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interferon alfa-2a (Proquiferon)

✓ Approved

Probiomed · IFNAR2 · 重组蛋白

什么是 interferon alfa-2a?

interferon alfa-2a 是一种重组蛋白,由Probiomed研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Intramuscular (IM) Injection、Subcutaneous Injection。

药物档案

商品名Proquiferon
公司Probiomed
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
状态Approved

作用机制

分子靶点

interferon alfa-2a 作用于 1 个分子靶点:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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

interferon alfa-2a 针对 8 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsAcquired immunodeficiency syndrome✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved

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相关研究文献

PubMedInorganic chemistry2026-10-26

Solution and Mechanochemical Reactions of a Diphosphene with Elemental Sulfur.

Kawase Yuria Y, Ito Kanta K, Omi Cocoro C, Ota Kei K et al.

The bulky Eind-substituted diphosphene, (Eind)P═P(Eind) (1a), reacted with an excess of elemental sulfur (S8) in solution at elevated temperatures to produce an isolable monomeric P(V) species, dithioxophosphorane, (Eind)P(═S)2 (4a), along with cleavage of the P═P double bond (Eind = 1,1,3,3,5,5,7,7-octaethyl-s-hydrindacen-4-yl). A three-membered P2S ring compound with formally P(II) centers, thiadiphosphirane, (Eind)P(S)P(Eind) (2a), was isolated as an intermediate in this solution-phase reaction. In contrast, mechanochemical treatment of 1a with S8 by ball milling under solid-state conditions afforded a P(I)/P(III) mixed-valent diphosphorus species, diphosphene sulfide, (Eind)(S═)P═P(Eind) (3a), which gradually isomerized to 2a at room temperature. The sulfurized products 2a, 3a, and 4a were characterized by 31P NMR spectroscopy, and the molecular structures of 2a and 4a were confirmed by single-crystal X-ray diffraction (SC-XRD) analysis. The structural and electronic properties of these sulfurized products were further investigated using density functional theory (DFT) calculations.

PMID 42929623
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PubMedClinics and practice2026-10-26

The Relationship Between Interferon Status and HPV Infection in Patients with Oral Epithelial Dysplasia: An Observational Study.

Khisamieva Guzel G, Sologova Diana D, Svitich Oxana O, Diachkova Ekaterina E et al.

Background/Objectives: Oral potentially malignant diseases (OPMDs) with signs of epithelial dysplasia are characterized by a high risk of malignancy. However, there are still no algorithms for their early diagnosis and prediction, due to the many possible predisposing factors, including human papillomavirus (HPV) infection and decreased immunity. There is a need to assess the relationship between the manifestations of oral epithelial dysplasia (OED), HPV invasion in the oral cavity, and interferon status to improve the identification and characterization of patients with different degrees of dysplasia. Methods: This study was designed and reported with reference to the STROBE checklist. The study aimed to assess the association between interferon status and HPV invasion in patients with OED. As per the inclusion and exclusion criteria, this observational study included 180 patients with histologically confirmed oral epithelial dysplasia associated with leukoplakia or oral lichen planus. Interferon (IFN) status was assessed by measuring serum interferon activity, spontaneous interferon production, IFN-α/β, and IFN-γ activity in peripheral blood. HPV DNA was detected and genotyped in biopsy specimens using polymerase chain reaction. Results: HPV-positive patients demonstrated significantly lower IFN-α/β and IFN-γ activity compared with HPV-negative patients (p < 0.001). Severe OED was more frequently observed in HPV-positive individuals, whereas mild dysplasia predominated among HPV-negative patients (p < 0.05). Interferon activity progressively decreased with increasing dysplasia severity, with the lowest IFN-α/β and IFN-γ activity detected in patients with severe dysplasia (p < 0.001 and p < 0.05, respectively). A significant positive correlation between IFN-α/β and IFN-γ activity was identified in patients with moderate dysplasia (p = 0.003). Multivariate binary logistic regression analysis demonstrated that HPV positivity (adjusted OR = 4.62, 95% CI: 2.18-9.79; p < 0.001) and reduced IFN-α/β activity (adjusted OR = 1.34 per 10-unit decrease, 95% CI: 1.14-1.58; p < 0.001) were independently associated with severe dysplasia. The multivariable model demonstrated acceptable discriminatory ability for identifying patients with severe dysplasia (AUC = 0.736), with a sensitivity of 89.4% and a specificity of 56.1%. Conclusions: The findings suggest that HPV-associated OED is linked to reduced interferon status, particularly lower IFN-α/β and IFN-γ activity in more severe dysplastic lesions. Combined assessment of interferon status and HPV detection may help identify patients at higher risk of severe OED.

