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Results for "

dovitinib

" in TargetMol Product Catalog
  • Inhibitors & Agonists
    7
    TargetMol | Activity
  • PROTAC Products
    3
    TargetMol | inventory
Dovitinib
T6289405169-16-6
Dovitinib (CHIR-258) (TKI258, CHIR258) is a multitargeted RTK inhibitor, mostly for class III (FLT3 c-Kit, IC50: 1 2 nM), also effective to class IV (FGFR1 3) and class V (VEGFR1-4) RTKs (IC50: 8-13 nM), less potent to EGFR, InsR, EphA2, c-Met, IGF-1R, Tie2, and HER2.
  • $39
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TargetMol | Inhibitor Sale
Dovitinib lactate
T7104692737-80-7
Dovitinib lactate (TKI-258 lactate)(TKI258) lactate is a potent inhibitor of fibroblast growth factor receptor 3 (FGFR3) (IC50 :5 nM).
  • $47
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Dovitinib-RIBOTAC TFA
T779302759351-69-2
Dovitinib RIBOTAC TFA effectively and selectively cleaves pre-miR-21, functioning as a targeted RNA degrader.
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Dovitinib-RIBOTAC
T779292759351-68-1
Dovitinib RIBOTAC is a potent, selective targeted RNA degrader that cleaves pre-miR-21.
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Dovitinib lactate hydrate
T6479915769-50-5
Dovitinib lactate hydrate (TKI258) is the Lactate of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3 c-Kit) with IC50 of 1 nM 2 nM, also potent to class IV (FGFR1 3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.
  • $50
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Dovitinib Dilactic Acid
T6193852433-84-2
Dovitinib Dilactic Acid (Dovitinib (TKI-258) Dilactic Acid) is the Dilactic acid of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3 c-Kit) with IC50 of 1 nM 2 nM, also potent to class IV (FGFR1 3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.
  • $75
4-6 weeks
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Pomalidomide-C5-Dovitinib
T814212732969-67-2
Pomalidomide-C5-Dovitinib (compound 2) is a PROTAC linking Pomalidomide and Dovitinib via a CRBN connector, exhibiting potent antiproliferative activity in FLT3-ITD+ acute myeloid leukemia (AML) cells. It promotes ubiquitin-proteasome-dependent degradation of FLT3-ITD and KIT proteins, thereby inhibiting their downstream signaling pathways and presenting research potential in FLT3-ITD+ AML [1].
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