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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

PubMedProtein & cell2026-07-27

CRISPR screening identifies GNPTAB as a noncanonical STING activator driving cellular senescence.

Yin Jian J, Gao Yizhou Y, Jing Yaobin Y, Jiang Xiaoyu X et al.

Cellular senescence is accompanied by profound lysosomal alterations, yet whether lysosome-associated factors actively drive aging remains unclear. Through a focused CRISPR/Cas9 screen in human mesenchymal progenitor cells (hMPCs), we identified N-acetylglucosamine-1-phosphotransferase subunits alpha and beta (GNPTAB), an enzyme responsible for lysosomal hydrolase targeting, as a potent regulator of cellular senescence. Genetic ablation of GNPTAB attenuated senescence, whereas its overexpression accelerated senescence. This pro-senescent function occurred independently of GNPTAB's canonical enzymatic role. Instead, GNPTAB binds to the innate immune adaptor stimulator of interferon genes (STING) via a specific interface (E1119), leading to activation of STING and its downstream TANK-binding kinase 1 (TBK1), as well as pro-inflammatory gene expression. A STING-binding-deficient GNPTAB mutant (E1119A) preserved canonical lysosomal functions but failed to induce senescence, while STING depletion abolished GNPTAB-driven senescence. Together, these findings uncover a new signaling pathway wherein GNPTAB engages STING to facilitate its activation, nominating this interface as a potential target for mitigating age-related cellular dysfunction.

PMID 42505080
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PubMedVaccines2026-07-27

Safety and Immunogenicity of the BNT162b2 COVID-19 Vaccine in Immunocompromised Participants 2 Years and Older: Results of an Open-Label Phase 2b Study.

Waghmare Alpana A, Dadhe Rucha R, Kobbe Robin R, Danziger-Isakov Lara L et al.

Background: The BNT162b2 vaccine is safe and effective for COVID-19 prevention. BNT162b2 safety and immunogenicity have been evaluated in immunocompromised individuals in real-world observational studies, particularly in pediatric populations, but not in clinical trials. Methods: This phase 2b single-arm trial descriptively evaluated a Dose 3 (age-appropriate) BNT162b2 primary series with a Dose 4 in immunocompromised individuals 2-<5, 5-<12, 12-<18, and ≥18 years of age without a previous clinical or microbiological COVID-19 diagnosis. Primary objectives were to describe immune responses, reactogenicity, and adverse events following vaccination. Results: Out of 124 participants enrolled, 119 received Dose 3 and 90 received Dose 4. Among participants without evidence of past SARS-CoV-2 infection, neutralizing geometric mean titers (GMTs) and geometric mean fold rises (GMFRs) against the SARS-CoV-2 ancestral strain ranged from 344.6 to 1584.4 and 7.9 to 36.4 at 1 month after Dose 3 and from 1474.0 to 4157.9 and 31.0 to 95.6 at 1 month after Dose 4, respectively, across age groups. Among participants with or without evidence of past infection, GMTs and GMFRs ranged from 787.1 to 2940.6 and 9.6 to 54.3 at 1 month after Dose 3 and from 1031.3 to 13,457.1 and 9.1 to 220.0 at 1 month after Dose 4. Percentages of participants with or without evidence of past SARS-CoV-2 infection achieving seroresponse ranged from 50.0 to 92.9% at 1 month after Dose 3, and from 75.0 to 100% and 33.3 to 100.0% at 1 and 6 months after Dose 4 across age groups, respectively. No new safety signals were identified. Conclusions: BNT162b2 was immunogenic, increasing GMTs in immunocompromised individuals ≥2 years old, particularly after Doses 3 and 4. GMT increases were generally similar across age groups and disease subsets. Three or four BNT162b2 doses had a favorable risk-benefit profile in this population.

PMID 42506639
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-07-27

Synthetic Toll-Like Receptors for Control of Innate Immunity With Far-Red Light.

Leopold Anna V AV, Verkhusha Vladislav V VV

Toll-like receptors (TLRs) are single-pass transmembrane proteins that initiate innate immune responses through recognition of pathogen-associated molecular patterns, including lipopolysaccharide, flagellin, and microbial nucleic acids. In mammals, TLRs are expressed in both immune and non-immune cells, where they activate cytokine expression through the myeloid differentiation primary response 88 (MyD88) signaling pathway and subsequently engage the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) or interferon regulatory factor 3 / interferon regulatory factor 7 (IRF3/IRF7) pathways. To enable optical control of TLR function, the extracellular domains of several homodimeric TLRs, including TLR3, TLR4, and TLR5, are replaced with the photosensory core module of the bacterial phytochrome DrBphP. The resulting chimeric receptors activate the NF-κB and IRF3/IRF7 pathways in mammalian cells in a far-red-light-dependent manner. The MyD88 pathway is further reprogrammed to induce caspase activation instead of cytokine production, thereby creating a synthetic system that links TLR stimulation to caspase signaling. This strategy establishes a versatile optogenetic platform for far-red-light control of innate immune and cell death pathways.

PMID 42504985
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PubMedACS nano2026-07-27

Personalized Autologous Vaccines Activate Stimulator of Interferon Gene and Suppress Dendritic Cell Programmed Death Ligand 1 to Potentiate Antitumor Immunity.

Yang Zhijuan Z, Han Huize H, Zhao Zhihao Z, Ding Lingwen L et al.

