Cancer Targeted Therapy

hsa-miR-3680-3p inhibitors are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA inhibitors have full-length nucleotide 2'-methoxy modification. The miRNA inhibitors strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning.

FGFR-IN-29 is an orally active pan-FGFR inhibitor that suppresses the kinase activities of FGFR1, FGFR2, FGFR3, and FGFR4. FGFR-IN-29 blocks the intracellular phosphorylation process of FGFR and arrests downstream tumor cell proliferation signaling. FGFR-IN-29 inhibits tumor growth in solid tumor xenograft mouse models. FGFR-IN-29 is applicable for cancer-related research.

The emergence of mutations in the BCR::ABL1 kinase domain (KD) impairs Imatinib Mesylate (HY-50946) binding capacity, thus contributing to Imatinib Mesylate resistance. Identification of these mutations is important for treatment decisions and precision medicine in chronic myeloid leukaemia (CML). ABL1 T315I Recombinant Human Active Protein Kinase is a recombinant ABL1 T315I protein that can be used to study ABL1 T315I-related functions.

25S-Anguivioside XV (Compound 8) is a steroidal glycoside. 25S-Anguivioside XV is isolated from the unripe berries of Solanum nigrum L. 25S-Anguivioside XV inhibits LPS-induced NO production with an IC₅₀ of 49.35 μM. 25S-Anguivioside XV exhibits antiproliferative activity against hepatoma cells.

hsa-miR-15b-3p antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

hsa-miR-4301 antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

hsa-miR-520e-5p inhibitors are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA inhibitors have full-length nucleotide 2'-methoxy modification. The miRNA inhibitors strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning.

hsa-miR-6829-3p antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

mmu-miR-21c antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

mmu-miR-669g antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

mmu-miR-7670-3p antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.

PI3K/mTOR Inhibitor-5 (compound 19a) is a potent and dual PI3K and mTOR inhibitor, with IC₅₀ values of 86.9 nM and 14.6 nM, respectively.

S2/IAPinh is a conjugate, which consist of an inhibitor for the apoptosis protein inhibitor (IAPinh) and a ligand for sigma 2 SW43. S2/IAPinh exhibits an anti-proliferative and apoptotic-inducing effect through degradation of the cellular inhibitor for apoptosis protein (clAP-1).

EGFR/Akt-IN-1 (compound 17) is a potent inhibitor of EGFR/Akt, with the IC₅₀s of 12.89 μM and 10.88 μM in A549 cells, respectively. EGFR/Akt-IN-1 arrestes the cell cycle at the S phase.

IBPR002 is an inhibitor of Aurora kinase A and Aurora kinase B, with IC₅₀ values of 41 nM and 17 nM, respectively. IBPR002 disrupts the nucleation and bundling of kinetochore microtubules, impairs the bipolarity of mitotic spindles, and promotes the binding of non-phosphorylated hepatoma up-regulated protein (HURP) to microtubules derived from the mother centrosome. IBPR002 reduces tumorigenesis levels in a colorectal cancer xenograft model using athymic nude mice. IBPR002 is applicable for research related to colorectal cancer.

Antitumor agent-195 (compound 16c) is a dual targeting agent of STAT3 and NQO1. Antitumor agent-195 significantly inhibits phosphorylation of STAT3 at Tyr705 at a concentration of 1 μM and effectively induce Apoptosis in MDAMB-231 and MDA-MB-468 breast cancer cells. Antitumor agent-195 as a NQO1 substrate strongly increases ROS generation and causes severe DNA damage in a dose-dependent manner. Antitumor agent-195 shows encouraging anti-tumor efficacy in the MDA-MB-231 xenograft model.

RET-IN-2 is a selective RET inhibitor with an IC₅₀ of 61.2 nM. RET-IN-2 inhibits the phosphorylation of RET and its downstream STAT3 and AKT proteins in BaF3/CCDC6-RET cells. RET-IN-2 inhibits the proliferation of RET fusion-positive cells. RET-IN-2 can be used for cancer-related research.

Biotin-PEG36-acid is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs.

XYD224 is a selective BRD9 PROTAC degrader with a DC₅₀ of 7.3 nM. XYD224 inhibits the proliferation of acute myeloid leukemia cells. XYD224 suppresses tumor growth in xenograft models. XYD224 is applicable for the research of acute myeloid leukemia (AML).

hsa-miR-4520-2-3p antagomirs are chemically-modified oligonucleotides that hybridize with mature miRNAs. The miRNA antagomirs have 2 phosphorothioates at the 5' end, 4 phosphorothioates at the 3' end, 1 cholesterol group at the 3' end, and full-length nucleotide 2'-methoxy modification. The miRNA antagomirs strongly compete with mature miRNAs to prevent the complementary pairing of miRNAs and their target genes, thereby inhibiting miRNAs from functioning. Stability of miRNA antagomirs appears to be significantly higher than miRNA inhibitors, they exhibits enhanced cellular uptake, stability and regulatory activity in vivo.