| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2803160801023 | 316080102 | IMATINIB ACCORD F.C.TAB 100MG/TAB BTx60 σε PVC/PVDC/alu blister | 392.11 | 398.00 | 464.07 |
| 05/2018 | 2803160802020 | 316080202 | IMATINIB ACCORD F.C.TAB 400MG/TAB BTx30 σε PVC/PVDC/alu blister | 709.34 | 720.00 | 812.81 |
| 05/2018 | 2803045901022 | 304590102 | IMATINIB TEVA F.C.TAB 100MG/TAB BTx60 σε OPA/AL/PVC/AL BLISTER OPA/AL/PVC/AL BLISTER | 392.33 | 398.22 | 464.32 |
| 05/2018 | 2803045901039 | 304590103 | IMATINIB TEVA F.C.TAB 100MG/TAB BTx60x1 σε OPA/AL/PVC/AL BLISTER OPA/AL/PVC/AL BLISTER | 392.33 | 398.22 | 464.32 |
| 05/2018 | 2803045901084 | 304590108 | IMATINIB TEVA F.C.TAB 100MG/TAB BTx60 σε PVC/PE/PVDC/PE/PVC/AL BLISTER PVC/PE/PVDC/PE/PVC/AL BLISTER | 392.33 | 398.22 | 464.32 |
| 05/2018 | 2803045901091 | 304590109 | IMATINIB TEVA F.C.TAB 100MG/TAB BTx60x1 σε PVC/PE/PVDC/PE/PVC/AL BLISTER PVC/PE/PVDC/PE/PVC/AL BLISTER | 392.33 | 398.22 | 464.32 |
| 05/2018 | 2803045902012 | 304590201 | IMATINIB TEVA F.C.TAB 400MG/TAB BTx30 σε OPA/AL/PVC/AL BLISTER OPA/AL/PVC/AL BLISTER | 709.56 | 720.22 | 813.06 |
| 05/2018 | 2803045902029 | 304590202 | IMATINIB TEVA F.C.TAB 400MG/TAB BTx30x1 σε OPA/AL/PVC/AL BLISTER OPA/AL/PVC/AL BLISTER | 709.56 | 720.22 | 813.06 |
| 05/2018 | 2803045902050 | 304590205 | IMATINIB TEVA F.C.TAB 400MG/TAB BTx30 σε PVC/PE/PVDC/PE/PVC/AL BLISTER PVC/PE/PVDC/PE/PVC/AL BLISTER | 709.56 | 720.22 | 813.06 |
| 05/2018 | 2803045902067 | 304590206 | IMATINIB TEVA F.C.TAB 400MG/TAB BTx30x1 σε PVC/PE/PVDC/PE/PVC/AL BLISTER PVC/PE/PVDC/PE/PVC/AL BLISTER | 709.56 | 720.22 | 813.06 |
For the treatment Philadelphia chromosome positive chronic myeloid leukemia (CML) and malignant gastrointestinal stromal tumors (GIST).
Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosine kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome abnormality in chronic myeloid leukemia (CML). It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia. Imatinib also inhibits the receptor tyrosine kinases for platelet derived growth factor (PDGF) and stem cell factor (SCF) - called c-kit. Imatinib was identified in the late 1990s by Dr Brian J. Druker. Its development is an excellent example of rational drug design. Soon after identification of the bcr-abl target, the search for an inhibitor began. Chemists used a high-throughput screen of chemical libraries to identify the molecule 2-phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.
Side effects include nausea, vomiting, diarrhea, loss of appetite, dry skin, hair loss, swelling (especially in the legs or around the eyes) and muscle cramps
Imatinib is well absorbed with mean absolute bioavailability is 98% with maximum levels achieved within 2-4 hours of dosing
18 hours for Imatinib, 40 hours for its major active metabolite, the N-desmethyl derivative
Imatinib elimination is predominately in the feces, mostly as metabolites.
* 8 L/h [50-year-old CML and GIST patient weighing 50 kg] * 14 L/h [50-year-old CML and GIST patient weighing 100 kg]