BIODRUGS生物药物
BIODRUGS(英文缩写 BIODRUGS),ISSN 1173-8804,eISSN 1179-190X,中文译名:生物药物 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.744 | Q1 |
| 2022 | 6.800 | Q1 |
| 2023 | 5.400 | Q1 |
| 2024 | 6.900 | Q1 |
| 2025 | 8.500 | Q1 |
BIODRUGS 最新收录文献
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1. From Reflection to Implementation: Tailored Clinical Development of a Pembrolizumab Biosimilar Candidate.
PMID:日期:2026-09-19Regulatory science increasingly recognizes that comparative efficacy studies may provide limited additional certainty to biosimilar development when high-resolution analytical, functional, and pharmacokinetic data robustly demonstrate similarity to the reference product. Modern structural and functional assays, combined with sensitive pharmacokinetic studies are capable of detecting differences with greater sensitivity than clinical efficacy endpoints. Accordingly, recent European Medicines Agency, US Food and Drug Administration, Medicines and Healthcare products Regulatory Agency, and Health Canada guidance suggest increasing alignment toward a "fit-for-purpose" pharmacokinetic-anchored clinical approach for biologics with well-characterizable structure and function. Pembrolizumab biosimilar development represents an early real‑world implementation of a streamlined clinical development approach. Its mechanism of action is well understood and driven by programmed cell death protein 1 (PD-1) receptor blockade with minimal reliance on fragment crystallizable-mediated effector functions, and its analytical traceability enables a detailed structure-function characterization. For this molecule, comparative pharmacokinetics provides a sensitive clinical measure of similarity that may be assessed in a multiple-dose pharmacokinetic equivalence study conducted in a sensitive patient population receiving adjuvant treatment following tumor resection. The comparative pharmacokinetic study design also provides a scientifically justified framework to assess safety and immunogenicity. In the development program of the pembrolizumab biosimilar candidate FYB206, scientific reasoning is used to illustrate how tailored pharmacokinetic-centered programs can maintain scientific rigor while reducing unnecessary clinical burden. More broadly, this approach may be considered applicable to other biologics with a well-defined mechanism of action, robust analytical accessibility, and sensitive functional assays, enabling scientifically proportionate and efficient biosimilar development. As FYB206 has not yet received regulatory approval; considerations presented herein reflect a forward‑looking scientific perspective based on the totality of available evidence.
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2. HLX11: A Pertuzumab Biosimilar.
2. HLX11：一种帕妥珠单抗生物类似药PMID:日期:2026-09-17HLX11 (pertuzumab-dpzb in the USA), marketed as POHERDY in the USA and EU and as HANBEIYOU in China, is a biosimilar of reference pertuzumab, an anti-human epidermal growth factor 2 (HER2) monoclonal antibody. It is approved for use in the same indications as reference pertuzumab: early or metastatic HER2-positive breast cancer. The physicochemical and functional properties of HLX11 are similar to reference pertuzumab, and pharmacokinetic equivalence has been shown in healthy individuals. HLX11 demonstrated equivalent clinical efficacy to EU-sourced reference pertuzumab in the neoadjuvant treatment of patients with HER2-positive, hormone-receptor negative, early stage or locally advanced breast cancer. The tolerability, safety and immunogenicity profiles of the two agents were also similar. No new safety or immunogenicity concerns were observed following a switch from neoadjuvant reference pertuzumab to adjuvant HLX11. The role of reference pertuzumab in the management of HER2-positive breast cancer is well established, and HLX11 provides an effective biosimilar alternative for patients requiring pertuzumab therapy.
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3. Plant-Based Systems for Producing Therapeutic Proteins: Current Status and Future Prospects.
