Cancer Targeted Therapy

mmu-miR-6999-3p 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.

rno-miR-327 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.

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 93 is a conjugate of E3 ligase ligand and linker, consisting of Thalidomide (HY-14658) and the corresponding Linker. E3 Ligase Ligand-linker Conjugate 93 can serve as a Cereblon ligand to recruit CRBN protein and serve as a key intermediate for the synthesis of complete PROTAC molecules.

PARP-1/2/7-IN-1 (compound 86) is a potent inhibitor of PARP-1/2/7, with the IC₅₀ of ＜ 10 nM.

PROTAC BRD4 Degrader-28 is a PROTAC degrader targeting BRD4, with a DC₅₀ of 5.4 nM for BRD4 in HEK293 cells. PROTAC BRD4 Degrader-28 binds to the CRBN E3 ubiquitin ligase, forms a ternary complex with BRD4, and thereby mediates the ubiquitination and proteasomal degradation of BRD4. PROTAC BRD4 Degrader-28 can be used in cancer research.

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.

HP1-IN-2 (Compound (R)-18) is a HP1/H3K9me3 interaction inhibitor with an IC₅₀ of 18.1 μM. HP1-IN-2 can be used for studying various cancers with overexpression of HP1.

OAT-4828 is an orally active ubiquitin-specific protease 7 (USP7) inhibitor with an IC₅₀ of 32 nM. OAT-4828 induces antileukemic activity in B-cell-derived non-Hodgkin's lymphoma models via inhibition of USP7. OAT-4828 is applicable to research related to chronic lymphocytic leukemia.

Rotundic acid (Standard) is the analytical standard of Rotundic acid (HY-N2217). This product is intended for research and analytical applications. Rotundic acid is an orally effective triterpenoid with a K_d value of 51.3 µM for PTP1B. Rotundic acid downregulates the AKT/mTOR pro-survival pathway and modulates the MAPK pathway. Rotundic acid induces cell cycle S-phase arrest, DNA damage and apoptosis; it inhibits migration, invasion, angiogenesis and proliferation of cancer cells. Rotundic acid improves leptin sensitivity, regulates gut microbiota and reduces cellular senescence. Rotundic acid can be used in research related to hepatocellular carcinoma, obesity, aging, acute lung injury and type 2 diabetes.

TJX7 is a recombinant antibody targeting CXCL13/BCA-1/BLC.

SM253 is an Hsp90 inhibitor that inhibits Hsp90-dependent protein folding. SM253 blocks chaperone function by binding to the N-middle linker region and the C-terminal M domain, reducing co-chaperone and client protein binding and activation. SM253 induces cancer cell apoptosis, activates caspase 3/7, causes cell cycle arrest and reduces cell proliferation, while decreasing Hsp90 client proteins such as AR, FKBP51, PSA, Cdk4, AKT, ERK, and p23, and reducing Hsp27/Hsp70 expression without inducing heat shock proteins. SM253 causes dose-dependent fibronectin loss in cells expressing LRP1. SM253 can be used for research on colon cancer, pancreatic cancer, and prostate cancer.

N-Desmethyl dosimertinib is the deuterium labeled N-Desmethyl dosimertinib.

(S)-PERK-IN-5 is the S-enantiomer of PERK-IN-5. (S)-PERK-IN-5 (example 39) is a PERK inhibitor, with an IC₅₀ of 0.101-0.250 μM.

Trastuzumab deruxtecan (DAR6) (T-DXd (DAR6); DS-8201 (DAR6); DS-8201a (DAR6)) is a low-drug-load derivative control preparation of Trastuzumab deruxtecan (HY-138298A) with a drug-to-antibody ratio (DAR) of 6. Trastuzumab deruxtecan (T-DXd; DS-8201a; DS-8201) is an anti-human epidermal growth factor receptor 2 (HER2) antibody-drug conjugate (ADC). Trastuzumab deruxtecan is composed of a humanized anti-HER2 antibody, an enzymatically cleavable peptide-linker, a topoisomerase I inhibitor (a toxin component of Dxd), and the drug-linker conjugate for ADC is Deruxtecan (HY-13631E). Trastuzumab deruxtecan can be used for the research of HER2-positive breast cancer and gastric cancer.

hsa-miR-3672 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-4774-5p 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-6732-5p 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-1249-5p 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-5121 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.