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ribavirin + PEG-IFNalpha-2a (Copegus + Pegasys / Pegasys + Copegus / Pegasys/Copegus)

✓ Approved

Roche · IFNAR2 · Small Molecule

What is ribavirin + PEG-IFNalpha-2a?

ribavirin + PEG-IFNalpha-2a is a small molecule developed by Roche. It is approved for therapeutic indications via injectable (others) or oral (po) or subcutaneous injection.

Drug Profile

Brand NamesCopegus + Pegasys, Pegasys + Copegus, Pegasys/Copegus
CompanyRoche
Drug ClassSmall Molecule
Molecular TargetIFNAR2
RouteInjectable (Others), Oral (PO), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Roche

Mechanism of Action

Molecular Targets

ribavirin + PEG-IFNalpha-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

ribavirin + PEG-IFNalpha-2a is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis C✓ Approved

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PubMedToxicology in vitro : an international journal published in association with BIBRA2026-05-24

Cellular responses to morpholinated curcumin derivatives in human muscle-invasive bladder cancer cells.

Kobylka Paulina P, Murias Marek M, Bakun Pawel P, Goslinski Tomasz T et al.

Curcumin is a well-known compound with anticancer properties, as demonstrated in preclinical studies. However, its clinical potential is limited by several drawbacks. Medicinal chemistry, therefore, offers the opportunity to develop curcumin derivatives through structural modifications. This study showed cytotoxic activity of curcumin derivatives in muscle-invasive bladder cancer cells (HT-1376). Cytotoxicity was assessed under normoxic and hypoxic conditions and compared with effects on human primary bladder epithelial cells (BdEC). The most promising compounds (2a and 2a-B) were further investigated in a 3D cell culture model. Mechanistic studies included the evaluation of lactate dehydrogenase release, cell cycle distribution, and induction of apoptosis and necrosis using luminescent-, colorimetric-, and fluorescence-based assays. Furthermore, the intracellular uptake was investigated using flow cytometry and confocal microscopy. Tested compounds showed greater cytotoxicity than curcumin, with enhanced effects under hypoxic conditions. The derivatives containing a keto-enol moiety showed greater selectivity for bladder cancer cells than curcumin. Compounds 2a and 2a-B also showed greater cytotoxicity in the 3D cell culture model than curcumin. Compounds 2a and 2a-B altered cell cycle progression, increasing the population of cells in the G2/M and S phases, and induced apoptosis in a time- and concentration-dependent manner. Comparative analysis with previously reported data identifies compound 2a as a promising candidate for further investigation due to its high selectivity for malignant versus normal bladder epithelial cells.

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A pH-responsive silver nanoparticle platform overcomes MEK inhibitor resistance in neurofibroma via triacsin C-mediated lipid metabolic reprogramming.

Xu Jiang J, Liu Longyan L, Liu Shuheng S, He Zesong Z et al.

To overcome resistance to MEK inhibitors such as selumetinib in neurofibroma, we developed a metabolism-targeted nanotherapeutic based on a pH-responsive silver nanoparticle platform (AgNP-PEG-TC) for delivering Triacsin C (TC), an inhibitor of long-chain acyl-CoA synthetases, to disrupt tumor-associated lipid metabolism. AgNP-PEG-TC was synthesized and characterized for its physicochemical properties, drug-loading efficiency, and pH-responsive release behavior. Its antitumor effects were assessed in human neurofibroma cells, including selumetinib-resistant cells, and in normal Schwann cells by examining proliferation, apoptosis, migration, and invasion. In vivo therapeutic efficacy and biosafety were evaluated in neurofibroma xenograft models. Bulk RNA sequencing, lipidomics, and protein analyses were performed to investigate the underlying mechanisms. AgNP-PEG-TC demonstrated stable colloidal properties and successful pH-sensitive release. It selectively reduced neurofibroma cell growth, migration, and invasion while promoting apoptosis, with minimal effects on normal cells. In xenograft models, AgNP-PEG-TC significantly inhibited tumor growth and showed good biocompatibility. Multi-omics analyses indicated that its antitumor activity was associated with ACSL4 downregulation, remodeling of arachidonic-acid-enriched phospholipids, enhanced lipid peroxidation, and increased lipid-droplet accumulation, suggesting heightened ferroptosis susceptibility. Notably, AgNP-PEG-TC synergized with MEK inhibitors and restored antitumor responses in resistant neurofibroma cells. These findings establish a metabolism-nanotechnology synergy in which AgNP-PEG-TC-mediated ACSL4 inhibition and lipid metabolic reprogramming resensitize MEK inhibitor-resistant neurofibromas to therapy. The platform functions as both a targeted drug carrier and a modulator of tumor lipid homeostasis, offering a promising combinatorial strategy.

