Table 1.
Tyrosine kinase inhibitors (TKIs) relevant to the treatment of MM.
| Name | TKI Generation | Target | Indication in Clinical | Trials (Author, Year) | Pt. No (MM No:%) |
Results [95% CI] | Note |
|---|---|---|---|---|---|---|---|
| Imatinib | 1st | KIT, BCR-ABL, 1 PDGFRA | 2 CML, KIT-positive 3 GISTs, Philadelphia chromosome-positive 4 ALL etc. | Guo (2011) [15] | 43 (11:25.6%) | PR (best response): 10 (23.3%) | exons 11 and 13 mutations predict the response to imatinib |
| Hodi (2013) [16] | 24 (17:70.8%) | 5 ORR:29% | |||||
| Nilotinib | 2nd overcome resistance of BCR-ABL mutants to imatinib |
KIT, BCR-ABL inhibitory activity to KIT mutations (exons 9, 11,13) |
CML | Carvajal (2015) [19] | 19 (12: 63%) | (Premedicated Pt with imatinib) 6 TTP (months): 3.4 OS (months): 14.2 |
Nilotinib may overcome acquired resistance to Imatinib |
| Lee (2015) [20] | 42 (12: 28.6%) | ORR: 16.7% [5.4–28.0] |
|||||
| Dasatinib | 2nd Multi-kinase TKI |
KIT, BCR-ABL, SRC family kinases | CML, Philadelphia chromosome-positive ALL | Kalinsky (2017) [21] | 73 (38: 52%) | Pt with PR (3: 5.9%) did not have KIT mutations |
superiority to imatinib was not shown |
1 PDGFRA: platelet-derived growth factor receptor alpha; 2 CML: chronic myelogenous leukemia; 3 GIST: gastrointestinal stromal tumors; 4 ALL: acute lymphoblastic leukemia; 5 ORR: objective response rate; 6 TTP: time to progression.