Browse result page of ThPDB2
This is the result page of the browse module of ThPDB2. This page gives the information about the query submitted by the user as per the browse category. Further details of the entries can be seen by clicking on the ID or THPP_ID. Further the user can sort the entries on the basis of various fields by clicking on the respective headers. The user can also download the results in various formats.
Tabular representation:
| ID | THPP_ID | Therapeutic Name | Sequence | Molecular Weight | Chemical Formula | Isoelectric Point | Hydrophobicity | Melting Point | Half Life | Description | Disease/Indication | Pharmacodynamics | Mechanism of Action | Toxicity | Metabolism | Absorption | Volume of Distribution | Clearance | Categories | Patent Number | Date of Issue | Date of Expiry | Drug Interaction | Target | Brand Name | Company | Brand Description | Prescribed for | Chemical Name | Formulation | Physical Appearance | Route of Administation | Recommended Dosage | Contraindication | Side Effects | Useful Links 1 | Useful Links 2 | Remarks |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10193 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | Antibodies in Flebogamma 5% may interfere with the response to live viral vaccines, such as measles, mumps, and rubella. Physicians should be informed of recent therapy with Immune Globulin Intravenous (Human) so that administration of live viral vaccine | 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 reg | Civacir | NA | NA | To prevent HCV infection in liver transplant patients; Prevent recurrence of hepatitis C-related liver disease in HCV positive liver transplant recipients or in patients who received an HCV-positive liver; Treat and prevent HCV infection | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10194 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Asceniv | Adma Biologics, Inc. | Adma Biologics, Inc. | used to treat the symptoms of Primary Immunodeficiency Syndrome (PI), Immune Thrombocytopenic Purpura (ITP), Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. | NA | The manufacturing process of ASCENIV employs three steps to remove/inactivate adventitious viruses to minimize the risk of virus transmission. The steps are "Precipitation and removal of fraction III" during cold ethanol fractionation, classical "solvent/detergent treatment" and "35 nm virus filtration." In compliance with current guidelines, the steps have been separately validated in a series of in vitro experiments for their capacity to inactivate or remove both enveloped and nonenveloped viruses. | clear to opalescent liquid, which is colorless to pale yellow. | Intravenous | The recommended dose of ASCENIV for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dose may be adjusted over time to achieve the desired trough levels and clinical response. | ASCENIV is contraindicated in: patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA-deficiency patients with antibodies to IgA and a history of hypersensitivity. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, fever, confusion, weakness, increased thirst or feeling hot, inability to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness of breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with severe headache, neck stiffness, eye pain, increased sensitivity to light, shortness of breath, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and welling and warmth, or discoloration in an arm or leg | Link | NA | NA |
| 10195 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Bivigam | Adma Biologics, Inc. | Adma Biologics, Inc. | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). This includes, but is not limited to, the humoral immune defect in common variable immunodeficiency (CVID), X-linked agammaglobulinemia, congenital agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies. | NA | The manufacturing process of BIVIGAM employs three steps to remove/inactivate adventitious viruses to minimize the risk of virus transmission. The steps are “Precipitation and removal of fraction III” during cold ethanol fractionation, classical “Solvent/detergent treatment” and “35 nm virus filtration”. In compliance with current guidelines, the steps have been separately validated in a series of in vitro experiments for their capacity to inactivate or remove both enveloped and non-enveloped viruses. Precipitation and removal of fraction III removes both enveloped and non-enveloped viruses, solvent/detergent treatment represents a virus inactivation step for enveloped viruses, and 35 nm virus filtration removes both enveloped and non-enveloped viruses by size exclusion. In addition to the steps above, low pH during several steps of the production process contributes to virus inactivation. The results of virus validation studies for BIVIGAM are shown in Table 3, expressed as log10 reduction factors. | sterile liquid | Intravenous infusion | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Link | NA | NA |
| 10196 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Flebogamma | Instituto Grifols SA | Instituto Grifols SA | It is indicated for replacement therapy in primary (inherited) humoral immunodeficiency disorders, such as common variable immunodeficiency, x-linked agammaglobulinemia, severe combined immunodeficiency, and Wiskott-Aldrich Syndrome. Flebogamma 5% is espe | NA | Flebogamma 5% contains 50 mg IgG per mL, 50 mg D-sorbitol per mL, and _ 6 mg/mL polyethylene glycol. There is no preservative in the formulation. The pH of the solution ranges from 5 to 6 and the osmolarity from 240 to 350 mOsm/L | Sterile, clear or slightly opalescent and colorless to pale yellow liquid | Intravenous infusion | Normally given as 300 to 600 mg/kg body weight subjects with primary humoral immunodeficiency disease (PID) every 3 or 4 weeks for 12 months. | Flebogamma 5% should not be administered to individuals with a history of severe or anaphylactic reactions to blood or blood-derived products. Individuals with selective IgA deficiency and demonstrable antibodies to IgA should not receive Flebogamma 5%. | Rash; itching; hives; difficulty breathing or swallowing; tightness in the chest; swelling of the mouth, hands, face, lips, eyes, throat, or tongue; bloating; calf pain or tenderness; chest pain; confusion; dark urine; decreased urination; fainting; fast or irregular heartbeat; fever or chills; increased or painful urination; numbness of an arm or a leg; one-sided weakness; red, swollen, blistered, or peeling skin; seizures; severe headache, dizziness, or stomach pain; shortness of breath or trouble breathing; speech problems; sweating; symptoms of kidney problems (eg, decreased urination, lower back or flank pain, swelling or bloating, sudden weight gain); unusual tiredness or weakness; vision problems; yellowing of the skin or eyes. | Link | NA | NA |
| 10197 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Cutaquig | Pfizer | Pfizer | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10198 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamastan | Grifols Therapeutics Llc | Grifols Therapeutics Llc | used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. | NA | In the manufacturing process of GAMASTAN, there are several steps with the capacity for viral inactivation or removal. The main steps of the manufacturing process that contribute to the virus clearance capacity are as follows: Caprylate precipitation/depth filtration Caprylate incubation Depth filtration Column chromatography Nanofiltration Low pH final container incubation | clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution | Intravenous | 0.1 mL/kg 0.2 mL/kg 0.2 mL/kg | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human). | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, itching, red, swollen, blistered, or peeling skin with or without fever, wheezing, tightness in the chest or throat, trouble breathing, swallowing, or talking, and unusual hoarseness | Link | NA | NA |
| 10199 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamunex | Talecris Biotherapeutics | Talecris Biotherapeutics | Gamunex-C is used to treat primary immunodeficiency (PI). This includes, but is not limited to, congenital agammaglobulinemia, common variable immunodeficiency, X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies. | NA | GAMUNEX (immune globulin intravenous human 10%) consists of 9%–11% protein in 0.16–0.24 M glycine. Not less than 98% of the protein has the electrophoretic mobility of gamma globulin. GAMUNEX (immune globulin intravenous human 10%) contains trace levels o | Sterile solution | Intravenous infusion | Treatment of Primary Humoral Immunodeficiency = The dose of GAMUNEX (immune globulin intravenous (human) 10%) for replacement therapy in primary immune deficiency diseases is 300 to 600 mg/kg body weight (3-6 mL/kg) administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical responses. | GAMUNEX (immune globulin intravenous (human) 10%) is contraindicated in individuals with acute severe hypersensitivity reactions to Immune Globulin (Human). GAMUNEX (immune globulin intravenous (human) 10%) contains trace amounts of IgA. It is contraindic in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. | Mild headache; dizziness; tired feeling; back pain, muscle cramps; minor chest pain; or flushing (warmth, redness, or tingly feeling). | Link | NA | NA |
| 10200 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 20 hours (mammalian reticulocytes, in vitro) | 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. | 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. | Used as 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. | 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 taggingor 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamimune N | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10577 | Th1118 | Sulodexide | NA | 5000-8000 | NA | NA | NA | NA | elimination half-life was 11.7 ± 2.0 h by IV route | A mixture of glycosaminoglycans (GAGs), composed of dermatan sulfate (DS) and fast moving heparin (FMH). | For the treatment of thrombosis. Also investigated for use/treatment in diabetic kidney disease, and neuropathy (diabetic). | The low molecular weight of both sulodexide fractions allows for extensive oral absorption compared to unfractionated heparin. The pharmacological effects of sulodexide differ substantially from other glycosaminoglycans and are mainly characterized by a prolonged half-life and reduced effect on global coagulation and bleeding parameters. Due to the presence of both glycosaminoglycan fractions, sulodexide potentiates the antiprotease activities of both antithrombin III and heparin cofactor II simultaneously. | Thrombin inhibition produced by sulodexide is due to the additive effect of its components, namely, heparin cofactor II (HCII) catalysis by dermatan sulfate and antithrombin-III catalysis by fast moving heparin (FMH). | Sulodexide seems to be well tolerated. Most adverse effects reported are related to the GI system and seem to be transient in nature. Among others adverse reactions are diarrhea, epigastralgia, dyspepsia, heartburn and dizziness. Allergic reactions, such as skin rash, have also been reported but are very rare. | It is mainly metabolized in the liver. | Sulodexide can be administered via the oral route, IV and IM routes. After oral dosing, the absorption rate being equivalent, the bioavailability is 40-60%. either calculated from the fast-moving heparin fraction or from the dermatan fraction. Bioavailability following IM administration is approximately 90%. After a rapid absorption in the intestine, the dermatan and heparin components start to appear in the plasma. Sulodexide is degraded after ingestion and loses its sulfate groups and both sulfated and unsulfated groups circulate in the blood for up to 24hours. AUC=22.83+/-4.44mg.h/L. | Cmax=516+/-77.54ng/mL, Tmax=1.33+/-0.58h, Vd=71.24+/-14.06L (b phase). Sulodexide reaches high concentrations in the plasma and is widely distributed in the endothelial layer. Binding to endothelial cell receptors in arteries and veins contributes to its rapid distribution profile. | 2.70+/-0.58L/h | Antithrombins and Fibrinolytic Agents and Hypoglycemic Agents and Anticoagulants and Hypolipidemic Agents | NA | NA | NA | NA | Heparin cofactor 2,Antithrombin-III | SULODEXIDE | Syntex S.A | Syntex S.A | Antithrombotic and antithrombin activity is of great pharmacologic interest and makes sulodexide a suitable drug for the prophylaxis and treatment of arterial and venous peripheral diseases | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10812 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | NA | NA | NA | NA | NA | .165 g/mL; 10 g/100mL; 12 g/1; 3 g/1; v; 1 g/10mL; 10 g/100mL; 5 g/50mL; .05 g/mL; 100 mg/mL | Injection; Injection, powder, lyophilized, for solution; Injection, solution. | intramuscular; intravenous; subcutaneous | NA | NA | NA | NA | NA | NA |
| 10813 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S43 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Bivigam | Kedrion Biopharma, Inc. | Kedrion Biopharma, Inc. | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 1 g/10mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10814 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S44 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Bivigam | Biotest Pharmaceuticals Corporation | Biotest Pharmaceuticals Corporation | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 10 g/100mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10815 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S45 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Bivigam | Biotest Pharmaceuticals Corporation | Biotest Pharmaceuticals Corporation | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 11 g/100mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10816 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S46 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | 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. | NA | 12 g/1 | injection, powder, lyophilized, for solution | Intravenous | 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. | 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. | 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. | Link | NA | NA |
| 10817 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S47 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | 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. | NA | 6 g/1 | injection, powder, lyophilized, for solution | Intravenous | 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. | 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. | 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. | Link | NA | NA |
| 10818 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S48 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | 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. | NA | 3 g/1 | injection, powder, lyophilized, for solution | Intravenous | 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. | 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. | 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. | Link | NA | NA |
| 10819 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S49 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Flebogamma Dif | GRIFOLS USA, LLC | GRIFOLS USA, LLC | NA | NA | 5 g/50mL | injection, solution | Intravenous | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) | Flebogamma 10% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 10% DIF is contraindicated in IgA deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Link | NA | NA |
| 10820 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S50 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Flebogamma Dif | GRIFOLS USA, LLC | GRIFOLS USA, LLC | NA | NA | .05 g/mL | injection, solution | Intravenous | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) | Flebogamma 10% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 10% DIF is contraindicated in IgA deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Link | NA | NA |
| 10821 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S51 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Gamastan | Cutter Med & Biol, Division Of Miles Canada Ltd. | Cutter Med & Biol, Division Of Miles Canada Ltd. | Passive immunization should be considered when vaccines for active immunization are not available, or in situations when vaccine has not been used prior to exposure to the infective agent or is contraindicated | NA | 0.165 | liquid | Intramuscular | For Hepatitis A- GamaSTAN® S/D in a dose of 0.02 mL/kg is recommended for household and institutional hepatitis A case contacts.; For measles- GamaSTAN® S/D should be given in a dose of 0.25 mL/kg to prevent or modify measles in a susceptible person exposed fewer than 6 days previously (1,2). A susceptible child who is exposed to measles and who is immunocompromised should receive a dose of 0.5 mL/kg (maximum dose, 15 mL) of GamaSTAN® S/D immediately (3). The dosage of Immune Globulin (Human) for exposed individuals who have underlying malignant disease should be 0.5 mL/kg or 15 mL maximum; For varicella- If Varicella-Zoster Immune Globulin (Human) is unavailable, GamaSTAN® S/D at a dose of 0.6 to 1.2 mL/kg, promptly given, may also modify varicella; For Rubella- Some studies suggest that the use of GamaSTAN® S/D in exposed, susceptible women can lessen the likelihood of infection and fetal damage; therefore, GamaSTAN® S/D at a dose of 0.55 mL/kg may benefit those women who will not consider a therapeutic abortion. | GamaSTAN® S/D should not be given to patients who are hypersensitive to this drug or to any ingredient in the formulation or component of the container. For a complete listing, see the Dosage Forms, Composition And Packaging section. GamaSTAN® S/D should not be given to persons with isolated immunoglobulin A (IgA) deficiency. Such persons have the potential for developing antibodies to IgA and could have anaphylactic reactions to subsequent administration of blood products that contain IgA (7). GamaSTAN® S/D should not be administered to patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections. | Local pain and tenderness at the injection site, urticaria, and angioedema may occur. Anaphylactic reactions, although rare, have been reported following the injection of human immune globulin preparations. Anaphylaxis is more likely to occur if GamaSTAN® S/D is given intravenously; therefore, GamaSTAN® S/D must be administered only intramuscularly. | Link | NA | NA |
| 10822 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S52 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Gamastan S/d | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Passive immunization should be considered when vaccines for active immunization are not available, or in situations when vaccine has not been used prior to exposure to the infective agent or is contraindicated | NA | .165 g/mL | injection | Intramuscular | For Hepatitis A- GamaSTAN® S/D in a dose of 0.02 mL/kg is recommended for household and institutional hepatitis A case contacts.; For measles- GamaSTAN® S/D should be given in a dose of 0.25 mL/kg to prevent or modify measles in a susceptible person exposed fewer than 6 days previously (1,2). A susceptible child who is exposed to measles and who is immunocompromised should receive a dose of 0.5 mL/kg (maximum dose, 15 mL) of GamaSTAN® S/D immediately (3). The dosage of Immune Globulin (Human) for exposed individuals who have underlying malignant disease should be 0.5 mL/kg or 15 mL maximum; For varicella- If Varicella-Zoster Immune Globulin (Human) is unavailable, GamaSTAN® S/D at a dose of 0.6 to 1.2 mL/kg, promptly given, may also modify varicella; For Rubella- Some studies suggest that the use of GamaSTAN® S/D in exposed, susceptible women can lessen the likelihood of infection and fetal damage; therefore, GamaSTAN® S/D at a dose of 0.55 mL/kg may benefit those women who will not consider a therapeutic abortion. | GamaSTAN® S/D should not be given to patients who are hypersensitive to this drug or to any ingredient in the formulation or component of the container. For a complete listing, see the Dosage Forms, Composition And Packaging section. GamaSTAN® S/D should not be given to persons with isolated immunoglobulin A (IgA) deficiency. Such persons have the potential for developing antibodies to IgA and could have anaphylactic reactions to subsequent administration of blood products that contain IgA (7). GamaSTAN® S/D should not be administered to patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections. | Local pain and tenderness at the injection site, urticaria, and angioedema may occur. Anaphylactic reactions, although rare, have been reported following the injection of human immune globulin preparations. Anaphylaxis is more likely to occur if GamaSTAN® S/D is given intravenously; therefore, GamaSTAN® S/D must be administered only intramuscularly. | Link | NA | NA |
