vegfr-2

CP-547632 is an orally available and potent, ATP-competitive dual inhibitor of VEGFR-2 and FGF kinase F with IC50s of 11 nM and 9 nM, respectively. CP-547632 is selective, with higher selectivity for VEGFR2 and bFGF than for EGFR, PDGFRβ and related tyrosine kinases (TKs). PDGFRβ and related tyrosine kinases (TKs) CP-547632 has antitumour activity.

JNJ-38158471 (CS-2660), a highly selective, orally available, well tolerated VEGFR2 inhibitor with IC50 of 40 nM, inhibits closely related tyrosine kinases such as Ret and Kit with IC50 of 180 nM and 500 nM.

5Z-7-Oxozeaenol (FR148083) is a potent, irreversible and selective inhibitor of transforming growth factor (TGF)-β-activated kinase 1 with IC50 of 8.1 nM for TAK1 and low activity against MEK1 with IC50 of 411 nM, it is also an inhibitor of VEGF-R2 with IC50 of 52 nM.

CGP60474 is an inhibitor of VEGFR-2 (IC50 = 84 nM) and an inhibitor of ATP-competitive PKC. CGP60474 is also a highly potent anti-endotoxemic agent and inhibits cyclin-dependent kinase (CDK) potently.

TIE-2/VEGFR-2 kinase-IN-5 (TIE-2 and VEGFR-2 tyrosine kinase receptor inhibitor) is a potent agent with anti-angiogenic activity, commonly used in biomedical research focused on angiogenesis.

VEGFR-2-IN-9 (KDR-in-4) is a potent KDR/VEGFR2 inhibitor with an IC50 of 7 nM, suitable for breast cancer research.

TIE-2/VEGFR-2 kinase-IN-1 is employed in the synthesis of TIE-2 and/or VEGFR-2 inhibitors for studying diseases associated with inappropriate angiogenesis [1].

CP-547632 hydrochloride is a well-tolerated and orally-bioavailable inhibitor of the VEGFR-2 and basic FGF kinases (IC50s: 11 nM and 9 nM) with antitumor efficacy.

Agerafenib hydrochloride, a highly potent inhibitor of BRAFV600E (Kd: 14 nM), demonstrates significant efficacy.

LXW7 is an octamer disulfide cyclic peptide and αvβ3 integrin ligand, acts as a potent and specific endothelial progenitor cells (EPCs) and endothelial cells (ECs) targeting ligand. LXW7 is a disulfide cyclic octa-peptide (cGRGDdvc) containing unnatural amino acids flanking both sides of the main functional motif.

VEGFR-2-IN-6 (WO 02/059110, example 64) is a potent inhibitor of VEGFR2, a crucial receptor involved in the regulation of angiogenesis [1].

VEGFR-2-IN-29 is a VEGFR2 inhibitor.

VEGFR-2/InhA-IN-1, a dual inhibitor based on pyrazole, targets InhA and VEGFR, exhibiting both anti-tuberculosis and anti-angiogenic properties. It demonstrates effective antibacterial activity against the Mycobacterium tuberculosis H37Rv strain (MIC = 6.25 μg/mL) and significantly suppresses VEGFR-2 activity (IC 50 = 15.27 nM).

VEGFR-2/AKT-IN-2 (Compound 5) is an inhibitor of VEGFR-2/AKT, with an IC50 of 0.061 μM for VEGFR in human liver cancer cells. It reduces total and phosphorylated AKT in cells, increases BAX and caspase-3 levels, and decreases Bcl-2, thereby inducing apoptosis. Additionally, VEGFR-2/AKT-IN-2 halts the cell cycle at the S phase and inhibits the growth of human liver cancer cells.

VEGFR-2/AURKA-IN-1 (compound 5e) is a thiazolidin-4-one derivative with antitumor activity against glioma (IC50: 6.43 μM in LN229 cells). This compound exhibits affinity for AURKA and VEGFR-2, acting as a potential ligand. VEGFR-2/AURKA-IN-1 induces DNA strand breaks, showcasing cytotoxicity and anticancer potential.

