tyrosine autophosphorylation

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.

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.

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.

LY2457546 is a highly potent, orally bioavailable multi-target anti-angiogenic tyrosine kinase inhibitor. It shows strong inhibitory activity against multiple targets including VEGFR2, PDGFRβ, FLT-3, Tie-2, and Eph family receptors, and is applied in cancer research such as leukemia.

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

(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.

3-Hydroxy Midostaurin (CGP 52421), a PKC412 metabolite, inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC50 values of approximately 132 nM in culture medium and 9.8 μM in plasma. Although less selective, it shows greater cytotoxicity compared to PKC412[1].

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].

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.

Tandutinib (CT53518) (MLN518, CT53518), an effective FLT3 antagonist (IC50: 0.22 μM), can also inhibit c-Kit and PDGFR, 15-20 fold higher potency for FLT3 versus CSF-1R and >100-fold selectivity for the same target versus FGFR, EGFR, and KDR.

3-Hydroxy Midostaurin-D5 is a deuterium-labeled 3-Hydroxy Midostaurin (T12610L) which is a metabolite of PKC412. PKC412 effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation (IC50s: 132 nM and 9.8 μM in culture medium and plasma).

Sunitinib (SU 11248) glucuronate is a multi-target receptor tyrosine kinase inhibitor with IC50 values of 80 nM for VEGFR2 and 2 nM for PDGFRβ. As an ATP-competitive inhibitor, it effectively suppresses Ire1α phosphorylation by inhibiting autophosphorylation and subsequent RNase activation.

EphB4-IN-1 is a selective tyrosine kinase inhibitor of EphB4, exhibiting an IC50 value range of 0.16-0.30 μM. It binds to the ATP-binding site of EphB4 in the DFG-in conformation, creating four stable intermolecular hydrogen bonds. Additionally, EphB4-IN-1 inhibits kinases such as Src, Abl1, Lck, and EGFR and prevents the autophosphorylation of EphB4. This compound is applicable in cancer research, including studies on non-small cell lung cancer.

The compound effectively and directly inhibits JAK2 tyrosine kinase autophosphorylation and specifically inhibits ligand-dependent JAK2 activation. It has no cytotoxicity at 100 μM. A 16-hour treatment with compound (1 μM) decreases JAK2 tyrosine autophos

PD-161570 is a potent and ATP-competitive human FGF-1 receptor inhibitor with an IC50 of 39.9 nM and a Ki of 42 nM. It also inhibits the PDGFR, EGFR, and c-Src tyrosine kinases with IC50 values of 310 nM, 240 nM, and 44 nM, respectively.

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).

Erlotinib-13C6 is a 13C-labeled Erlotinib. Erlotinib (T0373) is a directly acting EGFR tyrosine kinase inhibitor, with an IC50 of 2 nM for human EGFR[1].

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.

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.

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

AKN-028 acetate, a novel tyrosine kinase (TK) inhibitor, is a potent, orally active FMS-like receptor tyrosine kinase 3 (FLT3) inhibitor with an IC50 value of 6 nM. It inhibits FLT3 autophosphorylation and induces a dose-dependent cytotoxic response (mean IC50 = 1 μM). AKN-028 acetate also induces apoptosis by activation of caspase 3 and can be used in acute myeloid leukemia (AML) research [1].

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.

The growth factors, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) play major roles in enhanced smooth muscle cells growth in rodent blood vessels after vascular injury. Tyrosine kinase inhibition has been shown to be effective in blocking tyrosine phosphorylation at the PDGF and bFGF receptors in cultured fibroblast and vascular smooth muscle cells which in turn inhibits their proliferation[1]. CGP 53716 is a specific PDGFR tyrosine kinase inhibitor on SMC (smooth muscle cell) proliferation and migration in vitro and in neointimal formationin vivo[3]. CGP 53716 inhibited serum-induced cell growth in RASMC (rat aortic smooth muscle cells). And it completely blocked PDGF-BB tyrosine receptor autophosphorylation in RASMC and 3T3 cells, PDGF-BB-induced phosphorylation of mitogen-activated protein kinase at 1 μM in RASMC and inhibited PDGF-BB-induced c-Fos protein expression at 1 μM in RASMC; consistent with inhibition of PDGF-BB-induced DNA synthesis. Further, CGP 53716 inhibited PDGF-BB-, bFGF- and EGF-induced DNA synthesis in a concentration-dependent manner in each cell line. And it showed a 2- to 4-fold selectivity for PDGF-BB-stimulated DNA synthesis over bFGF or EGF in RASMC or 3T3 cells[1]. CGP 53716 inhibited dose dependently tyrosine phosphorylation of both the known PDGFRs: the PDGFR-α and PDGFR-β. After rat carotid artery ballooning injuryin vivo, the migration of alpha-actin-positive cells on the luminal side of internal elastic lamina was decreased with 50 mg/kg/day of CGP 53716 from 38 ± 10 (control group) to 4 ± 2. Intima/media ratio was inhibited by 40% after 14 days in the CGP 53716-treated group (P=0.028) after rat aortic denudation[3].

Genistein Diglucuronide is a metabolite of Genistein which exhibits specific inhibitory activity against tyrosine kinases including autophosphorylation of epidermal growth factor receptor kinase.