| 10823 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S53 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Hyqvia | Baxalta Us Inc. | Baxalta Us Inc. | HYQVIA is an immune globulin with a recombinant human hyaluronidase indicated for the treatment of Primary Immunodeficiency (PI) in adults. This includes, but is not limited to, common variable immunodeficiency (CVID), X-linked agammaglobulinemia, congenital agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies | NA | 160 U/mL | Liquid | Intravenous infusion | Administer HYQVIA at 300 to 600 mg/kg at 3 to 4 week intervals, after initial ramp-up. | In patients who have had a history of anaphylactic or severe systemic reactions to the administration of IgG.IgA deficient patients with antibodies to IgA and a history of hypersensitivity. patients with known systemic hypersensitivity to hyaluronidase or Recombinant Human Hyaluronidase of HYQVIA. | Common adverse reactions observed in clinical trials in > 5% of subjects were: local reactions, headache, antibody formation against recombinant human hyaluronidase (rHuPH20), fatigue, nausea, pyrexia, and vomiting. | Link | NA | NA |
| 10824 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S54 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | 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. | Iveegam Immuno 5000mg (iv) | Baxter Ag | Baxter Ag | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10865 | Th1226 | Dinutuximab | NA | 145000 | C6422H9982N1722O2008S48 | NA | NA | NA | The terminal half-life is 10 days | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | Dinutuximab is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | In vitro dinutuximab binds to neuroblastoma tumour cells and mediates the lysis of tumour cells via cell-mediated and complement-mediated cytotoxicity. | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. | The most common (incidence 15 %) grade 3 or 4 treatment-related adverse events in dinutuximab compared with standard therapy recipients were neuropathic pain (52 vs. 6 %), fever without neutropenia (39 vs. 6 %), any in-fection (39 vs. 22 %), hypokalaemia (35 vs. 2 %), hypersensitivity reactions (25 vs. 1 %), hyponatraemia (23 vs. 4 %), elevation of alanine transferase levels (23 vs. 3 %) and hypotension (18 vs. 0 %). Based on its mechanism of action, dinutuximab may cause fetal harm when administered to a pregnant woman however, there are no studies in pregnant women and no reproductive studies in animals to inform the drug-associated risk. Non-clinical studies suggest that dinutuximab-induced neuropathic pain is mediated by binding of the antibody to the GD2 antigen located on the surface of peripheral nerve fibers and myelin and subsequent induction of cell- and complement-mediated cytotoxicity. In clinical trials, 114 (85%) patients treated in the dinutuximab/RA group experienced pain despite pre-treatment with analgesics including morphine sulfate infusion. Severe (Grade 3) pain occurred in 68 (51%) patients in the dinutuximab/RA group compared to 5 (5%) patients in the RA group. Pain typically occurred during the dinutuximab infusion and was most commonly reported as abdominal pain, generalized pain, extremity pain, back pain, neuralgia, musculoskeletal chest pain, and arthralgia. | NA | NA | The mean volume of distribution at steady state (Vdss) is 5.4 L | The clearance is 0.21 L/day and increases with body size | Antibody, Immunosuppresive agent, Antineoplastic agent | US20140170155 | 18-02-2014 | 18-02-2038 | Severity of adverse effect can be increased while combining Dinutuximab with Acebutolol, Acetazolamide, Acetyldigitoxin, Aldesleukin, Aliskiren, Amifostine, Amiloride, Amiodarone, Amlodipine etc | GD2 disialoganglioside | unituxin | NA | NA | Unituxin (dinutuximab) is indicated, in combination with granulocyte- macrophage colony - stimulating factor (GM- CSF), interleukin- 2 (IL- 2) and 13- cis -retinoic acid (RA ), for the treatment of pediatric patients with high- risk neuroblastoma who achieve at least a partial response to prior first -line multiagent, multimodality therapy. | NA | 1 mL of concentrate contains 3.5 mg of dinutuximab | sterile, preservative-free, clear/colorless to slightly opalescent solution | Intravenous | The recommended dose of Unituxin is 17.5 mg/m2/day administered as an intravenous infusion over 10 to 20 hours for 4 consecutive days for a maximum of 5 cycles. | History of anaphylaxis to dinutuximab. | The most common serious adverse reactions (≥ 5%) are infections, infusion reactions, hypokalemia, hypotension, pain, fever, and capillary leak syndrome. | Link | NA | NA |
| 11149 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | Diethylstilbestrol,Chlorotrianisene,Conjugated estrogens,Estrone,Estradiol,Dienestrol,Ethinylestradiol,Mestranol,Estriol,Estrone sulfate,Quinestrol,Hexestrol,Tibolone,Synthetic Conjugated Estrogens, A,Synthetic Conjugated Estrogens, B,Polyestradiol phosphate,Esterified estrogens,Zeranol,Equol,Promestriene,Methallenestril,Epimestrol,Moxestrol,Estradiol acetate,Estradiol benzoate,Estradiol cypionate,Estradiol valerate,Biochanin A,Formononetin,Estetrol,Cetuximab,Omalizumab,Adalimumab,Abciximab,Gemtuzumab ozogamicin,Indium In-111 satumomab pendetide,Infliximab,Trastuzumab,Rituximab,Basiliximab,Muromonab,Digoxin Immune Fab (Ovine),Ibritumomab tiuxetan,Tositumomab,Alemtuzumab,Capromab pendetide,Efalizumab,Antithymocyte immunoglobulin (rabbit),Natalizumab,Palivizumab,Daclizumab,Bevacizumab,Technetium Tc-99m arcitumomab,Eculizumab,Panitumumab,Ranibizumab,Galiximab,Pexelizumab,Afelimomab,Epratuzumab,Bectumomab,Oregovomab,IGN311,Adecatumumab,Labetuzumab,Matuzumab,Fontolizumab,Bavituximab,CR002,Rozrolimupab,Girentuximab,Obiltoxaximab,XTL-001,NAV 1800,Briakinumab,Otelixizumab,AMG 108,Iratumumab,Enokizumab,Ramucirumab,Farletuzumab,Veltuzumab,Ustekinumab,Trastuzumab emtansine,PRO-542,TNX-901,Inotuzumab ozogamicin,RI 624,MYO-029,CT-011,Leronlimab,Glembatumumab vedotin,Olaratumab,IPH 2101,TB-402,Caplacizumab,IMC-1C11,Eldelumab,Lumiliximab,Canakinumab,Ipilimumab,Nimotuzumab,Clenoliximab,Tocilizumab,BIIB015,Sonepcizumab,Motavizumab,Elotuzumab,AVE9633,Carotuximab,XmAb 2513,Coltuximab ravtansine,Lucatumumab,Pertuzumab,Siplizumab,Apolizumab,Sibrotuzumab,Bivatuzumab,Lerdelimumab,Lexatumumab,Reslizumab,Teplizumab,Catumaxomab,Mepolizumab,Denosumab,Volociximab,Ofatumumab,Golimumab,Brentuximab vedotin,Belimumab,Raxibacumab,Obinutuzumab,Secukinumab,Vedolizumab,Nivolumab,Siltuximab,Pembrolizumab,Dulaglutide,Blinatumomab,Anthrax immune globulin human,Dinutuximab,Asfotase alfa,Idarucizumab,Alirocumab,Evolocumab,Antilymphocyte immunoglobulin (horse),Daratumumab,Necitumumab,Ixekizumab,Ravulizumab,Atezolizumab,Tetanus immune globulin, human,Eftrenonacog alfa,Human varicella-zoster immune globulin,Conatumumab,Tabalumab,Ficlatuzumab,Figitumumab,Durvalumab,Bapineuzumab,Depatuxizumab mafodotin,Onartuzumab,Solanezumab,Sarilumab,Tremelimumab,Brodalumab,Sirukumab,Lampalizumab,Guselkumab,Dalotuzumab,Emibetuzumab,Ublituximab,Ligelizumab,Seribantumab,Landogrozumab,Romosozumab,Vadastuximab talirine,Lebrikizumab,Varlilumab,Avelumab,Crenezumab,Rilotumumab,Anifrolumab,Ocrelizumab,Benralizumab,Gantenerumab,Visilizumab,Urelumab,Lorvotuzumab mertansine,Patritumab,Fulranumab,Tarextumab,Sotatercept,Gevokizumab,Duligotuzumab,Simtuzumab,Fasinumab,Dupilumab,Tralokinumab,Etrolizumab,Zalutumumab,Ganitumab,Etaracizumab,Polatuzumab vedotin,Inclacumab,Cixutumumab,Ascrinvacumab,Aducanumab,GS-5745,Vanucizumab,Labetuzumab govitecan,Tanezumab,Ensituximab,Fezakinumab,Dusigitumab,Fresolimumab,Indusatumab vedotin,Bococizumab,Mirvetuximab Soravtansine,Mogamulizumab,Plozalizumab,Inebilizumab,Mavrilimumab,Blosozumab,Bimagrumab,Dacetuzumab,Tovetumab,Lumretuzumab,Ibalizumab,Intetumumab,Carlumab,Demcizumab,Sifalimumab,Abituzumab,Ecromeximab,Naptumomab estafenatox,Crotedumab,Concizumab,Depatuxizumab,Rontalizumab,Amatuximab,Clazakizumab,Ozanezumab,Sacituzumab govitecan,Bimekizumab,Milatuzumab,Robatumumab,Rovalpituzumab tesirine,Namilumab,Racotumomab,Tregalizumab,Olokizumab,Bezlotoxumab,Edrecolomab,Nebacumab,Human cytomegalovirus immune globulin,Emicizumab,Sulesomab,Besilesomab,Tildrakizumab,Burosumab,Erenumab,Eptinezumab,Fremanezumab,Galcanezumab,Fanolesomab,Lecanemab,Lanadelumab,Cemiplimab,Emapalumab,Risankizumab,Camrelizumab,Setrusumab,Gancotamab,Anetumab ravtansine,Isatuximab,Icrucumab,Codrituzumab,Brolucizumab,Xentuzumab,Lintuzumab,Vobarilizumab,Parsatuzumab,Emactuzumab,Bevacizumab zirconium Zr-89,Refanezumab,Rozanolixizumab,Bermekimab,Pamrevlumab,Opicinumab,Trastuzumab deruxtecan,Margetuximab,Dalantercept,Pateclizumab,Gremubamab,Apomab,Tafasitamab,Ipafricept,Abrilumab,Frovocimab,Tezepelumab,Tigatuzumab,Telisotuzumab vedotin,Utomilumab,Zolbetuximab,Ponezumab,Asunercept,Suvratoxumab,Mitazalimab,Nemolizumab,Bleselumab,Gedivumab,Valanafusp alfa,Sofituzumab vedotin,Istiratumab,Pidilizumab,GMA-161,Ladiratuzumab vedotin,Tomaralimab,Vesencumab,Pinatuzumab vedotin,Lulizumab pegol,Lorukafusp alfa,Naratuximab emtansine,Zenocutuzumab,Atoltivimab,Maftivimab,Odesivimab,Belantamab mafodotin,Ansuvimab,Bamlanivimab,Hepatitis B immune globulin,Human Rho(D) immune globulin,Dostarlimab,Certolizumab pegol,Inolimomab,Pentaglobin,Abagovomab,Efungumab,Foralumab,Indatuximab ravtansine,Magrolimab,Olinvacimab,Actoxumab,Volagidemab,Bentracimab,Amivantamab,Ebola Zaire vaccine (live, attenuated),Imlifidase,Imdevimab,Casirivimab,Cilgavimab,Tixagevimab | 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 | Asceniv | Adma Biologics, Inc. | Adma Biologics, Inc. | Intravenous | 5 g/50mL | ASCENIV is contraindicated in: patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA-deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache, sinusitis, diarrhea, viral gastroenteritis, runny or stuffy nose, upper respiratory tract infection, bronchitis, nausea, fatigue, nosebleed, muscle spasms or pain, mouth and throat pain, pain in extremities, and itching | ASCENIV is a purified, sterile, ready-to-use preparation of concentrated human immunoglobulin G (IgG) antibodies. The product is a clear to opalescent liquid, which is colorless to pale yellow. The distribution of IgG subclasses is similar to that of normal plasma. The active ingredient is human immunoglobulin purified from source human plasma and processed using a modified classical Cohn Method 6 / Oncley Method 9 fractionation procedure. ASCENIV contains 100 ± 10 mg/mL protein, of which not less than 96% is human immunoglobulin obtained from source human plasma. It is formulated in water for injection containing 0.100-0.140 M sodium chloride, 0.20-0.29 M glycine, 0.15–0.25% polysorbate 80, with pH 4.0–4.6. ASCENIV contains ≤ 200 μg/mL of IgA. | Asceniv is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome (PI), Immune Thrombocytopenic Purpura (ITP), Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. Asceniv may be used alone or with other medications. | NA | ASCENIV is a purified, sterile, ready-to-use preparation of concentrated human immunoglobulin G (IgG) antibodies. The product is a clear to opalescent liquid, which is colorless to pale yellow. The distribution of IgG subclasses is similar to that of normal plasma. The active ingredient is human immunoglobulin purified from source human plasma and processed using a modified classical Cohn Method 6 / Oncley Method 9 fractionation procedure. ASCENIV contains 100 ± 10 mg/mL protein, of which not less than 96% is human immunoglobulin obtained from source human plasma. It is formulated in water for injection containing 0.100-0.140 M sodium chloride, 0.20-0.29 M glycine, 0.15–0.25% polysorbate 80, with pH 4.0–4.6. ASCENIV contains ≤ 200 μg/mL of IgA. | Link | Link | NA |
| 11150 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Antibodies | NA | NA | NA | NA | 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 | Bivigam | Kedrion Biopharma, Inc. | Kedrion Biopharma, Inc. | Intravenous | 1 g/10mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11151 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Antigen Neutralization | NA | NA | NA | NA | 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 | Bivigam | Adma Biologics, Inc. | Adma Biologics, Inc. | Intravenous | 5 g/50mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11152 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Blood Proteins | NA | NA | NA | NA | 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 | Bivigam | Adma Biologics, Inc. | Adma Biologics, Inc. | Intravenous | 10 g/100mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11153 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Globulins | NA | NA | NA | NA | 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 | Bivigam | ADMA Biologics, Inc | ADMA Biologics, Inc | Intravenous | 5 g/50mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11154 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Human Immunoglobulin G | NA | NA | NA | NA | 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 | Bivigam | ADMA Biologics, Inc | ADMA Biologics, Inc | Intravenous | 10 g/100mL | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | headache fatigue infusion site reaction nausea sinus infection increased blood pressure diarrhea dizziness tiredness back pain migraine muscle pain, and sore throat | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Bivigam [Immune Globulin Intravenous (Human), 10% Liquid] is an immune globulin used to treat primary humoral immunodeficiency (PI). | NA | 2. Cayco, A.V., M.A. Perazella, and J.P. Hayslett. Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature. J Am Soc Nephrol 1997; 8:1788-1794. | Link | Link | NA |
| 11155 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunoglobulin G | NA | NA | NA | NA | 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 | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Intravenous | 3 g/1 | 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. | 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. | Carimune® NF, Nanofiltered, Immune Globulin Intravenous (Human), is a sterile, highly purified polyvalent antibody product containing in concentrated form all the IgG antibodies which regularly occur in the donor population.15 This immunoglobulin preparation is produced by cold alcohol fractionation from the plasma of US donors. Part of the fractionation may be performed by another US-licensed manufacturer. Carimune® NF is made suitable for intravenous use by treatment at acid pH in the presence of trace amounts of pepsin. | 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. | NA | NA | Link | Link | NA |
| 11156 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunoglobulin Isotypes | NA | NA | NA | NA | 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 | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Intravenous | 6 g/1 | 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. | 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. | Carimune® NF, Nanofiltered, Immune Globulin Intravenous (Human), is a sterile, highly purified polyvalent antibody product containing in concentrated form all the IgG antibodies which regularly occur in the donor population.15 This immunoglobulin preparation is produced by cold alcohol fractionation from the plasma of US donors. Part of the fractionation may be performed by another US-licensed manufacturer. Carimune® NF is made suitable for intravenous use by treatment at acid pH in the presence of trace amounts of pepsin. | 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. | NA | NA | Link | Link | NA |
| 11157 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunoglobulins | NA | NA | NA | NA | 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 | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Intravenous | 12 g/1 | 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. | 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. | Carimune® NF, Nanofiltered, Immune Globulin Intravenous (Human), is a sterile, highly purified polyvalent antibody product containing in concentrated form all the IgG antibodies which regularly occur in the donor population.15 This immunoglobulin preparation is produced by cold alcohol fractionation from the plasma of US donors. Part of the fractionation may be performed by another US-licensed manufacturer. Carimune® NF is made suitable for intravenous use by treatment at acid pH in the presence of trace amounts of pepsin. | 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. | NA | NA | Link | Link | NA |
| 11158 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunoglobulins, Intravenous | NA | NA | NA | NA | 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 | Cutaquig | Octapharma USA Inc | Octapharma USA Inc | Subcutaneous | 165 mg/1mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11159 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunologic Factors | NA | NA | NA | NA | 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 | Cutaquig | Pfizer Laboratories Div Pfizer Inc | Pfizer Laboratories Div Pfizer Inc | Subcutaneous | 165 mg/1mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11160 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Immunoproteins | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 1 g / 6 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11161 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Passively Acquired Immunity | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 1.65 g / 10 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11162 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 2 g / 12 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11163 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Serum | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 3.3 g / 20 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11164 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | Serum Globulins | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 4 g / 24 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11165 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Cutaquig | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Subcutaneous | 8 g / 48 mL | CUTAQUIG is contraindicated: In patients who have had an anaphylactic or severe systemic reaction to the subcutaneous administration of human immune globulin or to any of the components of CUTAQUIG such as Polysorbate 80. In IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human globulin treatment. | local infusion site reactions (redness, swelling, itching), headache, fever, dermatitis, asthma, diarrhea, and cough. | Cutaquig (for injection under the skin) is used to treat primary immunodeficiency diseases. Cutaquig is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cutaquig may also... | Cutaquig is a prescription medicine used to treat the symptoms of Primary Humoral Immunodeficiency. Cutaquig may be used alone or with other medications. | NA | NA | Link | Link | NA |
| 11166 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Cuvitru | Baxalta Us Inc | Baxalta Us Inc | Subcutaneous | 200 mg/1mL | CUVITRU is contraindicated in patients who have had an anaphylactic or severe systemic hypersensitivity reaction to the subcutaneous administration of human immune globulin. CUVITRU is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human immune globulin treatment. | local injection site reactions (pain, redness, itching, swelling), headache, nausea, fatigue, diarrhea, vomiting, joint pain, and mouth and throat pain. | Cuvitru (for injection under the skin) is used to treat primary immunodeficiency diseases. Cuvitru is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cuvitru may also be... | Cuvitru is a prescription medicine used to treat the symptoms of Primary Immune Deficiency. Cuvitru may be used alone or with other medications. | NA | CUVITRU is a ready-for-use, sterile, liquid preparation of highly purified and concentrated immunoglobulin G (IgG) antibodies. The distribution of the IgG subclasses is similar to that of normal plasma. The Fc and Fab functions are maintained in CUVITRU. | Link | Link | NA |
| 11167 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Cuvitru | Takeda | Takeda | Subcutaneous | 200 mg / mL | CUVITRU is contraindicated in patients who have had an anaphylactic or severe systemic hypersensitivity reaction to the subcutaneous administration of human immune globulin. CUVITRU is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity to human immune globulin treatment. | local injection site reactions (pain, redness, itching, swelling), headache, nausea, fatigue, diarrhea, vomiting, joint pain, and mouth and throat pain. | Cuvitru (for injection under the skin) is used to treat primary immunodeficiency diseases. Cuvitru is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Cuvitru may also be... | Cuvitru is a prescription medicine used to treat the symptoms of Primary Immune Deficiency. Cuvitru may be used alone or with other medications. | NA | CUVITRU is a ready-for-use, sterile, liquid preparation of highly purified and concentrated immunoglobulin G (IgG) antibodies. The distribution of the IgG subclasses is similar to that of normal plasma. The Fc and Fab functions are maintained in CUVITRU. | Link | Link | NA |
