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immunoglobulin G

✓ Approved

Quimbiotec · 多克隆抗体 · 多克隆抗体

什么是 immunoglobulin G？

immunoglobulin G 是一种多克隆抗体，由Quimbiotec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

公司Quimbiotec
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, Quimbiotec

治疗适应症

immunoglobulin G 针对 4 个适应症，涉及 4 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersGuillain-Barre syndrome✓ Approved
Skin and subcutaneous tissue disordersPurpura✓ Approved
Immune system disordersImmunodeficiency✓ Approved
Infections and infestationsBorna virus infection✓ Approved

相关研究文献

PubMedJournal of medical virology2026-09-10

Molecular Evidence of Human T‑Cell Leukemia Virus Type 1 Transmission by Needlestick Injury in Healthcare Workers.

Tokunaga Masahito M, Kuramitsu Madoka M, Saito Masumichi M, Yoshimori Miyuki M et al.

Human T‑cell leukemia virus type 1 (HTLV‑1) is a retrovirus that spreads primarily through cell-to-cell transmission. Occupational transmission of HTLV-1 by needlestick injury is considered exceedingly rare, with no reported molecularly confirmed cases. We report two healthcare workers who experienced accidental needlestick injuries while caring for patients seropositive for HTLV‑1 and subsequently seroconverted. Full‑length HTLV‑1 proviral sequencing revealed complete nucleotide identity between source patients and infected nurses. These strains belonged to the HTLV-1 subtype 1a Japanese subgroup but were distinct from 315 previously registered strains. Proviral integration site analysis demonstrated nonoverlapping integration profiles between source patients and healthcare workers, providing direct evidence of de novo HTLV‑1 infection rather than expansion of transferred infected cells. Longitudinal analysis in one case showed dynamic clonal turnover between 5 and 14 months after transmission; > 90% of infected-cell clones were replaced, although the proviral load remained stable and low. Serological profiling revealed transiently elevated immunoglobulin M responses to Gag p19 peptides during early infection, followed by gradual immunoglobulin G maturation. These findings provide the first molecular confirmation of HTLV‑1 transmission via needlestick injury resulting in de novo infection, revealing an under-recognized occupational exposure route and supporting reconsideration of post-exposure testing strategies, particularly in endemic regions.

PMID 42720182
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PubMedCureus2026-09-10

Paraplegia Caused by IgG4-Related Hypertrophic Pachymeningitis With an Elevated Cerebrospinal Fluid Immunoglobulin G4 Concentration.

Doyama Hisaki H, Matsumoto Yasuko Y, Kurosaka Akiho A, Kobayashi Motoya M et al.

Immunoglobulin G4-related hypertrophic pachymeningitis (IgG4-RP) is a rare manifestation of immunoglobulin G4 (IgG4)-related disease and an uncommon cause of hypertrophic pachymeningitis (HP). Because serum IgG4 concentration is not necessarily elevated, the diagnosis of IgG4-RP is often challenging. We report a rare case of IgG4-RP in a 78-year-old woman presenting with complete paraplegia, sensory loss in the lower extremities, and bladder and rectal dysfunction. Gadolinium-enhanced magnetic resonance imaging showed enhancing spinal epidural lesions. A histopathological examination revealed dense lymphocyte and plasma-cell infiltration with fibrosis and increased IgG4-positive plasma cells, leading to the diagnosis of IgG4-RP. Although the serum IgG4 concentration was within the reference range, retrospective analysis of cerebrospinal fluid (CSF) showed a markedly elevated IgG4 concentration, with an increased IgG4 index and IgG4Loc. Glucocorticoid therapy resulted in radiological and neurological improvement. This case highlights the importance of considering IgG4-RP in patients with spinal HP even if serum IgG4 concentration is not elevated. Furthermore, CSF IgG4 measurement may contribute to the diagnosis of IgG4-RP, although further studies are required to establish its clinical utility.

PMID 42719365
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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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PubMedMedComm2026-09-10

Immunoglobulin Kappa Light Chain Produced by Cardiomyocytes and Participates in Maintaining Intercalated Disc Integrity.

Zhu Zhu Z, Sheng Yixuan Y, Chang Yun Y, Chang Yuan Y et al.

In this study, we unexpectedly found that the immunoglobulin kappa light chain (Igκ) was expressed in normal cardiomyocytes of mice and humans, especially in intercalated discs (ICDs). Cardiomyocyte-specific knockout of Igκ in mice results in reduced myocardial contraction, atrioventricular block (AV block), and even sudden death. Histological analysis revealed that Igκ knockout in cardiomyocytes leads to structural disorder of ICDs, dissemination of the cytoskeleton proteins desmin and F-actin, as well as the loss of desmoplakin (DSP), N-cadherin, and connexin 43 (Cx43) on ICDs. Mechanistically, Igκ can bind to and stabilize plectin, a cytoskeleton-cross-linking protein that facilitates the assembly of desmin‒actin networks that maintain normal cytoskeletal architecture. Igκ can also anchor desmin to the DSP through plectin, thereby stabilizing the integrity of the ICDs. This molecular interplay critically reinforces cardiomyocyte cohesion and maintains structural and functional homeostasises. Our findings are the first to identify cardiomyocyte-expressed Igκ as a novel ICD-related molecule that participates in cardiomyocyte contraction and conduction by stabilizing plectins. Importantly, this work extends current arrhythmogenic cardiomyopathy (ACM) pathogenic models by revealing that ablation of the non-desmosomal gene Igκ disrupts ICD integrity, uncovering a new mechanism for non-desmosomal gene-related ACM and highlighting Igκ as a potential target for therapeutic investigations.

