Lin28-let-7a antagonist 1 shows a clear antagonistic effect against the Lin28-let-7a interaction with an IC50 of 4.03 μM for Lin28A-let-7a-1 interaction.
PIN1 inhibitor 2 (compound 12) is a potent PIN1 inhibitor. PIN1 inhibitor 2 shows antitumor activity with an IC50 of 9.55 µM for MCF7 cells. PIN1 inhibitor 2 has the potential for the research of breast cancer[1].
RG-101 is a hepatocyte targeted N-acetylgalactosamine conjugated oligonucleotide that antagonises miR-122. miR-122 is an important host factor for hepatitis C virus (HCV) replication[1].
MIR96-IN-1 selectively inhibits biogenesis of microRNA-96, upregulating a protein target (FOXO1) and inducing apoptosis in cancer cells.Target: microRNA-96in vitro: MIR96-IN-1 inhibits biogenesis of its target precursor miRNA to varying extents : MIR96-IN-1 reduces the expression level of miR-96 by 90% at 40 μM. MIR96-IN-1 efficiently and selectively silences production of miR-96 at 40 μM while not affecting miR-182 or -183. Moreover, MIR96-IN-1 inhibits Drosha cleavage of pri-miR-96, as evidenced by an increase in the levels of pri-miR-96 and a reduction in levels of pre- and mature miR-96 in treated cells, as expected if MIR96-IN-1 binds to the Drosha site. [1]
Skullcapflavone I can be isolated from A. nallamalayana. Skullcapflavone I inhibits collagenase and elastase enzyme with IC50s of 106.74 μM and 186.70 μM. Skullcapflavone I has anticancer activities by down-regulating miR-23a[1].
Enoxacin-d8 (AT 2266-d8) is the deuterium labeled Enoxacin. Enoxacin (AT 2266), a fluoroquinolone, interferes with DNA replication and inhibits bacterial DNA gyrase (IC50=126 µg/ml) and topoisomerase IV (IC50=26.5 µg/ml). Enoxacin is a miRNA processing activator and enhances siRNA-mediated mRNA degradation and promotes the biogenesis of endogenous miRNAs. Enoxacin has potent activities against gram-positive and -negative bacteria. Enoxacin is a cancer-specific growth inhibitor that acts by enhancing TAR RNA-binding protein 2 (TRBP)-mediated microRNA processing[1][2][3][4].
TGP-377/421 (Targapre-miR-377/421) is a smalll molecule targets pre-miR-377 and inhibits its processing, binds to miR-377's Dicer processing site with Kd of 29 uM.TGP-377/421 inhibits the cellular biogenesis of miR-377 in HUVECs, reduced mature miR-377 levels in a dose-dependent fashion with IC50 of 5 uM, also inhibits miR-421.
Lademirsen (SAR339375; RG-012) is a highly specific antisense oligonucleotide (ASO) targeting miR-21. Lademirsen has the potential for Alport nephropathy research[1][2].
Miravirsen (SPC-3649), a β-d-oxy-locked nucleic acid-modified phosphorothioate antisense oligonucleotide, inhibit the biogenesis of miR-122. Miravirsen (SPC-3649) is used in the study for HCV infections[1].
Remlarsen (MRG-201), a miR-29b mimic, acts a miR-29b agonist. Remlarsen has the potential for preventiong formation of a fibrotic scar or cutaneous fibrosis[1].
MTL-CEPBA is a small activating RNA targeting for upregulation of C/EBPα. MTL-CEPBA has anti-inflammatory and anti-cancer activity[1].
SID 3712249 (MiR-544 Inhibitor 1) is an inhibitor of the biogenesis of microRNA-544 (miR-544). Target: MiR-544MiR-544 represses expression of mTOR, promoting tumor cell survival in a hypoxic environment. Inhibition of miR-544 processing with MiR-544 Inhibitor 1 caused apoptosis in triple negative breast cancer cells in response to hypoxic stress, sensitized their response to 5-fluorouracil, and blocked their growth after transplantion into immunodeficient mice. SID 3712249 (MiR-544 Inhibitor 1) is believed to bind directly to the precursor miRNA, blocking production of the mature microRNA and resulting in decreased miR-544, HIF-1α, and ATM transcripts. MiR-544 Inhibitor 1 was as selective and 25-fold more potent than a 2′-O-methyl RNA antagomir.
Targaprimir-96 is a potent inhibitor of microRNA-96 (miR-96) processing. Targaprimir-96 selectively modulates miR-96 production in cancer cells and triggers apoptosis. Targaprimir-96 binds primary miR-96 (pri-miR-96) with low nanomolar affinity. Targaprimir-96 directly engages pri-miR-96 in breast cancer cells and is ineffective on healthy breast cells[1].
Gypenoside LI, a gypenoside monomer, possesses anti-tumor activity. Gypenoside LI induces cell apoptosis, cell cycle and migration[1][2].
Thymidine 3',5'-diphosphate (Deoxythymidine 3′,5′-diphosphate; pdTp) tetrasodium is a selective small molecule inhibitor of staphylococcal nuclease and tudor domain containing 1 (SND1, the miRNA regulatory complex RISC subunit). Thymidine 3',5'-diphosphate tetrasodium exhibits anti-tumor efficacy in vivo[1].
LIN28 inhibitor LI71 is a potent and cell-permeable LIN28 inhibitor, which abolishes LIN28-mediated oligouridylation with an IC50 of 7 uM. LIN28 inhibitor LI71 directly binds the cold shock domain (CSD) to suppress LIN28’s activity against let-7 in leukemia cells and embryonic stem cells[1].
Targapremir-210 is a potent miR-210 inhibitor with an IC50 of 200 nM in MDA-MB-231 cells. Targapremir-210 binds to the Dicer site of the miR-210 hairpin precursor. This interaction inhibits production of the mature miRNA.
Cl-amidine TFA is an orally active peptidylarginine deminase (PAD) inhibitor, with IC50 values of 0.8 μM, 6.2 μM and 5.9 μM for PAD1, PAD3, and PAD4, respectively. Cl-amidine TFA induces apoptosis in cancer cells. Cl-amidine TFA induces microRNA (miR)-16 expression and causes cell cycle arrest. Cl-Amidine TFA prevents histone 3 citrullination and neutrophil extracellular trap formation, and improves survival in a murine sepsis model[1][2][3][4][5].
microRNA-21-IN-2 is a potential miR-21 inhibitor with an AC50 value of 3.29 μM. microRNA-21-IN-2 can be used for the research of cancer[1].
Pseudoprotodioscin, a furostanoside, inhibits SREBP1/2 and microRNA 33a/b levels and reduces the gene expression regarding the synthesis of cholesterol and triglycerides[1].