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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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

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

PubMedCognitive, affective & behavioral neuroscience2026-09-19

Who is to blame? Outcome controllability and error attribution differentially shape cognitive preparation and feedback evaluation.

Grote Luisa A LA, Schneider Daniel D, Wascher Edmund E, Arnau Stefan S

Sense of agency (SoA), the experience of controlling one's actions and their consequences, is crucial for self-representation and adaptive goal-directed behavior. Much of today's cognitive work is performed through interaction with systems that are not entirely reliable or are prone to operator error. Against this background, it is of particular interest to understand how perceived outcome-controllability and attribution of action-outcome disruptions feed back into cognitive processing as states of perceived agency. In this EEG study, we manipulated performance feedback in a color-discrimination task to dissociate self-attributed from system-attributed errors. Thirty-five participants completed blocks with veridical feedback, feedback suggesting increased error rates due to impaired personal performance, and feedback indicating malfunctioning response buttons. Behavioral performance was decomposed using the EZ-diffusion model, and time-frequency analyses focused on preparatory alpha and beta oscillations and feedback-locked theta activity. Both manipulated feedback conditions led to slower responses compared to veridical feedback. Diffusion modeling revealed that general performance slowing was driven by reduced drift rates, whereas differences between self- and system-attributed errors were reflected in nondecision time. In the EEG, manipulated feedback attenuated cue-related decreases in occipital alpha and sensorimotor beta power during the cue-target interval. In addition, system- versus self-attributed errors elicited stronger feedback-related midfrontal theta responses. Our findings suggest a functional dissociation within the agency inference process, where perceived controllability regulates preparatory investment of cognitive resources on a global level, while the attribution of action-outcome discrepancies seem to modulate evaluative processing.

PMID 42760470
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PubMedBMC gastroenterology2026-09-19

Leucine-rich alpha-2 glycoprotein as a predictor of primary non-response to anti-TNF-α therapy in biologic-naïve Egyptian IBD patients.

Amer Ibrahiem I, El Batae Hassan H, Elshaer Yasmine A YA, Sherief Dalia Elsayed DE et al.

Anti-tumor necrosis factor-α (anti-TNF-α) agents are a cornerstone in inflammatory bowel disease (IBD) therapy, yet primary non-response remains a significant practical challenge. Leucine-rich alpha-2 glycoprotein (LRG) has been recognized as a promising marker for disease activity. This study aimed to evaluate the predictive significance of pre-treatment serum LRG for response to anti-TNF-α therapy in biologic-naïve Egyptian IBD patients. In this prospective cohort study, 100 biologic-naïve IBD adult patients (50 Crohn's disease [CD], 50 ulcerative colitis [UC]) and 100 healthy controls were enrolled. Patients received induction therapy with adalimumab or infliximab. Clinical, biochemical, and endoscopic evaluations were conducted at baseline and at week 24. Response was defined by clinical indices and endoscopic improvement, while biochemical normalization was evaluated as a secondary, supportive parameter. IBD patients had significantly elevated baseline LRG levels compared to the healthy controls (p < 0.001). Responders' baseline LRG was substantially lower than that of non-responders in both UC (26.53 vs. 34.88 µg/mL; p = 0.008) and CD (26.03 vs. 35.07 µg/mL; p = 0.006). Receiver operating characteristic analysis revealed a cut-off of > 29 µg/mL for predicting non-response, yielding sensitivities of 74.2% and 80.0% with specificities of 69.57% and 65.71% for UC and CD, respectively and negative predictive values of 85.7% for UC and 88.5% for CD. Multivariate regression confirmed baseline LRG as an independent predictor of non-response. Baseline serum LRG levels > 29 µg/mL demonstrated moderate discriminatory ability for predicting primary non-response to anti-TNF-α therapy in Egyptian IBD patients. LRG may serve as a useful adjunctive biomarker for pre-treatment risk estimation and recognizing patients who may require alternative therapeutic strategies.