| 11168 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma | Grifols | Grifols | Intravenous | 0.5 g/10mL | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | headache fever shaking fast heart rate low blood pressure (hypotension) high blood pressure (hypertension) back pain muscle pain or aches chest pain nausea infusion site reactions pain in extremities chills vomiting increase in body temperature dizziness, and diarrhea | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Flebogamma is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIPD), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. Flebogamma may be used alone or with other medications. | NA | Flebogamma 5% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. The purification process includes cold ethanol fractionation, polyethylene glycol precipitation, ion exchange chromatography, low pH treatment, pasteurization, solvent detergent treatment, and Planova nanofiltration using 20 nanometer (nm) filters. | Link | Link | NA |
| 11169 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma 10% | Instituto Grifols, S.A. | Instituto Grifols, S.A. | Intravenous | 100 mg / mL | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11170 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma 5% | Instituto Grifols, S.A. | Instituto Grifols, S.A. | Intravenous | 50 mg / mL | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11171 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma DIF | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Intravenous | 0.05 g/1mL | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11172 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma Dif | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Intravenous | 5 g/50mL | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11173 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma Dif | Instituto Grifols, S.A. | Instituto Grifols, S.A. | Intravenous | 50 mg/ml | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11174 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Flebogamma Dif | Instituto Grifols, S.A. | Instituto Grifols, S.A. | Intravenous | 100 mg/ml | Flebogamma 5% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 5% DIF is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Flebogamma 10% DIF is a ready to use, sterile, clear or slightly opalescent and colorless to pale yellow, liquid preparation of purified immunoglobulin (IgG) obtained from human plasma pools. | NA | NA | NA | Link | Link | NA |
| 11175 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | GamaSTAN | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Intramuscular | 0.165 g/1mL | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human).11 [see WARNINGS AND PRECAUTIONS] IgA deficient patients with antibodies against IgA and a history of hypersensitivity.11 REFERENCES 11. Fudenberg HH. Sensitization to immunoglobulins and hazards of gamma globulin therapy. In: Merler E, editor. Immunoglobulins: biologic aspects and clinical uses. Washington, DC: National Academy of Sciences; 1970, p. 211-20. | local pain and tenderness at the injection site hives skin swelling allergic reactions, including anaphylaxis | Immune globulin is a sterile solution made from human plasma. It contains antibodies that protect you against infection from various diseases. Immune globulin intramuscular (IGIM, for injection into a muscle) is used to prevent infection with hepatitis A in people who travel to areas where this disease... | GamaStan is a prescription medicine used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. GamaStan may be used alone or with other medications. | NA | GAMASTAN is a clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution of polyvalent human immune globulin for intramuscular administration. GAMASTAN contains no preservative. GAMASTAN is prepared from pools of human plasma collected from healthy donors by a combination of cold ethanol fractionation, caprylate precipitation and filtration, caprylate incubation, anion-exchange chromatography, nanofiltration and low pH incubation. GAMASTAN consists of 15% to18% protein at pH of 4.1 to 4.8 in 0.16 to 0.26 M glycine. | Link | Link | NA |
| 11176 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamastan | Cutter Med & Biol, Division Of Miles Canada Ltd. | Cutter Med & Biol, Division Of Miles Canada Ltd. | Intramuscular | 0.165 | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human).11 [see WARNINGS AND PRECAUTIONS] IgA deficient patients with antibodies against IgA and a history of hypersensitivity.11 REFERENCES 11. Fudenberg HH. Sensitization to immunoglobulins and hazards of gamma globulin therapy. In: Merler E, editor. Immunoglobulins: biologic aspects and clinical uses. Washington, DC: National Academy of Sciences; 1970, p. 211-20. | local pain and tenderness at the injection site hives skin swelling allergic reactions, including anaphylaxis | Immune globulin is a sterile solution made from human plasma. It contains antibodies that protect you against infection from various diseases. Immune globulin intramuscular (IGIM, for injection into a muscle) is used to prevent infection with hepatitis A in people who travel to areas where this disease... | GamaStan is a prescription medicine used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. GamaStan may be used alone or with other medications. | NA | GAMASTAN is a clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution of polyvalent human immune globulin for intramuscular administration. GAMASTAN contains no preservative. GAMASTAN is prepared from pools of human plasma collected from healthy donors by a combination of cold ethanol fractionation, caprylate precipitation and filtration, caprylate incubation, anion-exchange chromatography, nanofiltration and low pH incubation. GAMASTAN consists of 15% to18% protein at pH of 4.1 to 4.8 in 0.16 to 0.26 M glycine. | Link | Link | NA |
| 11177 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamastan | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intramuscular | 0.18 | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human).11 [see WARNINGS AND PRECAUTIONS] IgA deficient patients with antibodies against IgA and a history of hypersensitivity.11 REFERENCES 11. Fudenberg HH. Sensitization to immunoglobulins and hazards of gamma globulin therapy. In: Merler E, editor. Immunoglobulins: biologic aspects and clinical uses. Washington, DC: National Academy of Sciences; 1970, p. 211-20. | local pain and tenderness at the injection site hives skin swelling allergic reactions, including anaphylaxis | Immune globulin is a sterile solution made from human plasma. It contains antibodies that protect you against infection from various diseases. Immune globulin intramuscular (IGIM, for injection into a muscle) is used to prevent infection with hepatitis A in people who travel to areas where this disease... | GamaStan is a prescription medicine used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. GamaStan may be used alone or with other medications. | NA | GAMASTAN is a clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution of polyvalent human immune globulin for intramuscular administration. GAMASTAN contains no preservative. GAMASTAN is prepared from pools of human plasma collected from healthy donors by a combination of cold ethanol fractionation, caprylate precipitation and filtration, caprylate incubation, anion-exchange chromatography, nanofiltration and low pH incubation. GAMASTAN consists of 15% to18% protein at pH of 4.1 to 4.8 in 0.16 to 0.26 M glycine. | Link | Link | NA |
| 11178 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamastan S/d | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intramuscular | 0.18 | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human). IgA deficient patients with antibodies against IgA and a history of hypersensitivity. | Local pain and tenderness at the injection site, urticaria, and angioedema may occur. Anaphylactic reactions, although rare, have been reported following the injection of human immune globulin preparations. Anaphylaxis is more likely to occur if GamaSTAN® S/D is given intravenously; therefore, GamaSTAN® S/D must be administered only intramuscularly. | NA | NA | NA | NA | Link | Link | NA |
| 11179 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamimune N 10% (iv) | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | Intravenous | 100 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11180 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamimune N 5% (iv) | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | Intravenous | 50 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11181 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamimune N Inj 5% (iv) | Cutter Med & Biol, Division Of Miles Canada Ltd. | Cutter Med & Biol, Division Of Miles Canada Ltd. | Intravenous | 50 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11182 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | GAMMAGARD Liquid | Baxalta US Inc. | Baxalta US Inc. | Intravenous; Subcutaneous | 100 mg/1mL | Hypersensitivity Reaction To Immune Globulins GAMMAGARD LIQUID is contraindicated in patients who have a history of anaphylactic or severe systemic hypersensitivity reactions to administration of human immune globulin. IgA Sensitive Patients With History Of Hypersensitivity Reactions GAMMAGARD LIQUID is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. Anaphylaxis has been reported with intravenous use of GAMMAGARD LIQUID and is theoretically possible following subcutaneous administration | flushing (warmth, redness, or tingly feeling), headache, dizziness, chills, muscle cramps, back or joint pain, minor chest pain, fever, nausea, vomiting, tiredness, or injection site reactions (pain, redness, and swelling) | NA | Gammagard Liquid is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, and Multifocal Motor Neuropathy. Gammagard Liquid may be used alone or with other medications. | NA | GAMMAGARD LIQUID Immune Globulin Intravenous (Human), 10% is a ready-for-use sterile, liquid preparation of highly purified and concentrated immunoglobulin G (IgG) antibodies. The distribution of the IgG subclasses is similar to that of normal plasma.1,2 The Fc and Fab functions are maintained in GAMMAGARD LIQUID. Pre-kallikrein activator activity is not detectable. GAMMAGARD LIQUID (immune globulin intravenous human 10%) contains 100 mg/mL protein. At least 98% of the protein is gammaglobulin, the average immunoglobulin A (IgA) concentration is 37µg/mL, and immunoglobulin M is present in trace amounts. GAMMAGARD LIQUID (immune globulin intravenous human 10%) contains a broad spectrum of IgG antibodies against bacterial and viral agents. Glycine (0.25M) serves as a stabilizing and buffering agent, and there are no added sugars, sodium or preservatives. The pH is 4.6 to 5.1. The osmolality is 240-300 mOsmol/kg, which is similar to physiological osmolality (285 to 295 mOsmol/kg).3 | Link | Link | NA |
| 11183 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | GAMMAGARD Liquid | Takeda | Takeda | Intravenous | 0.1 | Hypersensitivity Reaction To Immune Globulins GAMMAGARD LIQUID is contraindicated in patients who have a history of anaphylactic or severe systemic hypersensitivity reactions to administration of human immune globulin. IgA Sensitive Patients With History Of Hypersensitivity Reactions GAMMAGARD LIQUID is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. Anaphylaxis has been reported with intravenous use of GAMMAGARD LIQUID and is theoretically possible following subcutaneous administration | flushing (warmth, redness, or tingly feeling), headache, dizziness, chills, muscle cramps, back or joint pain, minor chest pain, fever, nausea, vomiting, tiredness, or injection site reactions (pain, redness, and swelling) | NA | Gammagard Liquid is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, and Multifocal Motor Neuropathy. Gammagard Liquid may be used alone or with other medications. | NA | GAMMAGARD LIQUID Immune Globulin Intravenous (Human), 10% is a ready-for-use sterile, liquid preparation of highly purified and concentrated immunoglobulin G (IgG) antibodies. The distribution of the IgG subclasses is similar to that of normal plasma.1,2 The Fc and Fab functions are maintained in GAMMAGARD LIQUID. Pre-kallikrein activator activity is not detectable. GAMMAGARD LIQUID (immune globulin intravenous human 10%) contains 100 mg/mL protein. At least 98% of the protein is gammaglobulin, the average immunoglobulin A (IgA) concentration is 37µg/mL, and immunoglobulin M is present in trace amounts. GAMMAGARD LIQUID (immune globulin intravenous human 10%) contains a broad spectrum of IgG antibodies against bacterial and viral agents. Glycine (0.25M) serves as a stabilizing and buffering agent, and there are no added sugars, sodium or preservatives. The pH is 4.6 to 5.1. The osmolality is 240-300 mOsmol/kg, which is similar to physiological osmolality (285 to 295 mOsmol/kg).3 | Link | Link | NA |
| 11184 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammagard S/d | Baxalta US Inc. | Baxalta US Inc. | Intravenous | 50 mg/1mL | GAMMAGARD S/D (immune globulin) is contraindicated in patients with selective IgA deficiency where the IgA deficiency is the only abnormality of concern (see INDICATIONS and WARNINGS). Patients may experience severe hypersensitivity reactions or anaphylaxis in the setting of detectable IgA levels following infusion of GAMMAGARD S/D (immune globulin) . The occurrence of severe hypersensitivity reactions or anaphylaxis under such conditions should prompt consideration of an alternative therapy. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, confusion, weakness, increased thirst, feeling hot, being unable to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness or breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with a severe headache, neck stiffness, eye pain, increased sensitivity to light, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and swelling and warmth or discoloration in an arm or leg | used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia and Multifocal Motor Neuropathy. | GAMMAGARD S/D, Immune Globulin Intravenous (Human) [IGIV] is a solvent/detergent treated, sterile, freeze-dried preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. | NA | NA | Link | Link | NA |
| 11185 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammagard S/d | Takeda | Takeda | Intravenous | 10 g / vial | GAMMAGARD S/D (immune globulin) is contraindicated in patients with selective IgA deficiency where the IgA deficiency is the only abnormality of concern (see INDICATIONS and WARNINGS). Patients may experience severe hypersensitivity reactions or anaphylaxis in the setting of detectable IgA levels following infusion of GAMMAGARD S/D (immune globulin) . The occurrence of severe hypersensitivity reactions or anaphylaxis under such conditions should prompt consideration of an alternative therapy. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, confusion, weakness, increased thirst, feeling hot, being unable to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness or breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with a severe headache, neck stiffness, eye pain, increased sensitivity to light, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and swelling and warmth or discoloration in an arm or leg | used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia and Multifocal Motor Neuropathy. | GAMMAGARD S/D, Immune Globulin Intravenous (Human) [IGIV] is a solvent/detergent treated, sterile, freeze-dried preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. | NA | NA | Link | Link | NA |
| 11186 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammagard S/d | Baxalta Canada Corporation | Baxalta Canada Corporation | Intravenous | 2.5 g / vial | GAMMAGARD S/D (immune globulin) is contraindicated in patients with selective IgA deficiency where the IgA deficiency is the only abnormality of concern (see INDICATIONS and WARNINGS). Patients may experience severe hypersensitivity reactions or anaphylaxis in the setting of detectable IgA levels following infusion of GAMMAGARD S/D (immune globulin) . The occurrence of severe hypersensitivity reactions or anaphylaxis under such conditions should prompt consideration of an alternative therapy. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, confusion, weakness, increased thirst, feeling hot, being unable to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness or breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with a severe headache, neck stiffness, eye pain, increased sensitivity to light, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and swelling and warmth or discoloration in an arm or leg | used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia and Multifocal Motor Neuropathy. | GAMMAGARD S/D, Immune Globulin Intravenous (Human) [IGIV] is a solvent/detergent treated, sterile, freeze-dried preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. | NA | NA | Link | Link | NA |
| 11187 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammagard S/d | Takeda | Takeda | Intravenous | 5 g / vial | GAMMAGARD S/D (immune globulin) is contraindicated in patients with selective IgA deficiency where the IgA deficiency is the only abnormality of concern (see INDICATIONS and WARNINGS). Patients may experience severe hypersensitivity reactions or anaphylaxis in the setting of detectable IgA levels following infusion of GAMMAGARD S/D (immune globulin) . The occurrence of severe hypersensitivity reactions or anaphylaxis under such conditions should prompt consideration of an alternative therapy. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, confusion, weakness, increased thirst, feeling hot, being unable to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness or breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with a severe headache, neck stiffness, eye pain, increased sensitivity to light, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and swelling and warmth or discoloration in an arm or leg | used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia and Multifocal Motor Neuropathy. | GAMMAGARD S/D, Immune Globulin Intravenous (Human) [IGIV] is a solvent/detergent treated, sterile, freeze-dried preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. | NA | NA | Link | Link | NA |
| 11188 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammagard S/d (iv) | Baxter Laboratories | Baxter Laboratories | Intravenous | 0.5 g / vial | GAMMAGARD S/D (immune globulin) is contraindicated in patients with selective IgA deficiency where the IgA deficiency is the only abnormality of concern (see INDICATIONS and WARNINGS). Patients may experience severe hypersensitivity reactions or anaphylaxis in the setting of detectable IgA levels following infusion of GAMMAGARD S/D (immune globulin) . The occurrence of severe hypersensitivity reactions or anaphylaxis under such conditions should prompt consideration of an alternative therapy. | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, nausea, lightheadedness, sweating, headache, pounding in your neck or ears, fever, chills, chest tightness, warmth or redness in your face, pale or yellowed skin, dark colored urine, confusion, weakness, increased thirst, feeling hot, being unable to urinate, heavy sweating, hot and dry skin, little or no urination, swelling, rapid weight gain, shortness or breath, chest pain, trouble breathing, blue colored lips, fingers, or toes, fever with a severe headache, neck stiffness, eye pain, increased sensitivity to light, chest pain with deep breathing, rapid heart rate, numbness or weakness on one side of the body, and swelling and warmth or discoloration in an arm or leg | used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia and Multifocal Motor Neuropathy. | GAMMAGARD S/D, Immune Globulin Intravenous (Human) [IGIV] is a solvent/detergent treated, sterile, freeze-dried preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. | NA | NA | Link | Link | NA |
