ENMD-2076 Tartrate is a multi-targeted kinase inhibitor with IC50s of 1.86, 14, 58.2, 15.9, 92.7, 70.8, 56.4 nM for Aurora A, Flt3, KDR/VEGFR2, Flt4/VEGFR3, FGFR1, FGFR2, Src, PDGFRα, respectively.
Dacomitinib is a specific and irreversible inhibitor of the ERBB family of kinases with IC50s of 6 nM, 45.7 nM and 73.7 nM for EGFR, ERBB2, and ERBB4, respectively.
Ibrutinib dimer is a Dimer of Ibrutinib. Ibrutinib dimer is an impurity of Ibrutinib[1]. Ibrutinib is a selective, irreversible Btk inhibitor with an IC50 of 0.5 nM[2].
Tandutinib (MLN518, CT53518) is a potent FLT3 antagonist with IC50 of 0.22 μM, also inhibits PDGFR and c-Kit, 15 to 20-fold higher potency for FLT3 versus CSF-1R and >100-fold selectivity for the same target versus FGFR, EGFR and KDR. IC50 value: 0.22 uM [1]Target: Flt3; PDGFRβ; c-Kitin vitro: Tandutinib has little activity against EGFR, FGFR, KDR, InsR, Src, Abl, PKC, PKA and MAPKs. Tandutinib inhibits IL-3-independent cell growth and FLT3-ITD autophosphorylation with an IC50 of 10-100 nM. Tandutinib also inhibits the proliferation of human leukemia Ba/F3 cells containing FLT3-ITD mutations with IC50 values of 10-30 nM, and the FLT3-ITD-positive Molm-13 and Molm-14 cells with an IC50 of 10 nM. In FLT3-ITD-positive Molm-14 cells but not the FLT3-ITD-negative THP-1 cells, Tandutinib treatment leads to significant apoptosis by 51% and 78% at 24 and 96 hours, respectively, due to specific FLT3 inhibition [1]. Tandutinib preferentially inhibits the growth of blast colonies from FLT3 ITD-positive compared with ITD-negative patients with AML, without affecting colony formation by normal human progenitor cells [2].in vivo: Oral administration of Tandutinib at 60 mg/kg bid significantly increases the survival in mice bearing Ba/F3 cells expressing W51 FLT3-ITD mutant, and gives a significant reduction in mortality in a mouse bone marrow transplantation model [1]. Tandutinib treatment at 180 mg/kg twice daily has mild toxicity toward normal hematopoiesis, however, it is a dose at which Tandutinib is effective in treating FLT3 ITD-positive leukemia in mice [2].
Zeteletinib (BOS-172738) shows selective inhibitory activity against RET, PDGFR, KIT, NTRK and FLT3 kinases. Zeteletinib has antitumor activity[1].
PDZ1i (113B7) is a specific inhibitor of MDA-9/Syntenin activity that inhibits MDA-9/Syntenin binding to EGFRvIII; selectively binds with micromolar affinity to the PDZ1 domain of MDA-9/Syntenin, with no affinity for PDZ2 domain of MDA-9/Syntenin; reduces invasion gains in GBM cells following radiation, inhibits crucial GBM signaling involving FAK and mutant EGFR, EGFRvIII, and abrogated gains in secreted proteases, MMP-2 and MMP-9, following radiation; results in smaller, less invasive tumors and enhanced survival in an in vivo glioma model.
Zalutumumab is a high affinity, completely human IgG1 monoclonal antibody targeting EGFR. Zalutumumab binds to domain III of the EGF receptor and acts by blocking the binding of EGF and by sterically interfering with the active conformation of the receptor. Zalutumumab binds with IgG and its Fab fragment with EC50s of 7 and 19 nM, respectively. Zalutumumab can be used for the research of cancer[1][2][3].
PKA-IN-1 is a potent and selective cyclic AMP-dependent protein kinase (PKA) catalytic subunit (cAK) inhibitor with an IC50 of 0.03 μM[1].
Barzolvolimab (CDX 0159) is a humanized anti-KIT IgG1 monoclonal antibody. Barzolvolimab specificity and potently inhibits KIT activation by SCF. Barzolvolimab can reduce skin mast cells and disease activity in chronic inducible urticaria[1].
GSK143 is an orally active and highly selective spleen tyrosine kinase (SYK) inhibitor with a pIC50 of 7.5. GSK143 inhibits phosphorylated Erk (pErk: pIC50=7.1)[1]. GSK143 reduces inflammation and prevents recruitment of immune cells in the intestinal muscularis in mice[2][3].
