北京若生智能科技有限公司
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IV

IVIG (BT 681 5% / IVIG 5%, Biotest / IVIG 10%, Biotest)

✓ Approved

Grifols, S.A. · 单克隆抗体 · 单克隆抗体

什么是 IVIG？

IVIG 是一种单克隆抗体，由Grifols, S.A.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BT 681 5%, IVIG 5%, Biotest, IVIG 10%, Biotest
公司Grifols, S.A.
药物类别单克隆抗体, 多克隆抗体, 抗体
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Grifols, S.A.

治疗适应症

IVIG 针对 8 个适应症，涉及 5 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersChronic inflammatory demyelinating polyradiculoneuropathy✓ Approved
Immune system disordersSelective IgG subclass deficiency✓ Approved
Nervous system disordersMultifocal motor neuropathy✓ Approved
Nervous system disordersGuillain-Barre syndrome✓ Approved
Blood and lymphatic system disordersThrombocytopenia✓ Approved

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相关研究文献

PubMedFrontiers in medicine2026-09-10

Case Report: Balancing immunosuppression and infection-intravenous immunoglobulin in anti-HMGCR immune-mediated necrotizing myopathy complicated by severe pneumonia.

Fu Jing J, Zhao Qiong Q, Lou Jing-Bo JB, Tang Gui-Hua GH et al.

A 65-year-old male with a 3-year history of atorvastatin use presented with progressive proximal muscle weakness, dysphagia, and markedly elevated creatine kinase (2,277 U/L). Initially misdiagnosed with polymyositis, he deteriorated with severe pneumonia, septicemia, and type I respiratory failure requiring mechanical ventilation. Interleukin-6 rose from 12.83 to 610.9 pg/mL during sepsis. After confirmation of anti-HMGCR antibody positivity (18 arbitrary units [AU], cutoff >10 AU) via line blot assay, we discontinued methotrexate, maintained methylprednisolone at 40 mg, and initiated intravenous immunoglobulin (IVIG) 0.4 g/kg/day for 5 days with broad-spectrum antibiotics. Within two weeks, proximal muscle strength (MRC scale) improved from 2/5 to 4/5, IL-6 normalized to 8.56 pg/mL, and respiratory failure resolved. This case suggests that IVIG may serve as a safe immunomodulatory bridge in critically ill IMNM patients with severe infections.

PMID 42718719
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PubMedFrontiers in medicine2026-09-10

Diagnostic challenge of GAD65-associated autoimmune encephalitis mimicking post-traumatic complications in an older adult: a case report.

Huang Xiuqing X, Zhang Qile Q, Huang Li L, Xu Jian J

Glutamic acid decarboxylase 65 (GAD65) antibody-associated autoimmune encephalitis is an uncommon immune-mediated neurological disorder with heterogeneous neuropsychiatric manifestations. Diagnosis is particularly challenging in older adults when symptoms of recent traumatic brain injury (TBI) overlap with structural or metabolic conditions. We report a 79-year-old man who developed recurrent headache, progressive confusion, abnormal behavior, poor oral intake, intermittent myoclonic jerks, and low-grade fever after TBI complicated by chronic subdural hematoma. Initial laboratory testing revealed hyponatremia, and the working diagnosis was post-traumatic brain syndrome with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although serum sodium was corrected and nocturnal agitation partially improved, persistent daytime confusion, cognitive impairment, behavioral abnormalities, and low-grade fever prompted further investigation. Cerebrospinal fluid (CSF) analysis showed mild inflammatory changes with pleocytosis and elevated protein. CSF metagenomic next-generation sequencing (mNGS) and paraneoplastic antibody testing were negative, whereas the autoimmune encephalitis panel was positive for GAD65 antibody at a titer of 1:32. Whole-body positron emission tomography-computed tomography (PET-CT) did not reveal malignancy. The diagnosis was therefore revised to GAD65 antibody-associated autoimmune encephalitis. Because high-dose corticosteroids were considered unsuitable owing to his history of gastric ulcer and previous gastrointestinal bleeding, he was treated with intravenous immunoglobulin (IVIG) at a total dose of 2 g/kg divided over 3 consecutive days followed by oral azathioprine 50 mg daily. His fever resolved within 1 week, and his mental status and responsiveness gradually improved. At 6-month follow-up, he had achieved near-baseline mental status, was able to walk with a cane, and was almost fully independent in daily activities, without relapse or serious treatment-related adverse events. This case highlights the diagnostic difficulty of recognizing autoimmune encephalitis after TBI. The clinical overlap between post- traumatic syndrome and immune-mediated brain injury often delays diagnosis, emphasizing the value of targeted CSF autoantibody testing in atypical cases. Traumatic brain injury may obscure the onset of GAD65-associated autoimmune encephalitis. Early recognition and a corticosteroid-sparing immunotherapy strategy (IVIG and azathioprine) can yield favorable outcomes in elderly patients with medical comorbidities.

