Drug Database
IN

interferon alpha 2b

✓ Approved

Helvetic Biopharma · IFNAR2 · Recombinant Proteins

What is interferon alpha 2b?

interferon alpha 2b is a recombinant proteins developed by Helvetic Biopharma. It is approved for therapeutic indications via injectable (others).

Drug Profile

CompanyHelvetic Biopharma
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, Helvetic Biopharma

Mechanism of Action

Molecular Targets

interferon alpha 2b acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

interferon alpha 2b is developed for 10 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
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

+5 more indications available with a free account

Sign up free to view all indications →

Related Research Articles

PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Experimental study on Qiangjing decoction modulating the expression of testis/epididymis-specific LncRNAs (Dmr/Mrhl/Tsx/HongrES2) and its regulatory mechanisms in oligoasthenospermic rats].

Bin Bin B, Lu Haiwang H, Wang Desheng D, Lin Siwei S et al.

Objective To investigate the therapeutic mechanism of Qiangjing decoction (QJD) in oligoasthenospermia model rats by regulating the expression of testis-specific long non-coding RNAs (LncRNAs) Dmr, Mrhl, Tsx, and epididymis-specific HongrES2. MethodsSixty sexually mature male Sprague-Dawley rats were randomly divided into the normal group, the model group, the Shengjing capsule group and the QJD group, with 15 rats in each group. Rat models of oligoasthenospermia were induced by intraperitoneal injection of cyclophosphamide (CTX). After successful modeling, the normal group received no intervention, the model group was given normal saline, and the QJD group and the Shengjing capsule group were administered the corresponding drugs for 38 consecutive days, sperm quality parameters were evaluated. Spermatogenic function was assessed by the method of testicular histomorphology. The mRNA expression levels of lncRNAs (Dmr, Mrhl, Tsx, HongrES2) and related genes (Sox8, Utf1, Wnt-2b, β-catenin, Gsk-3β, p68, Stra8) were detected by quantitative real-time PCR, while corresponding protein expression was analyzed by Western blot. Results In the normal group, the testicular tissue exhibited intact and regularly arranged seminiferous epithelium with active spermatogenesis. In the model group, the seminiferous epithelium showed partial detachment and disorganized arrangement, accompanied by a marked reduction in spermatozoa. In contrast, both the QJD group and the Shengjing capsule group displayed more layers of spermatogenic cells with relatively orderly arrangement, and abundant spermatozoa were observed. Sperm concentration and motility in the epididymis were markedly elevated following QJD treatment. Gene expression analysis revealed significant downregulation of Dmr, HongrES2, GSK-3β, and CES7 in the model group versus normal controls (P<0.05), while Tsx showed a non-significant decreasing trend. No significant differences were observed in Mrhl, Wnt-2b, β-catenin or Sox8 gene expression. QJD intervention significantly upregulated the expression of Dmr, HongrES2, GSK-3β, Tsx, CES7, and Wnt-2b. Protein expression of STRA8, SOX8, P68, UTF1, WNT-2b, β-CATENIN, GSK-3β and CES7 was significantly reduced in the model group but restored after QJD and Shengjing capsule treatment. Conclusion QJD may ameliorate oligoasthenospermia by upregulating testis-specific LncRNAs (Dmr, Mrhl, Tsx) and epididymis-specific HongrES2, thereby activating the Wnt-2b/β-catenin signaling pathway. This mechanism promotes spermatogonial proliferation and meiosis, while modulating key proteins (UTF1, CES7) crucial for spermatogenesis and maturation, ultimately improving sperm production and motility of rats with oligoasthenospermia.

PMID 43012205
Read full article →
PubMedScandinavian journal of immunology2026-11-11

Type I Interferonopathies in Inborn Errors of Immunity: Pathogenesis, Clinical phenotype, Diagnosis and Management.

Zeinali Fatemeh F, Rezaei Nima N, Yazdani Reza R

Type I interferonopathies represent a heterogeneous group of inborn errors of immunity (IEI), characterized by dysregulated and persistent activation of the Type I interferon pathway. These patients present a broad spectrum of clinical phenotypes involving the nervous system, skin, lungs, and haematopoietic system. Diagnosis is often challenging owing to overlap with other autoinflammatory and autoimmune conditions. In parallel with the expanding molecular spectrum of these disorders, their classification within IEI has continued to evolve. This review provides an updated synthesis of Type I interferonopathies in the context of the 2024 International Union of Immunological Societies (IUIS) classification, linking the underlying genetic defects and dysregulated interferon pathways to their characteristic and overlapping clinical phenotypes. Particular emphasis is placed on a practical diagnostic framework integrating clinical recognition, interferon-based biomarkers, and molecular testing, as well as on the transition from conventional immunomodulation toward pathway-directed therapies, including the growing clinical experience with Janus kinase inhibitors. This review integrates current knowledge on the pathogenesis, clinical features, diagnostic approaches, and treatment strategies in patients with Type I interferonopathies, providing an updated clinically oriented framework for their recognition, diagnosis, and management within the expanding spectrum of IEIs.

PMID 43009724
Read full article →
PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-11-11

Aryl Hydrocarbon Receptor Is Dispensable for the Early Transcriptional Response of Mouse Macrophages to Type I Interferon.

