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Ypeginterferon alpha-2b (PegBeron)

✓ Approved

Xiamen Amoytop Biotech Co.ltd · Recombinant Proteins · Recombinant Proteins

What is Ypeginterferon alpha-2b?

Ypeginterferon alpha-2b is a recombinant proteins developed by Xiamen Amoytop Biotech Co.ltd. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesPegBeron
CompanyXiamen Amoytop Biotech Co.ltd
Drug ClassRecombinant Proteins
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Xiamen Amoytop Biotech Co.ltd

Therapeutic Indications

Ypeginterferon alpha-2b is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Essential thrombocythaemiaPhase II

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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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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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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PubMedFrontiers in endocrinology2026-09-19

Increased HIF-2α and CD105 (endoglin) expression is associated with poor differentiation in pheochromocytomas and paragangliomas.

Günler Tuğba T, Çordan İlker İ

Reliable biomarkers reflecting tumor biology and histopathological risk status in pheochromocytomas and paragangliomas (PPGL) remain limited. In this study, the expression of biomarkers associated with hypoxia, angiogenesis, and proliferation was evaluated, and their associations with histopathological differentiation in PPGL were investigated. A total of 35 tumor foci from 31 patients with PPGL who were surgically treated were retrospectively examined. Expression levels of hypoxia-inducible factor-2 alpha (HIF-2α), vascular endothelial growth factor (VEGF), CD105 (endoglin), Ki-67, and succinate dehydrogenase subunit B (SDHB) were assessed using immunohistochemical methods. Associations between these markers and clinicopathological characteristics, Pheochromocytoma of the Adrenal Gland Scaled Score (PASS), and Grading System for Adrenal Pheochromocytoma and Paraganglioma (GAPP) scores were analyzed. HIF-2α expression, CD105 microvessel density (MVD) score, and Ki-67 proliferation index were significantly higher in poorly differentiated tumors compared with moderately/well-differentiated tumors (p<0.05 for all). In contrast, VEGF expression did not differ significantly between the groups. The GAPP score showed positive correlations with HIF-2α (r=0.48; p<0.01), CD105 (r=0.54; p<0.001), and Ki-67 (r=0.77; p<0.001). In univariate analyses, bilateral disease, HIF-2α expression, CD105 MVD score, and loss of SDHB expression were associated with higher GAPP scores. However, in multivariable regression analysis, only CD105 was independently associated with the GAPP score (β=0.04; p=0.026). Increased expression of CD105, HIF-2α, and Ki-67 was associated with poorer histopathological differentiation in PPGL. Among the biomarkers evaluated, only CD105 showed an independent association with the GAPP score, suggesting that tumor-associated neoangiogenesis may contribute to histopathological differentiation in PPGL. These findings support further investigation of CD105 as a potential biomarker for histopathological risk assessment. However, larger studies with long-term clinical outcome data are needed to establish its clinical prognostic value.

PMID 42760995
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PubMedFrontiers in medicine2026-09-19

Elevated ALT correlates with severe liver injury, monocyte infiltration, and Pro-inflammatory immune dysregulation in chronic hepatitis B virus infection.

Huang Jian J, Xu Ning N, Liang Xiuyan X, Cai Defeng D

Hepatitis B virus (HBV) infection remains a global health burden. Although alanine aminotransferase (ALT) is a well-established marker of liver injury, its relationship with immune infiltration, monocyte activation, and inflammatory immune skewing in chronic HBV infection remains incompletely understood. This study aimed to investigate the associations of ALT with liver injury, monocyte infiltration, and hepatic immune microenvironment dysregulation. A total of 192 HBV-infected patients and 37 healthy controls were enrolled. Serum ALT, AST, HBV seromarkers, HBV-DNA, alpha-fetoprotein (AFP), and serum fibrosis markers (COLIV, HA, PIIINP, LN) were measured. Univariate and multivariate regression analyses were used to adjust for confounders including age, sex, HBV-DNA, fibrosis markers, and HBeAg status. Transcriptomic data from the GSE84044 liver biopsy cohort (n = 105) were analyzed using the xCell algorithm to evaluate hepatic immune infiltration, macrophage polarization, and immune scores. Gene set enrichment analysis (GSEA) was performed to explore monocyte chemotaxis, activation, and WNT/β-catenin signaling pathway. Chronic hepatitis B (CHB) patients showed significantly elevated ALT and AST. Higher ALT levels were strongly associated with elevated fibrosis markers and AFP, indicating more severe liver injury. Peripheral monocytes count and intrahepatic monocyte infiltration were both significantly increased in high-ALT patients. However, after multivariate adjustment, ALT was no longer independently associated with monocyte infiltration, suggesting that the association was largely attributable to overall disease severity rather than a specific ALT-related association. GSEA showed that ALT was positively correlated with monocyte chemotaxis, activation, macrophage differentiation, and WNT/β-catenin signaling pathway. Immune landscape analysis revealed a pro-inflammatory immune profile in high-ALT patients, characterized by increased M1 macrophages, CD8+ T cells, and elevated immune scores, accompanied by decreased Tregs and Th1 cells. Elevated ALT in chronic HBV infection correlates with severe liver injury and a pro-inflammatory, dysregulated hepatic immune microenvironment characterized by enhanced monocyte infiltration and M1 macrophage polarization. Transcriptomic associations reveal a statistical link between WNT/β-catenin signaling activation and hepatic immune dysregulation in HBV-related liver injury; these correlative findings provide preliminary clues for developing immunomodulatory therapeutic strategies for CHB.

PMID 42761001
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