Pfizer's CP-547632 is a selective inhibitor of VEGFR-2 tyrosine kinase that was discovered during Pfizer's collaboration with OSI Pharmaceuticals. CP-547632, was identified as a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC(50) = 11 and 9 nM, respectively). It is selective relative to epidermal growth factor receptor, platelet-derived growth factor beta, and other related TKs. It also inhibits VEGF-stimulated autophosphorylation of VEGFR-2 in a whole cell assay with an IC(50) value of 6 nM. After oral administration of CP-547632 to mice bearing NIH3T3/H-ras tumors, VEGFR-2 phosphorylation in tumors was inhibited in a dose-dependent fashion (EC(50) = 590 ng/ml). CP-547,632 is a well-tolerated, orally-bioavailable inhibitor presently under clinical investigation for the treatment of human malignancies. CP-547632 is in phase I for the treatment of diabetic retinopathy and age-related macular degeneration.

Pfizer developed AG-013958, also known as AG-13958 for treatment of age-related macular degeneration (AMD). As a VEGFR tyrosine kinase inhibitor, AG13958 was targeted to FLT/TYK receptor inhibition.

Pfizer developed AG-013958, also known as AG-13958 for treatment of age-related macular degeneration (AMD). As a VEGFR tyrosine kinase inhibitor, AG13958 was targeted to FLT/TYK receptor inhibition.

Sodium tripolyphosphate hexahydrate (sodium trimetaphosphate) is used in laundry detergent as a detergent "builder". It may also be used as a buffering agent. It has been shown that fluoride varnishes containing sodium trimetaphosphate reduce enamel demineralization. Sodium trimetaphosphate enhances the effect of 250 p.p.m. fluoride toothpaste against enamel demineralization in vitro. It also demonstrated significant antimicrobial activity, especially against S. mutans, and may be considered a potential alternative for new dental materials.

Tezacitabine is a cytidine derivative patented by Merrell Dow Pharmaceuticals, Inc. as an antineoplastic and antiviral agent. Tezacitabine acts as irreversible ribonucleotide reductase inhibitor and DNA chain terminator. Tezacitabine shows as potent activity in a broad spectrum of tumor cell lines and in vivo tumor models, including human colon, prostate, and breast tumor xenografts, In clinical trials combination of Tezacitabine and 5-Fluorouracil exerts favor influences in patients with advanced solid tumors particularly in patients with esophageal and other gastrointestinal carcinomas.

DS-3032 (Milademetan) is an orally available, potent and selective inhibitor of the p53-MDM2 (murine double minute 2) interaction. Milademetan binds to, and prevents the binding of MDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. Milademetan is 10-fold more potent than the first-generation inhibitor nutlin-3a. By preventing this MDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This results in the restoration of p53 signaling and leads to the p53-mediated induction of tumor cell apoptosis. DS-3032 is currently being evaluated in three phase 1 clinical trials for solid and hematological malignancies, including acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML) in blast phase, lymphoma and myelodysplastic syndrome (MDS).

Motexafin lutetium is pentadentate aromatic metallotexaphyrin with photosensitizing properties patented by Pharmacyclics, Inc. as anticancer agent that enhances the cytotoxic potential of photodynamic therapy through several mechanisms, including depleting intracellular reducing metabolites that are necessary for repairing the oxidative damage induced by irradiation. Motexafin lutetium catalyzes the oxidation of intracellular reducing metabolites such as ascorbate, glutathione, nicotinamide adenine dinucleotide phosphate, and protein thiols, generating reactive oxygen species in a process known as futile redox cycling. The depletion (through oxidation) of these reducing metabolites removes the substrate necessary in a cell to repair oxidative damage induced by photodynamic therapy and, left unrepaired, such oxidative DNA damage is converted into lethal double-stranded breaks. Motexafin lutetium has the potential to combine the features of selective localization, ability to be activated by deeply penetrating far-red light, low incidence of skin photosensitization and water solubility. The product was in clinical development as a treatment for several types of solid tumors (as Lutrin), age-related macular degeneration (as Optrin), atherosclerosis and prevention of restenosis (as Antrin).