SU5204, a tyrosine kinase extracted from patent US5792783A, has IC50s of 4 and 51.5 μM for FLK-1 (VEGFR-2) and HER2, respectively.

(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC50s of 2.1, 0.008, and 1.2 µM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces regression of established tumors.

Syk-IN-4 is a potent, selective and orally bioavailable SYK with an IC50 of 0.31 nM. SYK has emerged as a potential target for autoimmunity and hematological cancers.

EMI56, the derivative of EMI1, displays greater potency toward mutant EGFR than EMI1. EMI56 inhibits EGFR triple mutants.

IBT6A hydrochloride is an impurity of Ibrutinib. IBT6A can be used in synthesis of IBT6A Ibrutinib dimer and IBT6A adduct. Ibrutinib is a selective, irreversible Btk with an IC50 of 0.5 nM.

IBT6A is an impurity of Ibrutinib. IBT6A can be used in synthesis of IBT6A Ibrutinib dimer and IBT6A adduct. Ibrutinib is a selective, irreversible Btk with an IC50 of 0.5 nM.

JNJ-38158471(KDR) is a well tolerated, orally available, highly selective VEGFR-2 inhibitor with IC50=40nM. It also inhibits closely related tyrosine kinases, Ret (180nM) and Kit (500nM). It has no significant activity (>1 microM) against VEGFR-1 and VEGF

SU-10994 is a novel VEGFR inhibitor.

Ningetinib is a potent, orally bioavailable inhibitor of tyrosine kinase with IC50 of 6.7 nM, 1.9 nM and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. Ningetinib exhibits antitumor activity.

Epertinib hydrochloride (S-222611 hydrochloride) is a potent, orally active, reversible, and selective tyrosine kinase inhibitor of EGFR, HER2 and HER4 with IC50 of 1.48 nM, 7.15 nM and 2.49 nM, respectively. Epertinib hydrochloride (S-222611 hydrochloride) exhibits antitumor activity.

MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB.

JNJ-28312141 is an orally active CSF1R inhibitor (Colony-stimulating factor-1 receptor, CRF1R) and also a FLT3 inhibitor.

A potent a+M7692nd highly selective Btk inhibitor with IC50 of 0.5 nM.

CB-988 is a potent, highly selective, non-covalent Btk inhibitor targering ibrutinib-resistant Btk C481S mutant (IC50=0.6 nM).

ABBV-105 (ABBV105) is a potent, selective, irreversible, covalent inhibitor of BTK with IC50 of 0.18 uM.

EGFR-IN-1 (compound 24) is an orally active and irreversible L858R/T790M mutant selective EGFR inhibitor. EGFR-IN-1 potently inhibits Gefitinib-resistant EGFR L858R, T790M with 100-fold selectivity over wild-type EGFR. EGFR-IN-1 displays strong antiproliferative activity against the H1975 cells and the first line mutant HCC827 cells. Antitumor activity.

Sitravatinib malate (MGCD516 malate) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC50s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively. Sitravatinib malate shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment.

Imatinib D4 (STI571 D4) is a deuterium labeled Imatinib (STI571). Imatinib is an orally bioavailable tyrosine kinases inhibitor that selectively inhibits BCR/ABL, v-Abl, PDGFR and c-kit kinase activity.

I-OMe-Tyrphostin AG 538 (I-OMe-AG 538) is a specific inhibitor of IGF-1R (insulin-like growth factor-1 receptor tyrosine kinase). I-OMe-Tyrphostin AG 538 inhibits IGF-1R-mediated signaling and is preferentially cytotoxic to nutrient-deprived PANC1 cells. I-OMe-Tyrphostin AG 538 is an ATP-competitive inhibitor of phosphatidylinositol-5-phosphate 4-kinase α (PI5P4Kα), with an IC50 of 1 µM.

CH6953755 is a potent, orally active and selective YES1 kinase (a member of the SRC family) inhibitor with an IC50 of 1.8 nM. CH6953755 inhibits YES1 kinase, leading to antitumor activity against YES1 Gene -amplified cancers in vitro and in vivo.

ALK/ROS1-IN-1 (compound 2e) is a potent and selective anti crizotinib-resistant ALK/ROS1 dual inhibitor, with IC50s of 0.174 μM and 0.530 μM for ALK and ROS1 enzyme, respectively.

Mutated EGFR-IN-3 (compound 3) is a potent, ATP-competitive and highly selective allosteric dibenzodiazepinone inhibitor of the EGFR(L858R/T790M) and EGFR(L858R/T790M/C797S) mutants with IC50 values of 12 nM and 13 nM, respectively.

FGFR4-IN-4 (compound 693) is a FGFR4 inhibitor with anti-tumor activity, extracted from patent WO2018113584A1.

c-Kit-IN-3 tartrate (Compound 18) is a potent c-KIT kinase inhibitor, which is potent and selective against BaF3-tel-c-KIT (IC50 of 4 nM) and a broad spectrum of drug-resistant mutants (IC50 of 8 nM for BaF3-tel-c-KIT-T670I) with improved bioavailability.

c-Kit-IN-3 L-tartrate (Compound 18) is a potent and selective c-KIT kinase inhibitor with an IC50s of 4 nM, 8 nM for c-KIT wt and c-KIT T670I, respectively. c-Kit-IN-3 L-tartrate displays great potencies against most of the gain-offunction mutations in the juxtamembrane domain, drugresistant mutations in the ATP binding pocket, and activation loops.

c-Kit-IN-3 (D-tartrate) (Compound 18) is a potent c-KIT kinase inhibitor, which is potent and selective against BaF3-tel-c-KIT (IC50 of 4 nM) and a broad spectrum of drug-resistant mutants (IC50 of 8 nM for BaF3-tel-c-KIT-T670I) with improved bioavailability.

c-Kit-IN-3 hydrochloride (Compound 18) is a potent c-KIT kinase inhibitor, which is potent and selective against BaF3-tel-c-KIT (IC50 of 4 nM) and a broad spectrum of drug-resistant mutants (IC50 of 8 nM for BaF3-tel-c-KIT-T670I) with improved bioavailability.

TGFβRI-IN-2 (compound 18) is a potent, selective and orally active (Activin-Like Kinase 5) ALK 5 inhibitor with pIC50 and pEC50 values of 7.6 and 6.63, respectively. TGFβRI-IN-2 can produce observed cardiac toxicity in vivo at high dose.

PKI-166 is a potent, selective and orally bioavailable EGFR tyrosine kinase inhibitor, with an IC50 of 0.7 nM.

BPI-9016M is a potent, orally active, and selective dual c-Met and AXL tyrosine kinases inhibitor. BPI-9016M suppresses tumor cell growth, migration and invasion of lung adenocarcinoma.