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Th1130 details

Primary information
ID 1604
ThPP ID Th1130
Therapeutic Peptide/Protein Name Brentuximab vedotin
Sequence Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification IIb
Molecular Weight 149200-151800
Chemical Formula C6476H9930N1690O2030S40
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life Terminal half-life is 4-6 days
Description Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection.
Indication/Disease Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution The steady state volume of distribution is 6-10 L.
Clearance MMAE is cleared by the liver but not quantitative studies have been performed.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction N.A.
Target Tumor necrosis factor receptor superfamily member 8
Information of corresponding available drug in the market
Brand Name Adcetris
Company Seattle Genetics
Brand Discription ADCETRIS (brentuximab vedotin) is a CD30-directed antibody-drug conjugate (ADC) consisting of three components: 1) the chimeric IgG1 antibody cAC10, specific for human CD30, 2) the microtubule disrupting agent MMAE, and 3) a protease-cleavable linker that covalently attaches MMAE to cAC10. Brentuximab vedotin has an approximate molecular weight of 153 kDa. Approximately 4 molecules of MMAE are attached to each antibody molecule. Brentuximab vedotin is produced by chemical conjugation of the antibody and small molecule components. The antibody is produced by mammalian (Chinese hamster ovary) cells, and the small molecule components are produced by chemical synthesis.
Prescribed for Hodgkin lymphoma (HL) after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates.
Chemical Name N.A.
Formulation Following reconstitution with 10.5 mL Sterile Water for Injection, USP, a solution containing 5 mg/mL brentuximab vedotin is produced. The reconstituted product contains 70 mg/mL trehalose dihydrate, 5.6 mg/mL sodium citrate dihydrate, 0.21 mg/mL citric acid monohydrate, and 0.20 mg/mL polysorbate 80 and water for injection. The pH is approximately 6.6.
Physcial Appearance ADCETRIS (brentuximab vedotin) for Injection is supplied as a sterile, white to off-white, preservative-free lyophilized cake or powder in single-use vials.
Route of Administration Intravenous infusion
Recommended Dosage Normal renal and hepatic function (1.8 mg/kg up to 180 mg), Mild (creatinine clearance > 50-80 mL/min) or moderate (creatinine clearance 30-50 mL/min) (1.8 mg/kg up to 180 mg), Severe (creatinine clearance less than 30 mL/min) (Avoid use), Mild (Child-Pugh A) (1.2 mg/kg up to 120 mg), Moderate (Child-Pugh B) or severe (Child-Pugh C) (Avoid use).
Contraindication concomitant bleomycin due to pulmonary toxicity
Side Effects Peripheral neuropathy, Anaphylaxis and Infusion Reactions, Hematologic Toxicities, Serious Infections and Opportunistic Infections, Tumor Lysis Syndrome, Increased Toxicity in the Presence of Severe Renal Impairment, Increased Toxicity in the Presence of Moderate or Severe Hepatic Impairment, Hepatotoxicity, Progressive Multifocal Leukoencephalopathy, Serious Dermatologic Reactions, Embryo-Fetal Toxicity
Useful Link http://www.rxlist.com/adcetris-drug.htm http://www.adcetris.com/ http://en.wikipedia.org/wiki/Brentuximab_vedotin
PubMed ID 25642958, 25641881, 25573987
3-D Structure Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID 1605
ThPP ID Th1130
Therapeutic Peptide/Protein Name Brentuximab vedotin
Sequence Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification IIb
Molecular Weight 149200-151800
Chemical Formula C6476H9930N1690O2030S40
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life Terminal half-life is 4-6 days
Description Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection
Indication/Disease Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution The steady state volume of distribution is 6-10 L.
Clearance MMAE is cleared by the liver but not quantitative studies have been performed.
Categories N.A.
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 N.A.
PubMed ID 25642958, 25641881, 25573987
3-D Structure Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID 1606
ThPP ID Th1130
Therapeutic Peptide/Protein Name Brentuximab vedotin
Sequence Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification IIb
Molecular Weight 149200-151800
Chemical Formula C6476H9930N1690O2030S40
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life Terminal half-life is 4-6 days
Description Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection
Indication/Disease Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution The steady state volume of distribution is 6-10 L.
Clearance MMAE is cleared by the liver but not quantitative studies have been performed.
Categories N.A.
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 N.A.
PubMed ID 25642958, 25641881, 25573987
3-D Structure Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID 1607
ThPP ID Th1130
Therapeutic Peptide/Protein Name Brentuximab vedotin
Sequence Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification IIb
Molecular Weight 149200-151800
Chemical Formula C6476H9930N1690O2030S40
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life Terminal half-life is 4-6 days
Description Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection.
Indication/Disease Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution The steady state volume of distribution is 6-10 L.
Clearance MMAE is cleared by the liver but not quantitative studies have been performed.
Categories N.A.
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 N.A.
PubMed ID 25642958, 25641881, 25573987
3-D Structure Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

