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interferon alpha 2b

✓ Approved

Helvetic Biopharma · IFNAR2 · 重组蛋白

什么是 interferon alpha 2b？

interferon alpha 2b 是一种重组蛋白，由Helvetic Biopharma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Helvetic Biopharma
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, Helvetic Biopharma

作用机制

分子靶点

interferon alpha 2b 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 alpha 2b 针对 10 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Basal cell carcinoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Bladder cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved

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相关研究文献

PubMedJournal of neurointerventional surgery2026-08-07

Thunderbolt System for acute ischemic stroke secondary to large vessel occlusion: primary results of the THUNDER study.

Fiorella David D, Woodward Keith K, Matouk Charles C, Levy Elad I EI et al.

THUNDER (Acute Ischemic Stroke Study With the Penumbra System Including Thunderbolt Aspiration Tubing) was the first study to evaluate the safety and effectiveness of a proprietary computer assisted vacuum thrombectomy (CAVT) system including modulated aspiration (Penumbra System with Thunderbolt; Penumbra, California, USA) in patients with emergent large vessel occlusion (ELVO). THUNDER was a single arm, prospective, multicenter study with core laboratory adjudication and oversight by a Clinical Events Committee and Data Safety Monitoring Board. The primary endpoint was post-Thunderbolt successful revascularization (modified Treatment in Cerebral Infarction (mTICI) 2b-3). Secondary endpoints included first pass mTICI 2b-3, post-Thunderbolt mTICI 2c-3, time to revascularization, symptomatic intracranial hemorrhages (sICH), device/procedure related serious adverse events (SAEs) within 24 hours, 90- day modified Rankin Score (mRS) 0-2, and all cause mortality. 216 patients were enrolled across 29 US centers (mean age 64.8 years, 45.4% women, median National Institutes of Health Stroke Scale score 15.0). The predefined performance goal was met, with post-Thunderbolt mTICI 2b-3 revascularization achieved in 87.5% (95% CI 82.3% to 91.6%; P<0.001). First pass mTICI 2b-3 was 64.8%. Post-Thunderbolt mTICI 2c-3 was 70.4%. Median time to revascularization was 20 min. Post-procedure, 83.0% of visualized clots were characterized as ingested. At 90 days, mRS 0-2 was 55.4%. Device/procedure related SAEs occurred in 2.8%, sICH in 0.9%, and the rate of all cause mortality at 90 days was 11.7%. The Thunderbolt system was safe and effective for the treatment of ELVO, achieving high revascularization and clot ingestion rates, short procedure times, and low complication rates. The first pass effect rate was numerically higher than those previously reported for large bore catheters and approximated those of ultra bore/super large bore devices. ClinicalTrials.gov NCT05437055.

PMID 42562636
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PubMedFrontiers in immunology2026-08-07

Human interferon-ω: an underappreciated type I interferon.

Chen Ruyue R

Interferon-ω (IFN-ω) is a member of the human type I interferon family that has historically been overshadowed by IFN-α and IFN-β. Recent human "natural perturbations", most notably selective neutralization of IFN-ω by autoantibodies in life-threatening viral infections, have renewed interest in this comparatively understudied cytokine and indicate that its antiviral activity may not always be fully compensated in defined clinical settings. This renewed focus has prompted reassessment of its single-gene organization, distinct antigenicity, intermediate receptor-binding kinetics, cellular sources, and regulatory mechanisms. In parallel, thymus-centered tolerance disorders, including autoimmune regulator (AIRE) deficiency, additional inborn errors of immune tolerance, and acquired "sick thymus" states, establish anti-IFN-ω autoantibodies as a stable, high-penetrance immunophenotype linking tolerance failure to durable cytokine-directed autoimmunity. Beyond antiviral defense, multi-omic studies in lupus-spectrum disease suggest tissue- and compartment-specific IFN-ω signals within broader type I interferon programs, yet endogenous IFN-ω remains rarely quantified with ligand-level resolution. This Review integrates current knowledge of IFN-ω from molecular regulation to human disease. Further progress will require subtype-resolved measurement, direct comparison with other type I interferons under matched conditions, and human genetic studies testing whether rare IFNW1 variants contribute to severe viral disease.

PMID 42563962
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PubMedCell insight2026-08-07

Febrile-range temperature selectively limits sustained pDC-Derived IFN-α via attenuation of STAT1-Dependent feedback signaling.

Xu Yangyang Y, Yang Hao H, Yang Lin L, Zhang Qing Q et al.