PMID 42718506
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PubMedFrontiers in immunology2026-09-10

X-linked hyper-IgM syndrome presenting as severe Pneumocystis pneumonia in a 6-month-old infant: a case report.

Guo Ying Y, He Xiaoli X, Zhang Lijun L, Li Mengting M et al.

X-linked hyper-immunoglobulin M (XHIGM) syndrome is a rare primary immunodeficiency caused by mutations in the CD40 ligand gene (CD40LG), characterized by defective T-cell-dependent B-cell class-switch recombination. Patients typically present with recurrent infections in early childhood, but diagnosis is often delayed due to heterogeneous clinical manifestations and the fact that serum IgM levels may remain within the normal range in a significant proportion of patients. Here we report a case of XHIGM in an infant whose diagnostic journey began with recurrent lymphadenitis and culminated in life-threatening Pneumocystis jirovecii pneumonia (PJP). A 6-month-old male infant was admitted with severe respiratory distress and hypoxemia. He had recurrent axillary lymphadenitis at 1 and 2 months of age and significant failure to thrive. Chest CT showed bilateral consolidative and interstitial opacities. Immunological evaluation revealed markedly decreased IgA, normal IgM and IgG, and profound T-cell lymphopenia. Sputum metagenomic sequencing identified Pneumocystis jirovecii. Whole-genome sequencing identified a hemizygous likely pathogenic CD40LG mutation (NM_000074.3:c.520C>T, p.Q174*); his mother was a carrier. He was treated with mechanical ventilation, trimethoprim-sulfamethoxazole (TMP-SMX), micafungin, corticosteroids, and intravenous immunoglobulin (IVIG), and was discharged after 36 days. In infants with recurrent or opportunistic infections, persistently low IgA and declining T-cell counts-even when initial screening appears normal-should raise suspicion for underlying immunodeficiency and prompt genetic evaluation. Early aggressive management and evaluation for hematopoietic stem cell transplantation are essential to improve outcomes.Serial immunological evaluation is essential in infants with recurrent or opportunistic infections, as persistently low IgA and declining T-cell counts-even when initial screening appears normal-should prompt genetic evaluation for underlying immunodeficiency. Early aggressive management and evaluation for hematopoietic stem cell transplantation are essential to improve outcomes.

PMID 42718418
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PubMedJournal of pharmacy practice2026-09-09

Management of Heparin-Induced Thrombocytopenia With Plasmapheresis and IVIG Prior to Heart Transplantation: A Case Report.

McCourt Natalie N, Blotske Kaitlin K, Wenninger Joseph J, Trujillo Toby T et al.

Background: Heparin-Induced Thrombocytopenia (HIT) is a serious immune-mediated complication characterized by anti-platelet factor 4 (PF4)/heparin antibodies that activate platelets, causing thrombocytopenia and a paradoxical prothrombotic state. Management requires immediate heparin discontinuation and alternative anticoagulation due to thrombotic risks. Case Presentation: We report a 36-year-old pregnant female with heart failure who developed HIT after heparin exposure during extracorporeal membrane oxygenation (ECMO) support and was subsequently evaluated for heart transplantation. Confirmed HIT led to switching anticoagulation to bivalirudin. Prior to transplantation, where intraoperative heparin is standard, she underwent plasmapheresis (PLEX) followed by intravenous immunoglobulin (IVIG) and corticosteroids to reduce circulating HIT antibodies. This immune-modulating approach enabled safe intraoperative heparin use without thrombotic complications. Post-transplant HIT assays were negative, with platelet recovery and stable coagulation parameters. Discussion: This case demonstrates that combined PLEX and IVIG can effectively lower pathogenic HIT antibodies, permitting necessary heparin administration in critical settings like heart transplantation. Conclusion: Given the lack of standardized guidelines for managing HIT when heparin exposure is unavoidable, this report highlights a promising strategy to mitigate risks and underscores the need for further research to optimize care in such complex clinical scenarios.

