Enzyme Modulators

<p>Inhibitor of NPM-ALK kinase</p>

<p>Inhibitor of acetylcholinesterase</p>

<p>Angiotensin-converting enzyme inhibitor; anti-hypertensive</p>

<p>Inhibitor of Abl and Src kinases; anti-proliferative; antineoplasticÂ</p>

<p>PI3K enzyme inhibitor</p>

<p>Inhibitor of DNA replication; inhibitor of theophylline and caffeine metabolism</p>

<p>Selective inhibitor histone methyltransferases SUV420H1 and SUV420H2 (IC50 values = 25 nM and 144 nM, respectively). Reduces histone H4K20me2 and H4K20me3 expression whilst increasing H4K20me1 global expression. Inhibits formation of p53-binding protein 1 (53BP1) foci upon ionizing radiation and reduces NHEJ-mediated DNA-break repair.</p>

<p>Inhibitor of CKD1, CDK2, and CDK4 serine/threonine kinases</p>

<p>Inhibitor of phosphodiesterase 7</p>

<p>Inhibitor of γ-secretase and Notch signalling</p>

<p>Ligand of plasminogen; used for bleeding control</p>

<p>An active product of vitamin A metabolism. Activates RXR and RAR receptor isoforms with high binding affinity. Induces differentiation of neural stem cells into neurons.</p>

<p>Anti-folate inhibitor of thymidylate synthase</p>

<p>Sumoylation inhibitor; reported to inhibit histone acetylation transferase</p>

<p>Topoisomerase I inhibitor</p>

<p>Small molecule antagonist of heparan sulfate that binds to glycosaminoglycans electrostatically. Surfen neutralised anti-coagulant activity of unfractionated and low molecular weight heparins, inhibited enzymatic sulfation and degradation reactions. Surfen also blocked signalling and cell adhesion to fibronectin that was triggered by heparan sulphate.</p>

<p>Binds to FK506 binding proteins (FKBPs) to form a complex that inhibits mammalian targets of rapamycin (mTOR). Blocks p70 S6 kinase activation by interleukin-2 and thereby inhibits proliferation of T cells. Induces differentiation of human pluripotent stem cells (hPSCs) to mesendoderm and blood progenitor cells.</p>

<p>Sorafenib is a drug that belongs to the class of multikinase inhibitors. It inhibits a number of kinases, including the Mcl-1 protein, which is involved in apoptosis along with blocking picolinic acid (PA), an endogenous metabolite involved in apoptosis signal transduction. Sorafenib also binds to epidermal growth factor receptor (EGFR) on the surface of cancer cells, inhibiting the production of proteins that are required for angiogenesis, thus blocking the formation of new blood vessels. Sorafenib may also inhibit P-glycoprotein (Pgp) activity. Overall, these cytotoxic effects give Sorafenib anti-tumor properties, inhibiting angiogenesis and cellular transformation, which are the two main processes of tumor growth and metastasis. Sorafenib has been shown to be effective against a range of solid tumors such as breast, prostate and lung cancers and is also used for the treatment of metastatic colorectal cancer and renal cell carcinoma. A combination therapy group found that sorafenib was more effective when used with interferon alfa-2b for the treatment of advanced renal cell carcinoma. Sorafenib also has the potential for drug interactions with other drugs that are metabolized by cytochrome P450 enzymes.</p>

<p>JAK2 inhibitor with potential antineoplastic activity</p>

<p>Inhibitor of HMG-CoA reductase</p>