Cancer Targeted Therapy

ISIS 5132 sodium scrambled negative control is the sequence scrambled negative control of ISIS 5132 sodium.

Anticancer agent 160 (Compound 6) is a natural product derived from Parthenium hysterophorus. Anticancer agent 160 is cytotoxic to HCT-116 cells, IC₅₀=5.0 μM.

ICT10336 is a hypoxia-responsive prodrug of ATR inhibitor, AZD6738 (HY-19323). ICT10336 is hypoxia-activated and specifically releases AZD6738 only in hypoxic conditions in vitro. This can inhibit ATR activation (T1989 and S428 phosphorylation) and subsequently abrogate HIF1a-mediated adaptation of hypoxic cancers cells, thus selectively inducing cell death in 2D and 3D cancer models. ICT10336 is a metabolic substrate of CYPOR activity.

VH032-NH-CO-CH2-NHBoc is a Boc-modified VH032 (HY-120217) that acts as a ligand for VHL to recruit von Hippel-Lindau (VHL) proteins. VH032-NH-CO-CH2-NHBoc will remove the Boc protection under acidic conditions, and connect with the target protein ligand through a linker to form a PROTAC molecule, which is a key intermediate for the synthesis of PROTAC based on VHL ligand.

Balsalazide-d₄ is deuterium labeled Balsalazide. Balsalazide could suppress colitis-associated carcinogenesis through modulation of IL-6/STAT3 pathway.

Acetic acid lead is a carboxylic acid and short-chain fatty acid (SCFAs). Magnesium acetate tetrahydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid lead exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid lead regulates energy metabolism. Acetic acid lead has anticancer activity against gastric cancer. Acetic acid lead induces writhing reaction and ulcerative colitis. Acetic acid lead can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain.

Ald-Ph-amido-PEG3-C1-Boc is an ADC linker, which belongs to a polyethylene glycol (PEG) linker.

hsa-miR-548au-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-6861-3p 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-3060-3p 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-6905-3p 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-8103 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.

HDAC6-IN-11 (Compound 9) is a selective HDAC6 inhibitor with the IC₅₀ value of 20.7 nM. HDAC6-IN-11 has more than 300-fold selectivity over HDAC other isoforms. HDAC6-IN-11 shows anti-proliferative activities against cancer cells.

3’-Deoxy-O6-methyl inosine 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.

CD38-IN-4 is a CD38 inhibitor. CD38-IN-4 inhibits CD38 hydrolase enzymatic activity through mixed inhibition kinetics, binding partially inside and partially outside the NAD⁺ catalytic pocket. CD38-IN-4 acts as a DNA-binding agent. CD38-IN-4 can be used for research on neuroblastoma.

Nonylbenzene-PEG5-OH is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs.

Trk-IN-6 shows excellent in vitro potency on a panel of TRK mutants (IC₅₀ = 0.2-0.7 nM).

m-PEG37-hydrazide is a PEG-based PROTAC linker can be used in the synthesis of PROTACs.

IRAK4-IN-13 (compound 21) is a potent and selective IRAK4 inhibitor with an IC₅₀ of 0.6 nM. IRAK4-IN-13 shows high metabolic clearance with human liver microsomes (HLM) intrinsic clearance is 96 µL/min/mg.

HDAC3/BRD4-IN-1 (compound 26n) is an inhibitor of HDAC3/BRD4 with an IC₅₀ of 8 nM for HDAC3 (IC₅₀s are 220 nM and 120 nM for HDAC1 and HDAC2, respectively). HDAC3/BRD4-IN-1 has anti-tumor and anti-proliferative effects by upregulating Ac-H3 and downregulating c-Myc. The half-life of HDAC3/BRD4-IN-1 in human liver microsomes is 29.36 min.