-months. Plasma metabolites for DQFS and HRH were analysed using ultra-high performance liquid chromatography-tandem mass spectrometry. Restricted maximum likelihood mixed-effect models were used to evaluate change in metabolites and dietary intake across the MNT intervention. Principle component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) plots were used to compare metabolite profiles between both studies. Five metabolites significantly changed between baseline and either the 3- or 6-month, with two metabolites [Ethylmalonate and Glycosyl-N-stearoyl-sphingosine (d18:1/18:0)] significantly reduced at both 3- and 6-months. Diet quality significantly increased across the intervention (p < 0.001). PCA and PLS-DA plots identified that post MNT intervention 3- and 6-month metabolic signatures aligned more closely with the "healthy" dietary pattern signature. Findings demonstrated that the metabolomic signature identified in the controlled DQFS feeding study can be used to map changes in diet quality in response to an MNT intervention in people at an elevated CVD risk. Future studies in larger, independent cohorts are warranted.

PMID 42259719
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PubMedAmerican journal of biological anthropology2026-06-09

Whole-Epiphysis Trabecular Bone in Tamarin Limbs Suggests Effects of Leaping Distance Alongside Non-Biomechanical Factors.

Nguyen Uyen U, Alfieri Fabio F, Veneziano Alessio A, Licht Annika A et al.

Beyond non-biomechanical factors, the trabecular architecture of long bone epiphyses variably underlies functional adaptations to locomotor behavior. A recent study, characterizing tamarin trabecular bone using traditional metrics derived from Volumes of Interest (VOIs), identified a preliminary relationship with leaping distance. We hypothesized that quantifying trabecular topological indices from whole epiphyses in the same system would enhance detection of locomotor signals. We analyzed μCT scans of humeral and tibial whole-epiphyseal trabecular bone in four tamarin species representing short- and long-distance leapers. We quantified topological indices-node density (NodDen), trabecular tortuosity (TrabTort), trabecular length (TrabLen), and fractal dimension (FD)-alongside traditional metrics-degree of anisotropy (DA) and bone volume fraction (BV/TV). We tested relationships between trabecular traits and leaping distance and assessed the effects of non-functional factors (sex and captivity). Long-distance leapers exhibited significantly higher NodDen in humeral and tibial epiphyses and increased distal humeral TrabTort. Regions of elevated NodDen were concentrated beneath the humeroscapular joint (proximal humerus) and occurred variably across other epiphyses. In contrast, DA, BV/TV, TrabLen, and FD were more strongly associated with sex and captivity. Higher loading magnitudes associated with longer leaps may increase NodDen and, more tentatively, TrabTort in tamarin limb epiphyses. However, locomotion-related signals were weaker than those linked to sex and captivity, suggesting that leaping distance affects specific trabecular traits, whereas the overall trabecular organization is driven by non-functional factors. Whole-epiphysis analyses and topological indices provide a valuable complement to traditional VOI-based approaches and metrics.

PMID 42259666
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PubMedJournal of minimal access surgery2026-06-09

Robotic single-site cholecystectomy with indocyanine green fluorescence for duplicated gallbladder.

Yoo Daegwang D

Symptomatic gallbladder (GB) duplication is a rare congenital anomaly that poses a significant surgical challenge due to anatomical variability, increasing the risk of bile duct injury or retained GB syndrome. We present the case of a 58-year-old woman with symptomatic cholelithiasis in a duplicated GB, who underwent a robotic single-site cholecystectomy using the da Vinci SP ® system. Intraoperative indocyanine green (ICG) fluorescence imaging was instrumental in delineating the biliary tree, enabling the successful resection of both GBs and their respective cystic ducts and arteries without complications. The articulated instruments of the robotic platform provided the dexterity required for precise dissection, particularly as one GB was partially embedded in the liver parenchyma. This case demonstrates that robotic single-site cholecystectomy with ICG fluorescence imaging is a safe, feasible and effective approach for managing GB duplication, enhancing anatomical identification to minimise surgical risks in aberrant biliary anatomy.

PMID 42262778
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