Pertuzumab (PBS), a humanized monoclonal antibody, is a HER2 dimerization inhibitor for the treatment of metastatic HER2-positive breast cancer.
H-89 is a potent inhibitor of cyclic AMP-dependent protein kinase (protein kinase A) with IC50 of 48 nM and has weak inhibition on PKG, PKC, Casein Kinase, and others kinases.
ASP3026 is a novel and selective inhibitor for ALK (anaplastic lymphoma kinase) with IC50 of 3.5 nM.
AG-13958 (AG-013958), a potent VEGFR tyrosine kinase inhibitor, is used for treatment of choroidal neovascularization associated with age-related macular degeneration (AMD)[1].
Iruplinalkib (WX-0593) is a potent, selective, and orally active inhibitor of ALK and ROS1 tyrosine kinase. Iruplinalkib (WX-0593) shows favorable safety and promising antitumor activity in advanced NSCLC with ALK or ROS1 rearrangement[1].
Vabametkib is a potent inhibitor of hepatocyte growth factor receptor (HGFR). Vabametkib inhibits Hs746T cells proliferation and inhibits c-Met with an IC50 value of 7 nM. Vabametkib can be used as an antineoplastic agent[1][2].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
NSC81111 is a potent and orally active EGFR-TK inhibitor with an IC50 of 0.15 nM. NSC81111 has anticaner effects[1].
Tivozanib hydrochloride hydrate is a potent and selective and orally active VEGFR tyrosine kinase inhibitor with IC50是of 0.21, 0.16, 0.24 nM for VEGFR-1, VEGFR-2, VEGFR-3, respectively. Tivozanib hydrochloride hydrate inhibits angiogenesis and vascular permeability in tumor tissues and shows antitumor activity. Tivozanib hydrochloride hydrate has the potential for the research of metastatic renal cell carcinoma (RCC) [1][2][3].
Futuximab is a chimeric monoclonal antibody targeting non-overlapping epitopes on EGFR. Futuximab has antineoplastic activity[1].
Picrasidine Q, an alkaloid component extracted from Angelica keiskei species, has the capacity of anti-cell transformation and anti-cancer. Picrasidine Q induces cell apoptosis and G1 phase arrest in human esophageal cancer cell lines, and directly inhibits FGFR2 kinase activity[1].
AT-533 is a potent Hsp90 and HSV inhibitor. AT-533 suppresses tumor growth and angiogenesis by blocking the HIF-1α/VEGF/VEGFR-2 signaling pathway. AT-533 also inhibits the activation of the downstream pathways, including Akt/mTOR/p70S6K, Erk1/2 and FAK. AT-533 inhibits the tube formation, cell migration, and invasion of human umbilical vein endothelial cells (HUVECs)[1][2][3].
FLT3-IN-16 is a potent FLT3 inhibitor with an IC50 of 1.1 μM. FLT3-IN-16 can be used for researching acute myeloid leukemia[1].
TAS0728 is a potent, selective, oral active, irreversible and covalent-binding HER2 inhibitor, binds to HER2 at C805, inhibits its kinase activity, with an IC50 of 13 nM. TAS0728 shows IC50s of 4.9, 8.5, 31, 65, 33, 25, 86 and 36 nM for BMX, HER4, BLK, EGFR, JAK3, SLK, LOK and human HER2, respectively. TAS0728 also inhibits the phosphorylation of HER2, HER3, and downstream effectors, shows no obvious effect on EGFR. Antitumor activity[1].
BMS-986142 is a potent and highly selective reversible inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 0.5 nM.
AZ-Dyrk1B-33 is a potent and selective Dyrk1B kinase inhibitor, with an IC50 of 7 nM[1].
Alectinib Hydrochloride (CH5424802 Hydrochloride) is a potent, selective, and orally available ALK inhibitor with IC50 of 1.9 nM, the dissociation constant (KD) value for ALK in an ATP-competitive manner is 2.4 nM using a competition-bind assay.
BMS-935177 is a potent and selective reversible inhibitor of Bruton’s tyrosine kinase (Btk) with an IC50 of 3 nM.
J-1048 is an activin receptor-like kinase 5 (ALK5) inhibitor. J-1048 can inhibit TAA-induced liver fibrosis in mice by explicitly blocking the TGF-β/Smad signaling pathway[1].
Enapotamab is an anti-AXL/UFO reference antibody. Enapotamab can be used to synthesis Bcl-xl inhibitor antibody-drug conjugates[1].