Cancer Targeted Therapy

hsa-miR-661 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-12187-3p 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-496a-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-7054-3p 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.

rno-miR-450b-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-3928-5p 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-501-5p 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.

hsa-miR-6784-3p 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.

mmu-miR-193a-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-6368 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-7231-5p 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.

MEK4 IN-4 is a MEK4 inhibitor (IC₅₀ = 0.041 μM) that inhibits the kinase catalytic activity of MEK4 via competitive blockade of ATP binding. MEK4 IN-4 can be used to investigate cell proliferative diseases and disorders associated with MEK4 activity, including cancer.

BTK-IN-32 (compound C2) is a potent inhibitor of BTK. BTK-IN-32 activates full-length BTK and smaller multidomain BTK fragments instead of the isolated kinase domain.

LSD1-IN-2 is a LSD1 inhibitor with an IC₅₀ of 0.5 μM. LSD1-IN-2 increases the levels of monomethylated and dimethylated histone H3 lysine 4 (H3K4me1/2) in cells. LSD1-IN-2 reactivates epigenetically silenced tumor suppressor genes. LSD1-IN-2 can be used in the research of colon cancer.

CK1δ-IN-10 (Compound 85) is the inhibitor for casein kinase 1 that inhibits CK1δ (CSNKID) with IC₅₀ of 0.255 μM.

PROTAC BRD2 BD1 Degrader-1 is a potent and selective BRD2 BD1 PROTAC degrader, with a DC₅₀ of 65 nM, an EC₅₀ of 423 nM, and a K_d of 69 nM against BRD2 BD1. PROTAC BRD2 BD1 Degrader-1 induces the formation of a ternary complex between the BET bromodomain and the VHL E3 ubiquitin ligase complex, triggering VCB-dependent degradation of the target bromodomain. PROTAC BRD2 BD1 Degrader-1 can be used in cancer research.

Pixantrone (BBR 2778 (free base)) hydrochloride, a mitoxantrone analog, is a topoisomerase II inhibitor and DNA intercalator, with anti-tumor activity.

EGFR-IN-187 (Compound 4d) is a selective EGFR inhibitor with an IC₅₀ of 25.41 μM. EGFR-IN-187 can cause cancer cells S amd G2/M phase arrest and induce apoptosis and autophagy. EGFR-IN-187 upregulates CCNE1, Bax, LC3B-II and P27 expression and downregulates CCNA1 and Bcl-2 levels. EGFR-IN-187 can be used for the research of cancer, such as lung cancer.

DBCO-PEG12-acid is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs. DBCO-PEG12-acid is a click chemistry reagent, it contains a DBCO group that can undergo strain-promoted alkyne-azide cycloaddition (SPAAC) with molecules containing Azide groups.

SynB1 is a cell-penetrating peptide with blood-brain barrier permeability, derived from the antimicrobial peptide Protegrin 1. SynB1 enhances the cellular uptake efficiency and cytoplasmic localization level of conjugated constructs. SynB1 can be used in studies related to rabies and glioblastoma.