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Chemical Structure Cat. No. Product Name CAS No.
Tuspetinib hydrate Chemical Structure
BCP49212 Tuspetinib hydrate 2758339-04-5
Tuspetinib (HM43239) is an orally active and selective FLT3 inhibitor with IC50s of 1.1 nM, 1.8 nM and 1.0 nM for FLT3 WT, FLT3 internal tandem duplication (ITD) and FLT3 D835Y kinases, respectively. Tuspetinib inhibits the kinase activity of FLT3 as a reversible type I inhibitor and modulates p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. Tuspetinib inhibits the proliferation and induces the apoptosis of leukemic cells.
HPK1-IN-2 Chemical Structure
BCP48923 HPK1-IN-2 2056122-11-1
HPK1-IN-2 is a potent and orally active inhibitor of hematopoietic progenitor kinase-1 (HPK1), Lck and Flt3. HPK1-IN-2 exhibits antitumor activity.
FLT3-IN-16 Chemical Structure
BCP48905 FLT3-IN-16 298207-49-5
FLT3-IN-16 is a inhibitor of Influenza Virus Polymerase.
KG5 Chemical Structure
BCP46930 KG5 877874-85-6
KG 5 is an orally available PDGFRß and B-Raf allosteric inhibitor.
MAX-40279 hemifumarate Chemical Structure
BCP46381 MAX-40279 hemifumarate 2388506-43-0
MAX-40279 hemifumarate is a dual and potent inhibitor of FLT3 kinase and FGFR kinase.
MAX-40279 hemiadipate Chemical Structure
BCP46003 MAX-40279 hemiadipate 2388506-44-1
MAX-40279 hemiadipate is a dual and potent inhibitor of FLT3 kinase and FGFR kinase.
MAX-40279 Chemical Structure
BCP46002 MAX-40279 2070931-57-4
MAX-40279 is an orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) and FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential antineoplastic activity.
FLT3-IN-3 Chemical Structure
BCP45355 FLT3-IN-3 2229050-90-0
FLT3-IN-3 is a potent and selective FLT3 inhibitor.
HM43239 Chemical Structure
BCP40967 HM43239 2569527-64-4
HM43239 is an orally active small molecule inhibitor of FLT3 that selectively inhibits not only FLT3 wild type, ITD mutants or TKD mutations, but also FLT3 ITD/TKD double mutations.
SB1317 Chemical Structure
BCP42651 SB1317 1204918-72-8
SB1317 is a novel small molecule potent CDK/JAK2/FLT3 inhibitor. Zotiraciclib may be useful for the treatment of cancer that crosses the blood brain barrier and acts by depleting Myc through the inhibition of cyclin-dependent kinase 9 (CDK9). It is one of a number of CDK inhibitors under investigation; others targeting CDK9 for the treatment of acute myeloid leukemia include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80 percent of glioblastomas characterized by this property.
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