PMID 42760552
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PubMedJournal of molecular medicine (Berlin, Germany)2026-09-19

MicroRNA-122 as a regulator and biomarker of liver disease.

Ahmadova Sara S, Wicik Zofia Z, Mucha Joanna J, Palatini Jeff J et al.

MicroRNA-122 (miR-122) is the most abundant liver-specific microRNA, comprising ~ 70% of the hepatic miRNA pool, and a central regulator of lipid metabolism, inflammation, fibrosis, viral replication, and hepatocarcinogenesis. This review synthesizes experimental, clinical, and molecular evidence on the role of miR-122 across the spectrum of liver disease, including metabolic dysfunction-associated fatty liver disease (MAFLD) and steatohepatitis (MASH), drug-induced acute liver injury, hepatitis B and C virus (HBV/HCV) infection, hepatocellular carcinoma (HCC), and colorectal cancer liver metastasis. Mechanistically, miR-122 governs hepatic lipogenesis through the Sirt1/LKB1/AMPK axis, modulates inflammation via LPS/TLR-4/FoxO3 signaling, and exerts tumor-suppressive and antiviral effects through Cyclin G1/p53, HO-1, NDRG3, GALNT10, PEG10, and NEGR1. A recurring theme is the compartment- and stage-dependent behavior of miR-122: hepatic expression declines with disease progression, whereas circulating levels rise with hepatocyte injury, reconciling apparently contradictory reports and underscoring the importance of specimen source and disease stage in biomarker interpretation. We further contrast the etiology-specific regulation of miR-122 in HBV- versus HCV-associated disease, in which epigenetic silencing and interferon-linked mechanisms drive divergent expression. Finally, we critically appraise the failed clinical translation of anti-miR-122 therapeutics (miravirsen, RG-101), highlighting viral resistance, safety liabilities, and the tumor-suppressor paradox that constrains inhibition-based strategies. Collectively, miR-122 emerges as a minimally invasive biomarker and a biologically informative, though therapeutically challenging, target in liver disease.

PMID 42760391
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PubMedWorld journal of surgical oncology2026-09-19

Stress-driven reprogramming of plasmacytoid dendritic cells in intrahepatic cholangiocarcinoma defines a reversible targetable immunosuppressive state.

Chen Mei-Ru MR, Xie Xiao-Li XL, Zhou Yan-Li YL, Tian Jin-Mei JM et al.

Plasmacytoid dendritic cells (pDCs) have been implicated in both restraining and promoting intrahepatic cholangiocarcinoma (iCCA), leaving their clinical relevance and therapeutic potential unresolved. Mendelian randomization was used to assess the causal association between circulating pDC levels and iCCA risk. Bulk and single-cell transcriptomic analyses were performed to characterize pDC-related programs and tumor-conditioned states, and multiplex immunofluorescence was used to define spatial distribution and clinical associations in iCCA tissues. To assess reversibility of stress-associated pDC features, IRE1α RNase activity was pharmacologically inhibited with 4µ8C under tumor-conditioned stress in vitro. Genetically predicted higher circulating pDC levels were associated with lower iCCA risk, consistent with a systemic protective association. In bulk cohorts, higher expression of pDC markers (CLEC4C, NRP1, IL3RA) was associated with an immune-inflamed microenvironment and improved survival in early-stage disease. Single-cell analyses indicated that intratumoral pDCs acquired stress-associated transcriptional programs, including enrichment of endoplasmic reticulum stress and unfolded protein response pathways. In vitro, 4µ8C reduced IRE1α-dependent XBP1 splicing and partially restored type I interferon-linked activation and pDC immunogenic readouts under tumor-conditioned stress. Spatial profiling further showed that higher intratumoral CD303⁺IRF7⁺ pDC activation was associated with advanced stage and poorer overall survival, whereas higher activation in adjacent non-tumor tissues correlated with more favorable outcomes. Together, these findings support a context-dependent, stress-associated pDC program in iCCA and provide a rationale for further evaluating the IRE1α-XBP1 stress axis as a potential approach to modulate pDC-associated immune states within the tumor microenvironment.

