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IV

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

✓ Approved

Grifols, S.A. · Monoclonal Antibodies · Monoclonal Antibodies

What is IVIG?

IVIG is a monoclonal antibodies developed by Grifols, S.A.. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesBT 681 5%, IVIG 5%, Biotest, IVIG 10%, Biotest
CompanyGrifols, S.A.
Drug ClassMonoclonal Antibodies, Polyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Grifols, S.A.

Therapeutic Indications

IVIG is developed for 8 unique indications across 5 therapeutic areas.

Therapeutic AreaConditionPhase
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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Related Research Articles

PubMedMedicine2026-07-25

Longitudinal changes in inflammatory markers and body weight in adults with primary immunodeficiency receiving immunoglobulin replacement therapy: A retrospective cohort study.

Akgul Balaban Yasemin Y, Inan Mustafa Ilker MI, Kalkan Fikriye F, Sonmez Ezgi E et al.

Immunoglobulin replacement therapy (IgRT) is the cornerstone of treatment for adults with primary immunodeficiency [primary immunodeficiency diseases (PID)]. Its role in infection prevention is well established. However, its effects on systemic inflammation and metabolic parameters remain incompletely understood. This study evaluated one-year changes in inflammatory indices and body weight in adults with PID receiving intravenous (IVIG) or subcutaneous (SCIG) immunoglobulin therapy. This retrospective study included 32 adults with PID. The cohort consisted predominantly of patients with common variable immunodeficiency, along with selected cases of Good syndrome and CTLA-4 insufficiency. Patients received intravenous immunoglobulin (IVIG) (n = 22) or SCIG (n = 10). Inflammatory markers [neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), neutrophil count] and body weight were assessed at baseline and after 12 months. Non-parametric tests were used due to sample size. Body weight increased significantly in both the IVIG (P = .01) and SCIG (P = .011) groups. In the IVIG group, CRP (P = .005), absolute neutrophil count (P = .017), and NLR (P = .034) decreased significantly. In the SCIG group, body weight increased significantly. However, changes in inflammatory markers were not significant. Platelet counts decreased (P = .012), while WBC counts increased (P = .016). IgRT was associated with increased body weight in adults with PID. This was consistent across both IVIG and SCIG groups. IVIG was also associated with reductions in inflammatory markers. These findings suggest that IgRT may have effects beyond infection prevention. Body weight may be a useful parameter during follow-up of adult PID patients.

PMID 42499116
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PubMedFrontiers in neurology2026-07-25

Anti-NMDA-receptor encephalitis and MOGAD associated optic neuritis: a case series.

