CEP-37440 is a novel potent and selective Dual FAK/ALK inhibitor with IC50 s of 2.3 nM (FAK) and 120 nM(ALK cellular IC50 in 75% human plasma).IC50 value: 2.3 nM (FAK); 120 nM (ALK cellular IC50 in 75% human plasma)Target: Dual FAK/ALKPreparation of fused bicyclic 2,4-diaminopyrimidine derivatives as a dual ALK and FAK inhibitorBy Jacobs, Martin J.; Ott, Gregory R. From PCT Int. Appl. (2013), WO 2013134353 A1 20130912.
DDR1-IN-6 is a selective Discoidin Domain Receptor family, member 1 (DDR1) inhibitor with an IC50 of 9.72 nM. DDR1-IN-6 inhibits auto-phosphorylation DDR1b (Y513) with an IC50 of 9.7 nM. DDR1-IN-6 has anti-cancer activity[1].
p60c-src substrate II is an efficient pentapeptide substrate for the tyrosine kinase pp60c-src[1].
Capillarisin, as a constituent from Artemisiae Capillaris herba, is found to exert anti-inflammatory and antioxidant properties. Capillarisin can be used for the research of asthma-mediated complications and can be a potential neuroprotectant against bupivacaine-induced neurotoxicity[1][2][3].
PF-04217903 methanesulfonate is a selective ATP-competitive c-Met inhibitor with IC50 of 4.8 nM, susceptible to oncogenic mutations (no activity to Y1230C mutant).IC50 value: 4.8 nM [1]Target: c-Metin vitro: Being more selective than staurosporine or PF-02341066, PF-04217903 displays >1000-fold selectivity for c-Met over a panel of 208 kinases, although more susceptible to oncogenic mutations of c-Met that attenuate potency than PF-02341066. In addition to WT c-Met, PF-04217903 displays similar potency to inhibit the activity of c-Met-H1094R, c-Met-R988C, and c-Met-T1010I with IC50 of 3.1 nM, 6.4 nM, and 6.7 nM, respectively, but has no inhibitory activity against c-Met-Y1230C with IC50 of >10 μM [1]. PF-04217903 in combination with sunitinib significantly inhibits endothelial cells, but not the tumor cells B16F1, Tib6, EL4, and LLC [2] PF-04217903 significantly inhibits the clonogenic growth of LXFA 526L and LXFA 1647L with IC50 values of 16 nM, and 13 nM, respectively, yielding an additive effect when in combination with cetuximab [3]. in vivo: Although unable to inhibit tumor growth in the sunitinib-sensitive B16F1 and Tib6 tumor models, the combination of PF-04217903 and sunitinib significantly inhibits tumor growth in sunitinib-resistant EL4, and LLC tumor models compared with sunitinib or PF-04217903 alone by significantly blocking vascular expansion, indicating a functional role for HGF/c-Met axis in the sunitinib-resistant tumors [2].
AG-1024 (Tyrphostin) inhibits IGF-1R autophosphorylation with IC50 of 7 μM, less potent to IR with IC50 of 57 μM.IC50 value: 7 uM (IGF-1R autophosphorylation); 57 uM (IR) [1]Target: IGF-1R; IRin vitro: AG-1024 blocks the IGF-1 receptor and IR autophosphorylation with IC50 of 7 μM and 57 μM, respectively. AG-1024 also inhibits the receptor tyrosine kinase activity towards exogenous substrates (TKA) with IC50 values of 18 μM and 80 μM, respectively [1]. Human breast cancer cell line MCF-7 exposure to Tyrphostin AG 1024 inhibited proliferation and induced apoptosis in a time-dependent manner, and the degree of growth inhibition for IC20 plus irradiation (4 Gy) was up to 50% compared to the control. Examination of Tyrphostin AG 1024 effects on radiation response demonstrated a marked enhancement in radiosensitivity and amplification of radiation-induced apoptosis [2]. AG-1024 significantly inhibits melanoma cell proliferation with an IC50 of <50 nM in the absence of serum, by blocking MAPK/ERK2 signaling, subsequently rapidly inducing pRb dephosphorylation and activation, and eventually the formation of growth suppressive pRb-E2F complexes [3].in vivo: Administration of AG-1024 at a dose of 30 μg for 10 days significantly inhibits the tumor growth of Ba/F3-p210 xenograft in mice [4].
MET kinase-IN-4 is an orally active Met kinase inhibitor. MET kinase-IN-4 has potent Met kinase inhibitory activity with an IC50 value of 1.9 nM. MET kinase-IN-4 can be used for the research of cancer[1].
SU5208 inhibits vascular endothelial growth factor receptor-2 (VEGFR2)[1].
HG-7-85-01 is a type II ATP competitive inhibitor of wild-type and gatekeeper mutations forms of Bcr-Abl, PDGFRα, Kit, and Src kinases. HG-7-85-01 inhibits T315I mutant Bcr-Abl kinase, KDR and RET with IC50s of 3 nM, 20 nM and 30 nM, and is only weak or no inhibition of other kinases (IC50>2 μM). HG-7-85-01 inhibits the cell proliferation, which is mediated by the induction of apoptosis, and inhibition of cell-cycle progression[1].
Afatinib (BIBW 2992) oxalate is an orally active, potent and irreversible dual specificity inhibitor of ErbB family (EGFR and HER2), with IC50 values of 0.5 nM, 0.4 nM, 10 nM and 14 nM for EGFRwt, EGFRL858R, EGFRL858R/T790M and HER2, respectively. Afatinib oxalate can be used for the research of esophageal squamous cell carcinoma (ESCC), non-small cell lung cancer (NSCLC) and gastric cancer[1][2][3][4].
