Angiogénese

<p>JAK2 JH2 binder-1: potent, selective, Ki=37.1 nM, potential for studying myeloproliferative neoplasms.</p>

<p>EGFR-IN-147 (compound ID-5841161) is a potent EGFR inhibitor, demonstrating a 14% inhibition rate at a concentration of 1μM. It holds promise for cancer research applications.</p>

VEGFR-2-IN-65 (Compound 07) functions as a VEGFR-2 inhibitor. It forms hydrogen bonds with Cys180 and can inhibit tube formation in HUVECs.

<p>Milpecitinib (Compound 21a) is a potent and selective Janus tyrosine kinase (JAK) inhibitor with anti-inflammatory properties. It shows promise for research in cancer and inflammatory diseases.</p>

<p>CDD-1115 is a potent and selective BMPR2 inhibitor, with an IC50 of 1.8 nM and a Kiapp of 6.2 nM. It effectively suppresses gene expression mediated by bone morphogenetic proteins (BMPs). BMPs regulate cellular processes in various tissue types, such as the kidneys, skeletal muscle, heart, and reproductive organs, and can induce ectopic bone formation.</p>

<p>DA-0157 is an orally active inhibitor targeting EGFR and ALK, designed to overcome resistance mutations in non-small cell lung cancer (NSCLC). It effectively inhibits the proliferation of Ba/F3-EGFR Del19/T790M/C797S (IC50= 6.9 nM), Ba/F3-EGFR WT (IC50= 0.83 μM), Ba/F3-EML4-ALK-L1196M (IC50= 5.5 nM), and Ba/F3-EML4-ALK (IC50= 7.4 nM). Additionally, DA-0157 inhibits CYP2D6 with an IC50 of 5.26 μM and demonstrates antitumor activity in mouse models.</p>

TTT 3002: oral FLT3 inhibitor for AML research, blocks D835 mutations, potent at 0.2 nM IC50.

BTK-IN-34 (compound 9h) functions as a selective BTK inhibitor, exhibiting antiproliferative effects in RAMOS cells by specifically targeting pBTK (Tyr223) while sparing upstream proteins such as Lyn and Syk in the BCR signaling pathway [1].

<p>EGFR-IN-48: potent EGFR inhibitor, oral, IC50: 0.193-66.7 nM, blocks EGFR mutants &amp; BaF3/PC-9 cell proliferation.</p>

Tarloxotinib bromide (TH-4000) is an irreversible inhibitor of EGFR/HER2.

FAK inhibitor7, a potent FAK inhibitor, demonstrates an IC50 of 3.58 nM. This compound effectively inhibits downstream signaling cascades of FAK (such as Src and AKT), which leads to cell cycle arrest at the G0/G1 phase and induces cytotoxic autophagy in ovarian cancer cells. Additionally, FAK inhibitor7 has been shown to suppress tumor metastasis and growth in ovarian cancer mouse models.

<p>MK-8457 is a dual inhibitor of SYK and ZAP70, valuable for rheumatoid arthritis research [1].</p>

FAK-IN-2: potent oral FAK inhibitor, IC50 35 nM, reduces tumor growth, migration, and induces cell death.

ALK/PI3K/AKT-IN-1 (Compound 45) effectively inhibits the proliferation of cancer cell lines A549, H1975, and PC9, with IC50 values of 0.44, 0.83, and 1.51 μM, respectively. This compound enhances the expression of p21 and p27, and decreases the activity of CDK2 and p-Rb, causing cell cycle arrest at the G1 phase. It suppresses the ALK/PI3K/AKT signaling pathway, promotes mitochondrial membrane potential depolarization, and induces apoptosis in A549 cells. Furthermore, ALK/PI3K/AKT-IN-1 inhibits the formation and growth of A549 cell spheres.

JAK1/TYK2-IN-3, orally active, selectively inhibits TYK2 (IC50: 6 nM), JAK1 (37 nM), JAK2 (140 nM), JAK3 (362 nM), and has anti-inflammatory effects.

JAK2-IN-11 (Example 6) is a JAK2 kinase inhibitor with potent antitumor activity, exhibiting an IC50 of ≤10 nM against JH2 BIND WT/V617F. This compound effectively suppresses tumor growth.

Compound 26F: potent enzyme inhibitor (IC50=28.2nM), low cytotoxicity (IC50=3.32μM), induces dose-dependent apoptosis in MDA-MB-231, blocks G0/G1 phase.

Antiallergic agent-1, an Src family kinase inhibitor, is a new and valuable lead compound with potential as an anti-allergic agent.

E7090 succinate inhibits FGFR1, FGFR2, and FGFR3 with IC50: 0.71, 0.50, 1.2 nM; less so FGFR4 at 120 nM.

<p>Siphonaxanthin is a carotenoid found in green algae, known for targeting the death receptor 5 (DR5) on cancer cells to induce apoptosis. In human leukemia HL-60 cells, it increases DR5 expression, reduces Bcl-2 levels, and activates caspase-3. It also inhibits fibroblast growth factor receptor-1 (FGFR-1) signaling in endothelial cells. Siphonaxanthin suppresses the proliferation, migration, and tubular formation of human umbilical vein endothelial cells (HUVECs), as well as the growth of microvessels in rat aorta rings. Additionally, it has anti-inflammatory properties by blocking the translocation of high-affinity IgE receptors (FcεRI) to lipid rafts in mast cells. Siphonaxanthin shows potential for research into diseases such as cancer, diabetic retinopathy, and rheumatoid arthritis.</p>