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peginterferon alfa-2b (Pegstat)

✓ Approved

Nanogen Biopharmaceutical · IFNAR2 · 重组蛋白

什么是 peginterferon alfa-2b？

peginterferon alfa-2b 是一种重组蛋白，由Nanogen Biopharmaceutical研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Pegstat
公司Nanogen Biopharmaceutical
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Nanogen Biopharmaceutical

作用机制

分子靶点

peginterferon alfa-2b 作用于 1 个分子靶点：

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

peginterferon alfa-2b 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Hepatobiliary disordersHepatic cirrhosis✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved

相关研究文献

PubMedHepatology (Baltimore, Md.)2026-10-26

A phase 2b/3 trial of saroglitazar in primary biliary cholangitis.

Vuppalanchi Raj R, Villamil Alejandra A, Yilmaz Yusuf Y, Idilman Ramazan R et al.

Saroglitazar, a dual PPAR alpha/gamma agonist, improved serum alkaline phosphatase (ALP) levels in patients with primary biliary cholangitis (PBC) in a phase 2a clinical trial. EPICS-III is a phase 2b/3 adaptive, double-blind, randomized controlled trial in patients with PBC who had an inadequate response to or were intolerant of ursodeoxycholic acid (UDCA). In phase 2b, 37 participants received placebo or saroglitazar magnesium 1 or 2 mg for 16 weeks. Saroglitazar magnesium 1 mg (0.97 mg of saroglitazar) was selected for phase 3, which randomized 148 patients to saroglitazar (n=97) or placebo (n=51) for 52 weeks. The primary endpoint was biochemical response at week 52, defined as ALP <1.67 x ULN with ≥15% reduction from baseline and total bilirubin below ULN; the key secondary endpoint was ALP normalization. Baseline characteristics in the phase 3 efficacy population were comparable except for higher baseline ALP and other liver biochemistries in the saroglitazar group. Biochemical response was achieved in 56.7% versus 9.8% with placebo (difference, 48.0%; 95% CI, 35.3 to 60.8; p<0.001). Among participants with baseline ALP ≤3xULN, biochemical response rates were 79.0% versus 14.3%, and 83.1% versus 14.7% in the per-protocol analysis. ALP normalization occurred in 8.2% with saroglitazar versus 0% with placebo (difference, 8.5%; 95% CI, 2.9 to 14; p=0.016). Among participants with baseline 5-D Itch score ≥12, the week-24 treatment difference was -3.2 points (95% CI, -5.66 to -0.82) but was not maintained at week 52. Adverse events occurred in 81.1% with saroglitazar versus 90.5% with placebo, and serious adverse events occurred in 6.3% and 11.1%, respectively. Saroglitazar 0.97 mg significantly improved biochemical response and ALP normalization and was well tolerated over 52 weeks.

PMID 42929426
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PubMedHepatology (Baltimore, Md.)2026-10-26

Phase 1b study of miricorilant in patients with presumed metabolic dysfunction-associated steatohepatitis (MASH).

Alkhouri Naim N, Rudraraju Madhavi M, Leibowitz Mark M, Jenders Robert A RA et al.

Miricorilant, an oral nonsteroidal selective glucocorticoid receptor modulator, is being investigated as a therapy that modulates hepatic cortisol activity in patients with metabolic dysfunction-associated steatohepatitis (MASH). This phase 1b study evaluated miricorilant's efficacy and safety. Seventy patients with presumed MASH received oral miricorilant daily (30-150 mg) or intermittent (100-200 mg once, twice, or thrice weekly) dosing regimens for 12 or 24 weeks. Across dosing regimens, reductions in relative liver fat content (LFC) ranged from 10.1% to 76.6%. Improvements in MASH liver function markers and the enhanced liver fibrosis (ELF) score were observed across regimens. Treatment-emergent adverse events (TEAE) leading to drug interruption/discontinuation occurred in 12.9% of patients (n=9) each; most were due to aminotransferase elevations during an excessively rapid drop in LFC (up to 70.2% at week 6) and in patients receiving daily dosing. Intermittent dosing enabled more patients to complete 12 weeks of treatment without discontinuation due to TEAEs. Intermittent dosing with miricorilant 100 mg twice weekly had the best benefit-risk profile; this cohort demonstrated a mean LFC reduction of 28.2% at week 12, with a corresponding decline in liver enzymes (ALT, -3.8 U/L; AST, -6.0 U/L). Patients in this cohort also had numerical improvement in lipid profiles, glycemic markers, and fibrosis biomarkers. Intermittent miricorilant dosing of 100 mg twice weekly achieved meaningful reductions in LFC and improved liver health markers with a favorable safety profile. This regimen is being evaluated in the phase 2b MONARCH study (NCT06108219).

PMID 42929711
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PubMedAddiction (Abingdon, England)2026-10-26

Polygenic prediction of cannabis-related outcomes: Evidence from the Avon Longitudinal Study of Parents and Children longitudinal cohort and the European gene-environment interaction case-control study.