| 11189 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammaked | Kedrion Biopharma, Inc. | Kedrion Biopharma, Inc. | Intravenous; Subcutaneous | 10 g/100mL | Hypersensitivity Reactions To Immune Globulins GAMMAKED is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA Sensitive Patients With History Of Hypersensitivity Reaction GAMMAKED is contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. | increased cough, runny nose, sore throat, headache, asthma, nausea, fever, diarrhea, sinusitis, local infusion site reactions, fatigue, upper respiratory tract infection, joint pain, bronchitis, depression, allergic dermatitis, migraine, muscle pain, viral infection, bruising, vomiting, rash, abdominal pain, back pain, indigestion, high blood pressure (hypertension), chills, and weakness | Gammaked (for injection into a vein or under the skin) is used to treat primary immunodeficiency. Gammaked is also used to increase platelets (blood clotting cells) in people with idiopathic thrombocytopenic purpura. Gammaked is also used to treat certain debilitating nerve disorders that cause muscle... | GAMMAKED is an immune globulin injection (human) 10% liquid that is indicated for the treatment of: | NA | Several of the individual production steps in the GAMMAKED manufacturing process have been shown to decrease TSE infectivity of that experimental model agent. TSE reduction steps include two depth filtrations (in sequence, a total of ≥ 6.6 log10 ). These studies provide reasonable assurance that low levels of CJD/vCJD agent infectivity, if present in the starting material, would be removed. | Link | Link | NA |
| 11190 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammaplex | Bio Products Laboratory Limited | Bio Products Laboratory Limited | Intravenous | 5 g/100mL | Gammaplex is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Gammaplex is contraindicated in patients with hereditary intolerance to fructose, also in infants and neonates for whom sucrose or fructose tolerance has not been established. Gammaplex is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | headache, fever, nasal congestion, fatigue, nausea, vomiting, high blood pressure (hypertension), low blood pressure (hypotension), rash, infusion site reaction, vomiting, muscle pain, chills, fast heart rate, chest pain/discomfort, pain, dizziness, general feeling of being unwell (malaise), pain or difficultly urinating, dry skin, itching, dehydration, and joint pain. | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Gammaplex is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome and Immune Thrombocytopenic Purpura. Gammaplex may be used alone or with other medications. | NA | Gammaplex is a ready to use sterile solution of polyclonal human Immunoglobulin G for intravenous administration that contains sorbitol, glycine and polysorbate 80 as stabilizers. Specifically, Gammaplex contains approximately 5 g normal human immunoglobulin and 5 g D-sorbitol in 100 mL of buffer solution containing: 0.6 g glycine, 0.2 g sodium acetate, 0.3 g sodium chloride and ~5 mg polysorbate 80. Immunoglobulin G purity is > 95%, the pH is in the range of 4.8 to 5.1, and osmolality is not less than 240 mOsmol/kg (typically 420 to 500 mOsmol/kg). The distribution of the four IgG subclasses is approximately 64% IgG1, 30% IgG2, 5% IgG3, and 1% IgG4. The content of IgA is lower than 10 μg/mL. The anti-D and anti-A/anti-B hemagglutinin content of the drug product is strictly controlled to specification. Gammaplex contains no reducing carbohydrate stabilizers (e.g. sucrose, maltose) and no preservative. | Link | Link | NA |
| 11191 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammaplex | Bio Products Laboratory Limited | Bio Products Laboratory Limited | Intravenous | 5 g/50mL | Gammaplex is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Gammaplex is contraindicated in patients with hereditary intolerance to fructose, also in infants and neonates for whom sucrose or fructose tolerance has not been established. Gammaplex is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity. | headache, fever, nasal congestion, fatigue, nausea, vomiting, high blood pressure (hypertension), low blood pressure (hypotension), rash, infusion site reaction, vomiting, muscle pain, chills, fast heart rate, chest pain/discomfort, pain, dizziness, general feeling of being unwell (malaise), pain or difficultly urinating, dry skin, itching, dehydration, and joint pain. | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Gammaplex is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome and Immune Thrombocytopenic Purpura. Gammaplex may be used alone or with other medications. | NA | Gammaplex is a ready to use sterile solution of polyclonal human Immunoglobulin G for intravenous administration that contains sorbitol, glycine and polysorbate 80 as stabilizers. Specifically, Gammaplex contains approximately 5 g normal human immunoglobulin and 5 g D-sorbitol in 100 mL of buffer solution containing: 0.6 g glycine, 0.2 g sodium acetate, 0.3 g sodium chloride and ~5 mg polysorbate 80. Immunoglobulin G purity is > 95%, the pH is in the range of 4.8 to 5.1, and osmolality is not less than 240 mOsmol/kg (typically 420 to 500 mOsmol/kg). The distribution of the four IgG subclasses is approximately 64% IgG1, 30% IgG2, 5% IgG3, and 1% IgG4. The content of IgA is lower than 10 μg/mL. The anti-D and anti-A/anti-B hemagglutinin content of the drug product is strictly controlled to specification. Gammaplex contains no reducing carbohydrate stabilizers (e.g. sucrose, maltose) and no preservative. | Link | Link | NA |
| 11192 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gammar Inj 165mg/ml | Armour Pharmaceutical Co. | Armour Pharmaceutical Co. | Intramuscular | 165 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11193 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamunex | Grifols | Grifols | Intravenous | 1 g/1g | GAMUNEX (immune globulin intravenous (human) 10%) is contraindicated in individuals with acute severe hypersensitivity reactions to Immune Globulin (Human). GAMUNEX (immune globulin intravenous (human) 10%) contains trace amounts of IgA. It is contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. | headache, fatigue, infusion site reaction, nausea, sinusitis, increased blood pressure, diarrhea, dizziness, tired feeling, lethargy, back pain, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Gamunex-C is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Gamunex-C injection is used to treat primary immunodeficiency (PI). This includes, but is not limited to, congenital agammaglobulinemia, common... | Gamunex is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy and before and after a Bone Marrow Transplant. Gamunex may be used alone or with other medications. | NA | GAMUNEX is made from large pools of human plasma by a combination of cold ethanol fractionation, caprylate precipitation and filtration, and anion-exchange chromatography. Isotonicity is achieved by the addition of glycine. GAMUNEX (immune globulin intravenous human 10%) is incubated in the final container (at the low pH of 4.0 – 4.3), for a minimum of 21 days at 23° to 27°C. The product is intended for intravenous administration. | Link | Link | NA |
| 11194 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamunex | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intravenous; Subcutaneous | 10 g / 100 mL | GAMUNEX (immune globulin intravenous (human) 10%) is contraindicated in individuals with acute severe hypersensitivity reactions to Immune Globulin (Human). GAMUNEX (immune globulin intravenous (human) 10%) contains trace amounts of IgA. It is contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. | headache, fatigue, infusion site reaction, nausea, sinusitis, increased blood pressure, diarrhea, dizziness, tired feeling, lethargy, back pain, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Gamunex-C is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Gamunex-C injection is used to treat primary immunodeficiency (PI). This includes, but is not limited to, congenital agammaglobulinemia, common... | Gamunex is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy and before and after a Bone Marrow Transplant. Gamunex may be used alone or with other medications. | NA | GAMUNEX is made from large pools of human plasma by a combination of cold ethanol fractionation, caprylate precipitation and filtration, and anion-exchange chromatography. Isotonicity is achieved by the addition of glycine. GAMUNEX (immune globulin intravenous human 10%) is incubated in the final container (at the low pH of 4.0 – 4.3), for a minimum of 21 days at 23° to 27°C. The product is intended for intravenous administration. | Link | Link | NA |
| 11195 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Gamunex-C | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Intravenous; Subcutaneous | 10 g/100mL | Hypersensitivity Reactions To Immune Globulins GAMUNEX-C is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA Sensitive Patients With History Of Hypersensitivity Reaction GAMUNEX-C is contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity. | headache fever chills high blood pressure skin rash nausea vomiting muscle spasm physical weakness loss of strength blurred vision tired feeling sore throat cough injection site reactions (redness, itching, and swelling of skin back pain joint pain pain in your arms or legs | NA | Gamunex-C is a prescription medicine used to treat the symptoms of Primary Immune Deficiency. Gamunex-C may be used alone or with other medications. | NA | GAMUNEX-C is a ready-to-use sterile, non-pyrogenic solution of human immune globulin protein for intravenous and subcutaneous (PI indication only) administration. GAMUNEX-C consists of 9%–11% protein in 0.16–0.24 M glycine. Not less than 98% of the protein has the electrophoretic mobility of gamma globulin. GAMUNEX-C contains trace levels of fragments, IgA (average 0.046 mg/mL), and IgM. The distribution of IgG subclasses is similar to that found in normal serum. GAMUNEX-C doses of 1 g/kg correspond to a glycine dose of 0.15 g/kg. While toxic effects of glycine administration have been reported, the doses and rates of administration were 3–4 fold greater than those for GAMUNEX-C. In another study it was demonstrated that intravenous bolus doses of 0.44 g/kg glycine were not associated with serious adverse effects.(20) Caprylate is a saturated medium-chain (C8) fatty acid of plant origin. Medium chain fatty acids are considered to be essentially non-toxic. Human subjects receiving medium chain fatty acids parenterally have tolerated doses of 3.0 to 9.0 g/kg/day for periods of several months without adverse effects.(21) Residual caprylate concentrations in the final container are no more than 0.216 g/L (1.3 mmol/L). The measured buffer capacity is 35 mEq/L and the osmolality is 258 mOsmol/kg solvent, which is close to physiological osmolality (285-295 mOsmol/kg). The pH of GAMUNEX-C is 4.0–4.5. GAMUNEX-C contains no preservative. GAMUNEX-C is not made with natural rubber latex. | Link | Link | NA |
| 11196 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hizentra | Csl Behring Ag | Csl Behring Ag | Subcutaneous | 0.2 g/1mL | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11197 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hizentra | Csl Behring | Csl Behring | Subcutaneous | 200 mg / mL | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11198 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hizentra | Csl Behring | Csl Behring | Subcutaneous | 200 mg/ml | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11199 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hyperrho S/d Full Dose | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intramuscular | 1500 unit / dose | None known. | NA | NA | NA | NA | NA | Link | Link | NA |
| 11200 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hyqvia | Baxalta US Inc. | Baxalta US Inc. | Subcutaneous | NA | HYQVIA is contraindicated in: Patients who have had a history of anaphylactic or severe systemic reactions to the administration of IgG. IgA deficient patients with antibodies to IgA and a history of hypersensitivity. Patients with known systemic hypersensitivity to hyaluronidase including Recombinant Human Hyaluronidase of HYQVIA. Patients with known systemic hypersensitivity to human albumin (in the hyaluronidase solution). | common variable immunodeficiency (CVID) X-linked agammaglobulinemia congenital agammaglobulinemia Wiskott- Aldrich syndrome, and severe combined immunodeficiencies. | Hyaluronidase is a genetically designed protein used as an aid in helping your body absorb other injected medications. Immune globulin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hyqvia are given... | HyQvia is a prescription medicine used to treat the symptoms of Primary Immune Deficiency. HyQvia may be used alone or with other medications. | NA | HYQVIA is a dual vial unit with one vial of Immune Globulin Infusion 10% (Human) and one vial of Recombinant Human Hyaluronidase. | Link | Link | NA |
| 11201 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Hyqvia | Baxalta Innovations Gmb H | Baxalta Innovations Gmb H | Subcutaneous | 100 mg/ml | HYQVIA is contraindicated in: Patients who have had a history of anaphylactic or severe systemic reactions to the administration of IgG. IgA deficient patients with antibodies to IgA and a history of hypersensitivity. Patients with known systemic hypersensitivity to hyaluronidase including Recombinant Human Hyaluronidase of HYQVIA. Patients with known systemic hypersensitivity to human albumin (in the hyaluronidase solution). | common variable immunodeficiency (CVID) X-linked agammaglobulinemia congenital agammaglobulinemia Wiskott- Aldrich syndrome, and severe combined immunodeficiencies. | Hyaluronidase is a genetically designed protein used as an aid in helping your body absorb other injected medications. Immune globulin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hyqvia are given... | HyQvia is a prescription medicine used to treat the symptoms of Primary Immune Deficiency. HyQvia may be used alone or with other medications. | NA | HYQVIA is a dual vial unit with one vial of Immune Globulin Infusion 10% (Human) and one vial of Recombinant Human Hyaluronidase. | Link | Link | NA |
| 11202 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Igivnex | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intravenous; Subcutaneous | 10 g / 100 mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11203 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Immune Globulin Intravenous (human) 5% | Bayer | Bayer | Intravenous | 50 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11204 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Immune Globulin Intravenous (human), 10% | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | Intravenous | 10 g / 100 mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11205 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Immune Globulin Intravenous (human), 5% | Talecris Biotherapeutics Inc | Talecris Biotherapeutics Inc | Intravenous | 5 g / 100 mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11206 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Immune Serum Globulin (human) | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Intramuscular | 0.18 | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11207 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Iveegam Immuno 5000mg (iv) | Baxter Ag | Baxter Ag | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11208 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Iypoly | Whoniz | Whoniz | Nasal | 0.15 g/100mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11209 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Kiovig | Takeda Manufacturing Austria Ag | Takeda Manufacturing Austria Ag | Intravenous | 100 mg/ml | NA | The most common side effects with Kiovig (seen in more than 1 patient in 10) are headache, hypertension (high blood pressure), nausea (feeling sick), rash, tiredness, local reactions such as pain, swelling or itching at the site of injection, and fever. Some side effects are more likely when using a high rate of infusion, in patients with low immunoglobulin levels, or in patients who have not received Kiovig before or for a long time. | NA | NA | NA | NA | Link | Link | NA |
| 11210 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam 10% | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Intravenous | 100 mg / mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11211 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam 5% | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Intravenous | 50 mg / mL | Octagam 5% liquid is contraindicated in patients who have acute severe hypersensitivity reactions to human immunoglobulin. Octagam 5% liquid contains trace amounts of IgA (not more than 0.2 mg/ml in a 5% solution). It is contraindicated in IgA deficient patients with antibodies against IgA and history of hypersensitivity (See DESCRIPTION). Octagam 5% liquid is contraindicated in patients with acute hypersensitivity reaction to corn. Octagam 5% liquid contains maltose, a disaccharide sugar which is derived from corn. Patients known to have corn allergies should avoid using Octagam 5% liquid. | The most serious adverse reactions observed with Octagam 5% liquid treatment have been immediate anaphylactic reactions, aseptic meningitis, and hemolytic anemia. The most common adverse reactions observed with Octagam 5% liquid treatment during clinical trial ( > 5%) were headache and nausea. | Immune Globulin Intravenous (Human), Octagam 5% liquid, is a solvent/detergent (S/D)-treated, sterile preparation of highly purified immunoglobulin G (IgG) derived from large pools of human plasma. Octagam 5% liquid is a solution for infusion which must be administered intravenously. | indicated for treatment of primary humoral immunodeficiency (PI). | NA | NA | Link | Link | NA |
| 11212 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam Immune Globulin (Human) | Octapharma Pharmazeutika Produktionsgesellschaft M.B.H. | Octapharma Pharmazeutika Produktionsgesellschaft M.B.H. | Intravenous | 50 mg/1mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11213 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam Immune Globulin (Human) | Octapharma Ab | Octapharma Ab | Intravenous | 50 mg/1mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11214 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam Immune Globulin (Human) | Octapharma USA Inc | Octapharma USA Inc | Intravenous | 100 mg/1mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11215 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Octagam Immune Globulin (Human) | Octapharma USA Inc | Octapharma USA Inc | Intravenous | 50 mg/1mL | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11216 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Panzyga | Octapharma USA Inc | Octapharma USA Inc | Intravenous | 100 mg/1mL | PANZYGA is contraindicated in patients who have a history of severe systemic hypersensitivity reactions, such as anaphylaxis, to human immunoglobulin. PANZYGA is contraindicated in IgA-deficient patients with antibodies against IgA and history of hypersensitivity. | headache, nausea, fever, fatigue, abdominal pain, vomiting, dizziness, anemia, dermatitis, and increased blood pressure. | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Panzyga is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. Panzyga may be used alone or with other medications. | NA | PANZYGA, Immune Globulin Intravenous (Human) – ifas 10% Liquid Preparation | Link | Link | NA |
| 11217 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Panzyga | Pfizer Laboratories Div Pfizer Inc | Pfizer Laboratories Div Pfizer Inc | Intravenous | 100 mg/1mL | PANZYGA is contraindicated in patients who have a history of severe systemic hypersensitivity reactions, such as anaphylaxis, to human immunoglobulin. PANZYGA is contraindicated in IgA-deficient patients with antibodies against IgA and history of hypersensitivity. | headache, nausea, fever, fatigue, abdominal pain, vomiting, dizziness, anemia, dermatitis, and increased blood pressure. | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Panzyga is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. Panzyga may be used alone or with other medications. | NA | PANZYGA, Immune Globulin Intravenous (Human) – ifas 10% Liquid Preparation | Link | Link | NA |
| 11218 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Panzyga | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | Intravenous | 100 mg / mL | PANZYGA is contraindicated in patients who have a history of severe systemic hypersensitivity reactions, such as anaphylaxis, to human immunoglobulin. PANZYGA is contraindicated in IgA-deficient patients with antibodies against IgA and history of hypersensitivity. | headache, nausea, fever, fatigue, abdominal pain, vomiting, dizziness, anemia, dermatitis, and increased blood pressure. | Immune globulin intravenous (IGIV, for injection into a vein) is used to treat primary immunodeficiency. IGIV is also used to increase platelets (blood clotting cells) in people with immune thrombocytopenic purpura. IGIV is also used in to help prevent certain infections in people with B-cell chronic... | Panzyga is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Bone Marrow Transplant, B-cell Chronic Lymphocytic Leukemia, Multifocal Motor Neuropathy, and Dermatomyositis. Panzyga may be used alone or with other medications. | NA | PANZYGA, Immune Globulin Intravenous (Human) – ifas 10% Liquid Preparation | Link | Link | NA |
