| Nomenclature | Janus kinase 1 | Janus kinase 2 | Janus kinase 3 | tyrosine kinase 2 |
| HGNC, UniProt | JAK1, P23458 | JAK2, O60674 | JAK3, P52333 | TYK2, P29597 |
| EC number | 2.7.10.2 | 2.7.10.2 | 2.7.10.2 | 2.7.10.2 |
| Common abreviation | JAK1 | JAK2 | JAK3 | Tyk2 |
| Inhibitors | ruxolitinib (pIC50 8.5–10.1) [203, 423], filgotinib (pIC50 8) [541] | NS‐018 (pIC50 9.1) [374], BMS‐911543 (pIC50 9) [420], AT‐9283 (pIC50 8.9) [230], XL019 (pIC50 8.7) [152], fedratinib (pIC50 8.5) [333, 566], gandotinib (pIC50 8.4) [330] | AT‐9283 (pIC50 9) [230] | – |
| Selective inhibitors | – | compound 1d (pIC50>9) [554] | – | – |
| Comments | – | The JAK2V617F mutation, which causes constitutive activation, plays an oncogenic role in the pathogenesis of the myeloproliferative disorders, polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis [64, 115]. Small molecule compounds which inhibit aberrant JAK2 activity are being developed as novel anti‐cancer pharmaceuticals. | – | – |
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