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anti-H5N1 avian influenza antibodies (Fabenflu / FBF001)

✓ Approved

Fab'entech · 多克隆抗体 · 多克隆抗体

什么是 anti-H5N1 avian influenza antibodies？

anti-H5N1 avian influenza antibodies 是一种多克隆抗体，由Fab'entech研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名Fabenflu, FBF001
公司Fab'entech
药物类别多克隆抗体, 抗体
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Fab'entech

治疗适应症

anti-H5N1 avian influenza antibodies 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsInfluenza✓ Approved

相关研究文献

PubMedNature communications2026-10-26

Extended dosing intervals enhance the durability of a self-amplifying mRNA vaccine against pandemic H5N1 influenza: a randomized, observer-blind, dose-finding Phase I study.

Pragalos Antoinette A AA, Pacciarini Filippo F, Jin Hongfan H, Hopkins Terri T et al.

Avian influenza poses a persistent pandemic threat, yet traditional vaccines face production delays. Self-amplifying mRNA (sa-mRNA) technology offers potential advantages, including rapid development, dose sparing, and enhanced, durable immunity. We evaluated ARCT-2304, a bicistronic sa-mRNA vaccine encoding H5N1 hemagglutinin (HA) and neuraminidase (NA), in a Phase 1 randomized, observer-blind trial (NCT06602531). Healthy adults (N = 212) received two doses of ARCT-2304 (1.5, 5, or 12 mcg) or control/placebo on a 4- or 8-week schedule. Primary outcomes evaluated safety and reactogenicity (solicited/unsolicited/serious adverse events [AEs]) and immunogenicity (HA inhibition and NA enzyme-linked lectin assays 28 days post-second dose). Immunogenicity results were benchmarked using serum from a prior study supporting licensure of an H5N1 vaccine. ARCT-2304 was well-tolerated, displaying mostly mild-to-moderate, transient, dose-dependent solicited AEs, with no safety concerns identified. Two doses elicited robust HA and NA humoral responses. An 8-week interval yielded higher magnitude and greater durability than a 4-week schedule, with neutralizing and anti-NA antibodies remaining significantly elevated 6-7 months post-second dose. ARCT-2304 also induced dose-dependent, Th1-polarized T-cell responses peaking at Day 29. These findings support advancing sa-mRNA platforms for pandemic influenza preparedness.

PMID 42928290
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PubMedAntibodies (Basel, Switzerland)2026-10-26

Targeting the Complement C1 Proteases Using Camelid-Derived Single Domain Antibodies: Production, Characterization and Possible Application for Tissue/Fluid Analysis.

Haut Nolwenn N, Rossi Véronique V, Peliconi Julie J, Reiser Jean-Baptiste JB et al.

The complement C1r and C1s proteases initiate the classical complement pathway within the C1 complex, but emerging evidence points to additional roles in tissues, including cell-intrinsic functions linked to cancer and connective tissue disorders. Few tools are available to explore these plasma and tissue-relevant functions. We report the first development and characterization of anti-C1r and anti-C1s VHH single-domain antibodies (nanobodies). A lama was immunized with the purified human C1r2/C1s2 tetramer. After phage display selection, two anti-C1r VHHs (C1rCl1, C1rCl6) and one anti-C1s VHH (C1sCl7) were produced in E. coli and characterized by ELISA, Western blot, SPR and size-exclusion chromatography using recombinant protease fragments and proenzyme forms. Functional impact on C1s activation was assessed by cleavage assay, and tissue applicability by immunohistochemistry on human skin sections. All three VHHs bound with high affinity to both active and proenzyme forms. Epitope mapping localized C1rCl1 and C1rCl6 to the CCP2 module of C1r, and C1sCl7 to the CCP1 module of C1s. The two anti-C1r VHHs recognize distinct, non-overlapping epitopes and can bind simultaneously to C1r. C1rCl1 mildly inhibited C1s activation by C1r. The VHH pair C1rCl1/C1rCl6 enabled sandwich ELISA detection of C1r in serum, plasma, and cell culture supernatant. Immunohistochemistry on human skin confirmed clean C1r staining in keratinocytes and fibroblasts, with a dissociated tissue distribution compared to C1s. These first anti-C1r and anti-C1s nanobodies constitute useful tools for detection in biological fluids and tissue staining, with potential applications in diseases where these proteases play a pathological role.