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IgA nephropathy is the most common primary glomerulonephritis worldwide, characterized by IgA deposition and a high risk of progression to kidney failure. While emerging therapies target IgA production or downstream inflammation, strategies to directly clear established IgA deposits from the kidney remain underexplored. Here, we evaluate a novel therapeutic IgA protease for its ability to clear glomerular IgA deposits and restore normal histology. The recombinant IgA protease was derived from Thomasclavelia ramosa (strain AK183), a human commensal bacterium presumed to have evolved for mutual tolerance within the microbiome with the host. The enzyme was PEGylated to reduce immunogenicity and prolong its half-life, producing the drug product PEG-AK183. We characterized its ex vivo potency and pharmacokinetic-pharmacodynamic profile in mice, then assessed therapeutic efficacy over eight weeks. In vitro, a single molecule of PEG-AK183 cleaved between 500 and 1000 hIgA1 molecules in 60 minutes, demonstrating high catalytic efficiency. A single injection into human IgA1 (hIgA1) transgenic mice induced complete clearance of serum hIgA1 for up to eight days. Following eight-week weekly treatments, PEG-AK183 reduced circulating IgA and immune complex levels by approximately 80% and completely cleared glomerular IgA and associated complement C3 deposits. This was accompanied by a 45.5% reduction in proteinuria and significant improvements in histopathological indices, including mesangial proliferation and endocapillary hypercellularity. No treatment-related adverse effects were observed, including abnormalities in intestinal plasma B cells, hepatotoxicity, or the anti-drug antibody development, supporting a favorable safety profile for long-term, repeated administration. Our preclinical study demonstrated that the engineered IgA degrader PEGAK183 is a potent, effective, and safe therapeutic in a humanized IgA nephropathy mouse model. By achieving sustained clearance of pathogenic IgA from both circulation and glomerular deposits, this IgA-protease-based therapy represents a promising candidate for the future treatment of IgA nephropathy.

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Efficacy and Safety of Pegylated Interferon as Rescue Therapy for Patients with Chronic Hepatitis B Who Failed to Achieve Functional Cure After Antisense Oligonucleotides or Small Interfering RNA: A Prospective, Multicentre, Open-Label Randomized Controlled Trial (SPHERE) Protocol.

Zhang Qiran Q, Sun Feng F, Sui Shulan S, Lin Jianmei J et al.

Although novel targeted therapies such as antisense oligonucleotides (ASO) or small interfering RNA (siRNA) can rapidly reduce hepatitis B surface antigen (HBsAg), only a subset of patients can achieve HBsAg seroclearance, and recurrence is common after discontinuation. This trial aims to evaluate the efficacy and safety of sequencing pegylated interferon alpha (Peg-IFNα) as rescue therapy for patients who have not achieved functional cure after initial therapy with ASO or siRNA. This is a prospective, multicentre, open-label, non-inferiority randomized controlled trial. Patients with chronic hepatitis B (CHB) who have previously completed a full course of ASO or siRNA therapy with HBsAg level of 1-500 IU/mL at screening will be enrolled. Participants will be randomized 1:1 to two arms: those in arm A (immediate treatment arm) will receive 24 weeks of Peg-IFNα starting at enrolment, followed by 24 weeks off-treatment observation; participants in arm B (delayed treatment arm) will firstly be observed for 24 weeks then followed by 24 weeks of Peg-IFNα treatment. At week 48, those with HBsAg seroclearance will enter a 48-week treatment-free follow-up, while those without seroclearance, regardless of initial arm, will receive an additional 24 weeks of Peg-IFNα, followed by 24 weeks off-treatment observation after week 72. The primary endpoint is the proportion of participants achieving HBV DNA < 20 IU/mL, HBsAg < 0.05 IU/mL and normal ALT at week 72. Secondary endpoints are HBsAg clearance rates, changes in clinical indicators, and safety evaluation results at other time points including weeks 24, 48 and 96. Sample size was calculated using Bayesian methods with the following parameters: experimental group response rate 0.57, control group response rate 0.47, non-inferiority margin 0.1, power 0.8, α = 0.05 and required posterior probability ≥ 80%. The single-group sample size was 33, and considering a 10% dropout rate, the total sample size was set to 72 (36 per group). Statistical analysis will be based on Bayesian non-inferiority test, with the primary judgment criterion being a posterior probability of ≥ 80% that the experimental group is non-inferior to the control group. Successful completion of this trial will provide a viable rescue treatment option for patients who have not met treatment goals after ASO or siRNA therapy. It may complete the future therapeutic framework, bringing more patients, especially those who are difficult-to-treat, within the scope of functional cure. ClinicalTrials.gov identifier NCT06923280.

