| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Side Effects | 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. |
| Primary information |
|---|
| ID | 1788 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S46 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Carimune Nanofiltered |
| Company | Csl Behring Ag |
| Brand Discription | 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. |
| Prescribed for | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. |
| Chemical Name | NA |
| Formulation | 12 g/1 |
| Physcial Appearance | injection, powder, lyophilized, for solution |
| Route of Administration | Intravenous |
| Recommended Dosage | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. |
| Contraindication | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. |
| Side Effects | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. |
| Useful Link | http://www.rxlist.com/carimune-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876903 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1789 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S47 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Carimune Nanofiltered |
| Company | Csl Behring Ag |
| Brand Discription | 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. |
| Prescribed for | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. |
| Chemical Name | NA |
| Formulation | 6 g/1 |
| Physcial Appearance | injection, powder, lyophilized, for solution |
| Route of Administration | Intravenous |
| Recommended Dosage | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. |
| Contraindication | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. |
| Side Effects | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. |
| Useful Link | http://www.rxlist.com/carimune-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876904 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1790 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S48 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Carimune Nanofiltered |
| Company | Csl Behring Ag |
| Brand Discription | 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. |
| Prescribed for | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. |
| Chemical Name | NA |
| Formulation | 3 g/1 |
| Physcial Appearance | injection, powder, lyophilized, for solution |
| Route of Administration | Intravenous |
| Recommended Dosage | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. |
| Contraindication | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. |
| Side Effects | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. |
| Useful Link | http://www.rxlist.com/carimune-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876905 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1791 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S49 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Flebogamma Dif |
| Company | GRIFOLS USA, LLC |
| Brand Discription | 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. |
| Prescribed for | NA |
| Chemical Name | NA |
| Formulation | 5 g/50mL |
| Physcial Appearance | injection, solution |
| Route of Administration | Intravenous |
| Recommended Dosage | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) |
| Contraindication | 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. |
| Side Effects | 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. |
| Useful Link | http://www.rxlist.com/flebogamma-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876906 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1792 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S50 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Flebogamma Dif |
| Company | GRIFOLS USA, LLC |
| Brand Discription | 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. |
| Prescribed for | NA |
| Chemical Name | NA |
| Formulation | .05 g/mL |
| Physcial Appearance | injection, solution |
| Route of Administration | Intravenous |
| Recommended Dosage | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) |
| Contraindication | 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. |
| Side Effects | 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. |
| Useful Link | http://www.rxlist.com/flebogamma-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876907 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1793 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S51 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Gamastan |
| Company | Cutter Med & Biol, Division Of Miles Canada Ltd. |
| Brand Discription | GamaSTAN® S/D treated with solvent/detergent is a sterile solution of immune globulin for intramuscular administration; it contains no preservative. GamaSTAN® S/D is prepared by cold ethanol fractionation from human plasma. The immune globulin is isolated from solubilized Cohn fraction II. The fraction II solution is adjusted to a final concentration of 0.3% tri-n-butyl phosphate (TNBP) and 0.2% sodium cholate. |
| Prescribed for | 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 |
| Chemical Name | NA |
| Formulation | 16.50% |
| Physcial Appearance | liquid |
| Route of Administration | Intramuscular |
| Recommended Dosage | 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. |
| Contraindication | 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. |
| Side Effects | 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. |
| Useful Link | http://www.rxlist.com/gamastan-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876908 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1794 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S52 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Gamastan S/d |
| Company | GRIFOLS USA, LLC |
| Brand Discription | GamaSTAN® S/D treated with solvent/detergent is a sterile solution of immune globulin for intramuscular administration; it contains no preservative. GamaSTAN® S/D is prepared by cold ethanol fractionation from human plasma. The immune globulin is isolated from solubilized Cohn fraction II. The fraction II solution is adjusted to a final concentration of 0.3% tri-n-butyl phosphate (TNBP) and 0.2% sodium cholate. |
| Prescribed for | 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 |
| Chemical Name | NA |
| Formulation | .165 g/mL |
| Physcial Appearance | injection |
| Route of Administration | Intramuscular |
| Recommended Dosage | 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. |
| Contraindication | 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. |
| Side Effects | 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. |
| Useful Link | http://www.rxlist.com/gamastan-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876909 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1795 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S53 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Hyqvia |
| Company | Baxalta Us Inc. |
| Brand Discription | HYQVIA is a dual vial unit with one vial of Immune Globulin Infusion 10% (Human) and one vial of Recombinant Human Hyaluronidase. |
| Prescribed for | 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 |
| Chemical Name | NA |
| Formulation | 160 U/mL |
| Physcial Appearance | Liquid |
| Route of Administration | Intravenous infusion |
| Recommended Dosage | Administer HYQVIA at 300 to 600 mg/kg at 3 to 4 week intervals, after initial ramp-up. |
| Contraindication | 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. |
| Side Effects | 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. |
| Useful Link | http://www.rxlist.com/hyqvia-drug.htm |
| PubMed ID | 20970960, 17911465, 16998749, 16876910 |
| 3-D Structure | Th1190 (View) or (Download) |
| Primary information |
|---|
| ID | 1796 |
| ThPP ID | Th1190 |
| Therapeutic Peptide/Protein Name | Immune Globulin Human |
| Sequence | IGG1: PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGK view full sequnce in fasta |
| Functional Classification | IIIb |
| Molecular Weight | 142682.3 |
| Chemical Formula | C6332H9826N1692O1980S54 |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting Point (℃) | NA |
| Half Life | >20 hours (mammalian reticulocytes, in vitro). |
| Description | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. |
| Indication/Disease | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. |
| Pharmacodynamics | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. |
| Mechanism of Action | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| Volume of Distribution | NA |
| Clearance | NA |
| Categories | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. |
| Target | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. |
| Information of corresponding available drug in the market |
|---|
| Brand Name | Iveegam Immuno 5000mg (iv) |
| Company | Baxter Ag |
| Brand Discription | NA |
| Prescribed for | NA |
| Chemical Name | NA |
| Formulation | NA |
| Physcial Appearance | NA |
| Route of Administration | NA |
| Recommended Dosage | NA |
| Contraindication | NA |
| Side Effects | NA |
| Useful Link | |
| PubMed ID | 20970960, 17911465, 16998749, 16876911 |
| 3-D Structure | Th1190 (View) or (Download) |