Clinical data | |
---|---|
Trade names | Bosulif |
License data | |
Routes of administration | By mouth |
ATC code | |
Legal status | |
Legal status | |
Pharmacokinetic data | |
Protein binding | 94–96% |
Metabolism | By CYP3A4, to inactive metabolites |
Elimination half-life | 22.5±1.7 hours |
Excretion | Fecal (91.3%) and kidney (3%) |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
ECHA InfoCard | 100.149.122 |
Chemical and physical data | |
Formula | C26H29Cl2N5O3 |
Molar mass | 530.45 g·mol−1 |
3D model ( JSmol) | |
| |
| |
(what is this?) (verify) |
Bosutinib, sold under the brand name Bosulif, is a small molecule BCR-ABL and src tyrosine kinase inhibitor used for the treatment of chronic myelogenous leukemia.[ medical citation needed]
Originally synthesized by Wyeth, it is being developed by Pfizer.[ citation needed]
It is an ATP-competitive Bcr-Abl tyrosine-kinase inhibitor with an additional inhibitory effect on Src family kinases (including Src, Lyn and Hck). [2] [3] It has also shown activity against the receptors for platelet derived growth factor and vascular endothelial growth factor. [4] Bosutinib inhibited 16 of 18 imatinib-resistant forms of Bcr-Abl expressed in murine myeloid cell lines, but did not inhibit T315I and V299L mutant cells. [2]
Bosutinib is metabolized through CYP3A4.
Bosutinib received US FDA and EU European Medicines Agency approval in September 2012, and March 2013, respectively for the treatment of adults with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy. [5] [6] [7] [8]
Bosutinib has two known absolute contraindications, which are: known hypersensitivity to bosutinib and liver impairment. [9] [10]
Bosutinib is both a substrate and an inhibitor of P-glycoprotein (P-gp) and CYP3A4. [2] Hence P-gp and CYP3A4 inhibitors may increase plasma levels of bosutinib. [2] Likewise CYP3A4 inducers may reduce plasma concentrations of bosutinib. [2] It may also alter the metabolism and uptake (into the GIT by means of its P-gp inhibitory effects) of other drugs that are substrates for P-gp and CYP3A4. [2]
{{
cite book}}
: |website=
ignored (
help)
Clinical data | |
---|---|
Trade names | Bosulif |
License data | |
Routes of administration | By mouth |
ATC code | |
Legal status | |
Legal status | |
Pharmacokinetic data | |
Protein binding | 94–96% |
Metabolism | By CYP3A4, to inactive metabolites |
Elimination half-life | 22.5±1.7 hours |
Excretion | Fecal (91.3%) and kidney (3%) |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
ECHA InfoCard | 100.149.122 |
Chemical and physical data | |
Formula | C26H29Cl2N5O3 |
Molar mass | 530.45 g·mol−1 |
3D model ( JSmol) | |
| |
| |
(what is this?) (verify) |
Bosutinib, sold under the brand name Bosulif, is a small molecule BCR-ABL and src tyrosine kinase inhibitor used for the treatment of chronic myelogenous leukemia.[ medical citation needed]
Originally synthesized by Wyeth, it is being developed by Pfizer.[ citation needed]
It is an ATP-competitive Bcr-Abl tyrosine-kinase inhibitor with an additional inhibitory effect on Src family kinases (including Src, Lyn and Hck). [2] [3] It has also shown activity against the receptors for platelet derived growth factor and vascular endothelial growth factor. [4] Bosutinib inhibited 16 of 18 imatinib-resistant forms of Bcr-Abl expressed in murine myeloid cell lines, but did not inhibit T315I and V299L mutant cells. [2]
Bosutinib is metabolized through CYP3A4.
Bosutinib received US FDA and EU European Medicines Agency approval in September 2012, and March 2013, respectively for the treatment of adults with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy. [5] [6] [7] [8]
Bosutinib has two known absolute contraindications, which are: known hypersensitivity to bosutinib and liver impairment. [9] [10]
Bosutinib is both a substrate and an inhibitor of P-glycoprotein (P-gp) and CYP3A4. [2] Hence P-gp and CYP3A4 inhibitors may increase plasma levels of bosutinib. [2] Likewise CYP3A4 inducers may reduce plasma concentrations of bosutinib. [2] It may also alter the metabolism and uptake (into the GIT by means of its P-gp inhibitory effects) of other drugs that are substrates for P-gp and CYP3A4. [2]
{{
cite book}}
: |website=
ignored (
help)