W56 (concentrations >200 μM) selectively inhibits Rac1 interaction with Rac1-specific GEFs TrioN, GEF-H1, and Tiam1, which activate subsequent G proteins. The peptide comprises residues 45-60 of the β3 region of the guanine nucleotide exchange factor (GEF) recognition/activation site of Rac1. W56 targets the Trp56 site of Rac1. It has implications in research of actin cytoskeleton reorganization, transcriptional activation of genes, stimulation of DNA synthesis, endocytic and exocytic membrane trafficking, regulation of translation, and pathologies such as cancer.
Wedelolactone inhibits NF-κB-mediated gene transcription in cells by blocking the phosphorylation and degradation of IκBα. Irreversible inhibitor of IKKα and β kinase activity (IC50 < 10 μM). Wedelolactone has no effects on p38 MAP kinase or Akt.
Wiskostatin is a selective inhibitor of N-WASP, a ubiquitously expressed member of the Wiskott-Aldrich Syndrome protein (WASp) family that regulates actin polymerization. Wiskostatin inhibits actin-dependent cellular functions, including migration, transmembrane transport and phagocytosis.
WKYMVm is a very potent agonist of formyl peptide receptor members FPR1/FPR2 (EC50 1 nM) and FPRL1/FPRL2 (75 pM and 3 nM, respectively). WKYMVm stimulation of leukocytes has been shown to elevate intracellular calcium, induce chemotaxis, superoxide generation, cell killing and phagocytosis.
Wortmannin is a potent and specific phosphatidylinositol 3-kinase (PI3-K) inhibitor with an IC50 of 2-4 nM. Inhibition of PI3-K/Akt signal transduction cascade enhances the apoptotic effects of radiation or serum withdrawal and blocks the antiapoptotic effect of cytokines. Inhibition of PI3-K by wortmannin also blocks many of the short-term metabolic effects induced by insulin receptor activation.
Wortmannin is a low molecular weight; hydrophobic fungal metabolite with a sterol-like structure produced by Penicilium fumiculosum.1,Inhibition of PI3K/Akt signal transduction cascade by wortmannin, enhances the apoptotic effects of radiation or serum withdrawal and blocks the antiapoptotic effect of cytokines.2,3 PI3K inhibition by wortmannin also blocks many of the short-term metabolic effects induced by insulin receptor activation.4 Research has demonstrated that wortmannin inhibits two enzymes from mitotical division, key regulators Polo-like kinase (Plk) family, Plk1 and Plk3. Wortmannin is a low-molecular-weight hydrophobic fungal metabolite with a sterol-like structure produced by Penicillium funiculosum.1 It is a selective inhibitor of phosphoinosidite 3-kinase. It interferes with Akt signal transduction cascade, enhancing the apoptotic effects of radiation or serum withdrawal and blocks the antiapoptotic effect of cytokines.2,3 Wortmannin is membrane-permeable, thus facilitating whole-cell studies of G-protein-coupled receptor and receptor tyrosine kinase signalling pathways. PI3K inhibition by wortmannin also blocks many of the short-term metabolic effects induced by insulin receptor activation.4 Research has demonstrated that wortmannin inhibits two mitotic enzymes, key regulators in the Polo-like kinase (Plk) family, Plk1 and Plk3.
WR99210 is a potent inhibitor of Plasmodium falciparum dihydrofolate reductase (DHFR), which is a major malarial drug target. It has subnanomolar potency for the wild type, double mutant and quadruple mutant dihydrofolate reductases.
WZ811 is a potent, specific antagonist of CXCR4 (IC50 = 0.3 nM). WZ811 blocks SDF-1 mediated changes in cellular cAMP levels in U87 glioma cells (IC50 = 1.2 nM) and Matirgel infiltration of MDA-MB-231 cells (IC50 = 5.2 nM).