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interferon (Shanferon)

✓ Approved

Sanofi S.A · IFNAR2 · Recombinant Proteins

What is interferon?

interferon is a recombinant proteins developed by Sanofi S.A. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesShanferon
CompanySanofi S.A
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

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 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic myeloid leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved

Related Research Articles

PubMedFrontiers in immunology2026-07-25

Spatial transcriptomics reveals molecular differences associated with malignant transformation in oral epithelial dysplasia.

Raja Naren N, Pathak Harsh B HB, Mitra Amrita A, Thomas Sufi Mary SM et al.

Oral epithelial dysplasia (OED) is a precancerous oral lesion with variable risk of progression to oral squamous cell carcinoma (OSCC). The molecular basis underlying this progression remains incompletely understood. To address this gap, this study applied spatial transcriptomics to characterize benign, OED and OSCC biopsies with a focus on the comparison between transforming and non-transforming OED. Spatial transcriptomic profiling was performed on 13 benign, 15 OED (8 transforming, 7 non-transforming), and 14 OSCC biopsies using the NanoString GeoMx Digital Spatial Profiler. Regions of interest were segmented into epithelial and immune-enriched compartments with morphological markers. Gene expression was measured using the GeoMx Cancer Transcriptome Atlas (~1, 800 genes) and differentially expressed genes (DEGs) were identified using linear mixed-effects modeling. Exploratory bioinformatic analyses were performed to provide biological context. Comparison of OED with and without transformation identified a limited set of 11 epithelial DEGs, including genes associated with antigen presentation and interferon signaling (e.g., B2M, STAT1, and CD74), while no significant DEGs were detected in immune-enriched regions. Pathway analyses indicated enrichment of immune- and interferon-related processes. Given the modest sample size and targeted gene panel, these findings should be considered exploratory in nature. This study provides spatially resolved, exploratory insights into molecular differences between OED lesions with distinct clinical outcomes. The results suggest altered epithelial-immune interactions in transforming lesions, though these findings require validation. Spatial transcriptomics may offer a useful framework for investigating early molecular changes in oral carcinogenesis.

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PubMedOpen forum infectious diseases2026-07-25

Associations Between QuantiFERON-TB Gold Plus IFNγ Concentrations and Progression to Symptomatic Tuberculosis in Global High-Burden TB Settings.

Sunshine Justine J, Shaffer Michael M, Han Linda L LL, Gaikwad Deepali D et al.

Predictive biomarkers for symptomatic tuberculosis (TB) progression would transform targeted prevention efforts. Although interferon-gamma release assays (IGRAs), including QuantiFERON® TB-Gold Plus (QFT-Plus), have been studied for this purpose, systematic evaluation of the QFT-Plus TB1 and TB2 Interferon-Gamma (IFNγ) concentrations remains limited, particularly in high-burden TB settings. Baseline TB1 and TB2 IFNγ concentrations from 5246 participants (ages 15-34 years) in TB-endemic regions were analyzed in relation to subsequent TB outcomes over a median of 525 days follow-up (NCT05190146). Participants were categorized as controls (no TB), suspected TB (no microbiological confirmation), or laboratory-confirmed TB, including a subset meeting a stringent case definition (≥2 positive microbiologic tests). Associations between baseline IFNγ concentrations and progression to symptomatic TB were assessed. In the full cohort (IGRA+/- participants), baseline TB2 IFNγ concentrations were significantly higher compared with controls among participants who developed suspected TB (P = .01), laboratory-confirmed TB (P = .01), or met the stringent case definition (P < .0001). In IGRA+ participants, baseline TB2 concentrations were significantly higher than controls in suspected (P = .01) and laboratory-confirmed (P = .02) groups. Associations with baseline TB1 IFNγ concentrations and TB progression were observed for participants meeting the stringent case definition within the full cohort (P = .001). Among stringent definition cases, TB2 concentrations achieved an area under the receiver operating characteristic curve of 0.84, with sensitivity of 80% and specificity of 78%. Quantitative IFNγ concentrations from QFT-Plus, particularly TB2, were associated with progression to symptomatic TB, met or exceeded WHO-recommended sensitivity and specificity thresholds for predictive biomarkers, and may support biomarker-based stratification in TB clinical research.

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PubMedSmart molecules : open access2026-07-25

Endocytosis-independent cytosolic entry of messenger RNA via fluorous bilayer zippering attenuating Toll-like receptor signaling and enables ischemic tissue salvage.

Wang Yue Y, Xie Haitao H, Xiang Guoqing G, Li Yanhua Y et al.

