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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

Related Research Articles

PubMedCureus2026-08-30

Treatment of Persistent Gastrocutaneous Fistula After Percutaneous Endoscopic Gastrostomy Using Endoscopic Suturing With Argon Plasma Coagulation: A Report of Two Cases.

Washington Miles J MJ, Washington Morris J MJ, Biswas Saptarshi S

Persistent gastrocutaneous fistula (PGCF) is an uncommon but often challenging complication following removal of a percutaneous endoscopic gastrostomy (PEG) tube. Prolonged PEG tube requirement leads to epithelialization of the PEG tube tract, resulting in a PGCF when the tube is removed. Several management options have been described for this complication, many of which demonstrate variable success rates. However, no definitive treatment for PGCF has been established. We report two adult male patients, aged 63 and 30 years, who developed PGCF after PEG tube removal following prolonged PEG placement. The first patient had persistent low-volume drainage for approximately one year after removal of the PEG tube, despite an attempt at external purse-string suture closure with simultaneous endoscopic clip placement. The second patient developed persistent high-volume drainage with peristomal skin breakdown despite local wound care and ostomy appliance placement for 3 months after removal of the PEG tube. Both patients underwent argon plasma coagulation of the fistula tract followed by endoscopic suture closure using the Boston Scientific OverStitch device (Boston Scientific Corporation, Marlborough, USA). In both cases, fistula drainage resolved within one week, with no documented recurrence during available follow-up. These cases are reported to highlight the technical feasibility of combined argon plasma coagulation and endoscopic suturing for selected chronic post-PEG PGCFs and to add to the limited published experience with this approach.

PMID 42668957
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PubMedMaterials today. Bio2026-08-30

Intranasal L-DOPA/TPP-engineered extracellular vesicles deliver icariin to ameliorate mitochondrial dysfunction with associated sphingolipid remodeling in Alzheimer's disease models.

Wu Beibei B, Wu Junyong J, Zhu Lemei L, Li An A et al.

Alzheimer's disease (AD) is associated with mitochondrial dysfunction, oxidative stress, and disrupted lipid homeostasis, but the therapeutic translation of mitochondrial-protective agents remains limited by inefficient brain delivery, insufficient neuronal selectivity, and poor subcellular precision. Here, we developed an intranasal extracellular vesicle formulation (L-DOPA/TPP-EV-ICA) by loading icariin (ICA) into mesenchymal stem cell-derived extracellular vesicles and post-inserting DSPE-PEG-Levodopa and TPP-PEG-PE to enhance nasal environment, neuronal association, and mitochondria-associated intracellular enrichment. The engineered vesicles retained EV-like morphology, showed measurable ICA encapsulation, and maintained colloidal stability under the tested storage and simulated nasal conditions. In a human nasal epithelial Transwell model, L-DOPA/TPP-EV-ICA showed greater neuronal uptake than unmodified EVs without detectable disruption of epithelial barrier integrity and exhibited preferential colocalization with mitochondria-associated structures after cellular internalization. In Aβ-injured neuronal cells, L-DOPA/TPP-EV-ICA treatment reduced mitochondrial oxidative stress and mPTP opening, improved membrane potential, and enhanced ATP production and redox-related parameters. Following intranasal administration, the engineered formulation generated stronger and more persistent brain-associated fluorescence and showed preferential association with NeuN-positive cells. In APP/PS1 mice, treatment improved cognitive performance, and attenuated histopathological and mitochondrial abnormalities. Integrated proteomic, metabolomic analyses, and protein-level analyses further identified treatment-associated alterations in sphingolipid-related pathways. These findings support L-DOPA/TPP-EV-ICA as a promising preclinical intranasal EV platform for improving mitochondrial function and modulating sphingolipid-associated alterations in AD-related models.

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PubMediScience2026-08-30

BOLD-100 treatment induces systemic lipid crosstalk in metastatic colorectal carcinoma patients in a combination treatment with FOLFOX.

Borutzki Yasmin Y, Hagn Gerhard G, Bileck Andrea A, Mohr Thomas T et al.

BOLD-100 (sodium trans-[tetrachlorobis(1H-indazole)ruthenate(III)]) is a clinical-stage anticancer drug candidate that targets glucose-regulated protein (GRP78) and impacts the endoplasmic reticulum (ER) stress responses in cancer cells. Despite expanding knowledge about its multimodal mechanism of action from preclinical studies, little is known about the metabolic effects of BOLD-100 in patients. This study is an exploratory analysis of the blood plasma from a subset of metastatic colorectal carcinoma (mCRC) patients who were participants in a phase 1b/2a dose-escalation study (NCT04421820) using a multi-omics strategy based on proteomic and lipid analyses. BOLD-100 treatment was found to exhibit systemic, dose-dependent effects that were more pronounced on the lipid level compared with the protein level. This study indicates that BOLD-100 affects lipid profiles and influences systemic lipid crosstalk, which, in combination with oxaliplatin, leucovorin, and fluorouracil (FOLFOX) chemotherapy may, at least partially, account for the superior clinical outcomes over established therapies in mCRC patients.

PMID 42668574
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PubMedPharmacogenetics and genomics2026-08-30

Prevalence and clinical impact of the uncommon DPYD c.257C>T (Pro86Leu) variant in a multiethnic cohort receiving fluoropyrimidine therapy.