| 11219 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring Ag | Csl Behring Ag | Intravenous | 5 g/50mL | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11220 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring Ag | Csl Behring Ag | Intravenous | 10 g/100mL | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11221 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring Ag | Csl Behring Ag | Intravenous | 20 g/200mL | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11222 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring Ag | Csl Behring Ag | Intravenous | 40 g/400mL | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11223 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring | Csl Behring | Intravenous | 0.1 | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11224 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Privigen | Csl Behring | Csl Behring | Intravenous | 100 mg/ml | Privigen is contraindicated in patients who have a history of anaphylactic or severe systemic reaction to the administration of human immune globulin. Privigen is contraindicated in patients with hyperprolinemia because it contains the stabilizer L-proline [see DESCRIPTION]. Privigen is contraindicated in IgA-deficient patients with antibodies to IgA and a history of hypersensitivity [see WARNINGS AND PRECAUTIONS]. | headache, back or joint pain, nausea, vomiting, fatigue, chills, fever, low levels of iron in the blood (anemia), dizziness, tired feeling, muscle cramps, minor chest pain, or flushing (warmth, redness, or tingly feeling) | Privigen ) is a sterile solution made from human plasma. It contains antibodies to help your body protect itself against infection from various diseases. Privigen is used as a replacement therapy for primary humoral immunodeficiency (PI). This includes, but is not limited to congenital agammaglobulinemia,... | Privigen I[mmune Globulin Intravenous (Human)] is a prescription medicine used to treat the symptoms of Primary Immunodeficiency Syndrome, Immune Thrombocytopenic Purpura, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and before and after a Bone Marrow Transplant. Privigen may be used alone or with other medications. | NA | Privigen is a ready-to-use, sterile, 10% protein liquid preparation of polyvalent human immunoglobulin G (IgG) for intravenous administration. Privigen has a purity of at least 98% IgG, consisting primarily of monomers. The balance consists of IgG dimers ( ≤ 12%), small amounts of fragments and polymers, and albumin. Privigen contains ≤ 25 mcg/mL IgA. The IgG subclass distribution (approximate mean values) is IgG1, 67.8%; IgG2, 28.7%; IgG3, 2.3%; and IgG4, 1.2%. Privigen has an osmolality of approximately 320 mOsmol/kg (range: 240 to 440) and a pH of 4.8 (range: 4.6 to 5.0). | Link | Link | NA |
| 11225 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Sandoglobulin Nf Liquid | Csl Behring | Csl Behring | Intravenous | 120 g / L | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 11226 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Vivaglobin | Csl Behring | Csl Behring | Subcutaneous | 160 mg/1mL | As with all immune globulin products, Vivaglobin® (immune globulin subcutaneous (human)) Immune Globulin Subcutaneous (Human) is contraindicated in individuals with a history of anaphylactic or severe systemic response to immune globulin preparations and in persons with selective immunoglobulin A (IgA) deficiency (serum IgA < 0.05 g/L) who have known antibody against IgA. | injection site reactions (mild swelling, redness, itching, bruising, pain, or warmth) that will usually lessen as your body adjusts to the medication headache upset stomach fever nausea vomiting stomach pain diarrhea bloating sore throat cough back pain itching or skin rash joint or muscle pain tiredness, or pain anywhere in the body | Vivaglobin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Vivaglobin subcutaneous (for injection under the skin) is used to treat primary immunodeficiency (PI). This includes, but is not limited to,... | Vivaglobin® Immune Globulin Subcutaneous (Human), is indicated for the treatment of patients with primary immune deficiency (PID). | NA | NA | Link | Link | NA |
| 11227 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Vivaglobin | Csl Behring | Csl Behring | Subcutaneous | 160 mg / mL | As with all immune globulin products, Vivaglobin® (immune globulin subcutaneous (human)) Immune Globulin Subcutaneous (Human) is contraindicated in individuals with a history of anaphylactic or severe systemic response to immune globulin preparations and in persons with selective immunoglobulin A (IgA) deficiency (serum IgA < 0.05 g/L) who have known antibody against IgA. | injection site reactions (mild swelling, redness, itching, bruising, pain, or warmth) that will usually lessen as your body adjusts to the medication headache upset stomach fever nausea vomiting stomach pain diarrhea bloating sore throat cough back pain itching or skin rash joint or muscle pain tiredness, or pain anywhere in the body | Vivaglobin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Vivaglobin subcutaneous (for injection under the skin) is used to treat primary immunodeficiency (PI). This includes, but is not limited to,... | Vivaglobin® Immune Globulin Subcutaneous (Human), is indicated for the treatment of patients with primary immune deficiency (PID). | NA | NA | Link | Link | NA |
| 11228 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Winrho | Cangene BioPharma, LLC | Cangene BioPharma, LLC | Intramuscular; Intravenous | 600 [iU]/1mL | WinRho 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. | 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 | NA | NA | NA | NA | Link | Link | NA |
| 11229 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Winrho | Cangene BioPharma, LLC | Cangene BioPharma, LLC | Intramuscular; Intravenous | 2500 [iU]/1mL | WinRho 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. | 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 | NA | NA | NA | NA | Link | Link | NA |
| 11230 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Winrho | Cangene BioPharma, LLC | Cangene BioPharma, LLC | Intramuscular; Intravenous | 5000 [iU]/1mL | WinRho 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. | 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 | NA | NA | NA | NA | Link | Link | NA |
| 11231 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Winrho | Cangene BioPharma, LLC | Cangene BioPharma, LLC | Intramuscular; Intravenous | 15000 [iU]/1mL | WinRho 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. | 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 | NA | NA | NA | NA | Link | Link | NA |
| 11232 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Winrho | Cangene BioPharma, LLC | Cangene BioPharma, LLC | Intramuscular; Intravenous | 1500 [iU]/1mL | WinRho 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. | 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 | NA | NA | NA | NA | Link | Link | NA |
| 11233 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Xembify | GRIFOLS USA, LLC | GRIFOLS USA, LLC | Subcutaneous | 200 mg/1mL | XEMBIFY is contraindicated in: Patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA deficient patients with antibodies against IgA and history of hypersensitivity to human immune globulin treatment. | infusion site reactions (redness, pain, swelling, bruising, hard lump itching, firmness, scabbing), cough, and diarrhea | Xembify (for injection under the skin) is used to treat primary immunodeficiency diseases. Xembify is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Xembify may also be... | XEMBIFY (immune globulin subcutaneous, human - klhw) is a 20% immune globulin solution for subcutaneous injection indicated for treatment of primary humoral immunodeficiency (PI) in patients 2 years of age and older. This includes, but is not limited to, congenital agammaglobulinemia, common variable immunodeficiency, X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies.1-4 | NA | Several of the individual production steps of the manufacturing process have been shown to decrease TSE infectivity of an experimental model agent. TSE reduction steps include depth filtrations (a total of ≥ 6.6 log10). These studies provide reasonable assurance that low levels of vCJD/CJD agent infectivity, if present in the starting material, would be removed. | Link | Link | NA |
| 11234 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | 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. | 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. | 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. | 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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 | Xembify | Grifols Therapeutics Llc | Grifols Therapeutics Llc | Subcutaneous | 0.2 | XEMBIFY is contraindicated in: Patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. IgA deficient patients with antibodies against IgA and history of hypersensitivity to human immune globulin treatment. | infusion site reactions (redness, pain, swelling, bruising, hard lump itching, firmness, scabbing), cough, and diarrhea | Xembify (for injection under the skin) is used to treat primary immunodeficiency diseases. Xembify is also used to treat chronic inflammatory demyelinating polyneuropathy (an autoimmune disorder in which the immune system attacks the nerves, causing muscle weakness and numbness). Xembify may also be... | XEMBIFY (immune globulin subcutaneous, human - klhw) is a 20% immune globulin solution for subcutaneous injection indicated for treatment of primary humoral immunodeficiency (PI) in patients 2 years of age and older. This includes, but is not limited to, congenital agammaglobulinemia, common variable immunodeficiency, X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies.1-4 | NA | Several of the individual production steps of the manufacturing process have been shown to decrease TSE infectivity of an experimental model agent. TSE reduction steps include depth filtrations (a total of ≥ 6.6 log10). These studies provide reasonable assurance that low levels of vCJD/CJD agent infectivity, if present in the starting material, would be removed. | Link | Link | NA |
| 14480 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | Uplizna | Horizon Therapeutics USA, Inc. | Horizon Therapeutics USA, Inc. | Intravenous | 10 mg/1mL | UPLIZNA is contraindicated in patients with: A history of a life-threatening infusion reaction to UPLIZNA Active hepatitis B infection | urinary tract infection (UTI), joint pain, headache, and back pain | Uplizna is a prescription medicine used to treat adults with neuromyelitis optic spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody positive. It is not known if Uplizna is safe or effective in children. | Uplizna (inebilizumab-cdon) is a CD19-directed cytolytic antibody used to treat neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 14481 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies | NA | NA | NA | NA | B-lymphocyte antigen CD19 | Uplizna | Viela Bio, Inc. | Viela Bio, Inc. | Intravenous | 10 mg/1mL | UPLIZNA is contraindicated in patients with: A history of a life-threatening infusion reaction to UPLIZNA Active hepatitis B infection | urinary tract infection (UTI), joint pain, headache, and back pain | Uplizna is a prescription medicine used to treat adults with neuromyelitis optic spectrum disorder (NMOSD) who are anti-aquaporin-4 (AQP4) antibody positive. It is not known if Uplizna is safe or effective in children. | Uplizna (inebilizumab-cdon) is a CD19-directed cytolytic antibody used to treat neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 14482 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies, Monoclonal | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14483 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14484 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Blood Proteins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14485 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Globulins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14486 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Immunoglobulins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14487 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Immunoproteins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14488 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Proteins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14489 | Th1507 | Inebilizumab | >Th1507_Inebilizumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSSSWMNWVRQAPGKGLEWVGRIYPGDGDTNYNVKFKGRFTISRDDSKNSLYLQMNSLKTEDTAVYYCARSGFITTVRDFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | NA | NA | NA | NA | Inebilizumab exhibits biphasic pharmacokinetics with a mean terminal half-life of 18 days.[L14315] The terminal half-life reported in phase I studies varied by dose but was typically close to 18 days, with a range of 6.8 to 18.7 days.[A214298, A214301] | Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD).[A214283, A214286] Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody [rituximab], which is also used to treat NMOSD, inebilizumab has broader specificity.[A214280, A214289, A214292, A214295, A214298, A214301] Inebilizumab was granted FDA approval on June 11, 2020, for the treatment of anti-aquaporin 4 positive NMOSD patients.[L14315] Given its mechanism of action and good safety profile, it may prove useful in the treatment of other conditions linked to autoimmune antibody production or B-cell malignancies.[A214280, A214295] | Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients.[L14315] | Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule.[A214280, A214289, A214292, L14315] Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended.[L14315] | Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation.[A214283, A214286] The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist.[A214283, A214286] The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss.[A214286] In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.[A214295] CD19 is a B-cell surface antigen expressed on most B-cells,[A214280] including the expanded population of CD27high CD38high CD180- CD19+ plasmablasts that are the origin of astrocytic AQP4-IgG in most NMOSD patients.[A214283, A214286] Inebilizumab binds to CD19 and, through one of several potential mechanisms, results in cell death.[A214280, A214289, A214292, L14315] Destruction of the specific AQP4-IgG-producing plasmablasts results in lower amounts of AQP4-IgG in the CNS and therefore slows neuronal damage and improves patient outcomes.[A214295] | Toxicity information regarding inebilizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as severe infusion reactions, infections, and arthralgia. Symptomatic and supportive measures are recommended. | Inebilizumab is a monoclonal antibody and is hence likely degraded through proteolysis.[L14315] | Inebilizumab is given intravenously and hence is immediately exposed to the systemic circulation. The mean reported Cmax following second dose 300 mg administration was 108 µg/mL, and the cumulative AUC following 26 weeks of treatment with two IV administrations was 2980 µg | Inebilizumab has an estimated central volume of distribution of 2.95L and a peripheral volume of distribution of 2.57L.[L14315] The steady-state volume of distribution in patients administered with a range of doses between 0.1 and 10.0 mg/kg ranged from 53.7 to 71.7 mL/kg.[A214301] | Inebilizumab has an estimated systemic clearance of 0.19 L/day.[L14315] In phase I studies, the reported clearance varied between 139-180 mL/day in one study,[A214298] and 3.5-6.2 mL/kg/day in another,[A214301] depending on the dose. | Serum Globulins | NA | NA | NA | NA | B-lymphocyte antigen CD19 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15122 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Alimentary Tract and Metabolism | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | Brineura | BioMarin Pharmaceutical Inc. | BioMarin Pharmaceutical Inc. | Intraventricular | 150 mg/5mL | Brineura is contraindicated in patients with:any sign or symptom of acute, unresolved localized infection on or around the device insertion site (e.g. cellulitis or abscess); or suspected or confirmed CNS infection (e.g. cloudy CSF or positive CSF gram stain, or meningitis) [see WARNINGS AND PRECAUTIONS].any acute intraventricular access device-related complication (e.g., leakage, extravasation of fluid, or device failure) [see WARNINGS AND PRECAUTIONS].ventriculoperitoneal shunts. | fever, ECG abnormalities, increased or decreased cerebrospinal fluid (CSF) protein, vomiting, seizures, hypersensitivity, blood clotting, headache, irritability, increased white blood cell count (pleocytosis), device-related infection, slow heart rate, feeling jittery, and low blood pressure (hypotension). | Brineura is used to slow the loss of ability to crawl or walk in children with symptoms of a rare genetic condition called ceroid lipofuscinosis type 2 disease (CLN2). Brineura is for use in children who are at least 3 years old. Brineura may help slow the loss of certain physical abilities in children... | Brineura (cerliponase alfa) injection is a hydrolytic lysosomal N-terminal tripeptidyl peptidase indicated to slow the loss of ambulation in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase1 (TPP1) deficiency. | NA | NA | Link | Link | NA |
| 15123 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | Brineura | Biomarin International Limited | Biomarin International Limited | Intracerebral | 150 mg / 5 mL | Brineura is contraindicated in patients with:any sign or symptom of acute, unresolved localized infection on or around the device insertion site (e.g. cellulitis or abscess); or suspected or confirmed CNS infection (e.g. cloudy CSF or positive CSF gram stain, or meningitis) [see WARNINGS AND PRECAUTIONS].any acute intraventricular access device-related complication (e.g., leakage, extravasation of fluid, or device failure) [see WARNINGS AND PRECAUTIONS].ventriculoperitoneal shunts. | fever, ECG abnormalities, increased or decreased cerebrospinal fluid (CSF) protein, vomiting, seizures, hypersensitivity, blood clotting, headache, irritability, increased white blood cell count (pleocytosis), device-related infection, slow heart rate, feeling jittery, and low blood pressure (hypotension). | Brineura is used to slow the loss of ability to crawl or walk in children with symptoms of a rare genetic condition called ceroid lipofuscinosis type 2 disease (CLN2). Brineura is for use in children who are at least 3 years old. Brineura may help slow the loss of certain physical abilities in children... | Brineura (cerliponase alfa) injection is a hydrolytic lysosomal N-terminal tripeptidyl peptidase indicated to slow the loss of ambulation in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase1 (TPP1) deficiency. | NA | NA | Link | Link | NA |
| 15124 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Enzymes | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | Brineura | Biomarin International Limited | Biomarin International Limited | Intracerebral | 150 mg | Brineura is contraindicated in patients with:any sign or symptom of acute, unresolved localized infection on or around the device insertion site (e.g. cellulitis or abscess); or suspected or confirmed CNS infection (e.g. cloudy CSF or positive CSF gram stain, or meningitis) [see WARNINGS AND PRECAUTIONS].any acute intraventricular access device-related complication (e.g., leakage, extravasation of fluid, or device failure) [see WARNINGS AND PRECAUTIONS].ventriculoperitoneal shunts. | fever, ECG abnormalities, increased or decreased cerebrospinal fluid (CSF) protein, vomiting, seizures, hypersensitivity, blood clotting, headache, irritability, increased white blood cell count (pleocytosis), device-related infection, slow heart rate, feeling jittery, and low blood pressure (hypotension). | Brineura is used to slow the loss of ability to crawl or walk in children with symptoms of a rare genetic condition called ceroid lipofuscinosis type 2 disease (CLN2). Brineura is for use in children who are at least 3 years old. Brineura may help slow the loss of certain physical abilities in children... | Brineura (cerliponase alfa) injection is a hydrolytic lysosomal N-terminal tripeptidyl peptidase indicated to slow the loss of ambulation in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase1 (TPP1) deficiency. | NA | NA | Link | Link | NA |