Piceatannol is a selective inhibitor of protein tyrosine kinase Syk. It could inhibit ICa,L, Ito, IKr, Ca2+ transients and Na+-Ca2+ exchange except IK1. Shows multiple biological activities such as anti-inflammatory, antiproliferative and immunomodulatory effects.In vitro: The treatment of human myeloid cells with piceatannol suppressed TNF-induced DNA binding activity of NF-κB. The effect of piceatannol was not restricted to myeloid cells, as TNF-induced NF-κB activation was also suppressed in lymphocyte and epithelial cells. Piceatannol also inhibited NF-κB activated by H2O2, PMA, LPS, okadaic acid, and ceramide. [1]
ALK-IN-9 (compound 40) is a potent ALK inhibitor. ALK-IN-9 inhibits cell proliferation with IC50s of <0.2 nM, <0.2 nM, 0.2 nM for Ba/F3-EML4-ALK, KM 12 (TPM3-TRKA), KG-l cell (OP2-FGFR1), respectively[1].
SU11652 is a potent receptor tyrosine kinase (RTK) inhibitor. SU11652 also inhibits several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit. SU11652 can be uesd for spontaneous cancers expressing Kit mutations research[1].
Henatinib is an orally active small-molecule multikinase inhibitor that has demonstrated broad and potent antitumor activities. Henatinib inhibits the activity of VEGFR-2, c-kit, PDGFR with IC50 values of 0.6 nM, 3.3 nM and 41.5 nM, respectively. Henatinib significantly inhibits VEGFR-2 phosphorylation and its downstream signal pathway in human umbilical vein endothelial cells (HUVECs)[1].
Insulin(human) is a peptide hormone that regulates the level of sugar (glucose) in the blood and that is produced by the beta cells of the pancreatic islets.
FAK-IN-8 (compound 5h) is a FAK inhibitor (IC50=5.32 µM). FAK-IN-8 has good anti-proliferative activity and can be used in cancer research[1].
CSF1R-IN-10 (Compound 48) is a CSF-1R inhibitor with an IC50 of 0.005 μM[1].
TL-895 is a potent, orally active, ATP-competitive, and highly selective irreversible BTK inhibitor with an IC50 and a Ki of 1.5 nM and 11.9 nM, respectively[1]. TL-895 is used be for JAKi-relapsed/refractory myelofibrosis, acute myeloid leukemia, COVID-19 and cancer research[2][3][4].
PPY-A is a potent T315I mutant and wild-type Abl kinases inhibitor with IC50s of 9 and 20 nM, respectively. PPY-A inhibits Ba⁄F3 cells transformed with wild-type Abl and Abl T315I mutantl with IC50s of 390 and 180 nM, respectively. PPY-A can be used for the research of chronic myeloid leukemia (CML)[1].
Ertumaxomab (Anti-Human CD22 Recombinant Antibody) is a bispecific antibody targeting HER2/neu and CD3. Ertumaxomab activates Fcγ type I/III-receptors, forming a tri-cell complex among tumour cell, T cell and accessory cell. Ertumaxomab has been used to research breast cancer[1].
WEHI-345 (analog) is a Src inhibitor, extracted from patent WO/2012003544A1, compound example 71.Target:SrcWEHI-345 (analog) is a protein kinase inhibitor. A family of proto-oncogenic TPKs referred to herein as SFKs (Src family kinases) have provided researchers with a better understanding of the mechanism of cancer as a disease state where normally healthy cellular signalling is disrupted.
Apatinib is a highly selective VEGFR2 inhibitor with an IC50 of 1 nM. Apatinib also potently suppresses the activities of Ret, c-Kit and c-Src with IC50s of 13, 429 and 530 nM, respectively.
Chrysotoxine is a dual inhibitor of Src/Akt. Chrysotoxine suppresses cancer stem cells (CSCs) phenotypes by down-regulating Src/Akt signaling. Chrysotoxine reduces cell viability and increases apoptosis level in H460 and H23 cells instead of non-tumor cell lines. Chrysotoxine shows rapid excretion and low bioavailability in rats. Chrysotoxine is used in cancer research[1][2].
EGFR mutant-IN-2 (Compound D51) is an EGFR mutant inhibitor. EGFR mutant-IN-2 inhibits the EGFRL858R/T790M/C797S mutant with an IC50 value of 14 nM. EGFR mutant-IN-2 inhibits the EGFRdel19/T790M/C797S mutant with an IC50 value of 62 nM. EGFR mutant-IN-2 has favorable PK parameters, safety properties, in vivo stability, and antitumor activity[1].
Gilteritinib-d8 is deuterium labeled Gilteritinib. Gilteritinib (ASP2215) is a potent and ATP-competitive FLT3/AXL inhibitor with IC50s of 0.29 nM/0.73 nM, respectively.
Radotinib-d6 is deuterium labeled Radotinib.
TL13-22 is a negative control for TL13-12 (HY-122582) and a potent ALK inhibitor with an IC50 of 0.54 nM. TL13-22 does not degrade ALK in cells[1].
JCN037 (JGK037) is non-covalent and BBB-penetrant EGFR tyrosine kinase inhibitor, with IC50 values of 2.49 nM, 3.95 nM, 4.48 nM for EGFR, p-wtEGFR and pEGFRvⅢ, respectively[1].
SCR-1481B1 (c-Met inhibitor 2) is a potent compound that has activity against cancers dependent upon Met activation and also has activity against cancers as a VEGFR inhibitor.
5'-Fluoroindirubinoxime (5’-FIO, compound 13), an Indirubin (HY-N0117) derivative, is a potent FLT3 inhibitor, with an IC50 of 15 nM[1].