PMID 42930034
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PubMedTransfusion2026-10-26

Blocking FcγRI and FcγRIII reduces RBC phagocytosis induced by patient-derived anti-E and anti-K alloantibodies in vitro.

Cabado Yaima Tundidor YT, Gonzalez Lazaro Gil LG, Noa Yeniley Ruiz YR, Oro Alequis Pavon AP et al.

Red blood cell (RBC) alloantibodies can cause hemolytic transfusion reactions and complicate compatible blood provision. Although antibody-opsonized RBCs are thought to be cleared partly through macrophage Fcγ receptor-mediated phagocytosis, the Fcγ receptors involved in phagocytosis induced by non-D alloantibodies remain incompletely defined. RBCs were sensitized with WHO anti-E or anti-C typing sera, or with plasma/serum from patients alloimmunized against RhE or K. Phagocytosis was assessed using THP-1-CD16A macrophages expressing FcγRI, FcγRIIA, and FcγRIII. Receptor involvement was evaluated using receptor-specific deglycosylated blocking monoclonal antibodies. RBCs sensitized with WHO anti-E or anti-C sera, or with patient-derived anti-E or anti-K alloantibodies, were phagocytosed by THP-1-CD16A macrophages. FcγRI or FcγRIII blockade reduced phagocytosis, although the magnitude of inhibition varied by antibody source and individual patient sample. FcγRIIA blockade produced little or no significant reduction across the conditions tested. Combined FcγRI and FcγRIII blockade produced the greatest inhibition with WHO reference sera, although inhibition was not fully additive. Patient-derived anti-E and anti-K samples showed a similar pattern. These findings support a functional contribution of FcγRI and FcγRIII to alloantibody-mediated RBC phagocytosis in this in vitro macrophage model, while suggesting a limited role for FcγRIIA under these experimental conditions.

PMID 42928980
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PubMedEpidemiology and infection2026-10-26

An investigation into post-pandemic ethnic group and deprivation inequalities in influenza and COVID-19 hospitalizations.

Scott Meg M, Browning Lucy L, Roberts Tirion T, De Boer Jessica J et al.

Health system decision-makers need evidence on how modifiable factors contribute to inequalities to inform effective interventions. We examined ethnic group and deprivation inequalities in influenza and COVID-19 hospitalizations in England (2023-2024) among vaccine-eligible individuals, using causal mediation analysis to assess the roles of deprivation, vaccination uptake and comorbidities. For influenza, hospitalization odds were highest among Pakistani and Bangladeshi groups, compared with White British individuals. Deprivation mediated 26% of the total ethnic group effect for the Pakistani group and 41% for the Bangladeshi group, whilst comorbidities contributed little. Ethnic group differences in COVID-19 hospitalizations were minimal in this post-pandemic period. For both infections, the most deprived group had disproportionately high hospitalization compared to the least deprived. For influenza, vaccination uptake mediated 17%-26% of deprivation effects, whilst for COVID-19, there were no meaningful residual deprivation inequalities after including vaccination uptake and comorbidities. Vaccination uptake and deprivation mediate a substantial proportion of inequalities in hospitalization for influenza and COVID-19 in the vaccine-eligible cohort. Improving vaccination coverage in under-vaccinated groups should remain a public health priority.

PMID 42929057
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PubMedAntibodies (Basel, Switzerland)2026-10-26

Complement in HER2-Positive Breast Cancer: A Conditionally Protective Mechanism Under Attack.

