Angiogenesis

VEGFR-2-IN-36 (compound 15) serves as a potent VEGFR-2 inhibitor, exhibiting an IC50 value of 0.067 μM, and acts as an apoptosis inducer with demonstrated

Mal-VC-PAB-(N-Me-amide-C3)-ADU-S100 triethylamine: an ISAC with anti-HER2, STING agonist ADU-S100, linker; for cancer research.

DSPE-PEG1000-A7R is a PEG compound consisting of DSPE and the tumor vasculature-targeting peptide (A7R). A7R exhibits high affinity and specificity for VEGFR-2, which is overexpressed in various tumors.

Abl Cytosolic Substrate is a substrate for Abelson tyrosine kinase (Abl ).

PROTAC VEGFR-2 degrader-1 shows minimal VEGFR-2 inhibition & low anti-proliferative effect on EA.hy926 cells.

Potent CDK inhibitor 3-Methylthienyl-carbonyl-JNJ-7706621, IC50: CDK1=6.4nM, CDK2=2nM, GSK-3=0.041μM; moderate on CDK4/VEGF-R2/FGF-R2.

FAK-IN-1 is a FAK inhibitor with anticancer activities (WO2020231726 (Example 27)).

EGFR-IN-162 (compound 20) is an effective EGFR inhibitor that enhances both early and late apoptosis (EGFR) as well as necrosis (necrosis). It shows potential for use in breast cancer research.

Potent BTK Degrader, IC50=5.1nM, CRBN-dependent, suppresses MCL; degrades Ibrutinib-resistant BTK, no kinases binding, reduces tumors in models.

EGFR-IN-144 (Compound 4B) inhibits EGFR (IC50=0.639 µg/mL) and tubulin polymerization (IC50=7.339 µg/mL). It exhibits cytotoxicity in various cancer cells with a GI50 at the nanomolar level. EGFR-IN-144 reduces the expression of mTOR, TNF-α, and IL-6, causes G1/S phase cell cycle arrest, and induces apoptosis.

AZ14240475 is a potent, selective, brain-penetrant inhibitor of EGFREx20Ins mutants (EGFREx20Ins mutants) with a pIC50 of 7.6, playing a significant role in cancer research.

EGFR-IN-151 (Compound 10) inhibits EGFR and its downstream signaling pathways ERK/STAT3. It effectively suppresses the proliferation of various lung cancer cells, with IC50 values of 11.7, 5.19, 7.32, and 1.53 μM for NCI-H1781, HCC827, NCI-H3255, and NCI-H1975, respectively. Additionally, EGFR-IN-151 hinders colony formation and cell migration in H1975, induces G1 phase cell cycle arrest, and triggers apoptosis in H1975 cells.

Gefitinib N-oxide hydrochloride is an N-oxide of EGFR inhibitor Gefitinib with IC50 of 2-37 nM.

BCPyr is a new candidate BTK degrader ( DC 50 = 800 nM).

PROTAC BTK Degrader-6 (Compound 15), with a DC50 of 3.18 nM, exhibits anti-inflammatory properties by inhibiting NF-κB activation and suppressing the expression

HSK205 is a dual FLT3 and haspin inhibitor, exhibiting potent antitumor activity [1], with an IC50 of 0.187 nM for FLT3.

CS-VIP 8 TFA is a selective allosteric inhibitor of the WDR5 protein (Ki= 0.008 μM). It induces a conformational change in the MLL1 complex, leading to the dissociation of MLL1 from the complex, thereby inhibiting the MLL1 histone methyltransferase activity and modulating HOX gene expression. CS-VIP 8 TFA shows potential for research in hematological disorders such as leukemia.

DSPE-PEG2000-GE11 is a PEG compound composed of DSPE and an EGFR-targeting peptide (GE11). GE11 is applicable for cancer cells that overexpress EGFR. DSPE-PEG2000-GE11 is utilized in drug delivery.

Si5-N14 is a key component of siloxane-linked lipid nanoparticles (SiLNP) with properties that enhance vascular repair and exhibit antitumor activity. In transgenic GFP mouse models, Si5-N14 mediates CRISPR-Cas9 editing. In Lewis lung carcinoma (LLC) tumor mouse models, it leads to the knockdown of vascular endothelial growth factor receptor 2 (VEGFR2), producing antitumor effects. Additionally, in mice with virus-induced lung injury, Si5-N14 facilitates the delivery of fibroblast growth factor-2 (FGF-2) mRNA, promoting vascular repair, oxygenation, and improved lung function. Si5-N14 shows potential for research in tumors, pneumonia, and cardiovascular diseases.

SNIPER(ABL)-049, a compound that conjugates Imatinib (ABL inhibitor) with Bestatin (IAP ligand) through a linker, effectively reduces BCR-ABL protein levels,