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immunoglobulin (Bivigam)

✓ Approved

ADMA Biologics, Inc. · Polyclonal Antibodies · Polyclonal Antibodies

What is immunoglobulin?

immunoglobulin is a polyclonal antibodies developed by ADMA Biologics, Inc.. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesBivigam
CompanyADMA Biologics, Inc.
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Therapeutic Indications

immunoglobulin is developed for 5 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersCombined immunodeficiency✓ Approved
Congenital, familial and genetic disordersWiskott-Aldrich syndrome✓ Approved
Immune system disordersSelective IgG subclass deficiency✓ Approved
Congenital, familial and genetic disordersBruton's agammaglobulinaemia✓ Approved
Immune system disordersImmunodeficiency✓ Approved

Related Research Articles

PubMed[Rinsho ketsueki] The Japanese journal of clinical hematology2026-08-30

[Intrathecal immunoglobulin administration for refractory viral central nervous system infection after allogeneic hematopoietic stem cell transplantation].

Matsuo Masaaki M, Kusakabe Shinsuke S, Kurashige Ryumei R, Fukushima Kentaro K et al.

Central nervous system (CNS) viral infections after allogeneic hematopoietic stem cell transplantation are associated with poor prognosis and have limited therapeutic options. We report three cases of refractory CNS viral infection treated by combination therapy with antiviral agents and intrathecal immunoglobulin administration. Case 1 involved cytomegalovirus encephalitis, Case 2 varicella zoster virus meningitis, and Case 3 human herpesvirus 6 encephalitis; all were resistant to antiviral agents. Two patients achieved viral DNA negativity in cerebrospinal fluid, and none experienced adverse events related to intrathecal injection. Although no intrathecal immunoglobulin products have been approved for use in Japan, our findings suggest that this treatment may be a viable option in selected refractory cases. Further studies are warranted to clarify the optimal agent, dosage, and schedule.

PubMedFood chemistry: X2026-08-30

Proteomic insights into goat milk serum proteins at varying altitudes in China.

Li Zhaomin Z, Wang Shanshan S, Cao Hanwen H, Yan Yingying Y et al.

Using Astral DIA quantitative proteomics, this study characterized serum protein profiles and potential functions of goat milk from different altitude regions. A total of 1446 proteins were identified, with 1268, 1256, and 1346 proteins detected in high-altitude, mid-altitude, and low-altitude samples, respectively. The high-altitude sample contained 34 unique proteins and showed higher abundances of α-lactalbumin, serum albumin, and polymeric immunoglobulin receptor, whereas the low-altitude sample contained 87 unique proteins and higher abundances of several immune-related proteins, including osteopontin, lactoferrin, immunoglobulin, lysozyme, xanthine oxidase, lactoperoxidase, and GLYCAM1. Differentially expressed analysis identified 453, 452, and 113 differential proteins in high-altitude vs. low-altitude, mid-altitude vs. low-altitude, and high-altitude vs. mid-altitude comparisons, respectively. KEGG analysis showed that carbohydrate metabolism was enriched in comparisons involving the low-altitude sample, whereas amino acid metabolism was enriched between high-altitude and mid-altitude samples. Notably, HIF-1 signaling pathway was enriched in the high-altitude sample, suggesting hypoxia-associated proteomic adaptation.

PubMed[Rinsho ketsueki] The Japanese journal of clinical hematology2026-08-30

[Predictors of treatment-free remission (TFR) and second TFR attempts in chronic myeloid leukemia].

Ureshino Hiroshi H

The introduction of tyrosine kinase inhibitors (TKIs) has made long-term survival achievable for patients with chronic myeloid leukemia (CML). In patients who achieve a deep molecular response, treatment-free remission (TFR), defined as sustained remission without molecular relapse after TKI discontinuation, has emerged as an important therapeutic goal. Accumulating evidence indicates that the establishment and maintenance of TFR are strongly influenced by host immunity, particularly immune surveillance mediated by natural killer (NK) cells. This review summarizes the clinical and immunological factors associated with successful TFR and discusses the potential of killer immunoglobulin-like receptor/human leukocyte antigen genetic polymorphisms as predictive biomarkers that regulate NK cell function and TFR outcomes. It also highlights immunomodulatory strategies using interferon-α, the feasibility of second attempts at TFR after initial discontinuation failure, and emerging therapeutic approaches targeting CML stem cells to achieve more durable disease control.

PubMedCureus2026-08-30

Lethargy With Reversible Bilateral Basal Ganglia and Substantia Nigra Lesions in Anti-N-Methyl-D-Aspartate Receptor Encephalitis: A Case Report.

Abe Daisuke D, Hidaka Masaoki M, Kumamoto Masaya M, Kanazawa Yuka Y et al.