Plasmacytoid dendritic cells (pDCs) are specialized sentinels of antiviral immunity and the dominant early source of interferon-α (IFN-α) during viral infection. While pDC-derived IFN-α restricts viral replication and provides a critical third signal for T cell activation, sustained type I interferon (IFN-I) signaling can drive immunopathology, and the physiological mechanisms that constrain this response remain incompletely understood. Here, we identify fever as a conserved host factor that selectively limits IFN-α production by pDCs. We show that febrile-range temperature does not impair early IFN-α induction but instead suppresses sustained IFN-α output in human and mouse pDCs. Mechanistically, elevated temperature attenuates signal transducer and activator of transcription 1 (STAT1) phosphorylation, thereby disrupting the IFN-I-dependent positive feedback loop required for IFN-I amplification following CpG-A stimulation. Pharmacological inhibition of protein phosphatase activity with okadaic acid (OA) restores STAT1 phosphorylation and rescues IFN-α production under febrile conditions. Together, these findings establish fever as a physiological regulator of pDC-derived IFN-I responses and reveal a temperature-dependent mechanism that constrains prolonged IFN-I production to prevent excessive immune activation.

PMID 42564948
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PubMedJournal of hazardous materials2026-08-07

Mechanistic insights into TNF-α and EGF-mediated vascular endothelial activation following PM2.5-induced alveolar injury.

Wu Tingting T, Li Zhigang Z, Yang Xinping X, Xu Rongrong R et al.

Fine particulate matter (PM2.5), a prevalent air pollutant, reaches pulmonary alveoli and triggers lung inflammation and systemic vascular dysfunction. The alveolar-vascular barrier enables local lung damage to spread to endothelium through soluble factors, making this model fit to analyze lung-systemic interactions. TNF-α and EGF separately dominate inflammatory cascades and endothelial regulation, yet their combined effects during PM2.5 toxicity are unclear. This research constructed a 3D alveolar-vascular barrier model with BEAS-2B, THP-1, and EA. hy926 cells were treated with 0 or 100 μg/mL SRM2786 PM2.5 for 24 h. PM2.5 enters alveolar epithelial cells via endocytosis, causing mitochondrial damage, cell apoptosis, and upregulated TNF-α, EGF, IL-8, TGF-α, and IL-1β. Extracellular TNF-α and EGF cross the barrier and activate the endothelial PI3K-Akt pathway. Increased Nrf2 and CYP1A1 verify progressive oxidative stress. This study illustrates inflammation- and oxidation-dependent crosstalk between alveolar injury and endothelial impairment, clarifying PM2.5 toxic mechanisms and aiding environmental toxicology studies and drug screening.

PMID 42561693
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PubMedFish & shellfish immunology2026-08-07

The fermentative product from Bacillus siamensis HU603 (6'-phospho macrolactin B) inhibits Micropterus salmoides rhabdovirus infection in vitro and in vivo.

Tong Xinhui X, Zhou Yan Y, Shao Qianhao Q, Qi Huan H et al.

Micropterus salmoides rhabdovirus (MSRV) poses a substantial challenge to the health and sustainability of largemouth bass aquaculture. It causes huge economic losses, particularly in juvenile fish. However, there are still no effective therapeutic strategies. Here, we evaluated the anti-MSRV activity of 6'-phospho macrolactin B (23 TH), a phosphorylated metabolite from Bacillus siamensis HU603 fermentation. In Epithelioma papulosum cyprini (EPC) cells, 23 TH exhibited low cytotoxicity and, at 40 mg/L, engendered a remarkable 98.11% inhibition of the MSRV nucleoprotein (N) expression. Further studies showed that 23 TH effectively suppressed virus-induced cytopathic effects and attenuated virus-induced apoptosis by preserving nuclear integrity and mitochondrial membrane potential. Mechanistically, 23 TH directly reduced viral infectivity following pre-incubation with MSRV, significantly inhibiting viral binding and internalization. Time-of-addition and removal assays showed that 23 TH acts mainly during the early stage of viral replication. In vivo, 23 TH treatment significantly improved survival rates of MSRV-infected fish (up to 76%), reduced viral load, and alleviated histopathological damage. Additionally, 23 TH markedly up-regulated antiviral-related genes level, including interferon-γ (IFN-γ), interferon regulatory factor 3 (IRF3), and IRF7, by 5.38-, 7.37-, and 6.05-fold, respectively. In summary, these findings confirm the antiviral potential of 23 TH and highlight its application as a promising therapeutic agent for controlling MSRV infection in aquaculture.

PMID 42551812
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PubMedJAMA2026-08-07

How Common Is Alpha-Gal Syndrome?

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