Detailed description page of THPdb

Details of Th1147 which contains 4 entries.

Entry 1
(1) Primary information
ID 1644
ThPP ID Th1147
Therapeutic Peptide/Protein Name Natalizumab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight N.A.
Chemical Formula N.A.
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) 61 (FAB fr
Half Life 11 Â± 4 days
Description Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease For treatment of multiple sclerosis.
Pharmacodynamics In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption N.A.
Volume of Distribution 5.7 Â± 1.9 L [Multiple Sclerosis (MS) Patients]
Clearance 16 Â± 5 mL/hour [patients with MS who did not haveÂ PMLÂ receiving the repeat IV administration of a 300 mg dose]
Categories Immunosuppressive agents
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction N.A.
Target N.A.
Information of corresponding available drug in the market
Brand Name Tysabri
Company Biogen Idec Inc.
Brand Discription Tysabri (natalizumab) is aÂ recombinantÂ humanized IgG4ÎºÂ monoclonal antibodyÂ produced in murineÂ myelomaÂ cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to Î±4-integrin. The molecular weight of natalizumab is 149 kilodaltons. Tysabri is supplied as a sterile, colorless, and clear to slightly opalescent concentrate for intravenous infusion.
Prescribed for ItÂ is indicated as monotherapy for the treatment of patients with relapsing forms ofÂ multiple sclerosis. Tysabri increases the risk ofÂ PML. ItÂ is indicated for inducing and maintaining clinical response and remission in adult patients with moderately to severely active Crohn's disease with evidence of inflammation who have had an inadequate response to, or are unable to tolerate, conventional CD therapies and inhibitors of TNF-Î±.
Chemical Name N.A.
Formulation Each 15 mL dose contains 300 mg natalizumab; 123 mg sodium chloride, USP; 17.0 mg sodium phosphate, monobasic, monohydrate, USP; 7.24 mg sodium phosphate, dibasic, heptahydrate, USP; 3.0 mg polysorbate 80, USP/NF, in water for injection, USP at pH 6.1.
Physcial Appearance Sterile, colorless, and clear to slightly opalescent concentrate
Route of Administration Intravenous infusion
Recommended Dosage The recommended dose of Tysabri for multiple sclerosis is 300 mg intravenous infusion over one hour every four weeks. The recommended dose of TysabriI for Crohn's disease is 300 mg intravenous infusion over one hour every four weeks. Tysabri should not be used with concomitant immunosuppressants (e.g., 6-mercaptopurine, azathioprine, cyclosporine, or methotrexate) or concomitant inhibitors of TNF-Î±. Aminosalicylates may be continued during treatment with Tysabri.
Contraindication Tysabri is contraindicated in patients who have or have hadprogressive multifocal leukoencephalopathyÂ (PML). It should not be administered to a patient who has had a hypersensitivity reaction to Tysabri. Observed reactions range from urticaria to anaphylaxis
Side Effects Progressive Multifocal LeukoencephalopathyÂ (PML), Hypersensitivity, Immunosuppression/Infections
Useful Link http://www.rxlist.com/tysabri-drug/side-effects-interactions.htm
PubMed ID 12510039
3-D Structure N.A.

Entry 2
(2) Primary information
ID 1645
ThPP ID Th1147
Therapeutic Peptide/Protein Name Natalizumab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight N.A.
Chemical Formula N.A.
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) 61 (FAB fr
Half Life 11 Â± 4 days
Description Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease For treatment of multiple sclerosis.
Pharmacodynamics In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption N.A.
Volume of Distribution 5.2 Â± 2.8 L [Crohnâ€™s Disease (CD) Patients]
Clearance 22 Â± 22 mL/hour [Patients with Crohnâ€™s Disease receiving the repeat IV administration of a 300 mg dose]
Categories Immunosuppressive agents
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction N.A.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company Elan Pharmaceuticals, Inc.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link http://www.drugbank.ca/drugs/DB00108
PubMed ID 12510039
3-D Structure N.A.

Entry 3
(3) Primary information
ID 1646
ThPP ID Th1147
Therapeutic Peptide/Protein Name Natalizumab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight N.A.
Chemical Formula N.A.
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) 61 (FAB fr
Half Life 11 Â± 4 days
Description Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease For treatment of multiple sclerosis.
Pharmacodynamics In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Immunosuppressive agents
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction N.A.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company Biogen Idec Canada Inc
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance Solution
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c5fdde91-1989-4dd2-9129-4f3323ea2962&
PubMed ID 12510039
3-D Structure N.A.

Entry 4
(4) Primary information
ID 1647
ThPP ID Th1147
Therapeutic Peptide/Protein Name Natalizumab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight N.A.
Chemical Formula N.A.
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) 61 (FAB fr
Half Life 11 Â± 4 days
Description Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease For treatment of multiple sclerosis.
Pharmacodynamics In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Immunosuppressive agents
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction N.A.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link http://www.drugs.com/mtm/natalizumab.html
PubMed ID 12510039
3-D Structure N.A.