PMID 42930365
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PubMedCells2026-10-26

Association of Cbl-Interacting Protein CIN85 with Protein Phosphatase 2A (PP2A) Partly Confer Neoplastic Properties to Human Leukemia Cell Lines.

Aldahami Malak Abdullah MA, Alfrayh Rawan Abdulrahman RA, Basmaeil Yasser Y, Bin Kulayb Haya Nasser HN et al.

Protein phosphatase 2A (PP2A) is a critical tumor suppressor frequently inactivated in hematological malignancies, yet the mechanisms underlying this dysregulation remain poorly defined. Here, we investigated a novel interaction between the PP2A catalytic subunit (PP2Ac) and the adaptor protein CIN85. Analyzing transcriptomic datasets from AML, CML, CLL, and ALL patients, alongside functional validation in K562 and THP1 leukemia cell lines via RT-qPCR, immunoblotting, phosphatase activity assays, pharmacological modulation (FTY720 and Okadaic acid), siRNA-mediated knockdown, and proliferation assays, we found that CML and CLL exhibit reduced PP2A and elevated CIN85, with activated AKT, SRC, and GSK-3β levels. Pharmacological activation of PP2A reduced AKT and GSK-3β phosphorylation, while inhibition had opposing effects, confirming PP2A's regulatory role. Crucially, CIN85 silencing markedly enhanced PP2A phosphatase activity without changing PP2Ac protein levels, leading to robust dephosphorylation of AKT, SRC, and GSK-3β and significantly suppressing leukemic cell proliferation. Collectively, these results identify CIN85 as a previously unrecognized endogenous negative regulator that directly suppresses PP2A function in leukemia. Importantly, disrupting the PP2Ac-CIN85 complex effectively restores PP2A tumor-suppressive activity, dampens oncogenic signaling, and inhibits growth, providing mechanistic clarity and positioning this protein-protein interface as one of the possible therapeutic targets for treating hematological cancers.

PMID 42929869
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PubMedCells2026-10-26

Antagonistic TGR5 and FXR Signaling Shapes STAT1-Dependent Interferon Responses in Intestinal Epithelial Cells.

Jia Huilin H, Wu Nannan N, Yan Yufeng Y, Kong Fanzhi F

Bile acids function not only as digestive metabolites but also as signaling molecules that influence mucosal immunity. However, how the bile acid receptors Takeda G-protein-coupled receptor 5 (TGR5; also known as GPBAR1) and farnesoid X receptor (FXR) coordinate intestinal epithelial interferon (IFN) responses remains incompletely understood. Here, we investigated the impact of TGR5 and FXR on IFN signaling in porcine IPEC-J2 and murine MODE-K intestinal epithelial cells. Pharmacological activation of TGR5 with INT-777 induced type I and type III IFNs together with multiple interferon-stimulated genes (ISGs), among which IFNλ3 and ISG15 showed the most prominent responses. Mechanistically, TGR5 enhanced STAT1 phosphorylation and nuclear accumulation, and both STAT1 silencing and pharmacological blockade of STAT1 phosphorylation attenuated TGR5-driven IFNλ3 and ISG15 expression. Inhibition of adenylate cyclase or protein kinase A further placed a cAMP-PKA-STAT1 axis downstream of TGR5. By contrast, activation of FXR with GW4064 suppressed poly(I:C)-induced IFNλ3 and ISG15 transcription and antagonized TGR5-mediated STAT1 activation and downstream gene expression. Confocal imaging further suggested that FXR restrains STAT1 nuclear trafficking through cytoplasmic colocalization with STAT1. Collectively, our findings identify a bile acid receptor rheostat in which TGR5 amplifies, whereas FXR dampens, epithelial IFN signaling through STAT1. This work provides a mechanistic framework for understanding how bile acid sensing may tune antiviral readiness at the intestinal mucosa.