VEGFR-2/STAT-3-IN-1 (Compound 9f) is a dual inhibitor targeting VEGFR-2 with an IC50 of 26.3 nM and STAT-3 with an IC50 of 5.63 nM. It suppresses the proliferation of cancer cells PANC1 and PC3, with IC50 values of 0.14 and 0.10 µM, respectively, and induces apoptosis in PC3 cells.

VEGFR-2/P-gp-IN-1 is a derivative of Licochalcone A, functioning as an orally active inhibitor of VEGFR-2 (IC50= 0.885 μM) and P-glycoprotein (P-gp). It combats tumor proliferation and overcomes chemotherapy resistance by simultaneously inhibiting VEGFR-2 kinase activity and the P-gp drug efflux pump. This compound suppresses the phosphorylation of VEGFR-2 and proteins in the downstream PI3K/AKT signaling pathway, induces apoptosis, arrests cells in the S phase, and inhibits invasive migration. Additionally, VEGFR-2/P-gp-IN-1 demonstrates potent in vivo antitumor activity in HeLa/DDP cell xenograft models and is applicable in cervical cancer research.

VEGFR-2 ligand-1, a derivative of Sorafenib, acts as a ligand for vascular endothelial growth factor receptor 2 (VEGFR2). It binds to the ATP-binding pocket of VEGFR2, forming hydrophobic interactions and hydrogen bonds with key binding site residues. VEGFR-2 ligand-1 is useful for research into angiogenesis-related diseases.

VEGFR-2/c-Met/EGFR-IN-1 is an inhibitor targeting VEGFR-2, c-Met, and EGFR with IC50 values of 0.014 μM, 0.072 μM, and 0.94 μM, respectively. c-Met-IN-27 inhibits angiogenesis in the chick embryo chorioallantoic membrane (CAM) assay, demonstrating in vivo anti-angiogenic activity. c-Met-IN-27 is applicable for research related to angiogenesis.

VEGFR-2/c-Met/EGFR-IN-2 is an inhibitor targeting VEGFR-2, c-Met, and EGFR, with IC50 values of 0.32 μM, 0.021 μM, and 9.3 μM, respectively. Known as c-Met-IN-27, this compound inhibits the proliferation of cancer cells and demonstrates anti-angiogenic activity in vivo by suppressing neovascularization in the chick embryo chorioallantoic membrane (CAM) assay. It is applicable in research related to breast and lung cancers.

VEGFR-2/DHFR-IN-2 (compound 5b) is a dual inhibitor targeting VEGFR-2 and DHFR, with respective IC50 values of 0.623 μM and 9.085 μM. It demonstrates potent cytotoxicity against C26, HepG2, and MCF7 cancer cell lines, with IC50 values ranging from 3.59 μM to 8.38 μM. VEGFR-2/DHFR-IN-2 holds promise for cancer research [1].

VEGFR-2/DHFR-IN-1 (compound 8b) is a chemical inhibitor of VEGFR-2 and DHFR, with IC50 values of 0.384 μM and 7.881 μM, respectively. It possesses effective antibacterial activity against pathogens including Escherichia coli, Streptococcus faecalis, Salmonella enterica, MSSA, and MRSA, with MIC values ranging from 8 to 16 μg/mL. Additionally, it exhibits potent cytotoxicity against cancer cell lines C26, HepG2, and MCF7, with IC50 values between 2.97 and 7.12 μM, making it a valuable tool for cancer research [1].

VEGFR-2/BRAF-IN-1, a dual inhibitor of VEGFR-2 and BRAF kinases, demonstrates potent inhibitory activity with IC50 values of 0.049 µM for VEGFR-2, 0.063 µM for BRAF V600E, and 0.005 µM for BRAF WT. It effectively induces apoptosis and arrests the cell cycle primarily at the G1/S phase.

VEGFR-2/BRAF-IN-2, as a dual VEGFR-2 and BRAF kinase inhibitor, exhibits potent IC50 values of 0.111 µM, 0.089 µM, and 0.071 µM against VEGFR-2, BRAF V600E, and BRAF WT, respectively. This compound effectively induces apoptosis and predominantly arrests the cell cycle in the G1 phase.