PMID:日期:2026-09-17Protein-based therapeutics have transformed modern disease treatment and now constitute a rapidly expanding segment of the pharmaceutical market. In this context, plant-based expression systems have emerged as a versatile alternative to conventional mammalian cell platforms for the production of recombinant proteins. Beyond their well-established advantages in cost, scalability, and biosafety, recent advances in transient expression technologies and plant cell culture systems have enabled rapid, high-yield production of complex biologics with increasing control over product quality. In particular, deconstructed viral vectors and Agrobacterium-mediated transient expression in plants enable rapid recombinant protein production, supporting their potential for applications requiring flexible and accelerated manufacturing. Concurrently, progress in host glycoengineering has enabled the generation of humanized and functionally tailored glycoforms, including antibody glycovariants with enhanced Fc-mediated effector functions. These advances have expanded the applicability of plant-based platforms to the production of monoclonal antibodies, antibody fragments, and emerging antibody-based modalities. In parallel, a broad range of single-chain therapeutic proteins, including enzymes, antimicrobial and antiviral agents, and proteins for inducing immune tolerance, have been successfully produced in plant systems as biologically active and functional therapeutics, demonstrating the broad utility of plant-based platforms across multiple therapeutic classes. This review provides a comprehensive overview of current plant-based production platforms, including whole-plant and plant cell suspension systems, and evaluates their comparative advantages and limitations relative to mammalian expression technologies. Recent progress in the development of therapeutic proteins, with an emphasis on monoclonal antibodies for passive immunization, is highlighted. Finally, the remaining technical, regulatory, and commercial challenges are discussed, along with future prospects for integrating plant-based systems into mainstream biopharmaceutical manufacturing.
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4. Beyond the Prevention of Anti-drug Antibody Formation with Uricase Therapy: Mechanistic Roles of DMARDs in Modifying Gout Flare Risk.
PMID:日期:2026-09-14Disease-modifying antirheumatic drugs (DMARDs) are immune-modifying agents that have shown efficacy in improving response rates and reducing infusion reactions associated with uricase therapy for uncontrolled gout by inhibiting anti-drug antibody (ADA) formation. However, increased gout flare rates following initiation of uricase therapy remain a concern, impacting patient quality of life and treatment adherence. Gout flares are an acute inflammatory reaction to monosodium urate crystals, driven by inflammasome activation. As such, it is possible that DMARDs could impact gout flare risk. In this hypothesis-generating narrative review, we have synthesized mechanistic data investigating the effects of the DMARDs methotrexate, mycophenolate mofetil, azathioprine, leflunomide, and sirolimus on mechanisms involved in gout flare such as NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome activation. The mechanisms by which DMARDs inhibit ADA formation appear to be distinct from those that may affect gout flares, but these may exist in balance with one another to form a distinct pharmacological profile for each agent. Paradoxically, preclinical evidence suggests that DMARDs may sometimes induce NLRP3 inflammasome activation, particularly at higher doses. We suggest that individual DMARDs' effect on inflammatory pathways relevant to gout flare may vary depending on the pathophysiological context and differences in their pharmacological profiles. Therefore, the inflammatory consequences of combining DMARDs with uricase therapy are likely to be specific to the individual agent. Understanding the mechanistic profile of each DMARD is key to optimizing both immunogenicity management and flare outcomes in patients receiving uricase therapy for uncontrolled gout.
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5. Biologic Therapies for Alleviating Neurodegeneration in Lysosomal Storage Diseases.
5. 缓解溶酶体贮积症神经退行性变的生物疗法PMID:日期:2026-09-14Lysosomal storage diseases (LSDs) are a group of rare inherited metabolic disorders characterized by lysosomal dysfunction and progressive accumulation of undegraded substrates, leading to multisystem involvement and, in many cases, severe neurodegeneration. Because the blood-brain barrier (BBB) restricts central nervous system (CNS) access for most therapeutic modalities, neurological manifestations remain the major unmet need across LSDs. In this review, we summarize current and emerging strategies aimed at correcting CNS pathology, including enzyme replacement therapy (ERT), adeno-associated virus (AAV)-mediated gene therapy, allogeneic hematopoietic stem cell transplantation (HSCT), and autologous HSCT with gene-modified hematopoietic stem cells. While ERT provides limited CNS benefits and allogeneic HSCT mitigates neurodegeneration only partially, their overall impact on CNS outcomes remains restricted. Newer approaches, such as BBB-shuttling ERTs, CNS-tropic AAV capsids, and genetically modified autologous hematopoietic stem and progenitor cells capable of sustained supraphysiological enzyme production, offer promising avenues for enhanced CNS delivery and cross-correction. Together, these advances underscore a shift toward integrated therapeutic strategies that combine systemic and CNS-directed interventions, with the potential to transform outcomes for patients with LSDs and other neurodegenerative disorders amenable to cross-correction.
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6. Biosimilars: A Virtuous Cycle of Sustainability and Innovation.