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PubMedBiomaterials2026-05-24

Janus TiO2-CoOX heterojunction enabling sonodynamic driving multi-pathway cell death for enhanced immune activation.

Cheng Ziyi Z, Ning Mingliang M, Zhu Yutong Y, Tian Ruizhi R et al.

Tumor heterogeneity induces resistance of programmed cell death (PCD), together with a highly immunosuppressive tumor microenvironment (TME), collectively constraining the efficacy of cancer therapies. Herein, a Janus TiO2-CoOX@PEG nanoplatform featuring a Z-scheme heterojunction was developed as a novel sonosensitizer, enabling efficient ultrasound-induced charge separation to boost sonodynamic therapy (SDT) activity. Moreover, the obtained TiO2-CoOX@PEG was endowed with multienzyme activity, including glutathione (GSH) oxidase- and catalase-like activities, which could regulate TME (e.g., relieve hypoxia), amplify oxidative stress, and collaboratively break intracellular redox homeostasis, thereby dismantling tumor defense barriers. More interestingly, upon ultrasound (US) irradiation, SDT together with chemodynamic therapy (CDT) was found to concurrently activate three programmed cell death pathways, i.e., apoptosis, ferroptosis, and pyroptosis to overcome tumor treatment resistance. This multiple death-pathway efficiently induced immunogenic cell death (ICD), promoting the release of damage-associated molecular patterns (DAMPs) and inflammatory cytokines. As a result, the in vivo tumor growth was significantly suppressed and the immunosuppressive TME was remodeled, as characterized by tumor-associated macrophages (TAMs) polarizing towards the M1 phenotype, maturation of dendritic cells (DCs), infiltration of abundant cytotoxic T lymphocytes (CTLs), and depletion of regulatory T cells (Tregs), which ultimately impeded the formation of distant lung metastases. Collectively, this work presents a sonodynamic-immunotherapeutic synergistic strategy based on Janus heterojunction nanoparticles to induce multi-pathway cell death and immune activation, offering a promising solution to overcome treatment resistance and achieve sustained systemic antitumor immunity.

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Genetic and phenotypic characterization of seedling drought tolerance in wheat with integrated analysis of trait variation and QTL mapping.

Zebarjad Aylin A, Sabouri Hossein H, Pezeshkian Zahra Z, Taliei Fakhtak F et al.

Wheat (Triticum aestivum L.) is a staple cereal crop highly vulnerable to drought stress, particularly during early seedling establishment, which limits productivity and yield stability. This study evaluated a recombinant inbred line population under well-watered and drought environments to dissect the morphological, physiological, and genetic bases of seedling drought tolerance. Drought stress severely reduced shoot and leaf biomass, while paradoxically enhancing root growth, suggesting adaptive resource reallocation to improve water foraging. Genetic variance analyses uncovered increased heritable variation for root traits under stress, alongside significant genotype-by-environment interactions, indicative of distinct adaptive responses. Multivariate analyses revealed an integrated stress-response network linking stay-gFreen phenotypes and biomass maintenance. Importantly, QTL mapping identified twelve drought-specific loci most notably on chromosomes 2A, 3B, 5A, and 6A as well as eight loci unique to non-stress conditions, underscoring environment-dependent genetic architectures. Major QTLs affecting seedling length, root length, and leaf senescence offer promising targets for marker-assisted breeding. Collectively, these results illuminate the complex, multigenic control of early-stage drought tolerance in wheat, providing a robust foundation for developing cultivars with improved resilience in water-limited environments and strengthening climate-smart breeding pipelines.

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