Carp Marie-Jeanne MJ, Ring Gil G, Waldhorn Ithai I, Shempliner Alexandra A et al.

Pre-emptive genotyping and genotype-guided dose adjustments are generally recommended for seven hypofunctional polymorphisms in the DPYD gene that are associated with fluoropyrimidine toxicity. However, targeted genotyping may miss uncommon and population-specific hypofunctional variants. Therefore, in 2021, we replaced conventional targeted genotyping with comprehensive DPYD exome sequencing. The objective of the current study was to identify uncommon hypofunctional variants and assess their association with fluoropyrimidine toxicity. In a cohort of 762 consecutive patients pre-emptively genotyped between 2021 and 2025, among the seven established risk variants, we identified *2A and HapB3 at their expected minor allele frequencies (MAF), but no carriers of any of the five other established risk variants. Interestingly, four patients were heterozygous for the rare missense c.257C>T variant (Pro86Leu; rs568132506), previously associated with fluoropyrimidine toxicity. The MAF (2.62 × 10-3) was similar to that previously described in Middle Eastern populations but 26-fold higher than in the gnomAD global population. Three of the carriers (75%) developed grade 3-4 fluoropyrimidine toxicity after one or two cycles, corresponding to a relative risk of 14.5 (95% confidence interval: 5.0-30.4, P = 0.0009) compared with a control cohort without hypofunctional DPYD variants. Our findings add to the growing body of evidence indicating that DPYD c.257C>T may be associated with severe fluoropyrimidine toxicity. Future studies should examine the clinical utility of including uncommon but potentially actionable variants, such as c.257C>T, into pre-emptive genotyping algorithms. This may be particularly important in multiethnic populations in which these variants can be more prevalent than those variants for which pre-emptive genotyping is generally recommended.

PMID 42669144
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PubMedPediatric research2026-08-30

Serum and urinary D-lactate in pediatric intestinal failure: clinical associations and reference values.

Halašová Rita R, Ibrahim Rana R, Balogová Stanislava S, Štichhauer Radek R et al.

D-lactate, produced by intestinal microbiota or derived from the methylglyoxal pathway and diet, is converted by D-lactate dehydrogenase (LDHD) to pyruvate, with several known pathogenic variants of the gene. This study compared serum and urinary D-lactate concentrations across five patient groups and established reference values in healthy children. In this cross-sectional study, 341 serum and urine samples from 129 pediatric patients were analyzed. The cohort comprised patients receiving home parenteral nutrition (PN, n = 19), after bowel adaptation (ADAPT, n = 28), with gastrostomy feeding (PEG, n = 13), other gastrointestinal disorders (GI, n = 14), and healthy controls (HC, n = 55). D-lactate was measured via enzymatic spectrophotometric assay. A genetic sub-analysis assessed pathogenic LDHD variants. Median serum and urinary D-lactate concentrations in healthy controls were 28.5 μmol/L (IQR 25-34.25) and 400 μmol/L (IQR 193-722), respectively. Both serum (p < 0.001) and urine (p = 0.011) D-lactate concentrations were higher in the ADAPT group compared to healthy controls. No pathogenic LDHD variants were identified. Children after bowel adaptation have higher serum and urine D-lactate concentrations compared to healthy controls. Reference values for serum and urinary D-lactate were defined. This is the first study to provide reference values for serum and urinary D-lactate concentrations in healthy children (serum: 28.5 µmol/L (IQR: 25-34.25 µmol/L); urine: 400 µmol/L (IQR: 193-722 µmol/L)). Children after bowel adaptation exhibited higher D-lactate concentrations in both serum and urine compared to healthy controls. Higher serum and urinary D-lactate levels were associated with the presence of an intestinal anastomosis.

PMID 42668282
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PubMedACS central science2026-08-29

A Tumor-Microenvironment-Responsive Chemically Masked IL‑2 Prodrug Potentiates PD‑1 Checkpoint Blockade and Elicits Robust Antitumor Efficacy.

Tan Linzhi L, Yang Yunwen Y, Zhao Kerui K, Zhou Jingjing J et al.

Interleukin-2 (IL-2) is a potent mediator of T-cell activation with significant potential for cancer immunotherapy, yet its clinical utility is severely constrained by its narrow therapeutic window. Here we report a chemically masked IL-2 prodrug (Cm-proIL2) that enables tumor-microenvironment-responsive cytokine activation through tumor-associated protease cleavage. Site-specific conjugation of a poly-(ethylene glycol) (PEG) moiety selectively masks peripheral receptor engagement, while PEG removal within the tumor microenvironment restores IL-2 receptor binding and reduces molecular size, thereby enhancing intratumoral lymphocyte penetration and effector T cell functionality. Building on this modular platform, we further engineered a PD-1-targeted nanobody fusion, PD1-Cm-proIL2, to enable the cis delivery of IL-2 activity to PD-1+ tumor-infiltrating T cells. PD1-Cm-proIL2 induces robust antitumor immunity, resulting in complete tumor regression and durable protection upon tumor rechallenge in a murine colorectal cancer model. Together, these findings demonstrate the feasibility of chemically masked, tumor-responsive cytokine activation as a strategy for improving the therapeutic index of IL-2-based immunotherapies.

PMID 42666916
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