PMID 42760567
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PubMedCell proliferation2026-09-19

Olfactory Tuft Cells Are Critical to Basal Inflammation, Innate Immune Response to Viral Infection, and Modulation of Quiescent Stem Cell Activation, Proliferation and Differentiation.

Zhang Sai-Sai SS, Wang Haiyan H, Yang Yi-Sen YS, Li Yi-Hong YH et al.

The olfactory mucosa serves as both a sensory organ and an immune barrier to protect against bacterial and viral invasion and other insults. It is unclear how different types of olfactory mucosal cells coordinate and contribute to these two functions. We set out to reveal the critical roles of a subset of microvillous cells of the mucosa, olfactory tuft cells, in protecting and reconstructing this vital olfactory sensory organ. We first validated the expression of canonical gustatory signalling proteins and other molecular markers in olfactory tuft cells. Genetic disruption of the Gng13 and Trpm5 genes that encode the two gustatory signalling proteins, G protein subunit Gγ13 and transient receptor potential ion channel Trpm5, respectively, resulted in elevated basal inflammation and enhanced activation of the quiescent stem cells-horizontal basal cells (HBCs) in the mucosa. Nasal infection of H1N1 influenza virus further exacerbated the inflammation and delayed the resolution of inflammation in the mutant mucosa, including more immune cell infiltration, augmented cytokine production and cell death, increased HBC proliferation and direct differentiation into tuft cells, and prolonged olfactory tuft cell hyperplasia. Cytokine treatment of the cultured olfactory epithelial organoids indicated that the cytokines that were found to be elevated in the mutant mucosa, including interleukin-4 (IL-4), IL-13 and interferon-γ (INF-γ), are able to stimulate HBC activation. Together, our results indicate that olfactory tuft cells play an important role in maintaining the baseline inflammation under the steady-state condition, and altering inflammatory magnitude and modulating HBC activation and differentiation in the olfactory mucosa following the viral infection. Our findings shed light on new roles of olfactory tuft cells in innate immune response, quiescent stem cell activation and neuroimmune interactions, and provide novel therapeutic targets for preventing and treating stem cell-related olfactory disorders such as chronic rhinosinusitis and long COVID.

PMID 42760864
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PubMedMedicine2026-09-19

The NF-κB pathway in inflammatory responses in preeclampsia: A systematic review and meta-analysis.

Zhang Hui H, Nong Yanhua Y, Huang Meiqi M, Wei Riyuan R et al.

Preeclampsia is a pregnancy-specific hypertensive disorder associated with systemic inflammation, endothelial dysfunction, and adverse maternal and fetal outcomes. The nuclear factor kappa B (NF-κB) signaling pathway has been implicated in inflammatory activation, but its role in preeclampsia remains incompletely defined. This systematic review and meta-analysis aimed to evaluate the association between NF-κB pathway activation and inflammatory responses in preeclampsia. This meta-analysis reviewed 15 peer-reviewed articles focusing on the involvement of the NF-κB pathway in preeclampsia. Quantitative assessments included changes in systolic and diastolic blood pressure and levels of key inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta, interleukin-6 (IL-6), and NF-κB. Systolic and diastolic blood pressure were significantly elevated in patients with preeclampsia. TNF-α and NF-κB levels were also significantly increased, indicating enhanced inflammatory activation associated with the disease. In contrast, interleukin-1 beta and IL-6 levels did not differ significantly, although IL-6 showed a nonsignificant trend toward increased levels. This meta-analysis suggests that NF-κB activation, together with increased TNF-α levels, may contribute to the inflammatory pathophysiology of preeclampsia. These findings support further investigation of NF-κB-related pathways, including Sirtuin 1-mediated regulation, as potential biomarkers and therapeutic targets.

PMID 42760699
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