Cancer Targeted Therapy

Pomalidomide-C16-azide is a PROTAC E3 ligase ligand-linker conjugate that can be used in studies related to PROTAC synthesis, such as serving as the E3+linker structure of PROTAC CDK9 degrader-13 (HY-184693).

α-Solanine (Standard) is the analytical standard of α-Solanine. This product is intended for research and analytical applications. α-solanine, a bioactive component and one of the major steroidal glycoalkaloids in Solanum nigrum, has been observed to inhibit growth and induce apoptosis in cancer cells.

DDR1-IN-11 (Compound 4) is an inhibitor of Discoidin domain receptor 1 (DDR1) with an IC₅₀ of 46.16 nM. DDR1-IN-11 can achieve an inhibition rate of 99.86% against Z-138 cells at a concentration of 10 μM, and it can be used in the research of acute myeloid leukemia (AML).

Ch-319 is a Triphenyltin (IV) carboxylate derivative. Ch-319 reduces androgen receptor expression, AKT and PRAS40 phosphorylation levels, and increases FOXO3a expression. Ch-319 increases Apoptosis. Ch-319 can be used in the research of prostate cancer.

hsa-miR-363-3p 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.

hsa-miR-4756-5p 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-670-5p 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-12193-3p 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-501-5p 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.

mmu-miR-7058-5p 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.

rno-miR-466b-2-3p 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.

N-(Azido-PEG4)-N-Boc-PEG4-Boc is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs. N-(Azido-PEG4)-N-Boc-PEG4-Boc is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. It can also undergo strain-promoted alkyne-azide cycloaddition (SPAAC) reactions with molecules containing DBCO or BCN groups.

Ulecaciclib is an orally activitive inhibitor of cyclin-dependent kinase (CDK), with K_i values of 0.62 μM (CDK2/Cyclin A), 0.2 nM (CDK4/Cyclin D1), 3 nM (CDK6/Cyclin D3), and 0.63 μM (CDK7/Cyclin H), respectively. Ulecaciclib can cross blood brain barrier and has good pharmacokinetic characteristics.

PROTAC TTK degrader-2 is a threonine tyrosine kinase (TTK) PROTAC degrader with a DC₅₀ of 3.1 nM in COLO-205 cells. PROTAC TTK degrader-2 induces proteasome-mediated degradation of TTK. It inhibits the proliferation of colorectal cancer cells. In colorectal cancer xenograft mouse models, PROTAC TTK degrader-2 mediates target degradation and exerts anticancer activity. PROTAC TTK degrader-2 can be used in colorectal cancer-related research.

ALK5-IN-25 (compound EX-02) is a potent ALK-5 inhibitor with an IC₅₀ ≤10 nM.ALK5-IN-25 also inhibits ALK-2 (selectivity ALK2/ALK5≤10). ALK5-IN-25 can be used for the research of cancer.

2′-Deoxy-8-(phenylmethoxy)guanosine is a purine nucleoside analog. Purine nucleoside analogs have broad antitumor activity targeting indolent lymphoid malignancies. Anticancer mechanisms in this process rely on inhibition of DNA synthesis, induction of apoptosis, etc.

ICMT-IN-51 (compound 43) is an inhibitor of ICMT (IC₅₀=0.55 μM).

aTAG 2139 (CFT-2139) is a bifunctional tag-targeted PROTAC-class degrader that induces the degradation of the MTH1 aTAG fusion protein by recruiting cereblon, with a DC₅₀ of 1.1 nM (in Jurkat T cells). aTAG 2139 is applicable to the research of CD19-positive cancers.

Puquitinib (XC-302 free base) is a multi-target inhibitor with the activity of inducing autophagy in nasopharyngeal carcinoma cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Puquitinib was able to inhibit the proliferation of CNE-2 cells, showing a dose-dependent antiproliferative effect. Puquitinib induced the formation of autophagosomes and autolysosomes in CNE-2 cells, which were observed by fluorescence microscopy and electron microscopy. Puquitinib promoted the formation of LC3-II and increased the expression of beclin 1, while reducing the level of p62. Puquitinib inhibited the PI3K/AKT/mTOR pathway by reducing the expression of p-AKT and p-mTOR. Puquitinib also induced apoptosis in CNE-2 cells, and when autophagy was inhibited, the apoptosis rate was reduced, which means that autophagy may interact with apoptosis to induce cell death.

hsa-miR-144-3p 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.