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recombinant human interferon alfa-2a

✓ Approved

BioGeneric Pharma · IFNAR2 · Recombinant Proteins

What is recombinant human interferon alfa-2a?

recombinant human interferon alfa-2a is a recombinant proteins developed by BioGeneric Pharma. It is approved for therapeutic indications via injectable (others).

Drug Profile

CompanyBioGeneric Pharma
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, BioGeneric Pharma

Mechanism of Action

Molecular Targets

recombinant human interferon alfa-2a 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

recombinant human interferon alfa-2a is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Neoplasm malignant✓ Approved

Related Research Articles

PubMedNature medicine2026-07-17

Englumafusp alfa plus glofitamab in B cell non-Hodgkin lymphoma: a phase 1 trial.

Hutchings Martin M, Dickinson Michael M, Gritti Giuseppe G, Carlo-Stella Carmelo C et al.

There is an unmet need for effective, off-the-shelf therapies for relapsed or refractory aggressive B cell non-Hodgkin lymphoma (B-NHL). Part 2 of the current study was an open-label, nonrandomized, phase 1 study of escalating doses of the CD19-4-1BBL co-stimulatory molecule, englumafusp alfa, in combination with glofitamab in patients with relapsed or refractory B-NHL. Obinutuzumab pretreatment was administered 7 days before the first glofitamab dose. Glofitamab step-up dosing in cycle 1 was followed by 11 cycles of glofitamab plus englumafusp alfa. Englumafusp alfa was administered at escalating doses, with the initial dose on cycle 2 day 8 (C2D8) or cycle 1 day 10 (C1D10). Primary objectives were to establish the maximum tolerated dose, and safety and tolerability. A total of 134 patients were enrolled, including 109 with aggressive B-NHL and 25 with indolent B-NHL. The maximum tolerated dose of englumafusp alfa was not reached; one dose-limiting toxicity occurred (grade 5 Pneumocystis jirovecii pneumonia). Adverse events were reported in 98.5% of all patients, with grade 3/4 adverse events in 59.0%. Grade 5 adverse events occurred in ten patients. In the subgroup of C2D8 patients with aggressive B-NHL (n = 83), overall response and complete metabolic response rates were 68.7% and 56.6%, respectively; among those without previous exposure to chimeric antigen receptor T cell therapy (n = 41), the corresponding rates were 73.2% and 65.9%. Pharmacodynamic changes following englumafusp alfa administration supported its co-stimulatory mode of action. These data demonstrate that the addition of englumafusp alfa to glofitamab is associated with encouraging efficacy and robust pharmacodynamic modulation, as well as a safety profile consistent with glofitamab monotherapy, in patients with relapsed or refractory B-NHL. CTIS identifier: 2022-502616-37-00 ; ClinicalTrials.gov identifier: NCT04077723 .

PMID 42463852
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PubMedbioRxiv : the preprint server for biology2026-07-17

Tracing developmental and adult hematopoiesis with an endogenous zebrafish runx1-2A-CreERT2 CRISPR knock-in.

Preston James A JA, Usha Masuma K MK, Ekker Stephen C SC, Clark Karl J KJ et al.

Zebrafish combines the power of genetics and unparalleled in vivo imaging for investigating the dynamics of vertebrate hematopoietic development. Across species, the transcription factor Runx1 is essential for definitive hematopoiesis. We generated a zebrafish runx1-2A-creERT2 CRISPR knock-in for tamoxifen-regulated Cre recombinase Runx1 lineage tracing and characterized its activity using the ubi:Switch recombinase-dependent fluorescence reporter, microscopic live imaging and flow cytometry. Tamoxifen treatment beginning at gastrula stage labeled all expected Runx1 lineages in the early embryo, including neuroectodermal olfactory placode and Rohan-Beard neurons, primitive hematopoietic blood cells, and nascent hematopoietic stem and progenitor cells (HSPCs) in the dorsal aorta. Runx1 HSPCs colonized the larval caudal hematopoietic tissue and thymus from three to five days of development. Timed tamoxifen induction of Cre activity allowed separation of Runx1 primitive hematopoiesis from definitive HSPC emergence and larval stem cell niche colonization. Flow cytometry of kidney marrow and peripheral blood from adults treated with tamoxifen at gastrula stage revealed Runx1 embryonic hematopoietic cells contributed to adult hematopoietic precursors, myeloid, lymphoid, and peripheral blood lineages. Labeling of all blood lineages was also effective by tamoxifen treatment of 5-month-old adults. The zebrafish runx1-2A-creERT2 line provides a powerful tool for precise spatial and temporal analysis of Runx1 progenitor mechanisms in developmental and adult hematopoiesis. zebrafish endogenous runx1-2A-creERT2 provides inducible Cre recombinase genetic analysis in all runx1 neuromesodermal and blood lineages zebrafish runx1-2A-creERT2 line enables in vivo spatial and temporal analysis of embryonic and adult hematopoiesis.

PMID 42465524
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PubMedInternational journal of oncology2026-07-17

[Retracted] Phenotypic characterization of human prostatic stromal cells in primary cultures derived from human tissue samples.

