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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

PubMedNature medicine2026-09-10

Myeloperoxidase inhibition with mitiperstat in heart failure with preserved or mildly reduced ejection fraction: a randomized phase 2b trial.

Lund Lars H LH, Lam Carolyn S P CSP, Pizzato Patricia Ely PE, Michaëlsson Erik E et al.

Myeloperoxidase (MPO)-derived oxidants reduce nitric oxide bioavailability and promote coronary microvascular dysfunction, cardiomyocyte stiffening and interstitial fibrosis-mechanisms implicated in the pathogenesis of heart failure with preserved and mildly reduced ejection fraction. Here, in a multicenter, randomized, double-blind, placebo-controlled, three-arm, parallel-group phase 2b trial of patients with heart failure and an ejection fraction of >40%, we evaluated whether treatment with the MPO inhibitor mitiperstat versus placebo for 48 weeks improved symptoms and exercise function at 16 weeks (the co-primary endpoints were the Kansas City Cardiomyopathy Questionnaire Total Symptom Score (KCCQ-TSS) and 6-minute walk distance (6MWD)). Secondary endpoints included changes in natriuretic peptides and inflammatory markers (up to 48 weeks) and echocardiographic parameters (up to 24 weeks). In total, 711 patients (45% women) were randomized 1:1:1 to mitiperstat 2.5 mg, mitiperstat 5 mg or placebo. Mitiperstat (pooled doses) did not improve KCCQ-TSS (placebo-corrected difference in mean change from baseline, -1.4 points (95% confidence interval (CI) -3.9, 1.2; P = 0.29), 6MWD (3.8 m (95% CI -3.1, 10.8)); P = 0.28) or any secondary endpoint. Adverse and serious adverse events, including infections, were similar among groups except for maculopapular rash (mitiperstat, 3.6%; placebo, 0.4%). These results indicate that mitiperstat was safe and well tolerated but did not improve symptoms or exercise function in chronic heart failure with preserved or mildly reduced ejection fraction. ClinicalTrials.gov registration: NCT04986202 .

PMID 42717033
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PubMedAllergy2026-09-10

Rademikibart for Asthma With Type 2 Biomarkers: Exploratory Subgroup Analyses From a Phase 2b Randomized Clinical Trial.

Wechsler Michael E ME, Akuthota Praveen P, Quart Barry B, Collazo Raúl R

Rademikibart, an IL-4Rα-targeting antibody, demonstrated efficacy in a Phase 2b trial of adults with moderate-to-severe uncontrolled asthma (NCT04773678). We report exploratory and predominantly post hoc subgroup analyses, according to baseline eosinophil count (EOS) and fractional exhaled nitric oxide (FeNO). Patients were randomized, double-blind, to rademikibart 150 mg or 300 mg Q2W (600-mg loading) or placebo, with medium-to-high dose inhaled corticosteroids and ≥ 1 reliever/controller. Up to eight EOS/FeNO subgroups were investigated, focusing on the following five: ≥ 300 cells/μL and ≥ 25 ppb (N = 80); ≥ 25 ppb (N = 142); ≥ 300 cells/μL (N = 129); ≥ 150 cells/μL (N = 247); 150- < 300 cells/μL (N = 118). Prebronchodilator FEV1 increased significantly at first assessment (Week 1) and was sustained throughout the 24-week treatment period. FEV1 and asthma control (ACQ-6) improvements were greatest when baseline EOS and FeNO were both elevated. At Week 1, after a 600-mg loading dose, placebo-adjusted FEV1 increased by 422 mL (≥ 300 cells/μL and ≥ 25 ppb), 339 mL (≥ 25 ppb), 324 mL (≥ 300 cells/μL), 227 mL (≥ 150 cells/μL), and 141 mL (150- < 300 cells/μL). At Week 24, with 300 mg Q2W, placebo-adjusted FEV1 increased by 519 mL (≥ 300 cells/μL and ≥ 25 ppb), 401 mL (≥ 25 ppb), 394 mL (≥ 300 cells/μL), 287 mL (≥ 150 cells/μL), and 159 mL (150- < 300 cells/μL). Exacerbations decreased by ≥ 63% per subgroup. Rademikibart was well tolerated. No eosinophilia (Preferred Term) was reported. Grade 1 eosinophil count increased did not lead to treatment discontinuation (n = 2). Rapid and sustained improvements were more pronounced in patients with type 2-high biomarkers than previously reported in the overall study population.