Parthasarathi Pooja P, Dattilo Michael M, Peragallo Jason J

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a well-recognized autoimmune condition that often presents with neuropsychiatric symptoms and seizures. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) often manifests as optic neuritis and, less frequently, as acute demyelinating encephalomyelitis or transverse myelitis. The co-occurrence of anti-NMDAR encephalitis and MOGAD is becoming increasingly recognized, but clinical series remain limited. We present three patients with anti-NMDAR encephalitis and MOGAD optic neuritis (ON): two men, aged 19 and 26, and one woman, aged 36. Clinical presentations, signs, investigations, and management of each case are discussed. The 26-year-old man presented with altered mental status and concurrent vision loss. The 36-year-old woman presented with altered mental status during the encephalitis episode and developed vision loss 4 months after encephalitis. The 19-year-old man with a prior history of altered mental status, diagnosed with NMDA encephalitis 9 years earlier, presented with headache and vision loss. Abnormal T2/FLAIR lesions in the brain and/or spinal cord during the encephalitis episode and unilateral or bilateral optic nerve enhancement during the optic neuritis episode were detected on brain and orbital magnetic resonance imaging (MRI) in all patients. All patients tested positive for cerebrospinal fluid (CSF) anti-NMDAR antibodies during the encephalitis episode and had positive serum MOG titers during the optic neuritis episode. Each patient presented with bilateral, asymmetrically reduced visual acuity and diminished color vision. One patient exhibited bilateral temporal optic nerve pallor, while two patients had bilateral optic nerve edema. The diagnostic work-up revealed positive serum MOG titers (1:100, 1:10,000, and 1:10,000 in the 36/F, 26/M, and 19/M, respectively). The 36-year-old woman was treated with intravenous (IV) steroids, plasma exchange (PLEX), and rituximab during the encephalitis episode. During the optic neuritis episode, she was treated with IV steroids, IV immunoglobulin (IVIG), and rituximab, followed by long-term rituximab maintenance therapy. The 19-year-old man was treated for encephalitis with IV steroids, IVIG, and rituximab. During his optic neuritis episode, he received IV steroids, IVIG, and tocilizumab, followed by long-term tocilizumab maintenance therapy. The 26-year-old man was treated with IV steroids, PLEX, and rituximab during the acute episode, followed by long-term IVIG maintenance therapy. After achieving 2 years of stability that prompted the discontinuation of IVIG, the patient experienced a MOG-IgG-positive relapse 5 months later. This relapse was marked by a seizure-like episode and the appearance of new lesions on MRI. The acute symptoms resolved after treatment with intravenous steroids and IVIG. Subsequently, the patient was initiated on an indefinite maintenance IVIG regimen. Visual acuity in all patients improved to their baseline levels following treatment. This series highlights the emerging overlap between anti-NMDAR encephalitis and MOGAD optic neuritis. Optic neuritis may occur months to years after encephalitis, underscoring the need for careful monitoring of patients with anti-NMDAR encephalitis who develop new visual symptoms. Dual autoimmunity may represent a distinct phenotype with implications for long-term immunotherapy.

PMID 42500388
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PubMedAmerican journal of medical genetics. Part A2026-07-25

Immune Modulatory Therapy for Severe Dengue Hemorrhagic Fever in a Patient With Mitochondrial Complex I Deficiency: A Case Report.

Iness Audra N AN, Walimbe Ameya S AS, Strouphauer Emily R ER, Hirano Michio M et al.

Dengue virus (DENV) poses a serious global health challenge, particularly in cases of dengue hemorrhagic fever (DHF). Patients with preexisting mitochondrial disorders may be at increased risk for complications due to the specific impact of DENV on mitochondrial-dependent cellular processes and immune function. We describe a 16-year-old male with known mitochondrial complex I deficiency caused by a homozygous likely pathogenic variant in NDUFV1 who subsequently developed DHF. His illness was marked by rapidly worsening weakness, respiratory distress, intracranial hemorrhage, and seizures. His clinical course was further complicated by encephalitis, arachnoiditis, and myelitis requiring extensive immunomodulation. He received corticosteroids, intravenous immunoglobulin (IVIG), and plasma exchange (PLEX), which led to improvement and partial recovery of functional status. This case highlights several rare complications of dengue fever, the impact of DENV on mitochondrial function, and underscores the complexity of managing infectious diseases in individuals with underlying mitochondrial disorders.

PMID 42499220
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PubMedDermatology and therapy2026-07-24

Necrobiotic Xanthogranuloma (NXG): Dermoscopic and Reflectance Confocal Microscopic Findings and Review of Treatment with Intravenous Immunoglobulin (IVIG).

Pawlus Zuzanna Z, Wojtowicz Irena I, Kaznowska Ewa E, Reich Adam A et al.

Necrobiotic xanthogranuloma (NXG) is a rare, chronic non-Langerhans cell histiocytosis strongly associated with paraproteinemia and hematologic disorders. This study aims to present a clinical case of NXG, with particular emphasis on the dermoscopic and reflectance confocal microscopic (RCM) findings, and to review the literature on the efficacy of intravenous immunoglobulin (IVIG) therapy in this condition. A 58-year-old woman presented with progressive yellow-orange plaques, showing irregular vessels and hemorrhagic dots on dermoscopy. RCM displayed multiple large refractive cells and smaller cells with horseshoe-like structures, corresponding to xanthomatous histiocytes and Touton cells, respectively. Diagnostic evaluation revealed monoclonal IgG gammopathy and an indolent B cell lymphoma. Long-term treatment with IVIG combined with systemic glucocorticosteroids resulted in partial improvement. A review of 16 cases with follow-up available indicates that IVIG is a highly effective therapeutic option for NXG, often leading to rapid and significant improvement or complete remission. However, long-term responses vary, and interruption of therapy may result in disease relapse, suggesting the importance of sustained treatment. In conclusion, NXG is a multisystem disease showing several characteristics in noninvasive imaging methods. Although IVIG appears highly effective, variability in treatment response highlights the need for individualized management and for further research to better understand disease pathogenesis.

PMID 42493693
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PubMedPediatric blood & cancer2026-07-24

Immunoglobulin Depletion and Recovery Following Blinatumomab in Infants With KMT2A-Rearranged ALL.

Vieira Martins Miguel M, de Lorenzo Paola P, Kotecha Rishi S RS, Attarbaschi Andishe A et al.

Adding blinatumomab to standard chemotherapy for infants with KMT2A-rearranged acute B-cell lymphoblastic leukemia (KMT2A-r B-ALL) improves outcomes. Although blinatumomab impairs immunoglobulin G (lgG) production, increasing infection susceptibility, IgG recovery remains poorly understood. Thirty infants received Interfant-06 protocol chemotherapy with one course of blinatumomab added post-induction. We screened 169 IgG levels post-blinatumomab and IVIg supplementation timepoints. An increase in IgG was subsequently noted until maintenance, where practically all available values returned to normal (>4 g/L). Blinatumomab leads to an IgG reduction, with near-complete recovery occurring before end of treatment. Future trials should monitor immunoglobulin recovery post-blinatumomab to guide infection-preventing strategies. Trial Registration: EudraCT no: 2016-004674-17.

PMID 42496646
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PubMedFrontiers in cellular neuroscience2026-07-24

Case Report: A case of paraneoplastic autoimmune encephalitis with concurrent anti-GABABR and anti-SOX1 antibody positivity.

Liu Feng F, Jiang Ye-Han YH, Hu Yu-Fang YF, Qin Jin-Guan JG et al.

Paraneoplastic autoimmune encephalitis (PAE) is most commonly associated with small cell lung cancer (SCLC). Anti-γ-aminobutyric acid B receptor (GABABR) antibodies underlie a treatable limbic syndrome, whereas anti-SRY-box transcription factor 1 (SOX1) antibodies serve as high-specificity onconeural biomarkers of SCLC-driven autoimmunity. The sequential emergence of these two antibodies during the longitudinal course of a single patient has rarely been documented. A 75-year-old man presented with episodic impaired consciousness, behavioural disturbance and rapid cognitive decline. Brain MRI showed bilateral hippocampal signal abnormalities. A cell-based assay (CBA) detected anti-GABABR antibodies at high titre in serum (1:3200) and cerebrospinal fluid (CSF; 1:1000), while a tissue-based assay (TBA) on rat brain confirmed a neuronal cell-surface staining pattern; the full paraneoplastic panel, including anti-SOX1, was negative, and initial tumour screening was unrevealing. A diagnosis of anti-GABABR encephalitis (initially regarded as non-paraneoplastic) was made and the patient improved with intravenous immunoglobulin (IVIG), high-dose corticosteroids and maintenance mycophenolate mofetil. During a refractory second relapse 5 months later, repeat CBA showed rising anti-GABABR titres (serum 1:10,000; CSF 1:1000) and newly positive anti-SOX1 antibodies (serum 1:100; CSF 1:1); a previously occult right superior mediastinal mass radiologically compatible with SCLC was identified on repeat chest CT. The diagnosis was revised to anti-GABABR/anti-SOX1 dual-antibody PAE (probable PNS by 2021 PNS-Care criteria). The family declined biopsy, PET/CT and antitumour therapy because of advanced age and frailty; repeated IVIG with continued immunosuppression achieved partial clinical stabilisation with persistent cognitive impairment. Apparently isolated anti-GABABR encephalitis can evolve into dual anti-GABABR/anti-SOX1 paraneoplastic disease, with the second antibody heralding an occult SCLC. Repeating both CBA-based and intracellular antibody panels at every clinical relapse, together with repeat thoracic imaging, is essential to avoid missing an evolving paraneoplastic aetiology.

PMID 42494433
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