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Factor IX (AlphaNine SD / AlphaNine)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · F9 · Cell-based Therapies

What is Factor IX?

Factor IX is a cell-based therapies developed by Mitsubishi Tanabe Pharma Corporation. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesAlphaNine SD, AlphaNine
CompanyMitsubishi Tanabe Pharma Corporation
Drug ClassCell-based Therapies
Molecular TargetF9
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

Factor IX acts on 1 molecular target:

F9coagulation factor IX (P19, F9 p22)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

Factor IX is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersExtravasation blood✓ Approved
Congenital, familial and genetic disordersFactor IX deficiency✓ Approved
Vascular disordersHaemorrhage✓ Approved

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Despite the established epidemiological synergy between Porphyromonas gingivalis-induced periodontitis and oral squamous cell carcinoma (OSCC), a critical gap remains in developing single-agent therapeutics that simultaneously neutralize bacterial virulence and suppress host oncogenic signaling. This study aimed to comprehensively evaluate Curcumin 4'-O-β-D-gentiobioside (COG) as a novel, dual-pathway phytochemical intervention targeting the keystone virulence factor RgpB while concurrently disrupting OSCC progression networks. A multi-modal computational approach was used, including network pharmacology, molecular docking, molecular dynamics simulations, and ADMET profiling. Anti-aging activity was predicted through pharmacological activity modeling. Network pharmacology identified Curcumin 4'-O-β-D-gentiobioside (COG; PubChem CID: 46926100) targeting hub genes (TNF, IL6, EGFR, AKT1), enriching immune regulation, apoptosis, and oxidative stress pathways (FDR < 0.05). Docking revealed strong binding to RgpB (XP GScore: - 9.867 kcal/mol), supported by hydrogen bonds and π-stacking. Molecular dynamics confirmed stability (RMSD: 1.0-1.5 Å; ΔG =  - 14 kcal/mol). COG downregulated pro-inflammatory (CXCL10, MAPK8) and oncogenic (MDM2, BCL2L1) mediators, while enhancing ER stress response (KDELC1, ATF4). ADMET analysis predicted high absorption, negligible neurotoxicity, and no hepatotoxicity/genotoxicity. Predicted anti-aging activities included senolytic, antioxidant, and NF-κB inhibition. These results position COG as a promising dual-agent that concurrently neutralizes RgpB virulence, disrupts chronic inflammation, and suppresses OSCC progression, addressing a critical unmet need in oral disease therapeutics. These findings warrant in vivo validation for translation into oral disease therapeutics.

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Effects of Mandala Coloring on Alpha Brain Activity and Anxiety Symptoms among Students at Universiti Sains Malaysia: A Randomized Controlled Trial.

Chang Xin Ni XN, Othman Azizah A, Yusoff Nasir N, Zulkifly Mohd Faizal Mohd MFM

University students commonly experience stress and anxiety, which can negatively affect their academic performance. Mandala coloring has gained attention as a therapeutic art-based activity that may help alleviate symptoms of anxiety. Changes in brain activity, particularly in the alpha power, are known to reflect psychological states and responses to interventions. This study investigated the effects of mandala coloring on alpha brain activity and anxiety symptoms among students at Universiti Sains Malaysia. In a randomized experimental study, sixty students aged 18 to 25 years (M=22.97, SD=1.03) with moderate to high anxiety levels were randomly assigned to either an intervention group (n=30), which colored a geometric mandala for 20 minutes, or a control group (n=30), which colored a blank circle. Brain activity was recorded using electroencephalography (EEG), and anxiety levels were assessed before and after the session using the Malay version of the Beck Anxiety Inventory. Data were analyzed using a mixed-design analysis of variance (ANOVA) with group (intervention vs. control) as the between-subjects factor, and time and brain regions as the within-subjects factor. Both groups showed reductions in anxiety symptoms over time, with no significant differences between groups (F(1; 56)=0.03, p=0.87). However, EEG changes across brain regions differed between groups, with mandala coloring leading to increased frontal alpha power (F(3; 156)=3.21, p=0.03). Mandala coloring was associated with increased frontal alpha power, suggesting enhanced relaxation and focused attention. Anxiety symptoms decreased in both coloring groups, indicating that coloring in general may support emotional regulation and well-being. Taken together, these findings suggest that coloring-based activities may serve as useful therapeutic tools for reducing anxiety and improving focus among university students.

