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IN

interferon (Alfaferone)

✓ Approved

Johnson & Johnson Services, Inc. · IFNAR2

What is interferon?

interferon is a therapeutic agent developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via others or injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesAlfaferone
CompanyJohnson & Johnson Services, Inc.
Molecular TargetIFNAR2
RouteOthers, Injectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Mechanism of Action

Molecular Targets

interferon acts on 1 molecular target:

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

interferon is developed for 9 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
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
Nervous system disordersMultiple sclerosis✓ Approved

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Related Research Articles

PubMedMaterials (Basel, Switzerland)2026-10-16

Preliminary Investigations into the Possibility of Using Hot Torsion Testing to Model Microstructural Evolution During Aluminum Extrusion.

Korczak Piotr P, Laber Konrad Błażej KB, Boczkal Sonia S, Leśniak Dariusz D et al.

This paper outlines preliminary findings from studies on the possibility of using hot torsion testing for the physical modeling of microstructural evolution during aluminum alloy extrusion processes. Accordingly, two plastic deformation processes were investigated: high-temperature torsion and extrusion. The studies were conducted within the temperature range characteristic of the extrusion of 16 mm diameter round profiles made of EN AW-6060 aluminum alloy, with different cooling rates after deformation. Physical modeling of both processes was preceded by numerical modeling with the finite element method (FEM) and a detailed analysis of the deformation conditions occurring during both processes. Thanks to the careful selection of thermoplastic forming parameters, comparable values of the strain, strain rate, and temperature of profiles suitable for direct microstructural comparison were obtained. The conducted studies made it possible to determine the influence of the applied thermoplastic forming parameters on the microstructural evolution of the tested material. Finite element method simulations revealed distinct strain gradients in both the hot torsion and extrusion processes. Metallographic analysis of the EN AW-6060 alloy showed a strong dependence of grain size and the degree of recrystallization on the thermoplastic processing temperature and the local strain level. The obtained results confirm that hot torsion testing, combined with the selection of representative regions based on FEM analysis, can serve as a supporting method for modeling microstructural evolution in industrial extrusion processes, provided that the thermomechanical conditions correspond to those occurring in the modeled process.

PMID 42882707
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PubMedNature metabolism2026-10-16

IRF7 signalling in tanycytes controls brain-body-immune response across the ovarian cycle.

Nampoothiri Sreekala S, Fernandois Daniela D, Journiac Nathalie N, Delahaye Fabien F et al.

Sex-specific differences in metabolic and immune function are shaped by endocrine-immune interactions, yet the complexity of this relationship remains poorly understood. Here, we identify an immune cell-like state of tanycytes, an ependymoglial cell type lining the third ventricle that mediates brain-body communication1,2 in both mice and humans. Using single-cell transcriptomics, we provide a high-resolution cellular map of the mouse and human mediobasal hypothalamus with cross-species comparison of tanycytes. We capture dynamic sex-, oestrous cycle- and high-fat diet-dependent transcriptomic changes in tanycytes, including a cyclic interferon response in tanycytes during the physiological oestrous cycle in female mice. We found that the oestrous cycle, with its changing hormonal milieu, especially oestradiol, affected the brain's immune responses, characterized by the temporal and cyclic expression of interferon regulatory factor 7 (Irf7) gene, as well as downstream interferon-stimulated genes such as Cxcl10 in tanycytes of female mice, which are associated with increased infiltration of leukocytes and cytokine responses. Irf7 expression in tanycytes of physiological males remained stable and markedly lower, suggesting a distinct immune activation pattern in the brains of cycling females. By targeting oestrogen and interferon signaling in tanycytes, we show that balanced, cyclic leukocyte infiltration into the median eminence may have a role in oestrous cycle maintenance, whereas Irf7 in tanycytes modulates circulating monocyte proportions, revealing brain-immune system communication through tanycytes. Our findings reveal an immune-associated role for tanycytes, with potential implications for understanding the endocrine and immunological mechanisms underlying sex-biased diseases.

PMID 42881274
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PubMedInternational journal of molecular sciences2026-10-16

ISG15 Is a Key Multidirectional Regulator of Cytosolic RNA- and DNA-Sensing Pathways and Type I Interferon Feedback Loops.

White Maleana G MG, Iordanskiy Sergey S

Activation of cytosolic RNA and DNA sensing pathways that normally recognize viral nucleic acids triggers the expression and release of type I interferons (IFN-I). This release drives the expression of interferon-stimulated genes (ISGs) that activate acute inflammation and counteract viral replication at various stages. Recent studies have highlighted how interferon-stimulated gene 15 (ISG15), a small, ubiquitin-like modifier, regulates cytosolic RNA and DNA sensing pathway proteins to control the antiviral response and inflammation. ISG15 is a multifunctional protein that acts as a secreted cytokine, binds freely to intracellular proteins, and covalently modifies proteins in a reversible process termed ISGylation. A dual regulatory molecule, ISG15 can both stabilize and destabilize proteins that promote and inhibit IFN-I signaling. Conversely, viruses have evolved strategies to disrupt and exploit ISG15-dependent antiviral responses to evade the host immune system. In this review, we examine how ISG15 regulates cytosolic RNA and DNA sensing pathway proteins to control IFN-I signaling and the antiviral response, highlighting it as a master regulator that fine-tunes IFN-I signaling and feedback. Recognizing the multifaceted action of ISG15 is essential for designing balanced therapeutic strategies across antiviral drug development, cancer immunotherapy, and chronic inflammatory disease management.