Spinazzola Edoardo E, Austin-Zimmerman Isabelle I, Trotta Giulia G, Li Zhikun Z et al.

Polygenic risk scores (PRSs) for cannabis use disorder (CUD), major depressive disorder (MDD), insomnia and chronic pain, and early age at cannabis initiation might be linked to problematic cannabis use. We tested whether: (1) higher PRS for CUD, MDD, insomnia and chronic pain are associated with earlier initiation and problematic cannabis use; (2) age at cannabis initiation explains more variance in problematic use than any single PRS; and (3) PRSs moderate the association between early initiation and problematic cannabis use. Observational study involving two cohorts: (1) the Avon Longitudinal Study of Parents and Children (ALSPAC) population-based birth cohort and (2) for conceptual replication, the EUropean Gene-Environment Interaction (EU-GEI) first-episode psychosis case-control study. (1) United Kingdom; (2b) 16 population-based catchment areas in Europe and 1 in Brazil, with FEP cases recruited from mental health services and controls from the general population of the same catchment areas. For ALSPAC, n = 8224 genotyped (51% male); subsamples with Cannabis Abuse Screening Test (CAST) at 17 years (n = 895), 20y (n = 1587), 24y (n = 836) and frequency of use at 24y (n = 2908). EU-GEI: n = 776 [controls: mean age 37.2, standard deviation (SD) = 13.5; 47% male] and 491 FEP cases (mean age 31.5, SD = 11.2; 62.5% male). Outcomes were self-reported lifetime and frequency of cannabis use and CAST score (problematic use questionnaire). Predictors were PRSs for CUD, MDD, insomnia and chronic pain. Models were adjusted for sex, age and genetic principal components (ALSPAC), and additionally for site and case-control status (EU-GEI). In ALSPAC, CUD PRS was associated with CAST score at 20 [beta coefficient (β) = 0.04, False Discovery Rate-corrected P-value (pFDR) = 0.03] and CAST at 24 years (β = 0.11, pFDR = 0.005). MDD PRS was associated with CAST scores at 17y (β = 0.1, pFDR = 0.002), 20y (β = 0.06, pFDR = 0.01) and 24y (β = 0.09, pFDR = 0.01). Pain PRS was associated with the CAST scores at 17y (β = 0.09, pFDR = 0.002), 20y (β = 0.07, pFDR < 0.001) and 24y (β = 0.09, pFDR = 0.005). In EU-GEI, CUD PRS (RRR = 1.82, pFDR = 0.001) and pain PRS (RRR = 1.27, pFDR = 0.007) were associated with weekly-to-daily use. The Relative Excess Risk due to Interaction RERI model showed evidence of additive interaction for CUD PRS, RERI = 2.4, P = 0.009, while MDD and schizophrenia PRS showed no evidence of additive interaction. Genetic liability, measured by polygenic risk scores, to cannabis use disorder, major depressive disorder, and chronic pain appears to be associated with heavier and more problematic cannabis use. Age at cannabis initiation explains more variance in problematic cannabis use than polygenic liability.

PMID 42929306
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PubMedResearch and practice in thrombosis and haemostasis2026-10-25

A screening assay for type 2B von Willebrand factor variants using an enzyme-linked immunosorbent assay based on recombinant wild-type glycoprotein Ib and ristocetin.

Pagliari Maria Teresa MT, Baronciani Luciano L, Colpani Paola P, Cozzi Giovanna G et al.

Type 2B von Willebrand disease (VWD) is caused by gain-of-function variants in the A1 domain of von Willebrand factor (VWF), leading to increased platelet binding, loss of high-molecular-weight multimers, and sometimes thrombocytopenia. Conventional diagnosis relies on ristocetin-induced platelet agglutination or molecular testing. To evaluate an in-house enzyme-linked immunosorbent assay (ELISA) based on a recombinant glycoprotein Ib wild-type (rGPIb-WT) fragment and ristocetin, as a screening tool to identify first-time referral patients requiring further evaluation for possible type 2B VWD. Plasma from 131 healthy controls and 31 type 2B patients was analyzed using rGPIb-WT ELISA at ristocetin concentrations of 0.06, 0.09, and 0.12 mg/mL. Optical density ratios of plasma sample to normal pooled plasma were used to generate receiver operating characteristic curves and define screening cut-offs. Plasma from 254 first-time referrals was tested. Positive samples were evaluated for platelet-dependent VWF activity over VWF antigen ratio (VWF:GPIbR/VWF:Ag) and VWF multimers. Candidate patients underwent VWF exon 28 Sanger sequencing. Twenty-six of 254 patients tested positive at least at 1 ristocetin concentration. Sixteen were considered candidates for type 2B VWD evaluation based on a VWF:GPIbR/VWF:Ag ratio <0.7 and/or an abnormal multimeric pattern. Type 2B variants were found in 12 of 16 sequenced patients. The remaining 10 patients showed ultra-large multimers or an increased proportion of high-molecular-weight multimers; 8 of these had a normal VWF:GPIbR/VWF:Ag ratio (>0.7). The rGPIb-WT ELISA positivity may reflect type 2B variants or the presence of larger multimers. Integrated with conventional assays, positivity may guide type 2B-directed evaluation.