Gravina Giovanni Luca GL, Mancini Andrea A, Ranieri Guido G, Di Pasquale Boris B et al.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding Figs. 2A and 4B (and possibly also Fig. 4A), certain of the gel lanes within these figure parts (showing numbered cultures) appeared to contain duplicated data (specifically, lanes 2‑4 and 8‑10 in Fig. 2A, lanes 5 and 6 in Fig. 4A, and lanes 1‑4 and 7‑10 in Fig. 4B). Upon performing an independent analysis of the data in this paper, it also came to light that the β‑actin data in Fig. 3A and the Desmin data in Fig. 3E had appeared in a previous paper published in American Journal of Pathology that featured entirely different authors, although comparing the affiliations of the papers, one of the universities was the same. Given the apparent duplications of data within this paper itself and the re‑use of data that had originally appeared in a different article, the Editor of International Journal of Oncology has decided that it should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The corresponding author, Claudio Festuccia, takes full responsibility for the raised concerns and clarifies that the other co-authors were not directly involved in the preparation of the submitted figures. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 42: 2116‑2122, 2013; DOI: 10.3892/ijo.2013.1892].

PMID 42464654
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PubMedbioRxiv : the preprint server for biology2026-07-17

Tetherin enforces an immunometabolic checkpoint that coordinates glycolytic and interferon signaling in adipocytes.

Cho Chung Hwan CH, Jang YoungUk Y, Warnock Aidan A, Yildiz Ramazan R et al.

Coordination between innate immune signaling and glucose metabolism is fundamental to organismal homeostasis, yet despite decades of study linking immunity and metabolism, the mechanisms by which metabolic cells restrain antiviral innate signaling while preserving glycolytic competence during overnutrition remain poorly defined. Here we identify Tetherin (BST2) as a unique cell-intrinsic immunometabolic checkpoint that couples restraint of type I interferon (IFN-I) signaling to preservation of glycolytic capacity in adipocytes. Tetherin localizes to endoplasmic reticulum and organizes an interactome enriched for antiviral sensing regulators and glycolytic control nodes in adipocytes. Mechanistically, Tetherin directly engages the ubiquitin-dependent degradation machinery NDFIP1 and RNF128 to terminate IRF3 activation, thereby limiting pro-inflammatory, anti-glycolytic signaling and protecting adipocytes from metabolic dysfunction. In parallel, multiomics integration reveals that Tetherin also acts as a scaffold that binds and spatially organizes and activates PFKFB3 to increase glycolytic capacity and restrain MAVS-IRF3 innate immune signalling. In vivo, adipocyte-specific loss of Tetherin amplifies high sucrose diet and high-fat-diet-induced glucose intolerance and liver steatosis, whereas overexpression of human Tetherin in adipocyte suppresses obesity-driven interferon signaling, restores glycolytic pathway, and improves metabolic homeostasis. Orthogonal perturbations in cancer and insulinoma cells further confirm an immunometabolic role for Tetherin. Together, these findings define Tetherin as a dual node immunometabolic checkpoint that couples restraint of antiviral innate inflammatory signaling to maintenance of glycolytic competence, thereby safeguarding adipocyte metabolic homeostasis.

PMID 42465282
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PubMedACG case reports journal2026-07-17

Colonic Ischemia Without Mesenteric Occlusion: A Case Implicating Interferon-β.

Siegel Alexander A, Tun Kyaw Min KM, Gamache Jennifer J, Kizer Robert R

Type I interferons are commonly used immunomodulatory agents. Interferon-α (interferon-α) has been associated with ischemic colitis, but cases linking interferon-β (IFN-β) to ischemic colitis are rare. We present a 66-year-old woman with multiple sclerosis treated with IFN-β who developed acute abdominal pain and diarrhea. Imaging demonstrated right-sided colonic inflammation with pneumatosis. Colonoscopy with tissue biopsy confirmed ischemic colitis, despite patent mesenteric vasculature on angiographic imaging. Her symptoms resolved after discontinuation of IFN-β. This case highlights IFN-β as a potential cause of nonocclusive ischemic colitis and underscores the importance of recognizing ischemic complications in patients treated with IFN-β.

PMID 42465814
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PubMedNature communications2026-07-17

Triple IFN pathway deficiency sensitizes mice to human respiratory virus infection independent of human viral receptor expression.

Fan Qinghong Q, Pan Meifang M, Jiang Mengling M, Feng Chengqian C et al.

Interferon (IFN) pathways form the innate barrier against viral invasion and partial deficiency in these pathways allows human virus infection. Whether a complete IFN pathway deficiency could confer the susceptibility to human viral infection independent of expressing the human viral receptor remains unknown. We develop an innate immunity severely deficient mouse model, designated AGL, which features one-step knock-out of the IFNAR, IFNGR and IFNLR. The AGL mice become susceptible to diverse representative human respiratory viruses, including adenovirus type 55 (HAdV-55; double-stranded DNA), human monkeypox virus (MPXV) clade IIb (double-stranded DNA), parainfluenza virus (PIV; negative-sense single-stranded RNA), and the clinically isolated SARS-CoV-2 delta variant (positive-sense single-stranded RNA). Our results suggest that the type III IFN pathway constitutes a backup layer of antiviral frontline beneath the type I and II IFN pathways. In addition, proof-of-concept studies testing MPXV and PIV antivirals highlight the translational value of AGL mice. The AGL mice, as a universal model, substantially enhance the ability to investigate both emerging and established viruses without the need for tailored mouse models.

PMID 42463654
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