A potent agonist of human STING and also weakly activates mouse STING. Suppresses the metastasis of human renal carcinoma cells.
Inhibits gene transcription driven by STAT3. Inhibits cancer cell stemness gene expression and blocks spherogenesis of stemness-high cancer cells isolated froma variety of cancer types.
Selectively inhibits the growth of cancer cells over normal cells. Induces non-apoptotice cell death in glioblastoma cells, and is active in vivo.
Plant growth inhibitor discovered using a resistance-gene-directed approach.
Important tool for exploring the physiology of Nav1.1 channels. Increases Nav1.1-mediated current in a concentration dependent manner.
Clinically useful anticonvulsant medication. Its mechanism of action is believed to be inhibition of Nav1.1 and Nav1.6 activation
Irreversible inhibitor of mitochondrial carnitine palmitoyl transferase 1 (CPT1). It is widely used to study fatty acid oxidation.
Inhibited HIF-mediated transcription in cells derived from glioma, breast, and prostate cancers. The mechanism of action is via down-regulation of HIF-1α protein synthesis accompanied by suppression of phosphorylation of eukaryotic translation initiation factor 4E binding protein 1 and p70 S6 kinase, key regulators of HIF-1α protein synthesis.
Blocks cell-surface localization and signaling of the epidermal growth factor receptor (EGFR) glycoprotein and selectively arrests proliferation only in cells dependent on EGFR for survival.
Inhibitor of the signaling molecule STING in mouse and human cells. It reduced systemic cytokine response in mice treated with the STING agonist 10-carboxymethyl-9-acridanone and showed efficacy in Trex-/- mice.
Inhibitor of the signaling molecule STING in mouse cells. It covalently binds to Cys91 of STING preventing activation via blockade of palmitoylation at Cys91.
Inhibitor of the signaling molecule STING in mouse cells. Covalently binds to Cys91 of STING preventing activation via blockade of palmitoylation at Cys91.
Selectively inhibits the kinase RIOK2 (Kd = 200 nM) causing disruption of ribosomal biogenesis and ribosomal stress.
Inhibitor of the histon acetyltransferases p300 and PCAF. Sensitizes cancer cells to ionizing radiation and suppresses proteins involved in invasion and angiogenesis.
Reversible inhibitor of the histone demethylase LSD1. Promotes autophagy in neuroblastoma cells.
Antiprotozoan drug currently used for malaria and giardiasis that has recently been investigated for treating lupus, as an anticancer agent, in inflammation, and as a female sterilization agent.
Widely used for signal amplification in fluorescent in situ hybridization (FISH) protocols. Can be used in catalyzed reporter deposition (CARD) signal amplification protocols in a variety of immunoassays in which, horseradish peroxidase catalyzed deposition of biotinyl tyramide is detected with labeled streptavidin.
MK-2206 is a potent and selective allosteric inhibitor of Akt that enhances antitumor efficacy of several standard chemotherapeutic agents.
Inhibits USP7 and the closely related USP47. Inhibits neuroblastoma growth via induction of p53-mediated apoptosis
Highly selective, potent, cell permeable inhibitor of Aurora A with off-target binding at GABAA. Induces apoptosis and autophagy in breast cancer and melanoma cells via suppression of activation of the p38 MAPK pathway
Potent inhibitor of the BET family of bromodomains with no activity at BAZ2B, SP140, ATAD2, CREBBO and PCAF. Inhibition of BET bromodomains results in downregulation of Myc transcription.
Potent and selective TRPC5 blocker with therapeutic benefit in a rat model of hypertensive proteineuric kidney disease. Active in vivo
LY2603618 inhibits Chk1, an important regulator of cellular response to DNA damage. It has been shown to cause dramtice suppression of cell growth in MCF-7 and MDA-MB-31 breast cancer cells
Potent inhibitor of Brd4 (IC50 = 100 nM). BI 2536 has been shown to suppress cMyc-expression in MM.1S multiple myeloma cells.
Protects cells from ferroptosis caused by iron catalyzed formation of free radicals from lipid peroxides. Treatment of several treatment-resistant cancer cell lines exhibiting a high mesenchymal state resulted in selective induction of ferroptosis
RS-1 has been used to exploit the RAD51 overexpression in cancerous cells by inducing lethality via genotoxic RAD51 protein complexes. RS-1 has also been found to a potent enhancer of CRISPR- and TALEN- based gene editing.
UNC0379 is a selective inhibitor of the lysine methyltransferase SETD8. Treatment of SY5Y and NGP neuroblastoma cell lines lead to activation of p53 and decreased tumor growth in an ex-vivo tumorigenicity assay.
An important tool for probing the involvement of AhR in the toxicity of various environmental toxins such as TCDD and other dioxins.
Significantly decreased IL-1β and IL-18 levels in LPS-stimulated human blood-derived macrophages as well as IL-1β release and caspase 1 activity in human blood neutrophils with no effect on TNFα levels.
Inhibits the cystine-glutamate antiporter, system Xc- leading to activation of an ER stress response. Inhibition of system Xc- leads to cysteine starvation, glutathione depletion and induction of ferroptosis.
Sensitizes cancer cells to carious chemotherapeutic agents
Prevents necroptosis, virus-induced necrosis and TLR3-induced necrosis.
NAcM-OPT is a potent and selective NEDD8 ligation inhibitor, IC50=80 nM (in vitro).
SBI-0206965 (1884220-36-3) is a potent and selective inhibitor of the autophagy kinase ULK-1, IC50=108 and 711 nM for ULK1 and 2 respectively.
Displays selective cytotoxic effects on human oral cancer cell lines. Inhibits hepatocellular carcinoma cell growth via modulation of the Wnt/β-catenin pathway.
KA can selectively kill high-glycolytic cancer cells via glucose dependent ATP depletion and been used in a predictive model for selective targeting of the Warburg effect, the most prominent hallmark of cancer cell metabolism.
SMED-1 displays strong synergism at 10 μM plus 1 mM Dex and exhibits little activity alone (IC50>20 μM).
A potent and selective fatty acid synthase (FASN) inhibitor acting via interfering with cofactor binding.