PMID 42717393
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PubMedBJS open2026-09-10

The iBRA-NET localization study: international IDEAL 2a/2b multicentre cohort study comparing the safety and effectiveness of wire- and radar-guided localization for impalpable breast lesions.

Dave Rajiv V RV, Morgan Jenna J, Lowes Simon S, Milligan Robert R et al.

Wire-guided localizations have been the historical standard for breast lesion localization; however, they have logistical constraints and can dislodge in the preoperative period. Radar-guided localization has the potential to uncouple localization from the day of surgery, but the technique needs to be evaluated in a direct comparison with wire-guided localization to ensure efficacy and safety. The iBRA-NET localization study is a prospective platform IDEAL 2a/2b study comparing wire-guided localization with new generation localization devices. This arm describes SCOUT® radar localization for impalpable breast lesions performed between June 2021 and December 2024, compared with a historical cohort of wire-guided localization performed between August 2018 and August 2020. Primary outcome was identification of the index lesion in the excision specimen. Secondary endpoints included safety (complications), margin re-excision, magnetic resonance imaging bloom size, and specimen weight. Data were accrued from 1297 radar localized patients in 27 units. Index lesion identification was 95.2% in radar-guided excisions versus 99.1% in wire-guided excisions (P = 0.001). In a sensitivity analysis excluding patients receiving neoadjuvant chemotherapy, identification rates were 98.9% versus 99.6% (P = 0.114). For a subset of patients having a simple lumpectomy for a unifocal, unilateral breast lesion with no neoadjuvant treatment (1627), positive margins were seen in the main excision specimen in 1003 (15.0%) wire-guided versus 624 (9.0%) radar-guided excisions (P < 0.001). Re-excision was required in 131 (13.2%) wire-guided versus 91 (14.7%) radar-guided excisions (P = 0.442). There was a significant difference in specimen weight/size2 (0.138 g/mm2 wire-guided localization versus 0.182 g/mm2 radar; P < 0.001). The median start time for surgery was earlier in the day for radar-guided localizations compared with wire-guided (12:27 versus 13:40; P < 0.001). All radar placements in axillary nodes (13) led to successful nodal retrieval. SCOUT® radar localizations are a safe and effective localization technique in both the breast and axilla, with outcomes comparable to wires. There were demonstrable logistical advantages in operative start time when using a radar reflector.

PMID 42720093
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PubMedNature communications2026-09-10

Structure and mechanism of human sphingosine-1-phosphate transporter MFSD2B.

Ahmed Shahbaz S, Huang Min M, Dai Yaxin Y, Yang Xuebo X et al.

Sphingosine-1-phosphate (S1P) is an essential signaling lipid that maintains vascular integrity and regulates immune cell trafficking. The major facilitator superfamily domain-containing protein 2B (MFSD2B) serves as the main S1P exporter in red blood cells and platelets; however, its structure and transport mechanism are unclear. Here, we report the 3.0 Å cryo-EM structure of human MFSD2B bound to S1P. S1P is captured in a distinctive binding state, deeply buried within the C-domain, with its sphingoid tail accommodated by a hydrophobic pocket and its phosphate group coordinated by a cluster of polar residues within the transporter's cavity. Mutagenesis and molecular dynamics simulations identify the TM2/TM11 lateral opening as the primary pathway for S1P translocation, with key charged residues acting as sequential anchors during transport. Furthermore, we demonstrate that MFSD2B functions as a uniporter, and that subtle rewiring of local charge networks can alter its coupling mechanism. Our work provides a molecular framework for understanding S1P transport mediated by MFSD2B in hematopoietic cells.