PMID 42884081
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PubMedEMBO reports2026-10-16

TREX1 limits anti-tumor immunity by degrading short cytosolic DNA molecules.

Yang Chun-Yen CY, Chami Bayan B, Ursino Chiara C, Johnson Silpa Mary SM et al.

TREX1 has recently emerged as a promising therapeutic target in cancer owing to its role in degrading cytosolic DNA and suppressing type I interferon signaling. However, the nature of the immunostimulatory DNA species degraded by TREX1 remains elusive. Here, we show that TREX1 deficiency in murine lung and melanoma tumor cells leads to a substantial, MRE11-dependent increase in short cytosolic DNA fragments that originate preferentially from transcriptionally active regions of the genome, without a corresponding increase in micronuclei. These fragments robustly activate interferon-stimulated genes and drive differentiation of pro-inflammatory macrophages. In syngeneic mice, tumors derived from Trex1-knockout cells exhibit delayed growth, increased sensitivity to anti-PD-1 immune checkpoint blockade, and extended survival. These effects depend on an intact immune system and foster durable anti-tumor memory. Together, our results reveal that short, transcription-derived cytosolic DNA fragments are key TREX1 substrates mediating immune activation in cancer, establishing TREX1 inhibition as a compelling strategy to enhance tumor immunogenicity.

PMID 42881257
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PubMedCommunications psychology2026-10-16

Task-specific theta enhancement and domain-general alpha/beta suppression as oscillatory signatures of cognitive flexibility.

Hülsemann Mareike M, Löffler Christoph C, Schubert Anna-Lena AL

Cognitive flexibility-the ability to adapt to changing situational or task demands-is a fundamental aspect of human cognition and a potential source of individual differences in higher-order cognitive abilities. To further understand the neural mechanisms underlying this ability, we examined event-related spectral perturbations (ERSP) in three cued switching tasks (parity/magnitude, global/local, number/letter) in a sample of 148 adults. Employing a data-driven approach that combined mass-univariate time-frequency analysis, cluster-based permutation testing, and latent change structural equation modeling, we identified two robust neural signatures: a transient frontal theta increase and a sustained alpha/beta suppression. Both effects were more pronounced in switch compared to repeat trials. Frontal theta reflected task-specific control processes, whereas parietal alpha/beta indexed domain-general attentional processes that persisted from cue onset through target processing-consistent with two-stage models of task switching. Notably, flexibility-related alpha/beta dynamics did not correlate with measures of intelligence or working memory capacity. However, stronger cue-elicited alpha/beta suppression correlated with reduced non-decision-time switch costs, indicating more effective task preparation, underscoring that alpha/beta suppression captures a neurally coherent but behaviorally distinct dimension of cognitive flexibility. These findings provide evidence that alpha/beta suppression constitutes a reliable, cross-task generalizable neural signature of attentional reconfiguration during task switching, while highlighting the multi-component nature of individual differences in cognitive flexibility.

PMID 42881249
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PubMedCells2026-10-16

Study of the Expression of Integrins in Smooth Myocytes of the Gastrointestinal Organs After Space Flight.

Samoilenko Tatyana T, Shishkina Viktoria V, Zolotaryova Svetlana S, Kostin Andrey A et al.

Spaceflight has crucial effects on living organisms, primarily due to weightlessness, which causes essential morphofunctional changes in the tissues of almost all body systems. Smooth muscle tissue is one of the main system-forming components of the gastrointestinal tract, which makes its study particularly relevant to space gastroenterology. Integrins are cell adhesion receptors expressed in practically all cell types, including smooth muscle cells. By mediating interactions with the extracellular matrix and intercellular signaling, smooth muscle cell integrins actively participate in adaptation to microgravity conditions. However, this aspect of smooth muscle tissue function has not been addressed in space gastroenterology until now. The aim of the study was to investigate the expressions of integrins alpha-5, alpha-2, and alpha-1 expression in smooth myocytes of the gastric and jejunal muscular layer in Mongolian gerbils (Meriones unguiculatus) after a 12-day spaceflight, which was part of the Foton M-3 project. We detected a slight increase in integrin alpha-1 expression, a trend toward decreased integrin alpha-2 expression, and a significant decrease in integrin alpha-5 expression in the gastric and jejunal muscularis propria in Mongolian gerbils from the spaceflight group, which may indicate weakened interactions between cells and the extracellular matrix and potentially lead to reduced smooth muscle contractility. Research on the fundamental role of integrins in the development of the digestive system adaptive mechanisms to zero-gravity conditions may be useful in developing preventive measures to mitigate the risk of gastrointestinal smooth muscle hypotrophy and maintain the health of astronauts during their professional activities aboard the ISS.

PMID 42882428
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