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a neuroinflammatory disorder characterized by a broad spectrum of neuropsychiatric symptoms, and the optimal treatment strategy for atypical or refractory cases has not been well established. We report the case of a 26-year-old woman with anti-NMDAR encephalitis associated with an ovarian teratoma who presented with acute psychiatric and neurological manifestations. The patient underwent tumor resection followed by first-line immunotherapies, including corticosteroids, intravenous immunoglobulin, and plasma exchange. Because of persistent neurological symptoms, second-line immunotherapy with cyclophosphamide was initiated, leading to gradual clinical improvement. However, she subsequently developed lethargy and upper-limb tremors, accompanied by bilateral basal ganglia and substantia nigra abnormalities on MRI. Notably, both her clinical symptoms and radiological abnormalities improved following an additional course of cyclophosphamide treatment. This report highlights a rare clinical and radiological manifestation and suggests that additional immunotherapy may be effective for delayed neurological worsening.

PubMedCureus2026-08-30

Unrecognized Charcot-Marie-Tooth Disease Unmasked by Chemotherapy-Induced Neurotoxicity.

Fernandes Isabel V IV, Melo Sara S, Sousa Gabriela M GM, Pazos Maria Isabel MI et al.

Chemotherapy-induced peripheral neuropathy (CIPN) is among the most prevalent and clinically significant toxicities from systemic cancer treatments, with taxanes being a leading cause. It is characterised by a length-dependent, predominantly sensory axonal neuropathy that can stabilise or improve after treatment discontinuation. However, the clinical course can be profoundly altered by underlying peripheral nerve pathology. We report the case of a 68-year-old woman with luminal B, HER2-negative breast cancer who developed severe peripheral neuropathy during adjuvant chemotherapy with doxorubicin/cyclophosphamide followed by weekly paclitaxel. Treatment was discontinued after 9 of 12 planned paclitaxel cycles due to grade 3 peripheral neuropathy ( Common Terminology Criteria for Adverse Events (CTCAE) v5.0). Despite cessation of the offending agent and initiation of duloxetine, symptoms continued to worsen, with progressive motor impairment and significant gait instability. Nerve conduction studies revealed a severe sensorimotor demyelinating polyneuropathy, atypical for the predominantly axonal pattern of taxane-induced CIPN. Inflammatory, infectious, paraneoplastic, and metabolic causes were excluded, and empirical corticosteroids and intravenous immunoglobulin proved ineffective. Genetic testing identified a peripheral myelin protein 22 (PMP22) duplication (17p11.2), confirming Charcot-Marie-Tooth disease type 1A (CMT1A), a hereditary demyelinating neuropathy previously subclinical. This case report underscores the value of serial clinical and electrophysiological assessment when neuropathy is atypical, disproportionately severe, or refractory to standard treatment.

PubMedKidney medicine2026-08-30

NSAID-Induced Acute Interstitial Nephritis Concurrent With IgA Vasculitis: A Case-Based Systematic Review.

Caputo Carmela C, Sessa Concetto C, Serio Vittorio V, Baciga Federica F et al.

Overlap between acute interstitial nephritis (AIN) and glomerulonephritis is uncommon and diagnostically challenging. We present the first pediatric case of clinically diagnosed immunoglobulin A vasculitis nephritis (IgAV-N) concurrent with nonsteroidal anti-inflammatory drug (NSAID)-induced AIN. A 14-year-old boy was hospitalized for recurrent gastroenteritis, purpura, and arthralgia treated with ibuprofen. After 5 days, he developed stage 3 acute kidney injury, subnephrotic proteinuria, hypertension, and oligoanuria. Kidney biopsy showed mild to moderate interstitial inflammation with tubulitis; immunofluorescence was negative for glomerular IgA, with nonspecific tubular C3 staining. After NSAID discontinuation, 10 dialysis sessions, and corticosteroids, kidney function recovered completely within 3 months. To support the clinical lesson highlighted by our case, we conducted a systematic review of biopsy-confirmed AIN-glomerulonephritis overlap. PubMed, Scopus, Web of Science, and Google Scholar were searched for biopsy-confirmed AIN with concurrent glomerulonephritis. Clinical features, etiologies, treatments, and outcomes were extracted. Systematic review identified 8 studies (12 patients). Drug-related AIN predominated (9 of 12), followed by infection (2 of 12) and autoimmune disease (1 of 12). Nephrotic-range proteinuria was described in 6, hematuria in 8, and hypersensitivity findings in 7 of the 12 patients. Complete recovery occurred in 7 and partial recovery in 3 patients, and dialysis was required in 2 of the 12 patients. NSAID-induced AIN concurrent with IgA vasculitis nephritis should be suspected in atypical acute kidney injury.

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