PMID 42719716
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PubMedJournal of ginseng research2026-09-10

Ginsenoside Rb1 ameliorates endothelial dysfunction in sepsis: Targeting the RhoA/ROCK pathway to modulate mitochondrial homeostasis and inflammation.

Shang Shixi S, Wang Jingju J, Huang Ying Y, Sun Lihua L et al.

Sepsis-induced endothelial dysfunction drives organ injury through microcirculatory failure, characterized by barrier disruption and heterogeneous blood flow. Ginsenoside Rb1 (G-Rb1), a bioactive ginseng constituent, exhibits potent anti-inflammatory and antioxidant properties. This study investigates whether G-Rb1 ameliorates sepsis by preserving endothelial barrier integrity via modulating mitochondrial homeostasis and inhibiting the RhoA/ROCK pathway. A murine cecal ligation and puncture (CLP) sepsis model and lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) were employed. Endothelial barrier function, mitochondrial dynamics, and inflammatory responses were assessed via histology, flow cytometry, Western blot, and Seahorse XF analysis. RhoA/ROCK inhibitor (Fasudil) and Drp1 inhibitor (Mdivi-1) served as mechanistic controls. G-Rb1 significantly improved survival in CLP mice and attenuated lung injury. It suppressed pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) in bronchoalveolar lavage fluid and rebalanced T cell percentage. In HUVECs, G-Rb1 restored endothelial junction proteins (VE-cadherin, ZO-1, Claudin-5), reduced ROS/MDA, and enhanced SOD/GSH/ATP levels. Mechanistically, G-Rb1 inhibited RhoA activation and ROCK-mediated Drp1 phosphorylation (Ser616), normalizing mitochondrial fission, membrane potential, and oxidative phosphorylation. G-Rb1 alleviates sepsis-induced endothelial dysfunction by suppressing the RhoA/ROCK/Drp1 axis, thereby restoring mitochondrial homeostasis and barrier integrity. These findings highlight G-Rb1 as a promising therapeutic candidate for sepsis management via dual modulation of cytoskeletal dynamics and mitochondrial quality control.

PMID 42719378
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PubMedJournal of magnetic resonance imaging : JMRI2026-09-10

Periventricular and Perivascular-Space Diffusion MRI Measures, Amyloid Abnormality, and Executive Decline in the Alzheimer's Disease Continuum: A Longitudinal Study.

Chen Cheng C, Gu Jialong J, Hu Qili Q, Alzheimer's Disease Neuroimaging Initiative et al.

Amyloid abnormality is a defining component of Alzheimer disease (AD) biology but does not fully account for variation in executive-function decline, which may also reflect white matter and periventricular injury. To compare periventricular diffusivity (PVeD), diffusion tensor image analysis along the perivascular space (ALPS), and G-Along Perivascular Space (G-ALPS), an algebraic variation of ALPS, as diffusion MRI measures in relation to amyloid abnormality and longitudinal executive-function decline. Retrospective. The imaging-baseline cohort included 1190 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) (70.6 ± 7.5 years; 666 female, 524 male). The primary analytic sample included 302 participants (70.6 ± 6.1 years; 168 female, 134 male). 3 T/diffusion-weighted spin-echo echo-planar imaging and 3D T1-weighted inversion-prepared gradient-echo imaging. PVeD, ALPS, and G-ALPS were evaluated in relation to cerebrospinal fluid Aβ42, amyloid positron emission tomography (PET) Centiloid, structural MRI measures, white matter hyperintensity (WMH), and longitudinal Alzheimer's Disease Neuroimaging Initiative Executive Function composite (ADNI-EF). Group comparisons, regression, longitudinal models, and bootstrap indirect-effect analyses with Benjamini-Hochberg correction were performed. All three diffusion MRI measures differed across diagnostic groups, with mean values of PVeD, ALPS, and G-ALPS showing lower levels in dementia than cognitively normal participants (PVeD: 0.456 ± 0.048 vs. 0.430 ± 0.047; ALPS: 1.291 ± 0.188 vs. 1.163 ± 0.186; G-ALPS: 1.757 ± 0.512 vs. 1.393 ± 0.467). G-ALPS showed the most consistent association with ADNI-EF trajectory (β = 0.031, 95% CI: 0.003-0.059). Exploratory models identified statistical indirect effects involving inverted CSF Aβ42, ADNI-EF decline, and PVeD (-0.0518), ALPS (-0.0407), or G-ALPS (-0.0460); all survived Benjamini-Hochberg correction, with a corresponding G-ALPS effect for amyloid PET Centiloid (-0.0169). Periventricular and perivascular-space diffusion MRI measures were associated with amyloid abnormality and executive-function decline, mainly in cognitively normal and mild cognitive impairment participants. 3. Stage 2.

PMID 42720233
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