| 15125 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Enzymes and Coenzymes | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15126 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Exopeptidases | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15127 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Hydrolases | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15128 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Hydrolytic Lysosomal N-terminal Tripeptidyl Peptidase | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15129 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Peptide Hydrolases | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15130 | Th1568 | Cerliponase alfa | >Th1568_Cerliponase_alfa SYSPEPDQRRTLPPGWVSLGRADPEEELSLTFALRQQNVERLSELVQAVSDPSSPQYGKYLTLENVADLVRPSPLTLHTVQKWLLAAGAQKCHSVITQDFLTCWLSIRQAELLLPGAEFHHYVGGPTETHVVRSPHPYQLPQALAPHVDFVGGLHRFPPTSSLRQRPEPQVTGTVGLHLGVTPSVIRKRYNLTSQDVGSGTSNNSQACAQFLEQYFHDSDLAQFMRLFGGNFAHQASVARVVGQQGRGRAGIEASLDVQYLMSAGANISTWVYSSPGRHEGQEPFLQWLMLLSNESALPHVHTVSYGDDEDSLSSAYIQRVNTELMKAAARGLTLLFASGDSGAGCWSVSGRHQFRPTFPASSPYVTTVGGTSFQEPFLITNEIVDYISGGGFSNVFPRPSYQEEAVTKFLSSSPHLPPSSYFNASGRAYPDVAALSDGYWVVSNRVPIPWVSGTSASTPVFGGILSLINEHRILSGRPPLGFLNPRLYQQHGAGLFDVTRGCHESCLDEEVEGQGFCSGPGWDPVTGWGTPNFPALLKTLLNP | 59 | NA | NA | NA | NA | Refer to FDA Label | Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). | Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death [L755]. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. | Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1. | The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as M6P/IGF2 receptor). Cerliponase alfa is activated in the lysosome under low pH conditions and the activated proteolytic form of rhTPP1 cleaves tripeptides from the N-terminus of stored proteins. | No data from carcinogenicity, genotoxicity, and fertility studies. Unwanted effects of cerliponase alfa treatment include pyrexia, ECG abnormalities, decreased CSF protein, seizure and hypersensitivity. | Predicted to be metabolized through peptide hydrolysis. | Refer to FDA Label | The estimated CSF volume of distribution of cerliponase alfa following intraventricular infusion of 300mg of Brineura (median Vss = 245 mL) exceeds the typical CSF volume (100 mL) [FDA label]. | Refer to FDA Label | Proteins | NA | NA | NA | NA | Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15330 | Th1588 | Cenegermin | >Th1588_Cenegermin SSSHPIFHRGEFSVCDSVSVWVGDKTTATDIKGKEVMVLGEVNINNSVFKQYFFETKCRDPNPVDSGCRGIDSKHWNSYCTTTHTFVKALTMDGKQAAWRFIRIDTACVCVLSRKAVR | NA | NA | NA | NA | NA | Half life data specific to human administration is not readily accessible or available [FDA Label]. | Cenegermin is a human beta-nerve growth factor (beta-ngf)-(1-118)- peptide (non-covalent dimer) produced in escherichia coli. It received European Union Approval in July, 2017 for the treatment of moderate to severe neurotrophic keratitis. Cenegermin received approval from the US FDA a year later in August of 2018 [L4563]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. The prevalence of neurotrophic keratitis has been estimated to be less than five in 10,000 individuals [L4563]. While the prevalence of neurotrophic keratitis is low, the impact of this serious condition and its associated sequelae on an individual patient can be debilitating. Many currently available therapeutic options for treating the condition involve surgical interventions - surgeries that are typically only palliative [L4563]. The approval of cenegermin consequently provides a novel topical treatment that has the potential capacity to offer total corneal healing for many patients who may use the agent [L4563]. In particular, cenegermin was granted Priority Review designation, under which the FDA’s goal is to take action on an application within six months of application filing where the agency determines that the drug, if approved, would provide a significant improvement in the safety or effectiveness of the treatment, diagnosis or prevention of a serious condition [L4563]. Cenegermin also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases [L4563]. | Cenegermin is indicated for the treatment of moderate (persistent epithelial defect) or severe (corneal ulcer) neurotrophic keratitis in adults [FDA Label, F1502]. | Little to no pharmacodynamic studies have yet been conducted in humans [FDA Label]. | Cenegermin is a recombinant form of human nerve growth factor [FDA Label, F1502, F1503]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. Nerve growth factor is subsequently an endogenous protein involved in the differentiation and maintenance of neurons, which acts through specific high-affinity (i.e., TrkA) and low-affinity (i.e. p75NTR) nerve growth factor receptors [FDA Label, F1502, F1503]. Nerve growth factor receptors are expressed in the anterior segment of the eye (cornea, conjunctiva, iris, ciliary body, and lens), by the lacrimal gland, and by posterior segment intraocular tissues [FDA Label, F1502, F1503]. The treatment with cenegermin, administered as eye drops, is intended to allow restoration of corneal integrity [FDA Label, F1502, F1503]. | There are no data from the use of cenegermin in pregnant women [FDA Label, F1502]. Systemic exposure to cenegermin is negligible or does not occur [F1502]. As a precautionary measure, it is preferable to avoid the use of OXERVATE during pregnancy [F1502]. It is not known whether cenegermin is excreted in human milk [FDA Label, F1502]. A risk to the suckling child cannot be excluded [F1502]. A decision must be made whether to discontinue breast-feeding or to discontinue/abstain from this therapy taking into account the benefit of breast feeding for the child and the benefit of therapy for the woman [F1502]. The safety and effectiveness of cenegermin have been established in the pediatric population [FDA Label]. Use of cenegermin in this population is supported by evidence from adequate and well controlled trials of cenegermin in adults with additional safety data in pediatric patients from 2 years of age and older [FDA Label]. Of the total number of subjects in clinical studies of cenegermin, 43.5 % were 65 years old and over [FDA Label]. No overall differences in safety or effectiveness were observed between elderly and younger adult patients [FDA Label]. There are no data on the effects of cenegermin on human fertility [FDA Label, F1502]. | Ocularly administered cenegermin is mainly eliminated by tear secretion and the remainder mostly biotransformed by local tissue proteases [F1502]. | Cenegermin is mostly removed from the eye with the tear production and through the naso-lacrimal duct; the minor portion that is absorbed occurs mostly in the conjunctiva and peri-orbital tissue and to a minor extent through the cornea following ocular administration [F1502]. Pharmacokinetic profiling of patients included in studies found no accumulation effect of cenegermin [F1502]. In general, the systemic absorption of cenegermin is negligible [F1502]. | After eye drop administration, cenegermin is distributed particularly in the anterior portion of the eye, although a study with radiolabelled cenegermin in rats has shown that it also reaches the retina and other posterior parts of the eye at doses significantly higher than those administered by eye drops in humans to treat neurotrophic keratitis [F1502]. At the ocular doses, cenegermin is not distributed throughout body tissues as there is no systemic absorption above the natural baseline levels [F1502]. | ALthough the systemic absorption of cenegermin is negligible in general [F1502], clearance data specific to human administration is not readily accessible or available [FDA Label]. | Ophthalmologicals | NA | NA | NA | NA | High affinity nerve growth factor receptor | Oxervate | Dompé farmaceutici S.p.A. | Dompé farmaceutici S.p.A. | Ophthalmic | 20 ug/1mL | None. | eye pain, eye redness, eye inflammation, and increased tearing | OXERVATE ophthalmic solution contains cenegermin-bkbj, a recombinant form of human nerve growth factor produced in Escherichia coli. | OXERVATE™(cenegermin-bkbj) ophthalmic solution 0.002% is indicated for the treatment of neurotrophic keratitis. | NA | NA | Link | Link | NA |
| 15331 | Th1588 | Cenegermin | >Th1588_Cenegermin SSSHPIFHRGEFSVCDSVSVWVGDKTTATDIKGKEVMVLGEVNINNSVFKQYFFETKCRDPNPVDSGCRGIDSKHWNSYCTTTHTFVKALTMDGKQAAWRFIRIDTACVCVLSRKAVR | NA | NA | NA | NA | NA | Half life data specific to human administration is not readily accessible or available [FDA Label]. | Cenegermin is a human beta-nerve growth factor (beta-ngf)-(1-118)- peptide (non-covalent dimer) produced in escherichia coli. It received European Union Approval in July, 2017 for the treatment of moderate to severe neurotrophic keratitis. Cenegermin received approval from the US FDA a year later in August of 2018 [L4563]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. The prevalence of neurotrophic keratitis has been estimated to be less than five in 10,000 individuals [L4563]. While the prevalence of neurotrophic keratitis is low, the impact of this serious condition and its associated sequelae on an individual patient can be debilitating. Many currently available therapeutic options for treating the condition involve surgical interventions - surgeries that are typically only palliative [L4563]. The approval of cenegermin consequently provides a novel topical treatment that has the potential capacity to offer total corneal healing for many patients who may use the agent [L4563]. In particular, cenegermin was granted Priority Review designation, under which the FDA’s goal is to take action on an application within six months of application filing where the agency determines that the drug, if approved, would provide a significant improvement in the safety or effectiveness of the treatment, diagnosis or prevention of a serious condition [L4563]. Cenegermin also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases [L4563]. | Cenegermin is indicated for the treatment of moderate (persistent epithelial defect) or severe (corneal ulcer) neurotrophic keratitis in adults [FDA Label, F1502]. | Little to no pharmacodynamic studies have yet been conducted in humans [FDA Label]. | Cenegermin is a recombinant form of human nerve growth factor [FDA Label, F1502, F1503]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. Nerve growth factor is subsequently an endogenous protein involved in the differentiation and maintenance of neurons, which acts through specific high-affinity (i.e., TrkA) and low-affinity (i.e. p75NTR) nerve growth factor receptors [FDA Label, F1502, F1503]. Nerve growth factor receptors are expressed in the anterior segment of the eye (cornea, conjunctiva, iris, ciliary body, and lens), by the lacrimal gland, and by posterior segment intraocular tissues [FDA Label, F1502, F1503]. The treatment with cenegermin, administered as eye drops, is intended to allow restoration of corneal integrity [FDA Label, F1502, F1503]. | There are no data from the use of cenegermin in pregnant women [FDA Label, F1502]. Systemic exposure to cenegermin is negligible or does not occur [F1502]. As a precautionary measure, it is preferable to avoid the use of OXERVATE during pregnancy [F1502]. It is not known whether cenegermin is excreted in human milk [FDA Label, F1502]. A risk to the suckling child cannot be excluded [F1502]. A decision must be made whether to discontinue breast-feeding or to discontinue/abstain from this therapy taking into account the benefit of breast feeding for the child and the benefit of therapy for the woman [F1502]. The safety and effectiveness of cenegermin have been established in the pediatric population [FDA Label]. Use of cenegermin in this population is supported by evidence from adequate and well controlled trials of cenegermin in adults with additional safety data in pediatric patients from 2 years of age and older [FDA Label]. Of the total number of subjects in clinical studies of cenegermin, 43.5 % were 65 years old and over [FDA Label]. No overall differences in safety or effectiveness were observed between elderly and younger adult patients [FDA Label]. There are no data on the effects of cenegermin on human fertility [FDA Label, F1502]. | Ocularly administered cenegermin is mainly eliminated by tear secretion and the remainder mostly biotransformed by local tissue proteases [F1502]. | Cenegermin is mostly removed from the eye with the tear production and through the naso-lacrimal duct; the minor portion that is absorbed occurs mostly in the conjunctiva and peri-orbital tissue and to a minor extent through the cornea following ocular administration [F1502]. Pharmacokinetic profiling of patients included in studies found no accumulation effect of cenegermin [F1502]. In general, the systemic absorption of cenegermin is negligible [F1502]. | After eye drop administration, cenegermin is distributed particularly in the anterior portion of the eye, although a study with radiolabelled cenegermin in rats has shown that it also reaches the retina and other posterior parts of the eye at doses significantly higher than those administered by eye drops in humans to treat neurotrophic keratitis [F1502]. At the ocular doses, cenegermin is not distributed throughout body tissues as there is no systemic absorption above the natural baseline levels [F1502]. | ALthough the systemic absorption of cenegermin is negligible in general [F1502], clearance data specific to human administration is not readily accessible or available [FDA Label]. | Recombinant Human Nerve Growth Factor | NA | NA | NA | NA | High affinity nerve growth factor receptor | Oxervate | Dompé farmaceutici S.p.A. | Dompé farmaceutici S.p.A. | Ophthalmic | 20 ug/1mL | None. | eye pain, eye redness, eye inflammation, and increased tearing | OXERVATE ophthalmic solution contains cenegermin-bkbj, a recombinant form of human nerve growth factor produced in Escherichia coli. | OXERVATE™(cenegermin-bkbj) ophthalmic solution 0.002% is indicated for the treatment of neurotrophic keratitis. | NA | NA | Link | Link | NA |
| 15332 | Th1588 | Cenegermin | >Th1588_Cenegermin SSSHPIFHRGEFSVCDSVSVWVGDKTTATDIKGKEVMVLGEVNINNSVFKQYFFETKCRDPNPVDSGCRGIDSKHWNSYCTTTHTFVKALTMDGKQAAWRFIRIDTACVCVLSRKAVR | NA | NA | NA | NA | NA | Half life data specific to human administration is not readily accessible or available [FDA Label]. | Cenegermin is a human beta-nerve growth factor (beta-ngf)-(1-118)- peptide (non-covalent dimer) produced in escherichia coli. It received European Union Approval in July, 2017 for the treatment of moderate to severe neurotrophic keratitis. Cenegermin received approval from the US FDA a year later in August of 2018 [L4563]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. The prevalence of neurotrophic keratitis has been estimated to be less than five in 10,000 individuals [L4563]. While the prevalence of neurotrophic keratitis is low, the impact of this serious condition and its associated sequelae on an individual patient can be debilitating. Many currently available therapeutic options for treating the condition involve surgical interventions - surgeries that are typically only palliative [L4563]. The approval of cenegermin consequently provides a novel topical treatment that has the potential capacity to offer total corneal healing for many patients who may use the agent [L4563]. In particular, cenegermin was granted Priority Review designation, under which the FDA’s goal is to take action on an application within six months of application filing where the agency determines that the drug, if approved, would provide a significant improvement in the safety or effectiveness of the treatment, diagnosis or prevention of a serious condition [L4563]. Cenegermin also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases [L4563]. | Cenegermin is indicated for the treatment of moderate (persistent epithelial defect) or severe (corneal ulcer) neurotrophic keratitis in adults [FDA Label, F1502]. | Little to no pharmacodynamic studies have yet been conducted in humans [FDA Label]. | Cenegermin is a recombinant form of human nerve growth factor [FDA Label, F1502, F1503]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. Nerve growth factor is subsequently an endogenous protein involved in the differentiation and maintenance of neurons, which acts through specific high-affinity (i.e., TrkA) and low-affinity (i.e. p75NTR) nerve growth factor receptors [FDA Label, F1502, F1503]. Nerve growth factor receptors are expressed in the anterior segment of the eye (cornea, conjunctiva, iris, ciliary body, and lens), by the lacrimal gland, and by posterior segment intraocular tissues [FDA Label, F1502, F1503]. The treatment with cenegermin, administered as eye drops, is intended to allow restoration of corneal integrity [FDA Label, F1502, F1503]. | There are no data from the use of cenegermin in pregnant women [FDA Label, F1502]. Systemic exposure to cenegermin is negligible or does not occur [F1502]. As a precautionary measure, it is preferable to avoid the use of OXERVATE during pregnancy [F1502]. It is not known whether cenegermin is excreted in human milk [FDA Label, F1502]. A risk to the suckling child cannot be excluded [F1502]. A decision must be made whether to discontinue breast-feeding or to discontinue/abstain from this therapy taking into account the benefit of breast feeding for the child and the benefit of therapy for the woman [F1502]. The safety and effectiveness of cenegermin have been established in the pediatric population [FDA Label]. Use of cenegermin in this population is supported by evidence from adequate and well controlled trials of cenegermin in adults with additional safety data in pediatric patients from 2 years of age and older [FDA Label]. Of the total number of subjects in clinical studies of cenegermin, 43.5 % were 65 years old and over [FDA Label]. No overall differences in safety or effectiveness were observed between elderly and younger adult patients [FDA Label]. There are no data on the effects of cenegermin on human fertility [FDA Label, F1502]. | Ocularly administered cenegermin is mainly eliminated by tear secretion and the remainder mostly biotransformed by local tissue proteases [F1502]. | Cenegermin is mostly removed from the eye with the tear production and through the naso-lacrimal duct; the minor portion that is absorbed occurs mostly in the conjunctiva and peri-orbital tissue and to a minor extent through the cornea following ocular administration [F1502]. Pharmacokinetic profiling of patients included in studies found no accumulation effect of cenegermin [F1502]. In general, the systemic absorption of cenegermin is negligible [F1502]. | After eye drop administration, cenegermin is distributed particularly in the anterior portion of the eye, although a study with radiolabelled cenegermin in rats has shown that it also reaches the retina and other posterior parts of the eye at doses significantly higher than those administered by eye drops in humans to treat neurotrophic keratitis [F1502]. At the ocular doses, cenegermin is not distributed throughout body tissues as there is no systemic absorption above the natural baseline levels [F1502]. | ALthough the systemic absorption of cenegermin is negligible in general [F1502], clearance data specific to human administration is not readily accessible or available [FDA Label]. | Sensory Organs | NA | NA | NA | NA | High affinity nerve growth factor receptor | Oxervate | Dompé farmaceutici S.p.A. | Dompé farmaceutici S.p.A. | Ophthalmic | 0.0002 | None. | eye pain, eye redness, eye inflammation, and increased tearing | OXERVATE ophthalmic solution contains cenegermin-bkbj, a recombinant form of human nerve growth factor produced in Escherichia coli. | OXERVATE™(cenegermin-bkbj) ophthalmic solution 0.002% is indicated for the treatment of neurotrophic keratitis. | NA | NA | Link | Link | NA |
