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Factor IX (AlphaNine SD / AlphaNine)

✓ Approved

Mitsubishi Tanabe Pharma Corporation · F9 · 细胞治疗

什么是 Factor IX?

Factor IX 是一种细胞治疗,由Mitsubishi Tanabe Pharma Corporation研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Intravenous (IV)。

药物档案

商品名AlphaNine SD, AlphaNine
公司Mitsubishi Tanabe Pharma Corporation
药物类别细胞治疗
分子靶点F9
给药途径Injectable (Others), Intravenous (IV)
状态Approved

作用机制

分子靶点

Factor IX 作用于 1 个分子靶点:

F9coagulation factor IX (P19, F9 p22)
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

Factor IX 针对 3 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersExtravasation blood✓ Approved
Congenital, familial and genetic disordersFactor IX deficiency✓ Approved
Vascular disordersHaemorrhage✓ Approved

相关研究文献

PubMedJournal of biochemical and molecular toxicology2026-10-26

Theranekron Attenuates Inflammation, Oxidative Stress Index, and Apoptosis in Lipopolysaccharide-Induced Cardiovascular Toxicity: Association With Hypoxia-Inducible Factor-1 Alpha-Related Gene Expression.

Savran Mehtap M, Asci Halil H, Imeci Orhan O, Oguzlar Furkan Cagri FC et al.

This study aimed to evaluate the possible protective effects of Theranekron, an extract derived from Tarantula cubensis venom, on cardiovascular damage induced by lipopolysaccharide (LPS) in an experimental rat model. A total of 32 male Wistar Albino rats were randomly divided into 4 groups: Control, Lipopolysaccharide, Lipopolysaccharide plus Theranekron, and Theranekron alone. Lipopolysaccharide administration caused pronounced histopathological changes in the heart and aorta, including endothelial sloughing, hyperemia, hemorrhage, and infiltration of inflammatory cells. These pathological findings were accompanied by elevated oxidative stress markers, increased tumor necrosis factor-alpha and inducible nitric oxide synthase immunoreactivity, and increased caspase-3 immunoreactivity. Additionally, genes associated with the hypoxia-inducible factor-1 alpha (HIF-1α) pathway-such as interleukin 6, signal transducer and activator of transcription 3 (STAT3), and vascular endothelial growth factor-were significantly upregulated in the lipopolysaccharide group. Theranekron pretreatment was associated with partial attenuation of oxidative stress imbalance, of inflammatory and apoptotic immunoreactivity, and of the upregulation of HIF-1α-related transcripts. Overall, these findings suggest that Theranekron may offer partial protection against early LPS-induced cardiovascular injury.

PMID 42929009
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PubMedSignal transduction and targeted therapy2026-10-26

Encapsulated mitochondrial transplantation: Advancing organelle therapeutics.

Yang Hae-Jun HJ, Jeong Pil-Soo PS, Kim Sun-Uk SU

PMID 42928347
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PubMedAutophagy2026-10-26

AKT1-phosphorylated TERT assembles a FOXO3-MYC transcriptional complex that drives ERphagy and proteostasis in post-mitotic RPE.

Babu Vishnu Suresh VS, Ghosh Sayan S, Bammidi Sridhar S, Jiwon Ryu R et al.