PMID 42717192
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PubMedChemistry & biodiversity2026-09-10

Clean Synthesis of N-4-Alkylamino-7-chloroquinoline Cyclic Imides: Influence of Lipophilicity on Antibacterial and Ecotoxicological Properties.

Luz-Filho Agenor P AP, Silva Thais C TC, Silva Matheus B MB, Sousa Abraão P AP et al.

Motivated by the promising antimicrobial and ecotoxicological effects of 4-alkylamino-7-chloroquinoline and N-alkylphthalimide derivatives, these privileged nuclei were linked to investigate how lipophilicity influences antibacterial activity and ecotoxicity. For this purpose, seven 4-alkylamino-7-chloroquinolines (2a-g) were prepared, of which four were used as precursors (2a-d) and reacted with different anhydrides. Using a clean synthetic approach, 4-alkylamino-7-chloroquinoline-succinimides (3a-d) and -phthalimides (5a-d) were obtained in yields of 60%-99% after only filtration with distilled water. In vitro assays were performed to determine the minimum inhibitory/bactericidal concentration (MIC/MBC) against Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus, and Streptococcus mutans. Lipophilicity (log P) and toxicity were predicted using the pkCSM program. In vitro toxicity tests on Artemia salina larvae were used as an indicator of ecotoxicity. 4-Alkylamino-7-chloroquinolines (2b, 2f, 2g) revealed a moderate MIC of 156.25 µg·mL-1 against Gram-(-) and Gram-(+) bacteria, whose predicted toxicity does not pose a potential risk to human health. Results indicate a correlation between increased lipophilicity and higher ecotoxicity, where less lipophilic compounds were less toxic to A. salina (LC50 133.01-777.50 µg·mL-1) than 4-alkylamino-7-chloroquinoline-phthalimides, suggesting further investigation of their cytotoxicity.

PMID 42720095
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PubMedACS applied bio materials2026-09-10

Aptamer-Functionalized DNA Frameworks as Targeted Drug Buffers for Concentration Regulation of Maytansine.

Jiang Dan D, Li Jiaojiao J, Xiao Ying Y, Xiong Qian Q et al.

Traditional chemotherapy often suffers from nonspecific distribution and poor drug concentration control, leading to compromised therapeutic efficacy and adverse effects. Mertansine (DM1), a potent cytotoxic agent with poor selectivity, dose-limiting toxicity, and a narrow therapeutic window, demands targeted delivery and precise concentration regulation for safety and efficacy. Herein, we constructed two Janus DNA triangular prism-based molecular buffers (3A-JTP-3S2 and A-MTP-3S2) for targeted DM1 delivery and concentration regulation. Both of the buffers integrate nucleolin-targeting aptamer (Apt-AS1411) for cancer cell recognition and DM1-specific aptamer (Apt-Seq2-X) for regulating DM1 concentration within a desired therapeutic range. When we evaluated their endocytic behaviors, 3A-JTP-3S2 was prone to lysosomal degradation via clathrin-mediated endocytosis. In contrast, A-MTP-3S2, a higher-order multivalent assembly built from 3A-JTP-3S2 units, forms an endocytosis-resistant DNA network that anchors onto cell membranes due to its enlarged size. We thus prioritized the latter for subsequent studies. A-MTP-3S2 delivered DM1 with favorable tumor-targeting ability across a total DM1 concentration (CDM1) range of 50-1000 nM, significantly killing A549 cancer cells (viability: 55.7 ± 8.15% - 50.84 ± 2.27%) while showing less impact on BEAS-2B normal cells (viability: 91.21 ± 2.72% - 76.31 ± 5.97%). Notably, even as CDM1 varied from 50 to 1000 nM, A-MTP-3S2 still maintained free DM1 at a relatively constant level (1-55 nM), confirming its great buffering capacity. Our work offers a facile strategy for simultaneous targeted delivery and precise concentration regulation of low-specific and high-toxic drugs.

PMID 42717662
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