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c-Met inhibitor
JNJ-38877618 is a novel potent, highly selective, orally bioavailable c-Met tyrosine kinase inhibitor with Kd of 1.2, 2.1 and 21 nM for WT, M1250T and Y1235D mutants MET, respectively. -
c-Met inhibitor
Glumetinib (SCC244) is a potent and highly selective c-Met kinase inhibitor with an IC50 of 0.42 nM. Glumetinib shows antitumor activity and a superior safety margin. -
CSF-1R inhibitor
TE-952 is a potent, oral active and selective Type II inhibitor of colony stimulating factor-1 receptor (CSF-1R or cFMS, type III receptor tyrosine kinase), with IC50 values of 13 nM and 261 nM for CSF1R and TrkA , respectively. Effective against a mouse collagen-induced model of arthritis. -
c-FMS inhibitor
c-Fms-IN-9 is a c-FMS inhibitor extracted from patent WO2014145023A1, Compound Example 7. c-Fms-IN-9 inhibits unphosphorylated c-FMS kinase (uFMS) and uKIT with IC50s of <0.01 μM and 0.1-1 μM, respectively. -
c-KIT inhibitor
c-Kit-IN-2 is a c-KIT inhibitor with an IC50 of 82 nM, shows superior antiproliferative activities against all the three GIST cell lines, GIST882, GIST430, and GIST48, with GI50s of 3, 1, and 2 nM, respectively. -
c-KIT T670I mutant inhibitor
CHMFL-KIT-033 is a potent and selective inhibitor of c-KIT T670I mutant for gastrointestinal stromal tumors (GISTs), with an IC50 of 0.045 μM. -
AXL Inhibitor
TP-0903 is a potent and selective Axl kinase inhibitor with IC50 of 27 nM. -
MET/VEGFR-2 inhibitor
BMS-817378 is a novel prodrug of the dual Met/VEGFR-2 inhibitor BMS-794833. -
EGFR inhibitor
Olafertinib (CK-101, RX518) is an epidermal growth factor receptor (EGFR) inhibitor.
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EGFR Inhibitor
AG-18 is an inhibitor of epidermal growth factor (EGF) receptor kinase with an IC50 value of 35 ,M in the human epidermoid carcinoma cell line A431. -
FGFR2 Inhibitor
Alofanib is a potent and selective allosteric inhibitor of FGFR2 with potential anticancer activity. -
FGFR inhibitor
Erdafitinib is a potent and selective orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. -
TRK inhibitor
Larotrectinib (LOXO-101, ARRY-470) is an orally bioavailable, potent, ATP-competitive inhibitor of TRKA, TRKB, and TRKC.
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ALK2 inhibitor
LDN-214117 is a selective and potent ALK2 inhibitor. LDN-214117 inhibited ALK2 most, with a biochemical IC50 of 24 nM. -
neuropilin-1/VEGF-A inhibitor
EG00229 is the first small molecule inhibitors of the neuropilin-1 and VEGF-A interaction with an IC50 of inhibition of 8 uM(125I-VEGF binding to PAE/NRP1 cells). -
TRK inhibitor
LOXO-101 is a small molecule that was designed to block the ATP binding site of the TRK family of receptors, with 2 to 20 nM cellular potency against the TRKA, TRKB, and TRKC kinases. -
Src inhibitor
T338C Src-IN-1 is a potent mutant-Src T338C inhibitor; exhibited the most potent inhibition of T338C(IC50=111 nM) relative to WT c-Src (10-fold increase). -
Src inhibitor
T338C Src-IN-2 is a potent mutant c-Src T338C kinase inhibitor with IC50 of 317 nM; also inhibits T338C/V323A and T338C/V323S with IC50 of 57 nM/19 nM. -
FLT3/KIT/PDGFRα/PDGFRβ inhibitor
AC710 Mesylate is a potent, selective PDGFR-family kinases inhibitor with Kd values of 0.6 nM/1.0 nM/1.3 nM/1.0 nM for FLT3/KIT/PDGFRα/PDGFRβ respectively. -
c-Met inhibitor
SCR-1481B1 is a potent compound that has activity against cancers dependent upon Met activation and also has activity against cancers as a VEGFR inhibitor.
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MET/Axl inhibitor
Glesatinib hydrochloride is an inhibitor of the MET and Axl receptor tyrosine kinase pathways, which drive tumour growth when altered. -
multi-kinase inhibitor
Flumatinib is a multi-kinase inhibitor with IC50 Values of 1.2 nM, 307.6 nM and 2662 nM for c-Abl, PDGFRbeta and c-Kit respectively. -
RTK inhibitor
Sitravatinib is a novel small molecule inhibitor targeting multiple RTKs involved in driving sarcoma cell growth. -
ALK/EGFR inhibitor
HG-14-10-04 is a potent and specific ALK inhibitor with IC50 of 20 nM. -
Her3 (ErbB3) ligand
TX1-85-1 is ErbB3 inhibitor. TX2-121-1 may exert Her3-dependent pharmacology through an allosteric mechanismthereby disrupting interactions between Her3 and other proteins such as Her3 or cMet consistent with results presented here and distinct from conventional kinase inhibitors, which block catalytic function.