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

(1) Primary information
Entry 1
ID	1644
ThPP ID	Th1147
Therapeutic Peptide/Protein Name	Natalizumab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	N.A.
Chemical Formula	N.A.
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	61 (FAB fr
Half Life	11 Â± 4 days
Description	Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease	For treatment of multiple sclerosis.
Pharmacodynamics	In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action	Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption	N.A.
Volume of Distribution	5.7 Â± 1.9 L [Multiple Sclerosis (MS) Patients]
Clearance	16 Â± 5 mL/hour [patients with MS who did not haveÂ PMLÂ receiving the repeat IV administration of a 300 mg dose]
Categories	Immunosuppressive agents
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	N.A.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	Tysabri
Company	Biogen Idec Inc.
Brand Discription	Tysabri (natalizumab) is aÂ recombinantÂ humanized IgG4ÎºÂ monoclonal antibodyÂ produced in murineÂ myelomaÂ cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to Î±4-integrin. The molecular weight of natalizumab is 149 kilodaltons. Tysabri is supplied as a sterile, colorless, and clear to slightly opalescent concentrate for intravenous infusion.
Prescribed for	ItÂ is indicated as monotherapy for the treatment of patients with relapsing forms ofÂ multiple sclerosis. Tysabri increases the risk ofÂ PML. ItÂ is indicated for inducing and maintaining clinical response and remission in adult patients with moderately to severely active Crohn's disease with evidence of inflammation who have had an inadequate response to, or are unable to tolerate, conventional CD therapies and inhibitors of TNF-Î±.
Chemical Name	N.A.
Formulation	Each 15 mL dose contains 300 mg natalizumab; 123 mg sodium chloride, USP; 17.0 mg sodium phosphate, monobasic, monohydrate, USP; 7.24 mg sodium phosphate, dibasic, heptahydrate, USP; 3.0 mg polysorbate 80, USP/NF, in water for injection, USP at pH 6.1.
Physcial Appearance	Sterile, colorless, and clear to slightly opalescent concentrate
Route of Administration	Intravenous infusion
Recommended Dosage	The recommended dose of Tysabri for multiple sclerosis is 300 mg intravenous infusion over one hour every four weeks. The recommended dose of TysabriI for Crohn's disease is 300 mg intravenous infusion over one hour every four weeks. Tysabri should not be used with concomitant immunosuppressants (e.g., 6-mercaptopurine, azathioprine, cyclosporine, or methotrexate) or concomitant inhibitors of TNF-Î±. Aminosalicylates may be continued during treatment with Tysabri.
Contraindication	Tysabri is contraindicated in patients who have or have hadprogressive multifocal leukoencephalopathyÂ (PML). It should not be administered to a patient who has had a hypersensitivity reaction to Tysabri. Observed reactions range from urticaria to anaphylaxis
Side Effects	Progressive Multifocal LeukoencephalopathyÂ (PML), Hypersensitivity, Immunosuppression/Infections
Useful Link	http://www.rxlist.com/tysabri-drug/side-effects-interactions.htm
PubMed ID	12510039
3-D Structure	N.A.

(2) Primary information
Entry 2
ID	1645
ThPP ID	Th1147
Therapeutic Peptide/Protein Name	Natalizumab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	N.A.
Chemical Formula	N.A.
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	61 (FAB fr
Half Life	11 Â± 4 days
Description	Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease	For treatment of multiple sclerosis.
Pharmacodynamics	In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action	Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption	N.A.
Volume of Distribution	5.2 Â± 2.8 L [Crohnâ€™s Disease (CD) Patients]
Clearance	22 Â± 22 mL/hour [Patients with Crohnâ€™s Disease receiving the repeat IV administration of a 300 mg dose]
Categories	Immunosuppressive agents
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	N.A.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	Elan Pharmaceuticals, Inc.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	http://www.drugbank.ca/drugs/DB00108
PubMed ID	12510039
3-D Structure	N.A.

(3) Primary information
Entry 3
ID	1646
ThPP ID	Th1147
Therapeutic Peptide/Protein Name	Natalizumab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	N.A.
Chemical Formula	N.A.
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	61 (FAB fr
Half Life	11 Â± 4 days
Description	Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease	For treatment of multiple sclerosis.
Pharmacodynamics	In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action	Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Immunosuppressive agents
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	N.A.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	Biogen Idec Canada Inc
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	Solution
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c5fdde91-1989-4dd2-9129-4f3323ea2962&
PubMed ID	12510039
3-D Structure	N.A.

(4) Primary information
Entry 4
ID	1647
ThPP ID	Th1147
Therapeutic Peptide/Protein Name	Natalizumab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	N.A.
Chemical Formula	N.A.
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	61 (FAB fr
Half Life	11 Â± 4 days
Description	Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006.
Indication/Disease	For treatment of multiple sclerosis.
Pharmacodynamics	In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Î±4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation.
Mechanism of Action	Binds to the Î±4-subunit of Î±4b 1 and Î±4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the Î±4-mediated adhesion of leukocytes to their counter-receptor(s).
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Immunosuppressive agents
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	N.A.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	http://www.drugs.com/mtm/natalizumab.html
PubMed ID	12510039
3-D Structure	N.A.