北京若生智能科技有限公司
Drug Database
RE

recombinant human interferon alfa-2a

✓ Approved

BioGeneric Pharma · IFNAR2 · 重组蛋白

什么是 recombinant human interferon alfa-2a？

recombinant human interferon alfa-2a 是一种重组蛋白，由BioGeneric Pharma研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

公司BioGeneric Pharma
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, BioGeneric Pharma

作用机制

分子靶点

recombinant human 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

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

治疗领域疾病/病症分期
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Neoplasm malignant✓ Approved

相关研究文献

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
阅读全文 →
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
阅读全文 →
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
阅读全文 →
PubMedCells2026-10-26

Immune Evasion Strategies of Human Poxviruses: A Roadmap for Engineering Low-Immunogenic CAR-Based and iPSC-Derived Cell Products.

Antonov Daniil O DO, Loguinova Marina Yu MY, Fan Hui H, Sazonova Elena V EV et al.

Allogeneic chimeric antigen receptor (CAR)-based cell products and induced pluripotent stem cell (iPSC)-derived regenerative grafts increasingly use multilayer immune engineering. Current strategies are strongest against direct human leukocyte antigen (HLA)-dependent recognition but incompletely address natural killer (NK)-cell counter-pressure, priming by recipient antigen-presenting cells, humoral and complement-mediated injury, inflammatory remodeling, blood- and tissue-interface damage, and terminal cell killing. Poxvirus research has characterized diverse immunomodulatory mechanisms relevant to these barriers. We review poxviral control of interferon signaling, antigen processing and presentation, T-cell activation, NK-cell surveillance, cytokine and chemokine networks, complement, inflammatory signaling, and regulated cell death, integrating viral mechanisms with human perturbation, cell-engineering, and transplantation evidence. A qualitative Tier 1-3 framework distinguishes mechanisms close to current cell-therapy practice from those requiring greater product-specific validation or control. The resulting design rules favor graded antigen-presentation control with paired NK validation, local or transient inflammatory buffering, interface-restricted complement protection, and survival enhancement only when independent eliminability is preserved. Selected poxviral proteins can act autonomously outside productive infection, but direct viral-protein expression remains a selective rather than default option. We propose a conditional defense-in-depth framework in which modules are added only when a residual barrier is demonstrated in the final therapeutic product.

PMID 42929874
阅读全文 →
PubMedGels (Basel, Switzerland)2026-10-26

From Biomarker to Trigger: Biological Calibration of Stimuli-Responsive Gels Toward Precision Periodontal Therapy.

Martinović Lovre L, Šantić Roko R, Kuliš Ena E, Martinović Dinko D et al.

Endogenous stimuli-responsive gels are designed to alter drug release or matrix behavior in periodontal sites, but their responsiveness is often demonstrated under conditions that may not represent the biological compartment encountered after placement. This comprehensive review examined whether proposed periodontal triggers have been biologically calibrated. Targeted searches of PubMed/MEDLINE, publisher websites, and backward and forward citations identified human studies measuring periodontal pH, proteases, redox conditions, oxygen tension, microbial metabolites, and glucose, together with gel studies using the same cues. Human pH measurements ranged from mildly acidic to alkaline and did not support a universal activation window. Protease-responsive systems had the strongest mechanistic rationale, although recombinant-enzyme testing was not equivalent to native-fluid cleavage. Hydrogen peroxide-responsive gels were generally evaluated under challenge conditions above the limited direct gingival crevicular fluid evidence and without physiological antioxidant buffering. Oxygen-generating systems did not directly sense local oxygen tension. Some glucose challenges overlapped reported human GCF measurements, but calibration to defined periodontal sites and treatment conditions remained unverified. Across trigger classes, preclinical efficacy seldom isolated responsiveness from payload and carrier effects. Future studies should use compartment- and treatment-matched measurements, realistic input-output testing under flow and buffering, patient-derived fluids, and controls that isolate cue-dependent material behavior.

PMID 42929931
阅读全文 →
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
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多recombinant human interferon alfa-2a