6. 生物类似药：可持续性与创新的良性循环PMID:日期:2026-09-14A biosimilar is a biological medicinal product developed to replicate a licensed originator-i.e., the reference product-with which it shares quality, efficacy, and safety. Marketed following expiry of the reference product's patent protection, biosimilars introduce competition that benefits patients and foster sustainability. In addition to such sustainability of healthcare systems, biosimilars confer a less widely recognized yet equally important benefit: they stimulate innovation. The European regulatory framework, pioneered by the European Medicines Agency and reinforced by other reference regulatory bodies, has unlocked this innovative potential. This paper examines how the development, manufacturing, commercialization, and clinical use of biosimilars generate advances in healthcare delivery. Drawing on available evidence and market experience, it proposes a classification of biosimilar-driven innovation into three domains: pharmaceutical innovation, technological innovation, and therapeutic innovation. Benefits wholly or partially attributable to biosimilars encompass both incremental and disruptive improvements within each domain. These include, for instance, the reinvestment of resources into novel therapies and technologies; therapeutic paradigm shifts supported by evidence and increasingly reflected in clinical guidelines; and enhanced formulations and delivery devices. Although relevant to all healthcare stakeholders, this paper is primarily directed at physicians. As key facilitators of biosimilar adoption, they will find that the innovative aspects of these medicines offer both compelling arguments to support broader prescribing and practical examples of how biosimilars can enhance clinical practice and improve patient outcomes.
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7. The Effect of Anti-drug Antibodies on the Bioavailability of Alglucosidase Alfa in Classic Infantile Pompe Disease.
7. 抗药抗体对经典型婴儿型庞贝病中阿葡糖苷酶α生物利用度的影响PMID:日期:2026-09-11The impact of anti‑drug antibodies (ADAs) on the bioavailability of recombinant human acid α-glucosidase (rhGAA) in classic infantile Pompe disease remains incompletely understood. The aim of this study was to investigate the effects of ADAs on the bioavailability of rhGAA in classic infantile Pompe disease. We analyzed 15 pharmacokinetic (PK) curves from 13 patients receiving rhGAA. High titers were defined as ≥ 1:31250. Alpha-glucosidase activity in plasma was measured using protein A beads to precipitate ADA-bound rhGAA, and sepharose as control. Neutralizing effects were assessed in fibroblasts and culture medium after incubation with patient sera and a fixed amount of rhGAA. Peak activity (C) and area under the curve (AUC) were calculated by non-compartmental analysis. rhGAA bioavailability was affected in six of nine high-titer patients (n = 1, 1:31,250; n = 5, ≥ 1:156,250). AUC was reduced by 11-52% in the protein A assay compared with sepharose (n = 5). Fibroblast uptake studies demonstrated neutralizing effects with intracellular enzyme activity reduced to 47-71% (n = 5). No ADA effect was detectable in three patients. At the group level, high-ADA patients showed significantly lower C in both assays and a lower AUC in the protein A assay compared with non-high-ADA patients. Slower infusion schemes, as management for infusion-associated reactions, correlated inversely with C (R = - 0.64), but not AUC. Immunomodulation eliminated the effects of ADAs, as shown in two patients. High ADAs have heterogenous effects on rhGAA bioavailability. Titers ≥1:156,250, mostly, had a measurable effect, capturing up to > 50% of infused rhGAA. A high titer, per se, did not imply neutralizing effects. Where available, functional assays, including PK curves and uptake studies, may contribute to characterize ADA effects.
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8. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.
PMID:日期:2026-09-02The MYC family oncoproteins, including MYC, MYCN, and MYCL, are potent drivers of tumorigenesis across a broad range of human cancers, frequently linked to aggressive tumor behavior, poor prognosis, and therapy resistance. They function as master transcriptional regulators that orchestrate gene expression programs governing nearly all aspects of tumor development. Despite their pivotal oncogenic role, they have long been considered "undruggable" due to their intrinsically disordered structure, lack of enzymatic activity, and the difficulty of targeting their protein-DNA and protein-protein interactions with conventional small-molecule approaches. Recent advances are beginning to overcome these challenges through innovative molecular strategies that either directly inhibit MYC activity or exploit MYC regulatory networks. Importantly, the first direct MYC inhibitor evaluated in humans, OMO-103, recently demonstrated promising antitumor activity in phase I clinical trials. Indirect approaches have focused on suppressing MYC transcription, translation, or stability by targeting upstream signaling pathways, as well as by exploiting MYC-associated cofactor interactions and synthetic lethal vulnerabilities to improve therapeutic specificity. In this review, we highlight the multifaceted roles of MYC in different cancer types and provide a comprehensive overview of current therapeutic strategies targeting MYC with a particular focus on epigenetic modifiers and metabolic vulnerabilities.