| 15333 | Th1588 | Cenegermin | >Th1588_Cenegermin SSSHPIFHRGEFSVCDSVSVWVGDKTTATDIKGKEVMVLGEVNINNSVFKQYFFETKCRDPNPVDSGCRGIDSKHWNSYCTTTHTFVKALTMDGKQAAWRFIRIDTACVCVLSRKAVR | NA | NA | NA | NA | NA | Half life data specific to human administration is not readily accessible or available [FDA Label]. | Cenegermin is a human beta-nerve growth factor (beta-ngf)-(1-118)- peptide (non-covalent dimer) produced in escherichia coli. It received European Union Approval in July, 2017 for the treatment of moderate to severe neurotrophic keratitis. Cenegermin received approval from the US FDA a year later in August of 2018 [L4563]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. The prevalence of neurotrophic keratitis has been estimated to be less than five in 10,000 individuals [L4563]. While the prevalence of neurotrophic keratitis is low, the impact of this serious condition and its associated sequelae on an individual patient can be debilitating. Many currently available therapeutic options for treating the condition involve surgical interventions - surgeries that are typically only palliative [L4563]. The approval of cenegermin consequently provides a novel topical treatment that has the potential capacity to offer total corneal healing for many patients who may use the agent [L4563]. In particular, cenegermin was granted Priority Review designation, under which the FDA’s goal is to take action on an application within six months of application filing where the agency determines that the drug, if approved, would provide a significant improvement in the safety or effectiveness of the treatment, diagnosis or prevention of a serious condition [L4563]. Cenegermin also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases [L4563]. | Cenegermin is indicated for the treatment of moderate (persistent epithelial defect) or severe (corneal ulcer) neurotrophic keratitis in adults [FDA Label, F1502]. | Little to no pharmacodynamic studies have yet been conducted in humans [FDA Label]. | Cenegermin is a recombinant form of human nerve growth factor [FDA Label, F1502, F1503]. Neurotrophic keratitis is a degenerative disease resulting from a loss of corneal sensation [L4563]. The loss of corneal sensation impairs corneal health causing progressive damage to the top layer of the cornea, including corneal thinning, ulceration, and perforation in severe cases [L4563]. Nerve growth factor is subsequently an endogenous protein involved in the differentiation and maintenance of neurons, which acts through specific high-affinity (i.e., TrkA) and low-affinity (i.e. p75NTR) nerve growth factor receptors [FDA Label, F1502, F1503]. Nerve growth factor receptors are expressed in the anterior segment of the eye (cornea, conjunctiva, iris, ciliary body, and lens), by the lacrimal gland, and by posterior segment intraocular tissues [FDA Label, F1502, F1503]. The treatment with cenegermin, administered as eye drops, is intended to allow restoration of corneal integrity [FDA Label, F1502, F1503]. | There are no data from the use of cenegermin in pregnant women [FDA Label, F1502]. Systemic exposure to cenegermin is negligible or does not occur [F1502]. As a precautionary measure, it is preferable to avoid the use of OXERVATE during pregnancy [F1502]. It is not known whether cenegermin is excreted in human milk [FDA Label, F1502]. A risk to the suckling child cannot be excluded [F1502]. A decision must be made whether to discontinue breast-feeding or to discontinue/abstain from this therapy taking into account the benefit of breast feeding for the child and the benefit of therapy for the woman [F1502]. The safety and effectiveness of cenegermin have been established in the pediatric population [FDA Label]. Use of cenegermin in this population is supported by evidence from adequate and well controlled trials of cenegermin in adults with additional safety data in pediatric patients from 2 years of age and older [FDA Label]. Of the total number of subjects in clinical studies of cenegermin, 43.5 % were 65 years old and over [FDA Label]. No overall differences in safety or effectiveness were observed between elderly and younger adult patients [FDA Label]. There are no data on the effects of cenegermin on human fertility [FDA Label, F1502]. | Ocularly administered cenegermin is mainly eliminated by tear secretion and the remainder mostly biotransformed by local tissue proteases [F1502]. | Cenegermin is mostly removed from the eye with the tear production and through the naso-lacrimal duct; the minor portion that is absorbed occurs mostly in the conjunctiva and peri-orbital tissue and to a minor extent through the cornea following ocular administration [F1502]. Pharmacokinetic profiling of patients included in studies found no accumulation effect of cenegermin [F1502]. In general, the systemic absorption of cenegermin is negligible [F1502]. | After eye drop administration, cenegermin is distributed particularly in the anterior portion of the eye, although a study with radiolabelled cenegermin in rats has shown that it also reaches the retina and other posterior parts of the eye at doses significantly higher than those administered by eye drops in humans to treat neurotrophic keratitis [F1502]. At the ocular doses, cenegermin is not distributed throughout body tissues as there is no systemic absorption above the natural baseline levels [F1502]. | ALthough the systemic absorption of cenegermin is negligible in general [F1502], clearance data specific to human administration is not readily accessible or available [FDA Label]. | NA | NA | NA | NA | NA | High affinity nerve growth factor receptor | Oxervate | Dompé farmaceutici S.p.A. | Dompé farmaceutici S.p.A. | Ophthalmic | 20 mcg/ml | None. | eye pain, eye redness, eye inflammation, and increased tearing | OXERVATE ophthalmic solution contains cenegermin-bkbj, a recombinant form of human nerve growth factor produced in Escherichia coli. | OXERVATE™(cenegermin-bkbj) ophthalmic solution 0.002% is indicated for the treatment of neurotrophic keratitis. | NA | NA | Link | Link | NA |
| 15909 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | Enspryng | Hoffmann La Roche | Hoffmann La Roche | Subcutaneous | 120 mg / mL | ENSPRYNG is contraindicated in patients with: A known hypersensitivity to satralizumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS] Active Hepatitis B infection [see WARNINGS AND PRECAUTIONS] Active or untreated latent tuberculosis [see WARNINGS AND PRECAUTIONS] | runny or stuffy nose, headache, upper respiratory tract infection, gastritis, rash, joint pain, extremity pain, fatigue, and nausea | Enspryng is a recombinant humanized monoclonal antibody targeting human interleukin-6 (IL-6) receptors. Enspryng is a prescription medicine used to treat adults with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare, chronic autoimmune disease that causes inflammation in the central nervous... | ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 15910 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Antibodies, Monoclonal | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | Enspryng | Roche Registration Gmb H | Roche Registration Gmb H | Subcutaneous | 120 mg | ENSPRYNG is contraindicated in patients with: A known hypersensitivity to satralizumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS] Active Hepatitis B infection [see WARNINGS AND PRECAUTIONS] Active or untreated latent tuberculosis [see WARNINGS AND PRECAUTIONS] | runny or stuffy nose, headache, upper respiratory tract infection, gastritis, rash, joint pain, extremity pain, fatigue, and nausea | Enspryng is a recombinant humanized monoclonal antibody targeting human interleukin-6 (IL-6) receptors. Enspryng is a prescription medicine used to treat adults with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare, chronic autoimmune disease that causes inflammation in the central nervous... | ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 15911 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | Enspryng | Genentech Inc. | Genentech Inc. | Subcutaneous | 120 mg/1mL | ENSPRYNG is contraindicated in patients with: A known hypersensitivity to satralizumab or any of the inactive ingredients [see WARNINGS AND PRECAUTIONS] Active Hepatitis B infection [see WARNINGS AND PRECAUTIONS] Active or untreated latent tuberculosis [see WARNINGS AND PRECAUTIONS] | runny or stuffy nose, headache, upper respiratory tract infection, gastritis, rash, joint pain, extremity pain, fatigue, and nausea | Enspryng is a recombinant humanized monoclonal antibody targeting human interleukin-6 (IL-6) receptors. Enspryng is a prescription medicine used to treat adults with neuromyelitis optica spectrum disorder (NMOSD). NMOSD is a rare, chronic autoimmune disease that causes inflammation in the central nervous... | ENSPRYNG is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive. | NA | NA | Link | Link | NA |
| 15912 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Blood Proteins | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15913 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Immunoglobulins | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15914 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Immunomodulatory Agents | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15915 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Interleukin-6 Receptor Antagonist | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15916 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Proteins | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15917 | Th1643 | Satralizumab | >Th1643_Satralizumab QVQLQESGPGLVKPSETLSLTCAVSGHSISHDHAWSWVRQPPGEGLEWIGFISYSGITNYNPSLQGRVTISRDNSKNTLYLQMNSLRAEDTAVYYCARSLARTTAMDYWGEGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSNFGTQTYTCNVDHKPSNTKVDKTVERKSCVECPPCPAPPVAGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTFRVVSVLTVVHQDWLNGKEYKCKVSNKGLPAPIEKTISKTKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPMLDSDGSFFLYSKLTVDKSRWQEGNVFSCSVMHEALHAHYTQKSLSLSP | 143000 | NA | NA | NA | NA | The terminal half-life of satralizumab is approximately 30 days (range 22-37 days).[L15536] | Satralizumab is a recombinant humanized monoclonal antibody targeted against human interleukin-6 (IL-6) receptors, similar to [tocilizumab], which is produced in Chinese hamster ovary cells and based on an IgG2 framework.[L15536] Satralizumab is used in the treatment of neuromyelitis optica spectrum disorder (NMOSD), a rare autoimmune inflammatory disorder of the central nervous system (CNS) involving demyelinating lesions in the optic nerve, spinal cord, brainstem, and cerebrum.[A218551] Some of the pro-inflammatory mechanisms involved in NMOSD are thought to be mediated, at least in part, by IL-6, including increased production of anti-aquaporin-4 (AQP4) autoantibodies and increased permeability of the blood-brain barrier, which allows for the passage of pro-inflammatory mediators into the CNS.[A218546,A218551] Satralizumab is thought to exert its therapeutic benefits by blocking IL-6 receptors and, subsequently, these inflammatory responses. Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] is uniquely formulated with "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner[A218551] - this allows satralizumab to bind an IL-6 receptor until it reaches an endosome, after which the drug may dissociate from the receptor and move back into the plasma to act again. This novel mechanism effectively increases the duration of action of satralizumab, as it allows for single drug molecules to interact with multiple endogenous IL-6 receptors prior to elimination. Satralizumab was first approved for use in Canada in June 2020 for the treatment of AQP4 antibody-positive patients with NMOSD.[A218551] It received subsequent approvals in Switzerland and Japan,[A218551] and was approved for use by the FDA in August 2020,[L15566] becoming the 3rd treatment to receive FDA approval for NMOSD (after [eculizumab] in June 2019 and [inebilizumab] in June 2020). | Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adult patients who are anti-aquaporin-4 (AQP4) antibody positive.[L15536] In Canada, it is also used in adolescent patients for the same indication.[L15546] | Enspryng®, a satralizumab formulation developed by Chugai Pharmaceutical and Roche,[L15536] utilizes a novel "recycling antibody technology" whereby the association of satralizumab to IL-6 receptors occurs in a pH-dependent manner.[A218551] Satralizumab-bound IL-6 receptors are taken up into cells and transported into endosomes, a relatively acidic environment in comparison to plasma (pH 5.5-6.0 vs. pH 7.4) - this decrease in pH allows satralizumab to dissociate from the IL-6 receptor and be recycled back into the plasma, where it can bind to another IL-6 receptor and repeat the process.[A218551] Satralizumab has been associated with an increased risk of infection, including serious and potentially fatal infections. It should not be administered to patients with active infections, including localized infections, until the infection resolves, and is contraindicated for use in patients with active hepatitis B or tuberculosis.[L15536] | Interleukin-6 (IL-6) is a pro-inflammatory cytokine[A218546] which has been implicated in the pathogenesis of NMOSD.[A218551] The inflammatory cascade triggered by IL-6 signaling is thought to result in the differentiation of T-cells into pro-inflammatory TH17 cells[A218551] and the differentiation of B-cells into plasmablasts producing AQP4 autoantibodies.[A218551,A218546] IL-6 may also play a role in increasing the permeability of the blood-brain barrier, thereby allowing penetration of autoantibodies and pro-inflammatory mediators into the central nervous system.[A218551,A218546] Satralizumab is a humanized monoclonal antibody targeted against human IL-6 receptors.[L15536] It binds to soluble and membrane-bound IL-6 receptors and prevents the signaling cascade, and subsequent pro-inflammatory effects, associated with its binding to endogenous IL-6. | There is no data regarding overdose of satralizumab. No serious adverse effects were noted in healthy adults receiving a single dose of 240mg subcutaneously in clinical trials.[L15546] Patients experiencing a suspected overdose should be treated with symptomatic and supportive measures as clinically indicated. | While the metabolism of satralizumab has not been studied directly,[L15536] monoclonal antibodies as a class are principally cleared by catabolism.[L15536,A216712] | The Cmax and AUC at steady-state, achieved after an 8-week loading period, were approximately 31.5 mcg/mL and 737 mcg.mL/day, respectively.[L15536] Average Ctrough concentrations were approximately 19 mcg/mL.[L15546] The bioavailability of satralizumab following subcutaneous injection has been reported to be between 78.5% and 85%.[L15536,L15546] | Satralizumab is subject to biphasic distribution - the estimated volume of distribution for the central and peripheral compartments are 3.46 L and 2.07 L, respectively.[L15546] | The total clearance of satralizumab is concentration-dependent and is estimated to be 0.0601-0.0679 L/day.[L15536,L15546] The inter-compartmental clearance was 0.336 L/day.[L15536] | Serum Globulins | NA | NA | NA | NA | Interleukin-6 receptor subunit alpha | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15990 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Agents that produce hypertension | NA | NA | NA | NA | GD2 disialoganglioside | Danyelza | Y-mAbs Therapeutics, Inc. | Y-mAbs Therapeutics, Inc. | Intravenous | 40 mg/10mL | DANYELZA is contraindicated in patients with a history of severe hypersensitivity reaction to naxitamab-gqgk. Reactions have included anaphylaxis [see WARNINGS AND PRECAUTIONS]. | infusion-related reactions occurring on the day of infusion or the day following an infusion (low blood pressure, bronchospasm, flushing, wheezing, stridor, hives, shortness of breath, fever, swelling of the face/lips/tongue, respiratory tract edema, chills, low blood oxygen, itching, and rash) pain (abdominal pain, pain in extremity, bone pain, neck pain, back pain, and musculoskeletal pain), fast heart rate, vomiting, cough, nausea, diarrhea, decreased appetite, high blood pressure (hypertension), fatigue, erythema multiforme, numbness and tingling of extremities, hives not occurring on the day of infusion or the day following an infusion, fever not occurring on the day of infusion or the day following an infusion, headache, injection site reaction, fluid retention (edema), anxiety, localized swelling, irritability, decreased lymphocytes, decreased neutrophils, decreased hemoglobin, decreased platelet count, decreased potassium, increased alanine aminotransferase, decreased glucose, decreased calcium, decreased albumin, decreased sodium, and decreased phosphate | NA | DANYELZA is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of pediatric patients 1 year of age and older and adult patients with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy. | NA | NA | Link | Link | NA |
| 15991 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15992 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Antibodies, Monoclonal | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15993 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Antibodies, Monoclonal, Humanized | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15994 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Blood Proteins | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15995 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Glycolipid Disialoganglioside-directed Antibody | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15996 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Glycolipid Disialoganglioside-directed Antibody Interactions | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15997 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Immunoglobulins | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15998 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Immunotherapy | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15999 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Neurotoxic agents | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16000 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Proteins | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16001 | Th1660 | Naxitamab | NA | 144000 | NA | NA | NA | NA | The mean terminal half-life of naxitamab is 8.2 days.[L24454] | Naxitamab (humanized 3F8, hu3F8) is an IgG1 monoclonal antibody directed against the oncofetal differentiation antigen GD2 disialoganglioside.[L24454,A224604] Normally expressed during fetal development and in mature neurons, pain fibers, and skin cells, GD2 constitutes a highly efficient target in the treatment of neuroblastoma - it is widely expressed across and within neuroblastomas (and other neuroectodermal tumors),[A224609] and is rarely subject to antigen loss.[A224604] The first anti-GD2-monoclonal IgG antibody to be approved by the FDA for the treatment of neuroblastoma was [dinutuximab] under the brand name Unituxin in 2015.[A224474] One stark disadvantage of this therapy is the requirement for concurrent use of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA).[L24929] Naxitamab-gqgk (Danyelza) was granted accelerated approval by the FDA in November 2020 for the treatment of high-risk relapsed/refractory neuroblastoma of the bone or bone marrow.[L24454] This approval requires naxitamab to be co-administered only with GM-CSF, a factor known to enhance the granulocyte-mediated antibody-dependent cytotoxicity of anti-GD2 therapies,[A224604] making the administration of naxitamab therapy markedly simpler than that of its predecessor. | Naxitamab-gqgk is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), for the treatment of patients 1 year of age and older with relapsed or refractory high-risk neuroblastoma in the bone or bone marrow who have demonstrated a partial response, minor response, or stable disease to prior therapy.[L24454] | In targeting cell surface glycoproteins (GD2) that occur on the surface of neuroendocrine tumors, naxitamab directs the immune system towards these cancerous cells and induces the activation of both complement-dependent and antibody-dependent cytotoxicity.[L24454] Naxitamab can cause serious infusion reactions - including hypotension, hypoxia, anaphylaxis, and cardiac arrest - that necessitate careful monitoring during therapy. All patients should be pre-medicated with intravenous corticosteroids (e.g. [methylprednisolone]) as well as an antihistamine, H2 receptor antagonist, acetaminophen, and an antiemetic prior to therapy to mitigate the risk and severity of infusion-related reactions. Naxitamab may also cause severe neurotoxicity, including significant neuropathic pain, transverse myelitis, reversible posterior leukoencephalopathy syndrome (RPLS), and ocular toxicities. Pain management should be implemented prior to and during therapy - patients should take a 12-day course of neuropathic pain prophylaxis (e.g. gabapentin) starting 4 days prior to infusion, and should receive oral opioids 45-60 minutes prior to infusion and intravenous opioids and/or ketamine as needed thereafter.[L24454] | Neuroblastomas are neuroendocrine tumors occurring in immature and developing cells of the nervous system and are the most common malignancy diagnosed in children <1 year of age.