autophosphorylation kinase

Quizartinib (AC220) is an inhibitor of FLT3 (Kd: 1.6 nM) and demonstrates high selectivity for FLT3 when tested against a panel of 227 additional kinases.

Prexasertib (LY2606368) is an inhibitor of checkpoint kinase 1 (chk1) with potential antineoplastic activity.

CGP77675 (ZINC1488120) is a potent and selective inhibitor of Src family kinase with IC50s of 5-20 and 40 nM for the phosphorylation of peptide substrates and autophosphorylation of purified Src. CGP77675 exhibits anticancer activity.

HNMPA is a membrane impermeable inhibitor of insulin receptor tyrosine kinase. HNMPA inhibits tyrosine and serine autophosphorylation by the human insulin receptor. HNMPA exhibits no effect on cyclic AMP-dependent protein kinase or protein kinase C activities.

AKN-028 is an orally active and potent FLT3 tyrosine kinase inhibitor ( IC 50 = 6 nM). AKN-028 causes dose-dependent inhibition of FLT3 autophosphorylation.

AST 487 (NVP-AST 487) is a RET kinase inhibitor, inhibiting RET autophosphorylation and activation of downstream effectors. It also can inhibit Flt-3.

RG13022 (Tyrphostin RG13022) is a tyrosine kinase inhibitor; inhibits the autophosphorylation reaction of the EGF receptor (IC50: 4 μM).

EGFR-IN-12 (EGFR Inhibitor) is a cell permeable and selective inhibitor of EGFR kinase (IC50: 21 nM) and blocks receptor autophosphorylation in cells.

GNE-9605 is a highly effective, specifical, and brain-penetrant LRRK2 inhibitor (IC50: 19 nM).

(Rac)-SAR131675 is an effective and specific VEGFR-3 inhibitor. It inhibited VEGFR-3 tyrosine kinase activity (IC50: 20 nmol L) and VEGFR-3 autophosphorylation (IC50: 45 nmol L) in HEK cells, respectively. SAR131675 is highly specific for VEGFR-3 versus 107 receptors, enzymes, ion channels, and 65 kinases. SAR131675 is a highly specific VEGFR-3-TK inhibitor with significant antitumoral and antimetastatic activities in vivo through inhibition of lymphangiogenesis and TAM invasion.

Erlotinib-13C6 (CP-358774-13C6) is a 13C-labeled Erlotinib. Erlotinib is a directly acting EGFR tyrosine kinase inhibitor, with an IC50 of 2 nM for human EGFR[1]. Erlotinib reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. Erlotinib is used for the treatment of non-small cell lung cancer[1].Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process[2]. [1]. Moyer JD, et al. Induction of apoptosis and cell cycle arrest by CP-358,774, an inhibitor of epidermal growth factor receptor tyrosine kinase. Cancer Res. 1997, 57(21), 4838-4848.[2]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.

IRE1α kinase-IN-1 is a highly selective IRE1α (ERN1) inhibitor, with an IC50 of 77 nM, displaying 100-fold selectivity over the IRE1β isoform. It inhibits ER stress-induced IRE1α oligomerization and autophosphorylation, as well as IRE1α RNase activity (IC50=80 nM).

Gefitinib impurity 1 is a compound derived from Gefitinib, a potent and selective EGFR tyrosine kinase inhibitor (IC 50 = 33 nM). This orally active compound selectively inhibits tumor cell growth stimulated by EGF (IC 50 = 54 nM) and inhibits EGFR autophosphorylation induced by EGF in tumor cells. Additionally, Gefitinib induces autophagy and exhibits antitumor activity.

Edicotinib, also known as JNJ-40346527, is a small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; FMS) with potential antineoplastic activity. FMS tyrosine kinase inhibitor JNJ-40346527 blocks the receptor-ligand interaction between FMS and its ligand CSF1, thereby preventing autophosphorylation of FMS. As a result, unphosphorylated FMS cannot activate FMS-mediated signaling pathways, thus potentially inhibiting cell proliferation in FMS-overexpressed tumor cells.

CEP-37440 is an effective and specific Dual FAK ALK inhibitor with IC50s of 120 nM(ALK cellular in 75% human plasma) and 2.3 nM (FAK).

Lestaurtinib (CEP 701) is an orally available and selective inhibitor of FMS-like tyrosine kinase-3 (FLT3, IC50: 0.9 nM), which inhibits FLT3 autophosphorylation in vitro.Lestaurtinib promotes the expression of c-MYC, inhibits the phosphorylation of RPTKs, and has high affinity for TrkA and JAK2. Lestaurtinib promotes c-MYC expression, inhibits phosphorylation of RPTKs, has a high affinity for TrkA and JAK2, induces apoptosis and cell growth arrest, and can be used to study leukemia.

BFH772, a structure analogue of BAW2881, is a potent and selective VEGF inhibitor. BFH772 is highly effective at targeting VEGFR2 kinase with an IC50 value of 3 nM. BFH772 inhibits the ligand induced autophosphorylation of RET, PDGFR, and KIT kinases, wit

ATH686 is an potent and selective Inhibitor of FLT3.

The pp60 (v-SRC) Autophosphorylation Site, Phosphorylated is a phosphorylated peptide derived from an EGFR substrate, used as a critical tool for quantifying phosphorylated substrates in the screening of EGFR Kinase inhibitors.

AG 1295, a selective inhibitor of platelet-derived growth factor receptor (PDGFR) tyrosine-kinase, effectively halts PDGFR autophosphorylation without impacting the autophosphorylation of the EGF receptor[1][2][3][4].

Gefitinib dihydrochloride is a potent, selective, orally active EGFR tyrosine kinase inhibitor (IC50: 33 nM). Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth with an IC50 value of 54 nM and blocks EGFR autophosphorylation in EGF-stimulated tumor cells. Gefitinib dihydrochloride induces autophagy and apoptosis, and can be used in studies of cancer-related diseases such as lung and breast cancer.

Dihydrogenistein is a derivative of Genistein -- a compound that exhibits specific inhibitory activity against tyrosine kinases including autophosphorylation of epidermal growth factor receptor kinase.

Tie2 Inhibitor 7 blocks Tie2 kinase activity with a Ki value of 1.3 μM.. It has been shown to inhibit angiopoietin 1-induced Tie2 autophosphorylation and downstream signaling with an IC50 value of 0.3 μM. This compound can prevent endothelial cell tube formation and aberrant vessel growth in a rat model of Matrigel-induced choroidal neovascularization.

Pirtobrutinib (LOXO-305) is an advanced BTK inhibitor that displays high selectivity and operates through a non-covalent mechanism. This compound effectively inhibits various BTK C481 substitution mutations, leading to tumor regression in BTK-dependent lymphoma tumors in mouse xenograft models. Furthermore, Pirtobrutinib exhibits remarkable selectivity for BTK, with more than a 300-fold difference compared to 370 other kinases tested. Notably, at a concentration of 1 μM, Pirtobrutinib demonstrates no significant inhibition of non-kinase off-targets.