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9. Comparison of the Risk of Acute Anterior Uveitis Flare Between Adalimumab and Subcutaneous Infliximab in Patients with Radiographic Axial Spondyloarthritis and Prior Acute Anterior Uveitis: A Randomized Controlled Trial.
PMID:日期:2026-08-28Acute anterior uveitis (AAU) is the most common extra-musculoskeletal manifestation of radiographic axial spondyloarthritis (r-axSpA) and is an important consideration when selecting biological therapy. Although adalimumab (ADA) and infliximab are commonly used in patients with r-axSpA and AAU, direct comparative evidence, particularly between ADA and subcutaneous infliximab (IFX-SC), remains limited. The objective of this study was to compare the risk of AAU flare between ADA and IFX-SC in patients with r-axSpA and a history of AAU. This multicenter, head-to-head, randomized, open-label trial enrolled patients with r-axSpA and a documented AAU event within the preceding 2 years. Participants were randomly assigned (1:1) to receive ADA (40 mg every 2 weeks) or IFX-SC (intravenous 5 mg/kg induction followed by subcutaneous 120 mg every 2 weeks) and were followed for 48 weeks. The primary endpoint was AAU flare occurrence. Hazard ratios (HRs) were estimated using Cox proportional hazards models. Secondary endpoints included changes in best-corrected visual acuity (BCVA), r-axSpA disease activity and functional indices, and safety outcomes. Fifty-six patients were randomized (ADA, n = 28; IFX-SC, n = 28). During follow-up, one AAU flare episode occurred in each group. The adjusted HR of IFX-SC (vs ADA) for an AAU flare was 0.496 (95% confidence interval 0.025-9.768, p = 0.645). No significant differences in secondary endpoints were observed between groups (right BCVA, p = 0.622; left BCVA, p = 0.306; Axial Spondyloarthritis Disease Activity Score, p = 0.293; Bath Ankylosing Spondylitis Disease Activity Index, p = 0.262; Bath Ankylosing Spondylitis Functional Index, p = 0.307). Adverse events were similar in frequency and severity, with no new safety signals identified. No statistically significant differences in AAU flare risk or secondary ocular and rheumatologic outcomes were observed between ADA and IFX-SC over 48 weeks in patients with r-axSpA and prior AAU. These findings suggest that IFX-SC may represent a potential alternative to ADA for AAU flare prevention as well as disease activity control in this population. Clinical Research Information Service (CRIS), Republic of Korea; KCT0007239.
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10. Targeting CD38 Across Autoimmune and Plasma Cell-Driven Immune-Mediated Diseases: Rationale, Clinical Evidence, and Emerging Therapeutic Landscape.
10. 跨自身免疫性和浆细胞驱动的免疫介导性疾病靶向CD38：理论基础、临床证据及新兴治疗格局PMID:日期:2026-08-18Autoimmune diseases remain a major cause of chronic morbidity despite substantial advances in targeted immunomodulatory therapies. In many autoantibody-mediated conditions, disease refractoriness and relapse are driven by long-lived plasma cells, which are largely resistant to conventional immunosuppression and upstream B cell-directed strategies. CD38, a surface molecule highly expressed on plasmablasts and plasma cells and functionally involved in immunometabolic regulation, has emerged as a promising therapeutic target to overcome this limitation. Clinical interest in anti-CD38 therapy has been catalyzed by experience in plasma cell dyscrasias, where anti-CD38 monoclonal antibodies induce rapid and profound depletion of antibody-secreting cells. Over recent years, accumulating reports and early-phase studies have explored the repurposing of CD38-directed therapies in severe, treatment-refractory autoimmune diseases. The most compelling evidence has emerged in lupus nephritis and immune thrombocytopenia, with additional proof-of-concept data in autoimmune cytopenias and plasma cell-driven renal disorders such as immunoglobulin light chain (AL) amyloidosis. These experiences suggest that targeting CD38 can lead to meaningful clinical and immunological improvement, often accompanied by rapid reductions in pathogenic autoantibody production. However, the current evidence base remains heterogeneous and largely derived from small cohorts, case series, and early-phase trials, and important questions remain regarding durability of response, optimal treatment strategies, and long-term safety, particularly with respect to hypogammaglobulinemia and infection risk. We summarize the biological rationale for CD38 targeting in autoimmunity and plasma cell-driven immune-mediated diseases, critically appraise the emerging clinical evidence across disease settings, and discuss key challenges and future directions for integrating plasma cell-directed therapies into immunological disease management.