Petkova Dobromira D, Kuleva Ivaila I, Stoyanova Zhasmin Z, Ilcheva Boryana B et al.

The therapeutic efficacy of anti-HER2 monoclonal antibodies in breast cancer has traditionally been attributed to direct inhibition of signaling and antibody-dependent cellular cytotoxicity (ADCC). Recent evidence, however, has established complement activation through the classical pathway as a possible adjunct mechanism underlying the synergistic activity of the trastuzumab and pertuzumab combination. This synergy is mediated by complement-dependent cytotoxicity (CDC) and complement-dependent cellular phagocytosis (CDCP), and is lost upon C1q deletion in preclinical models. Tumor cells evade complement-mediated killing through overexpression of membrane-bound complement regulatory proteins (mCRPs), particularly CD55 and CD59, which correlate with shorter disease-free survival in patients treated with trastuzumab. C1q itself plays a dual, context-dependent role: it acts as a complement-independent tumor suppressor in HER2-positive breast cancer while promoting tumor progression in most other malignancies. Emerging therapeutic strategies, including biparatopic antibodies such as zanidatamab, complement-redirecting immunoconjugates, and mCRP-targeting approaches, aim to overcome complement resistance and enhance antitumor immunity. On this basis, we propose that HER2-positive breast cancer represents a conditionally complement-protective tumor, in which the balance between antibody-directed complement activation and mCRP-mediated evasion determines treatment outcome. This review evaluates the current evidence linking complement to anti-HER2 therapy and highlights future directions for successful treatment.

PMID 42930033
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PubMedAntibodies (Basel, Switzerland)2026-10-26

Switching Beyond Rituximab in Primary Glomerular Diseases: A Systematic Review of Within-Patient Efficacy and Safety of Non-Rituximab Anti-CD20 Antibodies.

Martino Francesca K FK, Stefanelli Lucia F LF, Cattarin Leda L, Del Prete Dorella D et al.

Background/Objectives: Rituximab is widely used in primary glomerular diseases, but treatment may fail for several reasons, including primary non-response, incomplete response, relapse, intolerance or anti-rituximab antibodies. We assessed within-patient efficacy and safety after switching to another anti-CD20 antibody, considering the reason for switching. Methods: PubMed and Scopus were searched from inception to 15 May 2026 without language restrictions. Eligible reports included adults with primary glomerular disease treated with a non-rituximab anti-CD20 antibody after rituximab and reporting within-patient outcomes. Risk of bias was assessed with design-specific JBI tools and certainty with GRADE. Heterogeneity precluded meta-analysis, and findings were synthesized narratively. Results: A total of 309 patients were included across 43 studies: 283 had membranous nephropathy (MN), 18 had minimal change disease (MCD), 6 had focal segmental glomerulosclerosis (FSGS), and 2 had IgA nephropathy (IgAN). Obinutuzumab was the principal drug used, and the main reasons for switching were primary non-response, with immunization, relapse, or intolerance occurring less frequently. In MN, among the 262 patients with available response data, 217 achieved complete or partial remission, and relapse was rare. For MCD, 17 of 18 patients with active disease attained remission, and only one relapsed during follow-up. On the other hand, five out of the six FSGS patients responded, but three of them relapsed. The two patients with IgAN achieved either complete or partial remission. Notably, these results may not apply to conventional IgAN, since one biopsy showed contextually MCD and the other was proliferative and crescentic. Infusion-related reactions were the most frequent adverse events and were generally mild, while infections were the main issue during the follow-up. Evidence certainty for all outcomes was very low. Conclusions: Switching to a non-rituximab anti-CD20 antibody may be a feasible rescue strategy, most convincingly after intolerance, rituximab immunization, or relapse. The uncontrolled, very-low-certainty evidence precludes firm recommendations, and controlled studies are warranted.

PMID 42930037
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