A fundamental constraint of conventional messenger RNA (mRNA) delivery systems is their obligatory trafficking through endosomal-lysosomal compartments, wherein cargo degradation and activation of endosomal Toll-like receptors precipitate substantial translational attrition and deleterious inflammatory cascades. We herein report a chemically engineered platform that circumvents these limitations ab initio. Through strategic perfluoro-acylation of branched polyethyleneimine (PEI, 25 kDa) with pentafluoropropionic anhydride, we install approximately 26 fluoro-amide "zipper" moieties per polymer chain that orchestrate direct, energy-independent trans-bilayer translocation without recruitment of clathrin, caveolae, or lipid raft microdomains-thereby precluding lysosomal entrapment and catabolism. Bio-orthogonal copper-free click chemistry between azide- and dibenzocyclooctyne (DBCO)-terminated PEI-F derivatives, coupled with redox-labile disulfide crosslinkers, engenders polyplexes of exceptional extracellular stability that undergo quantitative glutathione-triggered disassembly within the cytosolic milieu. This endosome-evasive entry mechanism effectively sequesters single-stranded mRNA from Toll-like receptor 3, TLR7, and TLR8 surveillance, establishing a "TLR-attenuated" delivery paradigm characterized by undetectable interferon-α, interferon-β, TNF-α, and IL-6 induction. In human umbilical vein endothelial cells, GFP-mRNA transfection exceeds 90% fluorescent positivity with 4.8-fold superior luciferase expression relative to Lipofectamine™ 3000, whilst maintaining >95% viability. Therapeutic translatability is demonstrated in a murine hindlimb ischemia model, wherein a single 10 μg intramuscular dose of mVEGF-A polyplexes restores blood perfusion to 118% of baseline within 28 days-representing marked superiority over the commercial gold standard and effectuating complete tissue salvage without necrosis. Comprehensive hematological and immunological profiling corroborates the absence of hematotoxicity, systemic inflammation, or innate immune activation. This modular, purely synthetic platform resolves the classical stability-availability paradox whilst eliminating the immunogenic liabilities inherent to endocytic delivery, furnishing a readily translatable scaffold for precision regenerative medicine.

PMID 42500712
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PubMedCurrent opinion in immunology2026-07-25

Human endogenous retroviruses leading to autoimmune diseases.

Mercado-Celin María J MJ, Patiño-Arboleda Marcela M, Rios-Serna Lady J LJ, Bedoya-Duque Maria A MA et al.

Human endogenous retroviruses (HERVs) comprise approximately 8% of the human genome and were long regarded as inert remnants of ancestral retroviral infections. Increasing evidence indicates that HERVs are active genomic elements capable of influencing transcriptional programs, modulating immune responses, and contributing to disease pathogenesis. Under physiological conditions, HERV expression is tightly controlled by epigenetic mechanisms; however, infections, chronic inflammation, aging, and diverse environmental stimuli can promote HERV reactivation. HERV-derived RNAs and proteins engage innate immune sensors and trigger antiviral-like responses through mechanisms of viral mimicry, leading to activation of type I interferon and other inflammatory pathways. HERV dysregulation has been associated with disease-relevant immune pathways. This review summarizes recent advances linking HERVs to autoimmune disease pathogenesis and discusses their potential translational relevance as biomarkers and therapeutic targets.

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PubMedBiochemical and biophysical research communications2026-07-25

IFITM3 promotes triple-negative breast cancer progression by regulating β-catenin localization.

Kim Heeyeon H, Yu Youngim Y, Park Yuseon Y, Kim Haein H et al.

Interferon-induced transmembrane protein 3 (IFITM3) is best known as an antiviral protein, but accumulating evidence supports pro-tumorigenic functions across several cancers. Here, we examined IFITM3 in triple-negative breast cancer (TNBC). IFITM3 depletion suppressed MDA-MB-231 cell proliferation, migration, sphere formation, and xenograft tumor growth, whereas IFITM3 overexpression enhanced these phenotypes. IFITM3 depletion restored E-cadherin expression and increased membrane-associated E-cadherin-β-catenin complexes. These changes were accompanied by reduced nuclear active β-catenin and decreased Wnt/β-catenin transcriptional activity in cultured cells. Altered β-catenin localization was also observed in xenograft tumors. Conversely, IFITM3 overexpression enhanced WNT3a-responsive transcription and nuclear accumulation of active β-catenin. IFITM3 expression was elevated in breast tumors and was associated with shorter overall survival in a selected lymph-node-negative TNBC cohort. Together, these findings identify IFITM3 as a regulator of β-catenin localization and Wnt signaling that promotes epithelial-mesenchymal transition (EMT) and stem-like properties in TNBC cells.

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PubMedImmunity2026-07-25

Disease-associated microglia adopt stage-specific phenotypes that regulate T cell fate and immunity in glioma.

Qian Jiawen J, Wang Chen C, Zhang Yi Y, Li Congwen C et al.

Malignant gliomas are lethal brain tumors characterized by profound local immunosuppression and a radically remodeled myeloid landscape. Although these tumors mobilize resident microglia and infiltrating monocyte-derived macrophages, the mechanisms governing their phenotypic convergence and diversification remain elusive. Here, we integrated single-cell profiling and spatial transcriptomics of glioma-associated microglia in the GL261 model. We identified distinct microglial states that aligned with tumor architecture, most notably Cst7-expressing disease-associated microglia (DAMs) that aggregated at the tumor invasive margin and exhibited a conserved transcriptional signature shared across various central nervous system pathologies. Interferon-γ and toll-like receptor signaling sequentially tuned stage-specific DAM features, including transient MHC-II expression and sustained PD-L1 upregulation, thereby recalibrating the local immune equilibrium by reshaping bidirectional DAM-T cell interactions during glioma progression. Our findings highlight microglial state transitions as a stage-specific layer of immune regulation in glioma that shapes T cell fate and support targeting microglial plasticity to rebalance anti-tumor immunity.

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