Cancer vaccines have underperformed clinically, largely because antigen-specific CTL priming and expansion are constrained by insufficient costimulatory activation and increased DC-mediated coinhibition. Here, we present a personalized cancer vaccine platform, STAR, which engineers stimulator of interferon gene (STING)-activating autologous tumor-derived microvesicles (TMVs) to concurrently amplify costimulatory signaling and relieve DC coinhibition during antigen cross-presentation. TMVs provide broad tumor antigen cargo and intrinsic STING activity; loading manganese phosphate nanoparticles (MnPs) potentiates cGAS-STING signaling, drives DC maturation, and enhances antigen cross-presentation. Importantly, concurrent delivery of PD-L1-targeting siRNA (siPD-L1) effectively inhibits DC-associated PD-L1, freeing CD80 to engage CD28 and limiting PD-1/PD-L1 signaling and thereby significantly enhancing antigen-specific CD8+ T cells. In mouse models, STAR vaccination elicited durable prophylactic immunity and achieved substantial therapeutic efficacy against melanoma and colorectal tumors without additional immunotherapies. Notably, patient-specific STAR vaccines derived from surgically resected tumors effectively prevented postoperative recurrence and metastasis in aggressive melanoma and triple-negative breast cancer models, thereby highlighting their translational potential. Overall, the STAR vaccine platform offers a versatile and clinically applicable approach to enhancing personalized cancer immunotherapy across diverse cancer types.

PMID 42503762
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PubMedJournal of enzyme inhibition and medicinal chemistry2026-07-27

Virtual screening and experimental validation of a METTL3-targeting peptide with in vitro antiproliferative activity against non-small cell lung cancer cells.

Dai Ying Y, Wu Hanying H, Shen Yahui Y, Yang Fan F et al.

The METTL3-METTL14 protein-protein interaction (PPI) plays an important role in tumour progression, and disruption of this interaction has been explored as a potential strategy. In this study, four peptides were identified from a peptide database through virtual screening and molecular docking. Among them, peptide-1 showed the lowest Kd value among the tested peptides in MST analysis (Kd = 0.76 ± 0.02 μM). Binding mode analysis, molecular dynamics simulations, and MM/PBSA calculations suggested that peptide-1 might form a binding-related conformation with METTL3 under the simulated conditions. In lung cancer cells, peptide-1 showed growth-inhibitory activity, whereas weaker effects were observed in BEAS-2B cells. Peptide-1 also reduced the METTL3-METTL14-associated NanoBRET signal, decreased cellular m6A levels and JUNB mRNA expression, and its antiproliferative effect was attenuated by METTL3 knockdown. These findings suggest that peptide-1 may represent a METTL3-targeting peptide candidate for further evaluation.

PMID 42506933
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PubMedJournal of clinical microbiology2026-07-27

A comparative performance evaluation of the VIDAS cytomegalovirus (CMV) interferon-gamma release assay (IGRA) and T-SPOT CMV for measuring CMV-specific T-cell responses in allogeneic hematopoietic stem cell transplant recipients receiving letermovir prophylaxis.

Solano de la Asunción Carlos C, Colomer Ester E, Vázquez Lourdes L, Cadenas Irene García IG et al.

Assessment of cytomegalovirus (CMV) cell-mediated immunity (CMV-CMI) using standardized, commercially available interferon-gamma release assays (IGRAs) may improve the clinical management of CMV infection in allogeneic hematopoietic stem cell transplant recipients (allo-HCT). Studies comparing the performance of CMV IGRA assays have been conducted in this setting, revealing frequent discrepancies between assays. Here, we compared the performance of a newly released VIDAS CMV IGRA (bioMérieux) and the T-SPOT. CMV (Oxford Immunotec) was evaluated in a cohort of 85 allo-HCT recipients who received letermovir prophylaxis. A total of 107 whole blood samples were collected at either day +100 (n = 53) or day +180 (n = 54) after allo-HCT and analyzed in parallel. A moderate qualitative agreement between assays was observed (Cohen's kappa coefficient, 0.47; 95% CI, 0.30-0.63). Discrepant results were obtained in 29 specimens, most of which were collected at day +100. A moderate correlation (rho, 0.54; P < 0.001) was observed between T-SPOT pp65-SPC and IFN-γ levels measured by the VIDAS CMV assay, whereas the correlation was weaker for T-SPOT IE-1 SPC and VIDAS IFN-γ levels (rho, 0.32; P < 0.001). The previously described booster effect of CMV DNAemia on the magnitude of CMV-CMI was captured by the VIDAS CMV assay. Neither the qualitative nor the quantitative results obtained with either IGRA predicted protection from CMV DNAemia following LMV discontinuation. While our data support the validity of the VIDAS CMV assay for the assessment of CMV-CMI in allo-HCT, they reinforce the idea that results from commercially available IGRA assays are not interchangeable, particularly in allo-HCT recipients with impaired CMV-CMI reconstitution. This is the first study comparing a new interferon-gamma release assay (IGRA), the VIDAS cytomegalovirus (CMV), performed on whole blood and based on an enzyme-linked immunofluorescent assay detection technique, with a commercially available ELISpot assay (T-SPOT CMV) for measuring CMV-specific T-cell responses (CMV-CMI). Our cohort included allogeneic hematopoietic stem cell transplant recipients who underwent letermovir prophylaxis. In this clinical setting, tailoring the duration of LMV prophylaxis based on CMV-CMI at the time of drug discontinuation has emerged as a promising application of these assays. Our data revealed substantial qualitative and quantitative differences between the assays, which should be taken into consideration in future observational studies or clinical trials assessing the utility of IGRAs for individualizing LMV prophylaxis duration.

PMID 42506914
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