Tabtim-On Darawan D, Segura Elodie E

Type I interferon (IFN-I) signaling is essential in the homeostasis and activation of immune cells, and macrophages play a central role in the IFN-I system. Dysregulation leads to tissue damage and autoimmunity, and IFN-I signaling needs to be tightly fine-tuned. One reported mechanism involves interactions with the transcription factor aryl hydrocarbon receptor (AhR). However, it remains to be determined whether AhR is required for the early transcriptional response of macrophages to IFN-I. Here we used macrophages from genetically deficient mice to investigate the involvement of AhR in the induction of early IFN-I-driven responses. We show that constitutive AhR deficiency does not impair the canonical transcriptional response to IFN-I in bone marrow-derived macrophages nor the expression of IFN-stimulated molecules by peritoneal macrophages upon in vivo exposure. These findings contrast with observations made in other cell types, in particular astrocytes and lung cancer cells, and support the notion of a context-dependent crosstalk between AhR and IFN-I-dependent signaling.

PMID 43012672
Read full article →
PubMedBioscience reports2026-11-11

From genome guardian to immune modulator: the dual faces of DNA-PKcs.

Li Qiang Q, Zhan Pei-Wen PW, Hong Xian X, Qu Ying Y et al.

The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) has long been recognized as a genome guardian, serving as a master regulator of non-homologous end joining (NHEJ), safeguarding genomic integrity and enabling adaptive immunity through V(D)J recombination. Beyond this nuclear function, DNA-PKcs is now increasingly appreciated as a context-dependent immune modulator, acting at the interface between the DNA damage response and inflammatory signaling. This review synthesizes recent advances that redefine DNA-PKcs as a versatile "molecular integrator." We delineate its structural dynamics and multifaceted regulation, and dissect its dual function in the cytoplasm, where it can either potentiate or suppress the cyclic GMP-AMP synthase and stimulator of interferon genes (cGAS-STING) pathway and even initiate STING-independent interferon responses. We further explore how dysregulation of DNA-PKcs underpins a spectrum of pathologies, from immunodeficiency and autoimmunity to cancer and neurodegeneration. Finally, we discuss the translational promise of DNA-PKcs inhibitors, which not only act as classical chemo- and radio-sensitizers but also remodel the tumor microenvironment by activating antitumor immunity. Decoding the context-dependent logic behind these dual faces is therefore paramount for developing novel therapeutics that leverage DNA-PKcs across oncology, autoimmunity, and neurodegeneration.

PMID 43012527
Read full article →
PubMedAntimicrobial agents and chemotherapy2026-11-11

Rosmarinic acid exerts anti-CVB3 effects by inducing HO-1 via the SIRT1/AMPKα/Nrf2 pathway.

Huang Junbo J, Song Qing Q, Di Yanjun Y, Cheng Zhiyun Z et al.

Coxsackievirus B3 (CVB3) is the primary pathogen of viral myocarditis (VMC), and there is no specific therapy. Rosmarinic acid (RA) has anti-inflammatory and antioxidant properties, but its anti-CVB3 activity and mechanism remain unclear. This study examined the inhibitory effect of RA on CVB3 replication and VMC, and the underlying mechanism. In CVB3-infected HeLa cells and a mouse VMC model, RA blocked viral replication dose-dependently, with an EC50 of 26.49 μM and a selectivity index of 21.72, which was more effective than ribavirin. Time-of-addition experiments showed that RA interfered with the post-entry replication stage. Mechanistically, RA directly bound sirtuin 1 (SIRT1), with an affinity of -10.2 kcal/mol, increasing its conformational stability and inhibiting ubiquitin-proteasome degradation, thereby reversing CVB3-induced SIRT1 downregulation. Antiviral and anti-inflammatory effects of RA were abolished by SIRT1 knockdown. RA activated the AMPK/Nrf2/HO-1 cascade in a SIRT1-dependent manner. Notably, the HO-1 metabolite biliverdin (BV) stimulated STAT1/2 phosphorylation and interferon-stimulated gene expression. In vivo, RA effectively ameliorated CVB3-induced myocardial injury and restored SIRT1/AMPK/Nrf2/HO-1 expression. In conclusion, RA prevents CVB3 replication and VMC via direct binding and stabilization of SIRT1, activation of the SIRT1/AMPK/Nrf2/HO-1/BV signaling pathway, and stimulation of interferon response through STAT1/2.

PMID 43012511
Read full article →
PubMedAnalytical chemistry2026-11-11

Single-Cell ICP-MS Quantification of Intracellular Chromium and Cell-Surface TNFR2 for Assessing Cr(III/VI)-Induced Lung Epithelial Injury and COPD-Relevant Responses.

Lu Xinyi X, Chen Beibei B, He Man M, Hu Bin B

An integrated platform combining droplet microfluidics, lanthanide labeling, and inductively coupled plasma mass spectrometry (ICP-MS) was proposed to quantify intracellular heavy metal and cell-surface protein at single-cell resolution. The workflow performs parallel measurements on homologous single-cell subsets to establish statistical correlations between metal accumulation and functional protein responses. Using tumor necrosis factor receptor 2 (TNFR2) as a model protein, we investigated the effects of atmospheric particulate matter-associated heavy metals on human lung epithelial cells (BEAS-2B). Several heavy metals trigger TNFR2 upregulation, with Cr(VI) exerting the most pronounced effect. The Cr(VI)-induced increase in TNFR2 expression was associated with elevated TNF-α release, higher intracellular ROS, and reduced SOD activity but did not correlate directly with intracellular Cr accumulation, likely due to distinct cellular uptake mechanisms between Cr(III) and Cr(VI). High-concentration Cr(III) exposure, however, led to intracellular Cr enrichment and provoked inflammatory responses. Integration of differential gene expression, TNF-α release, and TNFR2 expression support TNFR2 as a potential indicator of metal-induced oxidative stress, epithelial injury, and COPD-relevant inflammatory responses. This single-cell dual-parameter approach provides a new strategy for linking metal uptake to functional protein responses in environmental toxicology.

PMID 43010549
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about interferon alpha 2b