PMID 42715353
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PubMedJournal of virology2026-09-09

MADCAP: isolation of novel nAb-naïve AAV capsids from metagenomic data.

Lyashenko Eugenia E, Torregrosa Tess T, Ysasi Alexandra B AB, Wu Jason J et al.

Gene therapy using adeno-associated virus (AAV) vectors offers promising treatment for genetic disorders, but significant limitations restrict clinical application. Current AAV serotypes exhibit strong liver tropism and require high doses for extra-hepatic targeting, and pre-existing antibodies (NAbs) exclude up to 50% of potential patients. Evolutionarily distant isolates can evade neutralization but typically transduce human tissues poorly and require extensive engineering. We developed MADCAP (Metagenomic AAV Discovery and Capsid Annotation Pipeline) to systematically mine metagenomic data for functional, clinically relevant AAV capsids. We hypothesized that these sources might contain capsids that do not circulate widely in humans, can transduce human cells, and avoid neutralization. We screened 4.2 million metagenomic samples and identified 139 novel AAV capsid isolates which were tested for viral capsid assembly, viability, neutralization evasion, and tissue transduction in non-human primates. While natural serotypes (AAV1, AAV2, AAV9) were neutralized at low dilutions of pooled human immunoglobulin (IVIG), 68% of tested MADCAP capsids exhibited minimal to undetectable neutralization even at supra-physiological IVIG concentrations. Systemically delivered MADCAP capsids effectively transduced multiple clinically relevant tissues in non-human primates. Two capsids, MC46 and MC55, demonstrated improved CNS tropism compared to AAV9 while maintaining comparable production yields. In passive transfer studies, MC46 retained full transduction efficiency in the presence of human antibodies, while AAV9 transduction was completely lost. This work establishes metagenomic mining as a powerful tool for accelerating AAV capsid discovery, identifying isolates with favorable tissue tropisms and resistance to broadly neutralizing antibodies. This work provides proof of concept that potentially clinically relevant AAVs can be isolated from metagenomic data. Our findings lay the groundwork for accelerated discovery of AAV capsids which could potentially increase the accessibility and effectiveness of AAV gene therapy.

PMID 42714164
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PubMedIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion2026-09-09

Flare-Ups in Chronic ITP: A Proposal for a Clinical Sub-Phenotype "Acute-on-Chronic ITP".

Wadhera Sarthak S, Jain Arihant A, Swain Rudra Narayan RN, Ray Debadrita D et al.

Immune thrombocytopenia (ITP) is a heterogeneous disorder with fluctuating platelet counts. Current classifications do not adequately capture acute exacerbations in stable chronic ITP patients. We describe two chronic ITP patients with long-term stable platelet counts who experienced sudden, symptomatic thrombocytopenic flares. Both were managed with short courses of corticosteroids or IVIg while continuing prior therapy. Outcomes were assessed clinically and hematologically over extended followup. Both patients showed rapid and sustained responses, returning to baseline platelet counts without long-term therapy escalation. These episodes were distinguishable from refractory ITP by their identifiable triggers, episodic course, and excellent response to short-term treatment. We propose diagnostic criteria, key differentiators from refractory ITP, and a management algorithm. Acute on Chronic ITP is a distinct clinical entity characterized by sudden platelet declines in stable ITP patients, responsive to shortterm therapy. Recognizing this phenotype may prevent overtreatment, reduce healthcare costs, and improve patient outcomes. Formal incorporation into future ITP guidelines is warranted.

PMID 42712615
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