PMID 42929875
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-26

Large Oncosomes Induce Pro-Metastatic Stromal-Myeloid Reprogramming.

Silva Taylon Felipe TF, Concato-Lopes Virginia Marcia VM, Bedier Fatima F, Newman Lauren L et al.

Bone metastasis can be facilitated by systemic remodeling, yet the tumor-derived signals that influence the bone marrow microenvironment remain incompletely understood. Large oncosomes (LOs) are atypically large (> 1 µm), tumor-derived extracellular vesicles shed by amoeboid cancer cells. Here, we demonstrate that LOs function as systemic mediators of metastatic niche formation by activating innate immune sensing in bone marrow mesenchymal stem cells (BM-MSCs). Systemic administration of LOs to immunocompetent tumor-bearing mice did not affect primary tumor growth but increased metastatic burden. LOs induced a robust, dose-dependent interferon-driven inflammatory program, characterized by interferon-stimulated genes and neutrophil chemokines. Mechanistically, this response was driven by LO-associated nucleic acids activating convergent cytosolic DNA- and RNA-sensing pathways in recipient stromal cells. LO-conditioned BM-MSCs promoted the accumulation and polarization of neutrophils toward an immunosuppressive, polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC)-like phenotype. In vivo, genetic suppression of LO shedding in tumor cells reduced PMN-MDSC accumulation in the bone marrow, which was reversed by systemic LO administration. Together, these findings support a model in which LO-associated signals reprogram the bone marrow microenvironment to support metastatic colonization, identifying a previously unrecognized mechanism linking tumor vesiculation to immune remodeling at distant sites.

PMID 42928450
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PubMedInorganic chemistry2026-10-26

Polar Ruddlesden-Popper Rare-Earth Aluminum Oxynitrides with Partial Anion Order.

Oró-Solé Judith J, Guarín Jhonatan R JR, Fina Ignasi I, Frontera Carlos C et al.

Anion order in heteroanionic compounds may induce electrical dipoles and the formation of noncentrosymmetric polar structures. The majority of perovskite oxynitrides are centrosymmetric, but some of them show high dielectric permittivities and ferroelectric response resulting from local anion order. Here, we report a study of polar, partially anion-ordered Nd2AlO3N and Sm2AlO3N n = 1 Ruddlesden-Popper oxynitrides, prepared by solid-state reaction in flowing N2 at 1500 °C. They crystallize in the noncentrosymmetric I4mm space group with parameters a = 3.703314(3) and c = 12.545382(14) Å for Nd2AlO3N and a = 3.674477(5) and c = 12.40414(3) Å for Sm2AlO3N. Neutron powder diffraction data of Nd2AlO3N indicate that oxygen occupies the equatorial sites 4b of the AlO5N octahedra, whereas both anions occupy two crystallographically independent 2a axial X2 and X3 sites, with different O/N populations (68/32 for X2 and 32/68 for X3) and a larger bond distance to the Al atom for the oxygen rich site. Dielectric permittivities of 260 and 150 are measured for Nd2AlO3N and Sm2AlO3N, respectively, and second-harmonic generation spectroscopy and scanning transmission electron microscopy furnish complementary evidence of the polar nature of both compounds. These results represent the first experimental demonstration of acentric functionalities in a Ruddlesden-Popper oxynitride.

PMID 42929632
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