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Alternative splicing is increasingly recognized as a critical layer of oncogenic regulation, yet the biological meaning of individual splicing factors remains highly context dependent. Serine/arginine-rich splicing factor 3 (SRSF3) has been widely described as an oncogenic splicing regulator in colorectal, cervical, lung, pancreatic, and other cancers; however, emerging evidence also suggests tumor-suppressive or context-specific functions in selected malignancies. This review critically evaluates current knowledge of SRSF3 in cancer by moving beyond a catalogue of downstream targets. We discuss how SRSF3 controls cancer-associated splicing programs, how these events intersect with signaling pathways, metabolism, immune regulation, and therapeutic resistance, and why the same factor may produce divergent biological outcomes depending on tumor lineage, RNA-binding partners, and target isoforms. We also examine unresolved controversies, including whether SRSF3 is a universal oncogenic driver or a context-dependent regulator, whether SRSF3 expression alone is sufficient as a biomarker, and how cancer-specific splicing events can be therapeutically targeted without disrupting essential RNA processing in normal tissues. Finally, we highlight translational barriers, including limited clinical validation, delivery challenges for RNA-based therapeutics, toxicity risks, and compensatory splicing networks. A more precise understanding of SRSF3-dependent splicing vulnerabilities may support future biomarker development and rational combination therapies.

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Exercise has profound beneficial effects on bone health, yet the molecular mechanisms that mediate mechanical force transduction remain incompletely understood. Exosomal noncoding RNAs (ncRNAs) have emerged as critical intercellular messengers that translate mechanical stimuli into coordinated signaling cascades within the bone microenvironment. The present review systematically synthesizes evidence demonstrating that exercise dynamically modulates exosomal ncRNA expression in a modality‑dependent and temporally regulated manner. These exercise‑induced exosomal ncRNAs orchestrate bone remodeling by activating osteogenic pathways such as the Wnt/β‑catenin pathway, suppressing osteoclastogenesis via receptor activator of nuclear factor κB (RANK) ligand (RANKL)/RANK/osteoprotegerin axis modulation, and coordinating multicellular interactions. Translational applications for sports‑related bone injuries are critically evaluated, including noninvasive biomarkers, personalized exercise prescriptions, and engineered exosome‑based therapeutics, alongside current limitations. Collectively, these findings support exercise‑induced exosomal ncRNAs as a central paradigm linking physical activity to skeletal adaptation.

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Validity and reliability of the Turkish version of the early symptom measurement of post-stroke depression short form (ESMPSD-SF).

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The present methodological study was conducted to adapt the Early Symptom Measurement of Post-Stroke Depression developed by Li et al.1 into Turkish and to examine its validity and reliability. This study was conducted between September and December 2025 with a final sample of 120 patients diagnosed with stroke. Data were collected using a Personal Information Form and the Early Symptom Measurement of Post-Stroke Depression-Short Form (ESMPSD-SF). Expert opinion was obtained to assess content validity, and the Content Validity Index (CVI) was calculated. Construct validity was evaluated using the Kaiser-Meyer-Olkin (KMO) test, Bartlett's test, and Confirmatory Factor Analysis (CFA). Reliability was assessed using Cronbach's alpha, item-total correlations, and the test-retest method, which was performed with 30 participants after a 15-day interval. Content validity was high (CVI = 0.99). The KMO value (0.848) and Bartlett's test (χ2 = 439.024; p < 0.001) confirmed suitability for factor analysis. CFA indicated good model fit (RMSEA = 0.028, CFI = 0.99, TLI = 0.99). The overall Cronbach's alpha coefficient was 0.845, indicating good internal consistency. Test-retest reliability was excellent (ICC = 0.993). The Turkish version of the ESMPSD-SF, consisting of four subscales and 12 items, was found to be a valid and reliable measurement tool for Turkish culture.

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Expanding the landscape of covalent drug discovery: irreversible targeting of non-cysteine residues.

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Covalent inhibitors have re-emerged as a powerful class of therapeutics due to their prolonged target engagement, ability to decouple pharmacokinetic availability from pharmacodynamic outcome, potential for high selectivity and ability to modulate traditionally 'undruggable' targets. Historically, cysteine residues have dominated covalent drug discovery owing to their unique nucleophilicity and relative scarcity in the proteome. However, the desire to broaden the chemical scope of covalent therapeutics has driven a surge of interest in irreversibly targeting other amino acid residues, such as lysine, serine, tyrosine, threonine and histidine. This review explores the outstanding questions and challenges in developing covalent inhibitors beyond cysteine, highlighting current warhead chemistries, strategies for achieving selectivity, proteomic mapping advances, assessment of the intrinsic reactivity of the electrophiles targeting non-cysteine residues and opportunities for expanding the druggable proteome. We also discuss future directions and the pharmacological implications of non-cysteine covalent modifications in therapeutic contexts.

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