Angiogenesis

JH-XI-10-02 selectively degrades CDK8 (IC50: 159 nM) through proteasome, sparing CDK8 mRNA and CDK19.

DSPE-PEG2000-A7R is a PEG compound consisting of DSPE and a tumor vasculature-targeting peptide (A7R). A7R exhibits high affinity and specificity for VEGFR-2, a receptor that is overexpressed in various tumors.

EGFR-IN-43 (17c) is a potent EGFR inhibitor with ER antagonist action, tamoxifen/endoxifen+gefitinib linkage, and strong anticancer activity.

Anticanceragent 271 (compound 5C) exhibits antiproliferative activity against lung cancer (A549), colon cancer (Caco-2) cell lines, and human lung fibroblasts (WI38), with an IC50 value of 9.18 μM for A549 cells. This compound can downregulate PI3K and mTOR gene expression and is applicable in cancer research.

ML228 activates HIF pathway and VEGF, with EC50 of 1μM, effective in vitro.

JAK-2/3-IN-1 inhibits JAK-2/3 isoforms with sub-250 nM Ki; from US patent US8163732B2.

BTK inhibitor 19 is a highly selective, covalent BTK inhibitor ( IC 50 = 2.7 nM).

EGFR/COX-2-IN-1 is an EGFR/COX-2 inhibitor that effectively targets EGFRWT, EGFRT790M, COX-1, and COX-2 with IC50 values of 0.12, 0.076, 20.1, and 1.52 μM, respectively. It inhibits MCF-7, HT-29, and A-549 cells with IC50 values of 1.20, 5.14, and 14.81 μM, respectively. The compound induces apoptosis by upregulating Bax protein and downregulating Bcl-2 protein levels. Additionally, EGFR/COX-2-IN-1 significantly increases the proportion of cells in the G2/M phase in MCF-7 cells, demonstrating a broad-spectrum antitumor effect.

Tyrosine Protein Kinase JAK 2 (Phospho-Tyr8, 9) is a peptide derived from mouse JAK2, specifically composed of amino acids 475 to 491.

Varlitinib Tosylate is a selective and potent inhibitor of ErbB1(EGFR) and ErbB2(HER2).

TYD-68 is a potent and selective CRBN-recruiting TYK2 PROTAC degrader, with a DC50 value of 0.42 nM. This compound effectively inhibits IL-12 and IFN-α-induced phosphorylation of STAT4 and STAT1, thereby blocking TYK2-dependent signaling pathways. TYD-68 is applicable in psoriasis research.

Lewis Y tetrasaccharide, a derivative of Lewis X, is an antigen linked to ovarian cancer metastasis and bad prognosis.

BW710 is an orally active inhibitor specifically targeting fibroblast growth factor receptor 2 (FGFR2). It effectively inhibits the proliferation of BaF3-FGFR2 cells with an IC50 value of 2.8 nM. BW710 completely suppresses FGFR2 enzymatic activity and demonstrates selectivity among 75 tyrosine kinases, including FGFR1, FGFR3, and FGFR4, at a 1 μM concentration. Additionally, BW710 impedes FGFR2 signaling and selectively inhibits the proliferation of cancer cells driven by FGFR2. It exhibits promising pharmacokinetic properties, with an oral bioavailability of 29% in mice.

SIAIS178 is a potent and selective degrader of BCR-ABL based on PROTAC technology (IC50 of 24 nM).

VnP-16 enhances bone formation by stimulating the differentiation and activity of osteoblasts via direct β1 integrin engagement, which subsequently activates

Amuvatinib HCl (MP470 HCl) is a multi-targeted oral tyrosine kinase inhibitor and hinders RAD51-mediated DNA repair, exhibiting anticancer properties.

Antifibrotic agent 1 is an orally active medication designed to treat idiopathic pulmonary fibrosis (IPF). It effectively mitigates IPF-related processes, including TGF-β-induced epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transition (FMT), as well as profibrotic M2 polarization. Antifibrotic agent 1 selectively inhibits CSF-1R, PDGFR-α, and Src family kinases (SFKs), while sparing VEGFR, FGFR, and Abl to minimize off-target toxicity. In a bleomycin (BLM)-induced pulmonary fibrosis mouse model, it demonstrates strong antifibrotic activity.

Src Inhibitor4 (Compound 18) is a derivative of KX-01 and functions as a Src inhibitor. It effectively disrupts tumor cells, damages microtubules, and induces cell cycle arrest, apoptosis, and immunogenic cell death. After introducing phenol or aniline functional groups, Src Inhibitor4 serves as a payload conjugation site for antibody-drug conjugates, showcasing antitumor activity.

PLM-101 is an anticancer compound orally active against acute myeloid leukemia by targeting FLT3 and RET.

Potent EGFR & HER2 degrader; DC50 of 39.2 nM in OVCAR8, 736 nM in HeLa; has lapatinib, VHL ligand; inhibits HER2+ breast cancer (IC50=102 nM for SKBr3).

Multi-kinase-IN-6 (compound 10e) is a multikinase inhibitor that effectively impedes the activity of TrkA, ALK2, c-KIT, EGFR, PIM1, CK2α, CHK1, and CDK2.

EGFR/BRAFV600E-IN-4 (Compound 10f) is a dual inhibitor of EGFR and BRAFV600E, with IC50 values of 61 nM and 43 nM, respectively. It halts the cell cycle, induces apoptosis in both early and late stages, and inhibits cancer cell growth in vitro, showing broad-spectrum anticancer activity.

Pomalidomide-C5-Dovitinib (compound 2) is a PROTAC that links Pomalidomide and Dovitinib via a CRBN connector, exhibiting potent antiproliferative activity in

MS9427: PROTAC EGFR degrader, 7.1 nM (WT), 4.3 nM (L858R); targets mutant via UPS and autophagy; inhibits NSCLC cell growth; anticancer research.

VSLRGDTRG acetate is a synthetic peptide of the RGD motif from cadherin17 (CDH17), capable of binding to α2β1 integrin and activating its signaling pathways. It facilitates the high-affinity conformational change of β1 integrin via the RGD motif, enhancing cell adhesion and phosphorylation of FAK and ERK1/2, thereby promoting tumor proliferation and metastasis. VSLRGDTRG acetate is applicable in research on cancers expressing CDH17, such as colon and pancreatic cancers.

Bevasiranib sodium, a siRNA, silences genes for VEGF, key in CNV pathogenesis and wet AMD precursor.

OK2, a specific inhibitor of the CCN2/EGFR interaction, effectively disrupts this interaction by binding to the CT domain of CCN2.

Axltide mimics mouse Insulin receptor substrate 1, amino acids 979-989 with sequence KKSRGDYMTMQIG.

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,

BTK degrader-1 (compound 1), a bifunctional degrader of Bruton's tyrosine kinase (BTK), demonstrates the capability to be conjugated with CD79b and exhibits anti-tumor effects [1].