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interferon gamma (Heberon Gamma R / Heberon Gamma)

✓ Approved

Heber Biotec · IFNG · Recombinant Proteins

What is interferon gamma?

interferon gamma is a recombinant proteins developed by Heber Biotec. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection.

Drug Profile

Brand NamesHeberon Gamma R, Heberon Gamma
CompanyHeber Biotec
Drug ClassRecombinant Proteins
Molecular TargetIFNG
RouteInjectable (Others), Intramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, Heber Biotec

Mechanism of Action

Molecular Targets

interferon gamma acts on 1 molecular target:

IFNGinterferon gamma (IMD69, IFI)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

interferon gamma is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Infections and infestationsDisseminated mycobacterium avium complex infectionPhase I

Related Research Articles

PubMedThe AAPS journal2026-09-19

Quantitative Characterization of Innate and Adaptive Pharmacology of Allogeneic anti-CD20 Chimeric Antigen Receptor (CAR) Vδ1 γδ T cells using Multiscale Mechanistic Modeling.

Desai Devam A DA, Elashkar Omar O, Cristofoletti Rodrigo R, Mugundu Ganesh G et al.

Gamma Delta (γδ) T Cells are currently being evaluated as a therapeutic alternative to traditional alpha-beta (αβ) T-cells due to their superior safety profile and enhanced tissue retention properties. The application of CAR technology to gamma delta (γδ) T cells presents a novel therapeutic avenue with the potential to overcome some limitations of conventional CAR T-cell therapies, such as targeting solid tumors and reducing on-target, off-tumor toxicities. The objective of this manuscript is development of a translational PK-PD framework to first characterize in vitro killing potential of un-transduced and CAR transduced anti- CD20 Vδ1 γδ T cells as well as development of an in vivo mechanistic CK-PD model designed to understand the complex dynamics of CAR γδ T cells and their interaction with IL-15 and tumor cells. All the preclinical and clinical datasets along with relevant information were digitized and obtained from the published work on Adicet Bio's AD-001. The developed model was able to estimate the in vitro killing potential of untransduced and CAR transduced anti- CD20 Vδ1 γδ T cells as well as expansion, tissue distribution, the impact of lymphodepletion and interleukin-15 (IL-15), and the tumor-killing potential of CAR-modified γδ T cells. These insights offer a deeper understanding of the potential therapeutic benefits and mechanisms of γδ T cells in immunotherapy, particularly in their application against various cancers. The development of this translational framework can be paramount in understanding the underlying dose-exposure-response relationship of CAR modified γδ T cell therapy and facilitate the discovery and development of these agents.

PMID 42760488
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PubMedMedicine2026-09-19

Reveal the diagnostic value of a neutrophil inflammation- and cell death-associated gene signature in rheumatoid arthritis.

Gu Chunsong C, Chen Yujia Y, Huang Wei W, Chai Yihui Y et al.

This study aimed to construct an artificial neural network (ANN) diagnostic model for rheumatoid arthritis (RA) based on a neutrophil inflammation- and cell death-associated gene signature derived from a previously reported neutrophil extracellular traps (NETs)-related gene set, and to explore its association with immune infiltration and inflammatory pathways. The GEO dataset GSE110169 was used as the training dataset to identify differentially expressed genes between RA patients and healthy controls. Genes derived from a previously published NETs-related gene set were used as the initial candidate genes. Candidate genes were further screened using a random forest algorithm, and an ANN diagnostic model was constructed using the selected feature genes. Model performance was assessed by 10-fold cross-validation and externally validated in GSE93272. Cell Type Identification By Estimating Relative Samples Of RNA Transcripts was used to estimate immune infiltration, and weighted gene co-expression network analysis, gene ontology, and Kyoto encyclopedia of genes and genomes analyses were performed to explore related biological functions. Eleven selected feature genes were retained for model construction: Wiskott-Aldrich syndrome protein-like actin nucleation promoting factor, MFN1, enolase-1, optic atrophy 1, CLEC7A, interleukin-8, S100A8, ACTN4, RIPK1, CASP1, and integrin-linked kinase. The ANN model achieved an area under the curve of 0.923 in the training dataset and 0.722 in the external validation dataset. Immune infiltration analysis suggested that these genes were associated with gamma delta T cells, macrophages M0, memory B cells, resting dendritic cells, and activated dendritic cells. Functional enrichment analysis indicated involvement in lysosome, osteoclast differentiation, hematopoietic cell lineage, chemokine signaling pathway, and Fc gamma R-mediated phagocytosis. This study developed an ANN diagnostic model based on an neutrophil inflammation- and cell death-associated gene signature with potential diagnostic value for RA. However, because direct NET markers were not experimentally evaluated, the selected genes should not be interpreted as NETs-specific biomarkers. Further experimental validation is required.

PMID 42760665
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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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PubMedCell biochemistry and biophysics2026-09-19

Acetone Extract of Annona Muricata Linn Leaf Counteracts Hyperglycemia-Associated Metabolic Dysregulation by Modulating Oxidative Stress and Hepatic Carbohydrate Metabolism in Streptozotocin-Induced Diabetic Rats.

Omiyale Benjamin Olusola BO, Ekundayo Bidemi Emmanuel BE, Olusola Olutosin Samuel OS, Idowu Olajumoke Tolulope OT et al.

Annona muricata is widely recognized for its rich phenolic composition and potent antioxidant activity, suggesting therapeutic potential in diabetes management. This study investigated the mechanistic antidiabetic effects of acetone extract of A. muricata leaf on hepatic carbohydrate metabolism, oxidative stress, and hepatic function in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in forty-two male Wistar rats by intraperitoneal injection of STZ (55 mg/kg). Diabetic animals (n = 7 per group) were treated with 25, 50, and 100 mg/kg of the extract (yield: 10.08% w/w) for 28 days, while metformin (200 mg/kg) served as the standard drug. Hepatic antioxidant enzyme activities, lipid peroxidation, serum albumin, lactate dehydrogenase (LDH), and histopathological alterations were evaluated to assess oxidative status and hepatic function, alongside the activities of key carbohydrate-metabolizing enzymes and mRNA expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) and glucose transporter 4 (GLUT4). Administration of the acetone extract significantly enhanced hepatic antioxidant defenses, as demonstrated by increased levels of glutathione and increased activities of antioxidant enzymes, accompanied by a marked reduction in lipid peroxidation. Additionally, the extract significantly restored serum albumin levels and reduced LDH activity, indicating improved hepatocellular integrity. Furthermore, the extract significantly impacted the activities of carbohydrate-metabolizing enzymes and restored the expression of PPAR-γ and GLUT4 toward physiological levels. These results suggest that the antidiabetic activity of A. muricata may be mediated by the attenuation of oxidative stress, preservation of hepatic function, and regulation of hepatic carbohydrate metabolism and glucose transporter signalling pathways, highlighting its potential as a promising phytotherapeutic agent for the management of diabetes.

PMID 42760481
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