The retinal pigment epithelium (RPE) sustains lifelong proteostasis under chronic stress, yet how post-mitotic cells activate macroautophagy/autophagy when canonical kinase pathways suppress it remains unresolved. Here we demonstrate that AKT1 (protein kinase B alpha), drives autophagy through a non-canonical transcriptional mechanism triggered by isoform imbalance. In RPE and age-related macular degeneration (AMD) models, AKT2 (protein kinase B beta) hyperactivation destabilizes MTORC2 (mechanistic target of rapamycin complex 2) and engages RPS6KB/S6K (ribosomal protein S6 kinase beta) -mediated IRS-1 (insulin Receptor Substrate 1) inhibition, creating a feedforward autophagic arrest. Compensatory AKT1 activation via MTORC2 phosphorylates TERT (telomerase reverse transcriptase) at serine 824, driving nuclear translocation that is independent of telomere maintenance. In the nucleus, TERT assembles with FOXO3 (forkhead Box O3) and MYC (MYC proto-oncogene, bHLH transcription factor) into a tripartite transcriptional complex that occupies the EIF2AK3/PERK promoter (eukaryotic translation initiation factor 2-alpha kinase 3/ protein kinase R-like endoplasmic reticulum kinase), enabling EIF2AK3 transcriptional activation. This activity converts the unfolded protein response from pro-apoptotic to cytoprotective: EIF2AK3-ATF4 (activating transcription factor 4) signaling promotes core autophagy machinery biogenesis and selective ERphagy through the receptors TEX264 (testis expressed 264) and CCPG1(cell cycle progression 1), which prevents pathological EIF2AK3 clustering and preserves tubular ER architecture in diseased RPE. Using C. elegans phosphorylation-deficient mutants, mouse models and AMD patient iPSC-RPE, we establish that AKT1-mediated TERT phosphorylation is an evolutionarily conserved prerequisite for FOXO/DAF-16 nuclear function and lysosomal homeostasis in post-mitotic cells, offering therapeutic potential through targeted pharmacologic inhibition of AKT2.Abbreviations: ACTB: actin, beta; AKT1: AKT serine/threonine kinase 1; AKT2: AKT serine/threonine kinase 2; ALP: autophagy-lysosomal pathway; AMD: age-related macular degeneration, ATF4: activating transcription factor 4; ATG3: autophagy related 3; ATG4B: autophagy related 4B cysteine peptidase; ATG7: autophagy related 7; CCPG1: cell cycle progression 1; CFH: complement factor H; C57BL/6J: C57 black 6J; DMSO: dimethyl sulfoxide; MYC: MYC proto-oncogene, bHLH transcription factor; EIF2A/eIF2α: eukaryotic translation initiation factor 2A; EIF2AK3/PERK: eukaryotic translation initiation factor 2 alpha kinase 3; ER: endoplasmic reticulum; ERN1/IRE-1α: endoplasmic reticulum to nucleus signaling 1; ERphagy: endoplasmic reticulum-selective autophagy; FOXO1: forkhead box O1; FOXO3: forkhead box O3; iPSC-RPE: induced pluripotent stem cell-derived retinal pigment epithelium; ITGB1/integrin β1: integrin subunit beta 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPKAP1/SIN1: MAPK associated protein 1; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; MTORC2: MTOR complex 2; PBS: phosphate-buffered saline; PI3K: phosphoinositide 3-kinase; RICTOR: RPTOR independent companion of MTOR complex 2; RPE: retinal pigment epithelium; RPTOR: regulatory associated protein of MTOR complex 1; SQSTM1/p62: sequestosome 1; TERT: telomerase reverse transcriptase; TEX264: testis expressed 264, ER-phagy receptor; UPR: unfolded protein response; VCL: vinculin; WT: wild type.

PMID 42929416
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PubMedThe British journal of dermatology2026-10-26

The Science of Skin Ageing Comes of Age: Molecular Insights, Precision Targets and Emerging Therapeutics.

McGrath John A JA

PMID 42929156
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PubMedBMC medical education2026-10-26

Psychometric evaluation of the Persian version of the school-to-work transition anxiety scale in senior nursing students.

Shahsavari Hooman H, Nadali Javad J, Ghasempour Saeed S, Mirhosseini Seyedmohammad S et al.

