Entry 1 |
(1) Primary information |
---|
ID | 1117 |
ThPP ID | Th1016 |
Therapeutic Peptide/Protein Name | Pegfilgrastim |
Sequence | MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVL view full sequnce in fasta |
Functional Classification | Ib |
Molecular Weight | 18802.8 |
Chemical Formula | C845H1343N223O243S9 |
Isoelectric Point | 5.65 |
Hydrophobicity | 0.209 |
Melting Point (℃) | 60 |
Half Life | 15-80 hours |
Description | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. |
Indication/Disease | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant |
Pharmacodynamics | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. |
Mechanism of Action | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase |
Toxicity | N.A. |
Metabolism | N.A. |
Absorption | N.A. |
Volume of Distribution | N.A. |
Clearance | Filgrastim is primarily eliminated by the kidney and neutrophils/neutrophil precursors; the latter presumably involves binding of the growth factor to the G-CSF receptor on the cell surface, internalization of the growth factor-receptor complexes via endo |
Categories | Immunosuppressive Agents |
Patents Number | CA1341537 |
Date of Issue | 31/07/07 |
Date of Expiry | 31/07/24 |
Drug Interaction | N.A. |
Target | Granulocyte colony-stimulating factor receptor,Neutrophil elastase |
Information of corresponding available drug in the market |
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Brand Name | Neulasta |
Company | Amgen Inc. |
Brand Discription | Neulasta is a covalent conjugate of recombinant methionyl human G-CSF/Filgrastim and monomethoxypolyethylene glycol. Filgrastim (175 amino acid, 19 kilodaltons (kD)) is a water-soluble protein. Filgrastim is obtained from the bacterial fermentation of a s |
Prescribed for | Neulasta is used to prevent neutropenia(lack of certain white blood cells caused by receiving chemotherapy). |
Chemical Name | N.A. |
Formulation | Supplied in 0.6 mL prefilled syringes. Each syringe contains 6 mg pegfilgrastim (based on protein weight) in a sterile, clear, colorless, preservative-free solution (pH 4.0) containing acetate (0.35 mg), polysorbate 20 (0.02 mg), sodium (0.02 mg), and sor |
Physcial Appearance | Solution |
Route of Administration | Subcutaneous Injection |
Recommended Dosage | Single subcutaneous injection of 6 mg administered once per chemotherapy cycle in adults. Do not administer Neulasta between 14 days before and 24 hours after administration of cytotoxic chemotherapy. |
Contraindication | Allergy, or having sickle cell disorder; chronic myeloid leukemia; myelodysplasia (also called preleukemia); or if you are allergic to latex. |
Side Effects | Bone pain; pain in your arms or legs; or bruising, swelling, pain, redness, or a hard lump where the injection was given. |
Useful Link | http://www.drugs.com/neulasta.html |
PubMed ID | 21456630, 25594147, 25581410, 25524005 |
3-D Structure | Th1016 (View) or (Download) |
Entry 2 |
(2) Primary information |
---|
ID | 1118 |
ThPP ID | Th1016 |
Therapeutic Peptide/Protein Name | Pegfilgrastim |
Sequence | MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVL view full sequnce in fasta |
Functional Classification | Ib |
Molecular Weight | 18802.8 |
Chemical Formula | C845H1343N223O243S9 |
Isoelectric Point | 5.65 |
Hydrophobicity | 0.209 |
Melting Point (℃) | 60 |
Half Life | 15-80 hours |
Description | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. |
Indication/Disease | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant |
Pharmacodynamics | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. |
Mechanism of Action | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase |
Toxicity | N.A. |
Metabolism | N.A. |
Absorption | N.A. |
Volume of Distribution | N.A. |
Clearance | Filgrastim is primarily eliminated by the kidney and neutrophils/neutrophil precursors; the latter presumably involves binding of the growth factor to the G-CSF receptor on the cell surface, internalization of the growth factor-receptor complexes via endo |
Categories | Antineutropenic Agents |
Patents Number | CA1339071 |
Date of Issue | 29/07/97 |
Date of Expiry | 29/07/14 |
Drug Interaction | N.A. |
Target | N.A. |
Information of corresponding available drug in the market |
---|
Brand Name | N.A. |
Company | N.A. |
Brand Discription | N.A. |
Prescribed for | N.A. |
Chemical Name | N.A. |
Formulation | N.A. |
Physcial Appearance | N.A. |
Route of Administration | N.A. |
Recommended Dosage | N.A. |
Contraindication | N.A. |
Side Effects | N.A. |
Useful Link | http://www.drugs.com/drug-interactions/pegfilgrastim,neulasta-index.html?filter=2&generic_only |
PubMed ID | 21456630, 25594147, 25581410, 25524005 |
3-D Structure | Th1016 (View) or (Download) |
Entry 3 |
(3) Primary information |
---|
ID | 1119 |
ThPP ID | Th1016 |
Therapeutic Peptide/Protein Name | Pegfilgrastim |
Sequence | MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVL view full sequnce in fasta |
Functional Classification | Ib |
Molecular Weight | 18802.8 |
Chemical Formula | C845H1343N223O243S9 |
Isoelectric Point | 5.65 |
Hydrophobicity | 0.209 |
Melting Point (℃) | 60 |
Half Life | 15-80 hours |
Description | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. |
Indication/Disease | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant |
Pharmacodynamics | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. |
Mechanism of Action | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase |
Toxicity | N.A. |
Metabolism | N.A. |
Absorption | N.A. |
Volume of Distribution | N.A. |
Clearance | Filgrastim is primarily eliminated by the kidney and neutrophils/neutrophil precursors; the latter presumably involves binding of the growth factor to the G-CSF receptor on the cell surface, internalization of the growth factor-receptor complexes via endo |
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 | http://www.rxlist.com/neulasta-drug/indications-dosage.htm |
PubMed ID | 21456630, 25594147, 25581410, 25524005 |
3-D Structure | Th1016 (View) or (Download) |