Cancer Targeted Therapy

KRAS inhibitor-38 (Example 18) is a KRAS inhibitor that effectively suppresses the activity of KRAS G12C, KRAS G12D, and KRAS G12V in vivo.

rno-miR-543-3p 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.

Erythrabyssin II (EL-19) is a potent late-stage autophagy inhibitor that blocks the fusion of autophagosome and lysosome. Erythrabyssin II leads to the accumulation of autophagic substrates and does not impair lysosomal pH or lysosomal enzyme activity. Erythrabyssin II suppresses ovarian cancer organoid activity and induces apoptosis. Erythrabyssin II can be used for the study of ovarian cancer.

2’-Bromo-2’-deoxy-5-methyluridine 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.

E3 Ligase Ligand-linker Conjugate 92 is a conjugate of E3 ligase ligand and linker, consisting of Thalidomide (HY-14658) and the corresponding Linker. E3 Ligase Ligand-linker Conjugate 92 can serve as a Cereblon ligand to recruit CRBN protein and serve as a key intermediate for the synthesis of complete PROTAC molecules.

HBV/HDV-IN-2 (Compd 143) is a HBV, HDV and PD-1/PD-L1 inhibitor, with an EC₅₀ of 35 nM for T cell activation.

mmu-miR-6414 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-7646-5p 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.

Valproic acid-d₄ (sodium) is the deuterium labeled Valproic acid. Valproic acid (VPA; 2-Propylpentanoic Acid) is an HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium salt is used in the treatment of epilepsy, bipolar disorder and prevention of migraine headaches.

Alendronate (sodium hydrate) (Standard) is the analytical standard of Alendronate (sodium hydrate). This product is intended for research and analytical applications. Alendronate (sodium hydrate) is a farnesyl diphosphate synthase inhibitor with IC₅₀ of 460 nM.

Azido-PEG3-Ala-Boc is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs. Azido-PEG3-Ala-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.

VEGFR-2-IN-28 (compound 12c) is a potent VEGFR-2 inhibitor with IC₅₀ value of 0.83 µM. VEGFR-2-IN-28 induces apoptosis and has anticancer activity.

PROTAC c-Met degrader-5 is an orally active c-Met PROTAC degrader. PROTAC c-Met degrader-5 induces c-Met degradation via Cullin-CRBN, with a DC₅₀ value of 0.32 nM, and inhibits the phosphorylation of c-Met and its downstream signaling molecule STAT3. PROTAC c-Met degrader-5 inhibits cancer cell proliferation, migration and invasion, induces apoptosis, alters cell cycle distribution, and suppresses the growth of EBC-1 xenograft tumors. PROTAC c-Met degrader-5 can be used to study MET-driven cancers as well as Tepotinib (HY-14721)-resistant cancers harboring c-Met^D1228N and c-Met^Y1230H mutations.

hsa-miR-924 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-3968 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.

Azo-PROTAC-4C-cis is a BCR-ABL PROTAC degrader, and its degradation efficiency of BCR-ABL is much lower than that of its trans isomer Azo-PROTAC-4C-trans (HY-180983). Azo-PROTAC-4C-cis is the product of the conformational transformation of Azo-PROTAC-4C-trans under ultraviolet (UV) light irradiation. Azo-PROTAC-4C-cis can be converted into highly active Azo-PROTAC-4C-trans under visible light, thereby initiating protein degradation. Azo-PROTAC-4C-cis can be used for the study of myeloid leukemia.

Tubulin polymerization-IN-93 is a β-tubulin polymerization inhibitor. Tubulin polymerization-IN-93 disrupts the microtubule network structure. Tubulin polymerization-IN-93 activates the spindle assembly checkpoint and promotes Mitotic catastrophe. Tubulin polymerization-IN-93 activates the mitochondrial Apoptotic pathway. Tubulin polymerization-IN-93 exhibits anticancer activity against acute myeloid leukemia.

hsa-miR-302b-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-4520-2-3p 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.

hsa-miR-5682 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.