PMID 42927241
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PubMedBMJ neurology open2026-10-25

Efficacy and safety of cipaglucosidase alfa plus miglustat in Japanese adults with late-onset Pompe disease: a case series from clinical trials.

Kobayashi Hiroshi H, Narita Aya A, Kawamoto Michi M, Saeki Junjiro J et al.

The safety and efficacy of cipaglucosidase alfa plus miglustat (cipa+mig) versus alglucosidase alfa plus placebo (alg+pbo) in late-onset Pompe disease (LOPD) were established in the randomised, double-blind, 52-week PROPEL study (NCT03729362) conducted across 24 countries, including Japan. An open-label extension (OLE; NCT04138277) is evaluating long-term cipa+mig outcomes. In Japan, cipa+mig was also available before marketing authorisation in an expanded access study (ATB200-19). This case series summarises the efficacy and safety of cipa+mig in Japanese patients in PROPEL, PROPEL OLE and ATB200-19. Endpoints included 6-minute walk distance (6MWD), forced vital capacity (FVC), biomarkers and safety. Cipa+mig (20 mg/kg intravenous cipa and 130-260 mg oral mig (weight-based dosing)) and alg+pbo (20 mg/kg intravenous alg and oral pbo) were given biweekly. Patients randomised to alg+pbo in PROPEL received cipa+mig in the OLE. Safety was assessed at every visit, and biomarkers at weeks 2, 4, 6, 12, 26, 38, 52 and every 26 weeks thereafter. Six patients from PROPEL/OLE (cipa+mig, n=2; alg+pbo, n=4; all enrolled in the OLE) and four from ATB200-19 were included. Two patients discontinued treatment: one in the OLE (anaphylactic reaction) and one in ATB200-19 (withdrawal of consent). For evaluable patients (n=8), 6MWD remained stable or improved from baseline to weeks 52 and 104. In PROPEL/OLE, FVC varied with most patients improving with cipa+mig treatment; in ATB200-19, FVC remained stable to week 104. In PROPEL/OLE and ATB200-19, biomarker levels improved or stabilised by week 104, including in the PROPEL switch group, where levels worsened at week 52 but improved after switching to cipa+mig. Seven patients experienced treatment-related adverse events. No deaths occurred. Although the number of patients was small, the efficacy and safety of cipa+mig in Japanese patients from PROPEL/OLE and ATB200-19 were generally sustained and durable responses consistent with positive results in the overall PROPEL population.

PMID 42921145
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PubMedJournal of biochemical and molecular toxicology2026-10-25

Sinensetin Induces Oxidative Stress-Mediated Apoptosis in Non-Small Cell Lung Cancer Cells by Suppressing Nrf2/ARE-Dependent Antioxidant Defense.

Li Junyan J, He Ruoyun R, He Jiake J, Ye Jian J et al.

Non-small cell lung cancer (NSCLC) cells frequently depend on Nrf2/ARE-driven antioxidant programs to maintain redox balance and evade apoptosis. This study investigated whether sinensetin, a naturally occurring polymethoxylated flavone, reduces NSCLC cell survival by interfering with this cytoprotective pathway. A549 and H1299 NSCLC cells and normal BEAS-2B bronchial epithelial cells were exposed to sinensetin. Cell viability was measured by MTT assay, apoptosis was quantified by Annexin V-FITC/PI flow cytometry, and pathway- and apoptosis-related proteins were analyzed by western blotting. Nrf2 distribution was evaluated by nuclear/cytoplasmic fractionation, ARE-dependent transcription was assessed using a dual-luciferase reporter system, and Nrf2 was silenced by shRNA. Intracellular ROS was measured by DCFH-DA, antioxidant rescue was assessed with N-acetyl-l-cysteine (NAC), Nrf2/ARE-related proteins were examined in BEAS-2B cells, and Nrf2 overexpression was used as a rescue approach in A549 cells. Sinensetin inhibited NSCLC cell growth, increased apoptosis, reduced total and nuclear Nrf2, decreased ARE reporter activity, and downregulated HO-1 and NQO1. Sinensetin also increased intracellular ROS, whereas NAC partially reduced ROS accumulation, restored cell viability, and decreased apoptosis. BEAS-2B cells showed comparatively modest Nrf2/ARE pathway changes. Nrf2 overexpression partially restored HO-1 and NQO1, reduced apoptotic signaling, and attenuated sinensetin-induced loss of viability and apoptosis. These results support a model in which sinensetin promotes oxidative stress-mediated apoptosis in NSCLC cells, at least in part, through suppression of Nrf2/ARE-dependent antioxidant defense.

PMID 42927620
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