Senior nursing students frequently encounter transition anxiety during internships, a phenomenon that adversely affects their mental health, academic performance, and the quality of patient care. Although Iran has introduced internship programs to reduce transition shock, their effectiveness remains unclear due to the lack of a validated Persian assessment tool. This study sought to evaluate the validity and reliability of the Persian adaptation of the school-to-work transition anxiety scale in nursing students. This methodological research was carried out to examine the structural validity and internal reliability of the scale, utilizing data gathered from October 2024 to May 2025. A total population sampling approach was used. All eligible final-year nursing students were identified using the official enrollment list maintained by the faculty's education office and were invited to participate. A total of 342 students participated and were divided into two independent samples: 171 participants for exploratory factor analysis (EFA) and 171 participants for confirmatory factor analysis (CFA). EFA, using the maximum likelihood extraction method with Promax rotation, was conducted to identify the latent factor structure. Subsequently, CFA was performed on the second independent sample to verify the proposed model. Convergent validity was assessed following the Fornell and Larcker approach by calculating the average variance extracted (AVE) and composite reliability (CR), while discriminant validity was evaluated using the Heterotrait-Monotrait (HTMT) ratio. Internal consistency was examined using Cronbach's alpha and McDonald's omega coefficients, and stability was assessed using the intraclass correlation coefficient (ICC). The study included 342 nursing students (55.85% male, mean age 22.81 ± 2.16 years, grade point average 16.83 ± 1.31). Qualitative face validity confirmed all items as clear, relevant, and important. Content validity was confirmed, with minor revisions to three items and the removal of five items (CVR > 0.56). EFA extracted four factors (58.71% variance), with two items removed due to low factor loadings. CFA supported model fit (χ²/DF = 1.665, RMSEA = 0.063, CFI = 0.917). Convergent validity was confirmed for "Interpersonal Interactions" and "Fear of Being Infected" factors based on AVE and CR values. Discriminant validity was confirmed, as all HTMT coefficients were below the 0.85 threshold. Internal consistency of all factors was confirmed by Cronbach's alpha and McDonald's omega values greater than 0.7, and the stability of the scale was confirmed by evaluation of the ICC with 0.75 acceptable threshold. The final Persian version comprised 24 items across the same four-factor structure as the original 31-item scale. The school-to-work transition anxiety scale demonstrated strong reliability and validity, confirming its suitability as a self-report instrument for assessing transition-related anxiety among final-year nursing students in Iran.

PMID 42928185
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PubMedJournal of biological engineering2026-10-26

A stealth-body Fc engineering platform enables complete effector silencing in antibody and ADC therapeutics.

Kim Suyeon S, Jo Migyeong M, Kyung Munsu M, Ko Woo Hyung WH et al.

The development of next-generation antibody therapeutics requires Fc scaffolds that suppress unwanted effector functions while preserving core developability attributes. Existing effector-attenuated Fc backbones, however, retain residual interactions with Fcγ receptors (FcγRs) and C1q, highlighting a persistent design limitation in achieving complete effector silencing without compromising glycosylation, FcRn-mediated persistence, and manufacturability. This is particularly relevant for formats in which Fc effector function is undesirable, including immune-engaging antibodies, CD47 blockers, and antibody-drug conjugates (ADCs). Accordingly, a robust Fc engineering framework enabling complete and transferable effector silencing across antibody modalities is required. We developed Stealth-Body (SB) Fc variants, a fully effector-silenced Fc platform that abolishes Fc-mediated immune engagement while maintaining native-like glycosylation, pharmacokinetics, and manufacturability. Using a CHO cell display system with directed evolution guided by cross-species sequence features from goat IgG, we identified human glycosylated IgG1 variants (SB1, SB5, SB6) that abrogated binding to all human FcγRs and C1q, and to all murine and cynomolgus FcγRs. SB Fc retained pH-dependent FcRn binding, antigen recognition, thermostability, and expression, with in vivo persistence comparable to wild-type IgG1. Incorporation of SB Fc into trastuzumab, rituximab, and ADCs abolished ADCC, ADCP, and CDC, while integration into a CD47-targeting IgG-CD40L fusion protein mitigated hematologic toxicity without impairing immune activation. Collectively, SB Fc variants represent a generalizable, effector-null Fc scaffold that enables complete and transferable silencing of Fc-mediated immune functions while preserving key developability attributes. This platform expands the therapeutic window of antibody therapeutics through precise control of Fc activity across diverse modalities.

PMID 42928316
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