[A224604] The GD2 disialoganglioside is a glycolipid found highly expressed on the surface of neuroectodermal tumors,[A224609] including neuroblastomas. GD2 exhibits high density and homogeneity across neuroblastomas and a rare occurrence of antigen loss,[A224604] making it a desirable target in the treatment of these cancers. Naxitamab is an IgG1 monoclonal antibody directed against GD2 disialogangliosides - it binds to GD2 on the surface of neuroblastoma cells and induces both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC),[L24454] the latter of which is enhanced by co-administration with GM-CSF.[A224604] | Data regarding overdose of naxitamab are unavailable. In the event of an overdose, patients should be treated with symptomatic and supportive measures. | While the metabolism of naxitamab has not been studied directly,[L24454] monoclonal antibodies as a class are principally metabolized to smaller peptides via catabolic processes.[L24454,A216712] | The mean plasma concentration of naxitamab following an intravenous infusion of 3 mg/kg over 30 minutes was 57.4 µg/mL.[L24454] The AUC of naxitamab appears to correlate with body size.[A224474] | NA | The clearance of naxitamab appears to be correlated inversely with body weight.[L24454] | Serum Globulins | NA | NA | NA | NA | GD2 disialoganglioside | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16283 | Th1793 | Equine Botulinum Neurotoxin E Immune FAB2 | >Th1793_Equine_Botulinum_Neurotoxin_E_Immune_FAB2 MPKINSFNYNDPVNDRTILYIKPGGCQEFYKSFNIMKNIWIIPERNVIGTTPQDFHPPTSLKNGDSSYYDPNYLQSDEEKDRFLKIVTKIFNRINNNLSGGILLEELSKANPYLGNDNTPDNQFHIGDASAVEIKFSNGSQDILLPNVIIMGAEPDLFETNSSNISLRNNYMPSNHRFGSIAIVTFSPEYSFRFNDNCMNEFIQDPALTLMHELIHSLHGLYGAKGITTKYTITQKQNPLITNIRGTNIEEFLTFGGTDLNIITSAQSNDIYTNLLADYKKIASKLSKVQVSNPLLNPYKDVFEAKYGLDKDASGIYSVNINKFNDIFKKLYSFTEFDLRTKFQVKCRQTYIGQYKYFKLSNLLNDSIYNISEGYNINNLKVNFRGQNANLNPRIITPITGRGLVKKIIRFCKNIVSVKGIRKSICIEINNGELFFVASENSYNDDNINTPKEIDDTVTSNNNYENDLDQVILNFNSESAPGLSDEKLNLTIQNDAYIPKYDSNGTSDIEQHDVNELNVFFYLDAQKVPEGENNVNLTSSIDTALLEQPKIYTFFSSEFINNVNKPVQAALFVSWIQQVLVDFTTEANQKSTVDKIADISIVVPYIGLALNIGNEAQKGNFKDALELLGAGILLEFEPELLIPTILVFTIKSFLGSSDNKNKVIKAINNALKERDEKWKEVYSFIVSNWMTKINTQFNKRKEQMYQALQNQVNAIKTIIESKYNSYTLEEKNELTNKYDIKQIENELNQKVSIAMNNIDRFLTESSISYLMKIINEVKINKLREYDENVKTYLLNYIIQHGSILGESQQELNSMVTDTLNNSIPFKLSSYTDDKILISYFNKFFKRIKSSSVLNMRYKNDKYVDTSGYDSNININGDVYKYPTNKNQFGIYNDKLSEVNISQNDYIIYDNKYKNFSISFWVRIPNYDNKIVNVNNEYTIINCMRDNNSGWKVSLNHNEIIWTFEDNRGINQKLAFNYGNANGISDYINKWIFVTITNDRLGDSKLYINGNLIDQKSILNLGNIHVSDNILFKIVNCSYTRYIGIRYFNIFDKELDETEIQTLYSNEPNTNILKDFWGNYLLYDKEYYLLNVLKPNNFIDRRKDSTLSINNIRSTILLANRLYSGIKVKIQRVNNSSTNDNLVRKNDQVYINFVASKTHLFPLYADTATTNKEKTIKISSSGNRFNQVVVMNSVGNCTMNFKNNNGNNIGLLGFKADTVVASTWYYTHMRDHTNSNGCFWNFISEEHGWQEK | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin E Immune FAB2 was observed to have a mean half life of 7.75 h after administration of one vial and 7.32 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin E Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype E. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes E in adults and pediatric patients. | Equine Botulinum Neurotoxin E Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype E in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin E Immune FAB2 binds to botulinum toxin serotype E to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin E Immune FAB2 is a mix of polyclonal antibodies for botulinum toxin type E [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin E Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin E Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 5100 Units produced a mean Cmax of 0.94 Units/mL. Administration of two vials produced a mean Cmax of 1.75 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin E Immune FAB2 was found to have a mean Vd of 14.172 L after administration of one vial and 11.596 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin E Immune FAB2 was observed to have a mean clearance rate of 1250 mL/h after administration of one vial and 1110 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type E | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16284 | Th1794 | Equine Botulinum Neurotoxin C Immune FAB2 | >Th1794_Equine_Botulinum_Neurotoxin_C_Immune_FAB2 MPITINNFNYSDPVDNKNILYLDTHLNTLANEPEKAFRITGNIWVIPDRFSRNSNPNLNKPPRVTSPKSGYYDPNYLSTDSDKDTFLKEIIKLFKRINSREIGEELIYRLSTDIPFPGNNNTPINTFDFDVDFNSVDVKTRQGNNWVKTGSINPSVIITGPRENIIDPETSTFKLTNNTFAAQEGFGALSIISISPRFMLTYSNATNDVGEGRFSKSEFCMDPILILMHELNHAMHNLYGIAIPNDQTISSVTSNIFYSQYNVKLEYAEIYAFGGPTIDLIPKSARKYFEEKALDYYRSIAKRLNSITTANPSSFNKYIGEYKQKLIRKYRFVVESSGEVTVNRNKFVELYNELTQIFTEFNYAKIYNVQNRKIYLSNVYTPVTANILDDNVYDIQNGFNIPKSNLNVLFMGQNLSRNPALRKVNPENMLYLFTKFCHKAIDGRSLYNKTLDCRELLVKNTDLPFIGDISDVKTDIFLRKDINEETEVIYYPDNVSVDQVILSKNTSEHGQLDLLYPSIDSESEILPGENQVFYDNRTQNVDYLNSYYYLESQKLSDNVEDFTFTRSIEEALDNSAKVYTYFPTLANKVNAGVQGGLFLMWANDVVEDFTTNILRKDTLDKISDVSAIIPYIGPALNISNSVRRGNFTEAFAVTGVTILLEAFPEFTIPALGAFVIYSKVQERNEIIKTIDNCLEQRIKRWKDSYEWMMGTWLSRIITQFNNISYQMYDSLNYQAGAIKAKIDLEYKKYSGSDKENIKSQVENLKNSLDVKISEAMNNINKFIRECSVTYLFKNMLPKVIDELNEFDRNTKAKLINLIDSHNIILVGEVDKLKAKVNNSFQNTIPFNIFSYTNNSLLKDIINEYFNNINDSKILSLQNRKNTLVDTSGYNAEVSEEGDVQLNPIFPFDFKLGSSGEDRGKVIVTQNENIVYNSMYESFSISFWIRINKWVSNLPGYTIIDSVKNNSGWSIGIISNFLVFTLKQNEDSEQSINFSYDISNNAPGYNKWFFVTVTNNMMGNMKIYINGKLIDTIKVKELTGINFSKTITFEINKIPDTGLITSDSDNINMWIRDFYIFAKELDGKDINILFNSLQYTNVVKDYWGNDLRYNKEYYMVNIDYLNRYMYANSRQIVFNTRRNNNDFNEGYKIIIKRIRGNTNDTRVRGGDILYFDMTINNKAYNLFMKNETMYADNHSTEDIYAIGLREQTKDINDNIIFQIQPMNNTYYYASQIFKSNFNGENISGICSIGTYRFRLGGDWYRHNYLVPTVKQGNYASLLESTSTHWGFVPVSE | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin C Immune FAB2 was observed to have a mean half life of 29.6 h after administration of one vial and 45.6 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin C Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype C. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes C in adults and pediatric patients. | Equine Botulinum Neurotoxin C Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype C in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin C Immune FAB2 binds to botulinum toxin serotype C to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin C Immune FAB2 is a mix of polyclonal antibodies for botulinum toxin type C [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin C Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin C Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 3000 Units produced a mean Cmax of 2.26 Units/mL. Administration of two vials produced a mean Cmax of 4.89 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin C Immune FAB2 was found to have a mean Vd of 6.066 L after administration of one vial and 8.486 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin C Immune FAB2 was observed to have a mean clearance rate of 144 mL/h after administration of one vial and 127 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type C1 | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16285 | Th1795 | Equine Botulinum Neurotoxin G Immune FAB2 | >Th1795_Equine_Botulinum_Neurotoxin_G_Immune_FAB2 MPVNIKXFNYNDPINNDDIIMMEPFNDPGPGTYYKAFRIIDRIWIVPERFTYGFQPDQFNASTGVFSKDVYEYYDPTYLKTDAEKDKFLKTMIKLFNRINSKPSGQRLLDMIVDAIPYLGNASTPPDKFAANVANVSINKKIIQPGAEDQIKGLMTNLIIFGPGPVLSDNFTDSMIMNGHSPISEGFGARMMIRFCPSCLNVFNNVQENKDTSIFSRRAYFADPALTLMHELIHVLHGLYGIKISNLPITPNTKEFFMQHSDPVQAEELYTFGGHDPSVISPSTDMNIYNKALQNFQDIANRLNIVSSAQGSGIDISLYKQIYKNKYDFVEDPNGKYSVDKDKFDKLYKALMFGFTETNLAGEYGIKTRYSYFSEYLPPIKTEKLLDNTIYTQNEGFNIASKNLKTEFNGQNKAVNKEAYEEISLEHLVIYRIAMCKPVMYKNTGKSEQCIIVNNEDLFFIANKDSFSKDLAKAETIAYNTQNNTIENNFSIDQLILDNDLSSGIDLPNENTEPFTNFDDIDIPVYIKQSALKKIFVDGDSLFEYLHAQTFPSNIENLQLTNSLNDALRNNNKVYTFFSTNLVEKANTVVGASLFVNWVKGVIDDFTSESTQKSTIDKVSDVSIIIPYIGPALNVGNETAKENFKNAFEIGGAAILMEFIPELIVPIVGFFTLESYVGNKGHIIMTISNALKKRDQKWTDMYGLIVSQWLSTVNTQFYTIKERMYNALNNQSQAIEKIIEDQYNRYSEEDKMNINIDFNDIDFKLNQSINLAINNIDDFINQCSISYLMNRMIPLAVKKLKDFDDNLKRDLLEYIDTNELYLLDEVNILKSKVNRHLKDSIPFDLSLYTKDTILIQVFNNYISNISSNAILSLSYRGGRLIDSSGYGATMNVGSDVIFNDIGNGQFKLNNSENSNITAHQSKFVVYDSMFDNFSINFWVRTPKYNNNDIQTYLQNEYTIISCIKNDSGWKVSIKGNRIIWTLIDVNAKSKSIFFEYSIKDNISDYINKWFSITITNDRLGNANIYINGSLKKSEKILNLDRINSSNDIDFKLINCTDTTKFVWIKDFNIFGRELNATEVSSLYWIQSSTNTLKDFWGNPLRYDTQYYLFNQGMQNIYIKYFSKASMGETAPRTNFNNAAINYQNLYLGLRFIIKKASNSRNINNDNIVREGDYIYLNIDNISDESYRVYVLVNSKEIQTQLFLAPINDDPTFYDVLQIKKYYEKTTYNCQILCEKDTKTFGLFGIGKFVKDYGYVWDTYDNYFCISQWYLRRISENINKLRLGCNWQFIPVDEGWTE | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin G Immune FAB2 was observed to have a mean half life of 11.70 h after administration of one vial and 14.70 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin G Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype G. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes G in adults and pediatric patients. | Equine Botulinum Neurotoxin G Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype G in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin G Immune FAB2 binds to botulinum toxin serotype G to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin G Immune FAB2 is a mix of polyclonal antibodies for botulinum toxin type G [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin G Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin G Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 600 Units produced a mean Cmax of 0.59 Units/mL. Administration of two vials produced a mean Cmax of 1.19 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin G Immune FAB2 was found to have a mean Vd of 2.372 L after administration of one vial and 3.063 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin G Immune FAB2 was observed to have a mean clearance rate of 149 mL/h after administration of one vial and 144 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type G | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16286 | Th1796 | Equine Botulinum Neurotoxin A Immune FAB2 | NA | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin A Immune FAB2 was observed to have a mean half life of 8.64 h after administration of one vial and 10.20 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin A Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype A. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes A in adults and pediatric patients. | Equine Botulinum Neurotoxin A Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype A in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin A Immune FAB2 binds to botulinum toxin serotype A to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin A Immune FAB2 is a mix of polyclonal antibodies for [DB00083] [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin A Immune FAB2 may produce anapylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with prexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin A Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 4500 Units produced a mean Cmax of 2.69 Units/mL. Administration of two vials produced a mean Cmax of 6.23 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin A Immune FAB2 was found to have a mean Vd of 3.637 L after administration of one vial and 3.993 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin A Immune FAB2 was observed to have a mean clearance rate of 293 mL/h after administration of one vial and 285 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type A | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16287 | Th1797 | Equine Botulinum Neurotoxin F Immune FAB2 | >Th1797_Equine_Botulinum_Neurotoxin_F_Immune_FAB2 MPVAINSFNYNDPVNDDTILYMQIPYEEKSKKYYKAFEIMRNVWIIPERNTIGTNPSDFDPPASLKNGSSAYYDPNYLTTDAEKDRYLKTTIKLFKRINSNPAGKVLLQEISYAKPYLGNDHTPIDEFSPVTRTTSVNIKLSTNVESSMLLNLLVLGAGPDIFESCCYPVRKLIDPDVVYDPSNYGFGSINIVTFSPEYEYTFNDISGGHNSSTESFIADPAISLAHELIHALHGLYGARGVTYEETIEVKQAPLMIAEKPIRLEEFLTFGGQDLNIITSAMKEKIYNNLLANYEKIATRLSEVNSAPPEYDINEYKDYFQWKYGLDKNADGSYTVNENKFNEIYKKLYSFTESDLANKFKVKCRNTYFIKYEFLKVPNLLDDDIYTVSEGFNIGNLAVNNRGQSIKLNPKIIDSIPDKGLVEKIVKFCKSVIPRKGTKAPPRLCIRVNNSELFFVASESSYNENDINTPKEIDDTTNLNNNYRNNLDEVILDYNSQTIPQISNRTLNTLVQDNSYVPRYDSNGTSEIEEYDVVDFNVFFYLHAQKVPEGETNISLTSSIDTALLEESKDIFFSSEFIDTINKPVNAALFIDWISKVIRDFTTEATQKSTVDKIADISLIVPYVGLALNIIIEAEKGNFEEAFELLGVGILLEFVPELTIPVILVFTIKSYIDSYENKNKAIKAINNSLIEREAKWKEIYSWIVSNWLTRINTQFNKRKEQMYQALQNQVDAIKTAIEYKYNNYTSDEKNRLESEYNINNIEEELNKKVSLAMKNIERFMTESSISYLMKLINEAKVGKLKKYDNHVKSDLLNYILDHRSILGEQTNELSDLVTSTLNSSIPFELSSYTNDKILIIYFNRLYKKIKDSSILDMRYENNKFIDISGYGSNISINGNVYIYSTNRNQFGIYNSRLSEVNIAQNNDIIYNSRYQNFSISFWVRIPKHYKPMNHNREYTIINCMGNNNSGWKISLRTVRDCEIIWTLQDTSGNKENLIFRYEELNRISNYINKWIFVTITNNRLGNSRIYINGNLIVEKSISNLGDIHVSDNILFKIVGCDDETYVGIRYFKVFNTELDKTEIETLYSNEPDPSILKNYWGNYLLYNKKYYLFNLLRKDKYITLNSGILNINQQRGVTEGSVFLNYKLYEGVEVIIRKNGPIDISNTDNFVRKNDLAYINVVDRGVEYRLYADTKSEKEKIIRTSNLNDSLGQIIVMDSIGNNCTMNFQNNNGSNIGLLGFHSNNLVASSWYYNNIRRNTSSNGCFWSSISKENGWKE | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin F Immune FAB2 was observed to have a mean half life of 14.10 h after administration of one vial and 18.20 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin F Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype F. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes F in adults and pediatric patients. | Equine Botulinum Neurotoxin F Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype F in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin F Immune FAB2 binds to botulinum toxin serotype F to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin F Immune FAB2 is a mix of polyclonal antibodies for botulinum toxin type F [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin F Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin F Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 3000 Units produced a mean Cmax of 2.37 Units/mL. Administration of two vials produced a mean Cmax of 4.29 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin F Immune FAB2 was found to have a mean Vd of 3.413 L after administration of one vial and 4.334 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin F Immune FAB2 was observed to have a mean clearance rate of 169 mL/h after administration of one vial and 168 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type F | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16288 | Th1798 | Equine Botulinum Neurotoxin D Immune FAB2 | >Th1798_Equine_Botulinum_Neurotoxin_D_Immune_FAB2 MTWPVKDFNYSDPVNDNDILYLRIPQNKLITTPVKAFMITQNIWVIPERFSSDTNPSLSKPPRPTSKYQSYYDPSYLSTDEQKDTFLKGIIKLFKRINERDIGKKLINYLVVGSPFMGDSSTPEDTFDFTRHTTNIAVEKFENGSWKVTNIITPSVLIFGPLPNILDYTASLTLQGQQSNPSFEGFGTLSILKVAPEFLLTFSDVTSNQSSAVLGKSIFCMDPVIALMHELTHSLHQLYGINIPSDKRIRPQVSEGFFSQDGPNVQFEELYTFGGLDVEIIPQIERSQLREKALGHYKDIAKRLNNINKTIPSSWISNIDKYKKIFSEKYNFDKDNTGNFVVNIDKFNSLYSDLTNVMSEVVYSSQYNVKNRTHYFSRHYLPVFANILDDNIYTIRDGFNLTNKGFNIENSGQNIERNPALQKLSSESVVDLFTKVCLRLTKNSRDDSTCIKVKNNRLPYVADKDSISQEIFENKIITDETNVQNYSDKFSLDESILDGQVPINPEIVDPLLPNVNMEPLNLPGEEIVFYDDITKYVDYLNSYYYLESQKLSNNVENITLTTSVEEALGYSNKIYTFLPSLAEKVNKGVQAGLFLNWANEVVEDFTTNIMKKDTLDKISDVSVIIPYIGPALNIGNSALRGNFNQAFATAGVAFLLEGFPEFTIPALGVFTFYSSIQEREKIIKTIENCLEQRVKRWKDSYQWMVSNWLSRITTQFNHINYQMYDSLSYQADAIKAKIDLEYKKYSGSDKENIKSQVENLKNSLDVKISEAMNNINKFIRECSVTYLFKNMLPKVIDELNKFDLRTKTELINLIDSHNIILVGEVDRLKAKVNESFENTMPFNIFSYTNNSLLKDIINEYFNSINDSKILSLQNKKNALVDTSGYNAEVRVGDNVQLNTIYTNDFKLSSSGDKIIVNLNNNILYSAIYENSSVSFWIKISKDLTNSHNEYTIINSIEQNSGWKLCIRNGNIEWILQDVNRKYKSLIFDYSESLSHTGYTNKWFFVTITNNIMGYMKLYINGELKQSQKIEDLDEVKLDKTIVFGIDENIDENQMLWIRDFNIFSKELSNEDINIVYEGQILRNVIKDYWGNPLKFDTEYYIINDNYIDRYIAPESNVLVLVQYPDRSKLYTGNPITIKSVSDKNPYSRILNGDNIILHMLYNSRKYMIIRDTDTIYATQGGECSQNCVYALKLQSNLGNYGIGIFSIKNIVSKNKYCSQIFSSFRENTMLLADIYKPWRFSFKNAYTPVAVTNYETKLLSTSSFWKFISRDPGWVE | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin D Immune FAB2 was observed to have a mean half life of 7.51 h after administration of one vial and 7.77 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin D Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype D. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes D in adults and pediatric patients. | Equine Botulinum Neurotoxin D Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype D in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin D Immune FAB2 binds to botulinum toxin serotype D to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin D Immune FAB2 is a mix of polyclonal antibodies for botulinum toxin type D [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin D Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin D Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 600 Units produced a mean Cmax of 0.81 Units/mL. Administration of two vials produced a mean Cmax of 1.60 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin D Immune FAB2 was found to have a mean Vd of 1.465 L after administration of one vial and 1.653 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin D Immune FAB2 was observed to have a mean clearance rate of 137 mL/h after administration of one vial and 151 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type D | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 16289 | Th1799 | Equine Botulinum Neurotoxin B Immune FAB2 | >Th1799_Equine_Botulinum_Neurotoxin_B_Immune_FAB2 MPVTINNFNYNDPIDNNNIIMMEPPFARGTGRYYKAFKITDRIWIIPERYTFGYKPEDFNKSSGIFNRDVCEYYDPDYLNTNDKKNIFLQTMIKLFNRIKSKPLGEKLLEMIINGIPYLGDRRVPLEEFNTNIASVTVNKLISNPGEVERKKGIFANLIIFGPGPVLNENETIDIGIQNHFASREGFGGIMQMKFCPEYVSVFNNVQENKGASIFNRRGYFSDPALILMHELIHVLHGLYGIKVDDLPIVPNEKKFFMQSTDAIQAEELYTFGGQDPSIITPSTDKSIYDKVLQNFRGIVDRLNKVLVCISDPNININIYKNKFKDKYKFVEDSEGKYSIDVESFDKLYKSLMFGFTETNIAENYKIKTRASYFSDSLPPVKIKNLLDNEIYTIEEGFNISDKDMEKEYRGQNKAINKQAYEEISKEHLAVYKIQMCKSVKAPGICIDVDNEDLFFIADKNSFSDDLSKNERIEYNTQSNYIENDFPINELILDTDLISKIELPSENTESLTDFNVDVPVYEKQPAIKKIFTDENTIFQYLYSQTFPLDIRDISLTSSFDDALLFSNKVYSFFSMDYIKTANKVVEAGLFAGWVKQIVNDFVIEANKSNTMDKIADISLIVPYIGLALNVGNETAKGNFENAFEIAGASILLEFIPELLIPVVGAFLLESYIDNKNKIIKTIDNALTKRNEKWSDMYGLIVAQWLSTVNTQFYTIKEGMYKALNYQAQALEEIIKYRYNIYSEKEKSNINIDFNDINSKLNEGINQAIDNINNFINGCSVSYLMKKMIPLAVEKLLDFDNTLKKNLLNYIDENKLYLIGSAEYEKSKVNKYLKTIMPFDLSIYTNDTILIEMFNKYNSEILNNIILNLRYKDNNLIDLSGYGAKVEVYDGVELNDKNQFKLTSSANSKIRVTQNQNIIFNSVFLDFSVSFWIRIPKYKNDGIQNYIHNEYTIINCMKNNSGWKISIRGNRIIWTLIDINGKTKSVFFEYNIREDISEYINRWFFVTITNNLNNAKIYINGKLESNTDIKDIREVIANGEIIFKLDGDIDRTQFIWMKYFSIFNTELSQSNIEERYKIQSYSEYLKDFWGNPLMYNKEYYMFNAGNKNSYIKLKKDSPVGEILTRSKYNQNSKYINYRDLYIGEKFIIRRKSNSQSINDDIVRKEDYIYLDFFNLNQEWRVYTYKYFKKEEEKLFLAPISDSDEFYNTIQIKEYDEQPTYSCQLLFKKDEESTDEIGLIGIHRFYESGIVFEEYKDYFCISKWYLKEVKRKPYNLKLGCNWQFIPKDEGWTE | NA | NA | NA | NA | NA | Equine Botulinum Neurotoxin B Immune FAB2 was observed to have a mean half life of 34.2 h after administration of one vial and 57.1 h after two vials [FDA Label]. | Equine Botulinum Neurotoxin B Immune FAB2 is composed of a mixture of immune globulin fragments purified from plasma of horses that were previously immunized with botulinum toxin serotype B. It is intravenously administered for the treatment of symptomatic botulism following documented or suspected exposure to botulinum neurotoxin serotypes B in adults and pediatric patients. | Equine Botulinum Neurotoxin B Immune FAB2 is indicted for use in documented or suspected exposure to botulinum toxin serotype B in adults and pediatric patients [FDA Label]. | Equine Botulinum Neurotoxin B Immune FAB2 binds to botulinum toxin serotype B to prevent toxicity [FDA Label]. | Equine Botulinum Neurotoxin B Immune FAB2 is a mix of polyclonal antibodies for [DB00042] [FDA Label]. It binds to the toxin with high-affinity and prevents binding to ganglioside anchorage sites and membrane-bound receptors on cholinergic nerve terminals. This prevents internalization of the toxin into the cell and ultimately prevents it from exerting its toxic effects. Due to the long-lasting effects of botulinum toxin, the antibodies must be administered before symptoms present to prevent toxicity. | Equine Botulinum Neurotoxin B Immune FAB2 may produce anaphylaxis or anaphylactoid reactions particularly in patients who have previously been exposed to equine-derived antivenom or antitoxins or patient with preexisting hypersensitivity to horses, asthma, or hay fever [FDA Label]. Serum sickness reactions may present 10-21 days after infusion. Various infusion reactions may occur dependent on the rate of infusion. These include chills, fever, headaches, nausea, and vomiting. Arthralgia, myalgia, and vasovagal reactions may also occur independently of infusion rate. Because the antibodies are derived from equine plasma there is a risk of infectious disease transmission although this is controlled through manufacturing processes. | There is no metabolism data available. Equine Botulinum Neurotoxin B Immune FAB2 is assumed to be broken down similarly to other proteins and antibodies in systemic circulation. | Administration of one vial of containing at least 3300 Units produced a mean Cmax of 1.90 Units/mL. Administration of two vials produced a mean Cmax of 4.28 Units/mL [FDA Label]. | Equine Botulinum Neurotoxin B Immune FAB2 was found to have a mean Vd of 9.607 L after administration of one vial and 14.865 L after two vials [FDA Label]. | Equine Botulinum Neurotoxin B Immune FAB2 was observed to have a mean clearance rate of 196 mL/h after administration of one vial and 181 mL/h after two. | NA | NA | NA | NA | NA | Botulinum neurotoxin type B | Bat | Emergent BioSolutions Canada Inc. | Emergent BioSolutions Canada Inc. | Intravenous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |