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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

PubMedThe American journal of managed care2026-06-08

Socioeconomic and racial disparities in Guillain-Barré syndrome.

Altun Yagiz M YM, Bader Edward R ER, Yan Siyu S, Gluck Lauren L

Guillain-Barré syndrome (GBS) is a rapidly progressive neuromuscular disorder that often requires intensive care and immunomodulatory therapy. Despite standardized treatment approaches, access to care and outcomes may be influenced by social determinants of health. We evaluated associations between socioeconomic and racial factors and inpatient interventions and outcomes in GBS in the US. Retrospective cohort study. This retrospective cohort study used data from the National Inpatient Sample (2016-2021) to identify hospitalizations with a primary diagnosis of GBS ( International Statistical Classification of Diseases, Tenth Revision code G61.0). Multivariable logistic regression models assessed associations between demographic and socioeconomic variables and 5 prespecified outcomes: in-hospital mortality, nonroutine discharge, prolonged hospitalization, receipt of intravenous immunoglobulin (IVIG), and receipt of plasmapheresis. We analyzed 45,515 GBS-related hospitalizations (patients' mean age, 50.7 years; 46.0% female). After adjusting for covariates, higher zip code income was associated with reduced inpatient mortality (OR per quartile, 0.80; 95% CI, 0.66-0.98). Admission to private investor-owned hospitals was associated with lower IVIG or plasmapheresis use, an effect not seen when analyzing only privately insured patients. Black patients were less likely to receive plasmapheresis (OR, 0.75; 95% CI, 0.59-0.95). Black and Native American patients had higher odds of nonroutine discharge (Black: OR, 1.26; 95% CI, 1.06-1.51; Native American: OR, 2.16; 95% CI, 1.20-3.88). Medicare coverage was associated with higher odds of nonroutine discharge (OR, 1.90; 95% CI, 1.62-2.23), and Medicaid coverage was associated with prolonged hospitalization (OR, 1.73; 95% CI, 1.48-2.02). Self-pay was linked to reduced odds of nonroutine discharge but longer hospitalization (OR, 0.53; 95% CI, 0.43-0.66). This study reveals socioeconomic, racial, and institutional disparities in GBS hospitalization outcomes despite standardized treatment guidelines. These findings highlight the need for equity-focused strategies to ensure timely and consistent care for patients with acute neurologic conditions.

PMID 42258266
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PubMedClinical case reports2026-06-08

ECMO Support in Paraneoplastic Pemphigus With Respiratory Failure: A Case Report With Immune Cell Monitoring.

Li Lu L, Chen Danxia D, Jin Linzi L, Shu Qinqin Q et al.

Paraneoplastic pemphigus (PNP) is a life-threatening autoimmune blistering disease with a mortality rate of 70%-90%, driven largely by respiratory complications such as bronchiolitis obliterans. Managing respiratory failure in these patients remains exceptionally difficult. We report a 33-year-old male with follicular dendritic cell sarcoma who developed severe PNP complicated by type II respiratory failure and obstructive bronchiolitis requiring veno-venous extracorporeal membrane oxygenation (ECMO) support. The patient's PNP skin lesions improved during a treatment course that included ECMO support, intravenous immunoglobulin (IVIG), immunosuppressants, hemodialysis, and plasma exchange. Serial immune cell subset monitoring showed a rising CD4/CD8 ratio (+94.8%) and Helper T cells (+33.8%), alongside declining NK cells (-48.2%), T lymphocytes (-17.7%), and Suppressor T cells (-31.6%). This case illustrates successful short-term management of severe PNP with respiratory failure through multidisciplinary care, including ECMO. Because multiple interventions were administered concurrently, improvement cannot be attributed to any single therapy. Serial immune-cell monitoring may help track treatment response in this setting.

PMID 42256927
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PubMedBrain : a journal of neurology2026-06-08

Septin multimer autoantibodies in severe motor neuropathy mimicking lower motor neuron disease.

Arlt Friederike A FA, Miske Ramona R, Appeltshauser Luise L, Zinnow Viktoria V et al.

Severe neuropathies with predominant involvement of motor fibers can resemble lower motor neuron disease (LMND) phenotypes. Given the fatal prognosis of LMND, identifying underlying autoimmune syndromes is crucial to provide treatment options to patients. We investigated a novel autoantibody binding pattern observed on murine teased sciatic nerve fibers. Target antigens were identified using immunoprecipitation combined with mass spectrometry. Target specificity of these autoantibodies was validated in cell-based assays, neutralization assays, and knock-out models. A retrospective study cohort consisting of different neuropathies (chronic inflammatory demyelinating polyradiculopathy n=86, Guillain-Barré syndrome n=37, multifocal motor neuropathy n=18, diabetic neuropathy n=30, other inflammatory neuropathies n=10), amyotrophic lateral sclerosis (n=50), multiple sclerosis (n=50), and healthy controls (n=50) was negative for septin multimer autoantibodies. Histopathological analysis of skin and sural nerve including electron microscopy was performed in one seropositive patient, and autoantibody binding was characterized in vitro. Extensive immunotherapy was initiated in one patient, with clinical and serological follow-up over four years. Among 3,543 total samples tested, three patients (two male, one female) - diagnosed with the LMND variant of amyotrophic lateral sclerosis (ages 65, 72, and 79, respectively) - showed a novel and distinct autoantibody binding pattern of indirect immunofluorescence staining on peripheral nerves, targeting Schmidt-Lanterman incisures (SLIs), paranodes, and the abaxonal myelin. Target identification and validation revealed septin multimers as autoantibody epitopes. Despite the primarily intracellular location of septins, autoantibody binding was evident in living myelinated dorsal root ganglia, primarily at SLIs ("incisuropathy"). Septin multimer autoantibodies further initiated complement deposition on fixed and permeabilized cell-based assays. Sural nerve and skin biopsies showed inflammation, myelin and axonal pathology. Extensive immunotherapy in one patient was followed by disease stabilization over three years. The other two patients died of rapid disease progression: One of them received no immunotherapy while the other had ineffective treatments with single administrations of IVIG and rituximab. Our data suggest that septin multimer autoimmunity occurs in severe motor predominant neuropathies which can clinically resemble a neurodegenerative LMND. Screening for septin multimer autoantibodies should be considered in patients presenting with this phenotype. Follow-up studies need to determine the direct pathogenicity of septin multimer autoantibodies, their potential as a biomarker of an autoimmune syndrome, and responses to immunotherapy in larger cohorts.

PMID 42252093
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PubMedJournal of thrombosis and haemostasis : JTH2026-06-06

Management of anticoagulation in patients with heparin-induced thrombocytopenia requiring cardiac surgery with cardiopulmonary bypass: Guidance from the ISTH SSC on Perioperative and Critical Care Haemostasis and Thrombosis.

Pishko Allyson M AM, Frere Corinne C, Maier Cheryl L CL, Levy Jerrold H JH et al.

Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse drug reaction characterized by thrombocytopenia and a high risk of thrombosis. Patients with HIT and a need for cardiac surgery with cardiopulmonary bypass (CPB) represent a challenging group, as anticoagulation with unfractionated heparin (UFH) is the primary treatment choice. We conducted a systematic review evaluating intraoperative anticoagulation strategies for patients with a history of HIT who required cardiac surgery with CPB. Guidance statements were generated through consensus of the writing group. Of 1732 screened articles, 30 studies were included. Strategies evaluated were (1) direct thrombin inhibitors; (2) UFH after preoperative or intraoperative therapeutic plasma exchange (TPE); (3) UFH in combination with a potent antiplatelet agent; and (4) Heparin re-exposure in patients with negative functional assays. Of these, bivalirudin has the strongest supporting data and appears effective; still, its association with increased bleeding and practical limitations, including a lack of a reversal agent, limit its use. TPE with or without IVIG reduces anti-PF4/heparin antibody titers and allows for intraoperative UFH use, although protocols are heterogeneous. Use of potent antiplatelet agents with UFH re-exposure show promise but carry risks of bleeding and hypotension. Thus, alternative strategies of using UFH in combination with TPE or potent antiplatelet agents may be considered on a case-by-case basis. For patients with negative functional assays, evidence suggests that limited intraoperative UFH re-exposure carries a low risk of HIT recurrence, provided postoperative monitoring is performed. These guidance statements provide a framework for multidisciplinary decision-making in a complex clinical scenario.

PMID 42248416
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PubMedStem cell reports2026-06-05

Intravenous immunoglobulin enhances intestinal stem cell regeneration to mitigate radiation-induced enteritis via promoting β-catenin nuclear translocation.

He Jia J, Chu Tiancheng T, Fu Ping P, Jiang Peng P et al.

Radiation-induced enteritis (RIE), a common adverse effect after radiotherapy for pelvic, abdominal, and retroperitoneal tumors, has no effective treatment. Our previous study showed that intravenous immunoglobulin (IVIg) ameliorated radiation toxicity. Here, we investigated the role of IVIg in enhancing intestinal stem cell (ISC) regeneration to mitigate RIE and its underlying mechanism. In a mouse RIE model, IVIg improved tissue repair, reduced intestinal epithelial apoptosis and pyroptosis, decreased inflammatory factors, enhanced antioxidant capacity, and alleviated DNA damage. Notably, IVIg promoted the proliferation of OLFM4+ and LGR5+ ISCs in crypts and mitigated radiation-induced enteroid damage in vitro. Lineage tracing revealed that IVIg enhanced LGR5+ ISCs and their daughter cell survival. Mechanistically, IVIg promoted β-catenin nuclear translocation, and the β-catenin inhibitor MSAB diminished IVIg's radioprotective effects. Collectively, IVIg combats RIE by enhancing ISC regeneration via β-catenin nuclear translocation, highlighting its potential as an RIE therapeutic candidate.

PMID 42242214
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PubMedImmunology letters2026-06-05

Characterization of innate immune cells with regulatory functions in subjects with a remote history of Kawasaki disease who lack natural regulatory T cell specificities.

Song Jaeyoon J, Ruedas Montero Ruben E RE, Hernandez Sophia Y SY, Tremoulet Adriana H AH et al.

Kawasaki disease (KD) is an acute pediatric vasculitis of the coronary arteries. In the acute phase, natural regulatory T cells (nTreg) that recognize peptides of the heavy constant region of IgG (Fc), an important nTreg specificity in humans, are poorly expanded. Intravenous immunoglobulin therapy (IVIG) restores the expansion of Fc-specific nTreg, by providing high concentrations of Fc. However, Fc-specific nTreg wane over time, shortly after IVIG. Here we explored the mechanism that prevents the undesirable activation of pro-inflammatory T cells in healthy subjects with a remote history of KD, studied years after IVIG. Indeed, we characterized several innate immune cells that secreted two suppressive cytokines, interleukin-1 receptor antagonist (IL-1Ra) and IL-10. When studied side-by-side with healthy controls, we did not find differences within the immune monitoring between the two cohorts. Of interest, classical monocytes were activated and expanded in an Fc-dependent manner, secreted IL-1Ra and IL-10, and polarized toward regulatory DC. The results suggested that IgG concentrations play a role in the differentiation of monocytes, unveiling a mechanism for immune regulation.

PMID 42242631
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