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Th1124 details

Primary information
ID 1576
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
Categories N.A.
Patents Number US6268343
Date of Issue 23/08/01
Date of Expiry 23/08/21
Drug Interaction N.A.
Target Glucagon-like peptide 1 receptor
Information of corresponding available drug in the market
Brand Name Saxenda
Company Novo Nordisk
Brand Discription Saxenda contains liraglutide, an analog of human GLP-1 and acts as a GLP-1 receptor agonist. The peptide precursor of liraglutide, produced by a process that includes expression of recombinant DNA in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751.2 Daltons.
Prescribed for obese
Chemical Name N.A.
Formulation Each 1 mL of Saxenda solution contains 6 mg of liraglutide and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection. Each pre-filled pen contains a 3 mL solution of Saxenda equivalent to 18 mg liraglutide (free-base, anhydrous).
Physcial Appearance Saxenda is a clear, colorless solution
Route of Administration Subcutaneous
Recommended Dosage 3 mg daily
Contraindication medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2 , hypersensitivity, Pregnancy
Side Effects Risk of Thyroid C-Cell Tumors, Acute Pancreatitis, Acute Gallbladder, Risk for Hypoglycemia with Concomitant Use of Anti-Diabetic Therapy , Heart Rate Increase, Renal Impairment, Hypersensitivity Reactions, Suicidal Behavior and Ideation.
Useful Link http://www.rxlist.com/saxenda-drug.htm https://www.saxenda.com/ http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427913.htm
PubMed ID 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1577
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
Categories N.A.
Patents Number CA2264243
Date of Issue 06/10/08
Date of Expiry 23/08/21
Drug Interaction N.A.
Target N.A.
Information of corresponding available drug in the market
Brand Name Victoza
Company Novo Nordisk
Brand Discription Victoza contains liraglutide, an analog of human GLP-1 and acts as a GLP-1 receptor agonist. The peptide precursor of liraglutide, produced by a process that includes expression of recombinant DNA in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751.2 Daltons.
Prescribed for type 2 diabetes mellitus
Chemical Name N.A.
Formulation Each 1 mL of Victoza solution contains 6 mg of liraglutide. Each pre-filled pen contains a 3 mL solution of Victoza equivalent to 18 mg liraglutide (free-base, anhydrous) and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection.
Physcial Appearance Victoza is a clear, colorless solution.
Route of Administration Subcutaneous
Recommended Dosage 0.6 mg per day for one week. The 0.6 mg dose is a starting dose intended to reduce gastrointestinal symptoms during initial titration, and is not effective for glycemic control. After one week at 0.6 mg per day, the dose should be increased to 1.2 mg. If the 1.2 mg dose does not result in acceptable glycemic control, the dose can be increased to 1.8 mg.
Contraindication medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2, prior serious hypersensitivity reaction to Victoza.
Side Effects Nausea, Diarrhea, Vomiting, Constipation, Headache
Useful Link http://www.rxlist.com/victoza-drug.htm http://www.victoza.com/ http://www.drugs.com/victoza.html
PubMed ID 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1578
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1579
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1580
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1581
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

Primary information
ID 1582
ThPP ID Th1124
Therapeutic Peptide/Protein Name Liraglutide
Sequence HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification Ib
Molecular Weight 3751.2
Chemical Formula C172H265N43O51
Isoelectric Point N.A.
Hydrophobicity N.A.
Melting Point (℃) N.A.
Half Life approx. 13 hrs
Description Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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 25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure Th1124 (View) or (Download)

