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| Primary information |
|---|
| ID | 10816 |
| Therapeutic ID | Th1190 |
| Protein Name | Immune Globulin Human |
| Sequence | >Th1190_Immune_Globulin_Human
PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL
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| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S46 |
| Isoelectric Point | 8.13 |
| Hydrophobicity | -0.331 |
| Melting point | 61 °C (FAB fragment), 71 °C (whole mAb) |
| Half-life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Brand Name | Carimune Nanofiltered |
| Company | Csl Behring Ag |
| Brand Description | Csl Behring Ag |
| Prescribed For | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. |
| Chemical Name | NA |
| Formulation | 12 g/1 |
| Physical Appearance | injection, powder, lyophilized, for solution |
| Route of Administration | Intravenous |
| Recommended Dosage | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. |
| Contraindication | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. |
| Side Effects | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. |
| Useful Link 1 | Link |
| Useful Link 2 | NA |
| Remarks | NA |