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11228 details
Primary information
ID11228
Therapeutic IDTh1243
Protein NameHuman immunoglobulin G
Sequence>Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL
Molecular Weight142682.3
Chemical FormulaC6332H9826N1692O1980S42
Isoelectric Point8.13
Hydrophobicity-0.331
Melting point61 °C (FAB fragment), 71 °C (whole mAb)
Half-life>20 hours (mammalian reticulocytes, in vitro).
DescriptionIntravenous 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/DiseaseIVIg 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.
PharmacodynamicsUsed 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 ActionIVIg 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.
ToxicityNA
MetabolismNA
AbsorptionNA
NA
ClearanceNA
CategoriesNA
Patents NumberNA
Date of IssueNA
Date of ExpiryNA
Drug InteractionNA
TargetHigh 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 NameWinrho
CompanyCangene BioPharma, LLC
Brand DescriptionCangene BioPharma, LLC
Prescribed ForIntramuscular; Intravenous
Chemical Name600 [iU]/1mL
FormulationWinRho SDF is contraindicated in: Patients who have had known anaphylactic or severe systemic reaction to the administration of human immune globulin products. IgA-deficient patients with antibodies to IgA or a history of hypersensitivity reaction to WinRho SDF or any of its components. Patients with autoimmune hemolytic anemia, with pre-existing hemolysis or at high risk for hemolysis. Infants for the suppression of Rho (D) isoimmunization.
Physical Appearance hives, difficulty breathing, swelling of your face, lips, tongue, or throat, rash, lightheadedness, chest tightness, fever, chills, shaking, back pain, unusual weakness, red or pink urine, pale or yellowed skin, dark colored urine, rapid breathing, rapid heart rate, confusion, shortness of breath, little or no urinating, swelling, rapid weight gain, sudden numbness or weakness, slurred speech, problems with vision or balance, chest pain, coughing up blood, and swelling with redness and warmth in one or both legs
Route of AdministrationNA
Recommended DosageNA
ContraindicationNA
Side EffectsNA
Useful Link 1Link
Useful Link 2Link
RemarksNA