Primary information
ID	1604
ThPP ID	Th1130
Therapeutic Peptide/Protein Name	Brentuximab vedotin
Sequence	Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification	IIb
Molecular Weight	149200-151800
Chemical Formula	C6476H9930N1690O2030S40
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	Terminal half-life is 4-6 days
Description	Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection.
Indication/Disease	Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics	Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action	Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity	The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism	Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption	Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution	The steady state volume of distribution is 6-10 L.
Clearance	MMAE is cleared by the liver but not quantitative studies have been performed.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	N.A.
Target	Tumor necrosis factor receptor superfamily member 8
Information of corresponding available drug in the market
Brand Name	Adcetris
Company	Seattle Genetics
Brand Discription	ADCETRIS (brentuximab vedotin) is a CD30-directed antibody-drug conjugate (ADC) consisting of three components: 1) the chimeric IgG1 antibody cAC10, specific for human CD30, 2) the microtubule disrupting agent MMAE, and 3) a protease-cleavable linker that covalently attaches MMAE to cAC10. Brentuximab vedotin has an approximate molecular weight of 153 kDa. Approximately 4 molecules of MMAE are attached to each antibody molecule. Brentuximab vedotin is produced by chemical conjugation of the antibody and small molecule components. The antibody is produced by mammalian (Chinese hamster ovary) cells, and the small molecule components are produced by chemical synthesis.
Prescribed for	Hodgkin lymphoma (HL) after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates.
Chemical Name	N.A.
Formulation	Following reconstitution with 10.5 mL Sterile Water for Injection, USP, a solution containing 5 mg/mL brentuximab vedotin is produced. The reconstituted product contains 70 mg/mL trehalose dihydrate, 5.6 mg/mL sodium citrate dihydrate, 0.21 mg/mL citric acid monohydrate, and 0.20 mg/mL polysorbate 80 and water for injection. The pH is approximately 6.6.
Physcial Appearance	ADCETRIS (brentuximab vedotin) for Injection is supplied as a sterile, white to off-white, preservative-free lyophilized cake or powder in single-use vials.
Route of Administration	Intravenous infusion
Recommended Dosage	Normal renal and hepatic function (1.8 mg/kg up to 180 mg), Mild (creatinine clearance > 50-80 mL/min) or moderate (creatinine clearance 30-50 mL/min) (1.8 mg/kg up to 180 mg), Severe (creatinine clearance less than 30 mL/min) (Avoid use), Mild (Child-Pugh A) (1.2 mg/kg up to 120 mg), Moderate (Child-Pugh B) or severe (Child-Pugh C) (Avoid use).
Contraindication	concomitant bleomycin due to pulmonary toxicity
Side Effects	Peripheral neuropathy, Anaphylaxis and Infusion Reactions, Hematologic Toxicities, Serious Infections and Opportunistic Infections, Tumor Lysis Syndrome, Increased Toxicity in the Presence of Severe Renal Impairment, Increased Toxicity in the Presence of Moderate or Severe Hepatic Impairment, Hepatotoxicity, Progressive Multifocal Leukoencephalopathy, Serious Dermatologic Reactions, Embryo-Fetal Toxicity
Useful Link	http://www.rxlist.com/adcetris-drug.htm http://www.adcetris.com/ http://en.wikipedia.org/wiki/Brentuximab_vedotin
PubMed ID	25642958, 25641881, 25573987
3-D Structure	Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID	1605
ThPP ID	Th1130
Therapeutic Peptide/Protein Name	Brentuximab vedotin
Sequence	Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification	IIb
Molecular Weight	149200-151800
Chemical Formula	C6476H9930N1690O2030S40
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	Terminal half-life is 4-6 days
Description	Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection
Indication/Disease	Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics	Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action	Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity	The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism	Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption	Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution	The steady state volume of distribution is 6-10 L.
Clearance	MMAE is cleared by the liver but not quantitative studies have been performed.
Categories	N.A.
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	N.A.
PubMed ID	25642958, 25641881, 25573987
3-D Structure	Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID	1606
ThPP ID	Th1130
Therapeutic Peptide/Protein Name	Brentuximab vedotin
Sequence	Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification	IIb
Molecular Weight	149200-151800
Chemical Formula	C6476H9930N1690O2030S40
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	Terminal half-life is 4-6 days
Description	Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection
Indication/Disease	Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics	Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action	Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity	The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism	Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption	Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution	The steady state volume of distribution is 6-10 L.
Clearance	MMAE is cleared by the liver but not quantitative studies have been performed.
Categories	N.A.
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	N.A.
PubMed ID	25642958, 25641881, 25573987
3-D Structure	Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)

Primary information
ID	1607
ThPP ID	Th1130
Therapeutic Peptide/Protein Name	Brentuximab vedotin
Sequence	Heavy chain:QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK view full sequnce in fasta
Functional Classification	IIb
Molecular Weight	149200-151800
Chemical Formula	C6476H9930N1690O2030S40
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	Terminal half-life is 4-6 days
Description	Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection.
Indication/Disease	Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Pharmacodynamics	Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network.
Mechanism of Action	Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network.
Toxicity	The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy. Other toxicities include bone marrow suppression, infusion reactions, peripheral neuropathy, Stevens-Johnson syndrome, and tumor lysis syndrome.
Metabolism	Only a small fraction of MMAE is metabolized primarily via oxidation by CYP3A4 and CYP3A5.
Absorption	Brentuximab vedotin is administered only as an Intravenous infusion so absorption is 100%.
Volume of Distribution	The steady state volume of distribution is 6-10 L.
Clearance	MMAE is cleared by the liver but not quantitative studies have been performed.
Categories	N.A.
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	N.A.
PubMed ID	25642958, 25641881, 25573987
3-D Structure	Th1130 Heavy chain or (Download), Th1130 Light chain (View) or (Download)