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

Primary information
ID	1576
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
Categories	N.A.
Patents Number	US6268343
Date of Issue	23/08/01
Date of Expiry	23/08/21
Drug Interaction	N.A.
Target	Glucagon-like peptide 1 receptor
Information of corresponding available drug in the market
Brand Name	Saxenda
Company	Novo Nordisk
Brand Discription	Saxenda contains liraglutide, an analog of human GLP-1 and acts as a GLP-1 receptor agonist. The peptide precursor of liraglutide, produced by a process that includes expression of recombinant DNA in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751.2 Daltons.
Prescribed for	obese
Chemical Name	N.A.
Formulation	Each 1 mL of Saxenda solution contains 6 mg of liraglutide and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection. Each pre-filled pen contains a 3 mL solution of Saxenda equivalent to 18 mg liraglutide (free-base, anhydrous).
Physcial Appearance	Saxenda is a clear, colorless solution
Route of Administration	Subcutaneous
Recommended Dosage	3 mg daily
Contraindication	medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2 , hypersensitivity, Pregnancy
Side Effects	Risk of Thyroid C-Cell Tumors, Acute Pancreatitis, Acute Gallbladder, Risk for Hypoglycemia with Concomitant Use of Anti-Diabetic Therapy , Heart Rate Increase, Renal Impairment, Hypersensitivity Reactions, Suicidal Behavior and Ideation.
Useful Link	http://www.rxlist.com/saxenda-drug.htm https://www.saxenda.com/ http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427913.htm
PubMed ID	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1577
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
Categories	N.A.
Patents Number	CA2264243
Date of Issue	06/10/08
Date of Expiry	23/08/21
Drug Interaction	N.A.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	Victoza
Company	Novo Nordisk
Brand Discription	Victoza contains liraglutide, an analog of human GLP-1 and acts as a GLP-1 receptor agonist. The peptide precursor of liraglutide, produced by a process that includes expression of recombinant DNA in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751.2 Daltons.
Prescribed for	type 2 diabetes mellitus
Chemical Name	N.A.
Formulation	Each 1 mL of Victoza solution contains 6 mg of liraglutide. Each pre-filled pen contains a 3 mL solution of Victoza equivalent to 18 mg liraglutide (free-base, anhydrous) and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection.
Physcial Appearance	Victoza is a clear, colorless solution.
Route of Administration	Subcutaneous
Recommended Dosage	0.6 mg per day for one week. The 0.6 mg dose is a starting dose intended to reduce gastrointestinal symptoms during initial titration, and is not effective for glycemic control. After one week at 0.6 mg per day, the dose should be increased to 1.2 mg. If the 1.2 mg dose does not result in acceptable glycemic control, the dose can be increased to 1.8 mg.
Contraindication	medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2, prior serious hypersensitivity reaction to Victoza.
Side Effects	Nausea, Diarrhea, Vomiting, Constipation, Headache
Useful Link	http://www.rxlist.com/victoza-drug.htm http://www.victoza.com/ http://www.drugs.com/victoza.html
PubMed ID	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1578
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1579
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1580
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1581
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

Primary information
ID	1582
ThPP ID	Th1124
Therapeutic Peptide/Protein Name	Liraglutide
Sequence	HAEGTFTSDVSSYLEGQAAKEEFIIAWLVKGRG view full sequnce in fasta
Functional Classification	Ib
Molecular Weight	3751.2
Chemical Formula	C172H265N43O51
Isoelectric Point	N.A.
Hydrophobicity	N.A.
Melting Point (℃)	N.A.
Half Life	approx. 13 hrs
Description	Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor.
Indication/Disease	For use in/treatment of diabetes mellitus type 2.
Pharmacodynamics	Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11Ã¢â‚¬â€œ15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1.
Mechanism of Action	Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide.
Toxicity	In a clinical trial, one patient with type 2 diabetes experienced a single overdose of Victoza 17.4 mg subcutaneous (10 times the maximum recommended dose). Effects of the overdose included severe nausea and vomiting requiring hospitalization. No hypoglycemia was reported. The patient recovered without complications. In the event of overdosage, appropriate supportive treatment should be initiated according to the patient's clinical signs and symptoms. RISK OF THYROID C-CELL TUMORS
Metabolism	During the initial 24 hours following administration of a single [3H]-liraglutide dose to healthy subjects, the major component in plasma was intact liraglutide. Liraglutide is endogenously metabolized in a similar manner to large proteins without a specific organ as a major route of elimination.
Absorption	Maximum concentrations of liraglutide are achieved at 8-12 hours after dose. The mean peak and total exposures of liraglutide were 35 ng/mL and 960 ngÂ·h/mL, respectively, for a subQ single dose of 0.6 mg. After subcutaneous single dose administrations, Cmax and AUC of liraglutide increased proportionally over the therapeutic dose range of 0.6 mg to 1.8 mg. At 1.8 mg Victoza, the average steady state concentration of liraglutide over 24 hours was approximately 128 ng/mL AUC0-âˆž was equivalent between upper arm and abdomen, and between upper arm and thigh. AUC0-âˆž from thigh was 22% lower than that from abdomen. Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%.
Volume of Distribution	SubQ 0.6 mg is approximately 13LIntravenous is approximately 0.07L/kg
Clearance	The mean apparent clearance following subcutaneous administration of a single dose of liraglutide is approximately 1.2 L/h
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	25656058, 25650514, 25626486, 25625650, 25619391, 25614699, 20709939, 19343230, 19041364
3-D Structure	Th1124 (View) or (Download)

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