This project investigates the effectiveness of drugs which specifically block activity of the cancer-promoting genes known as the ‘PI3K-Pathway†in ovarian cancer cells.

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Background: Activation of the PI3K pathway is implicated in a number of tumour types, including haematological malignancies. Agents that target this pathway at different levels (e.g. RTK, PI3K, mTOR etc) have shown promising activity in preclinical models and in early phase trials. We have therefore investigated the activity of novel, potent, pan- and isoform-selective PI3K pathway inhibitors in lymphoma and myeloma models. Methods: Compounds studied included those with selectivity for mTOR (INK128, mTOR IC50 1.6 nM), PI3Kδ/γ (INK713, INK1048, IC50s ,10 nM for δ/γ isoforms, ,50 nM for others) and PI3Kδ/γ/β (INK1138, IC50s ,10 nM for each isoform). IC87114 (δ- selective), GDC-0941 (α/δ selective), rapamycin and doxorubicin were included as comparators. Agents were studied in a panel of lymphoma and myeloma cell lines, in normal PBMCs and in primary tumours cultured with stromal cells. Effects on cell viability and proliferation were assessed using the Guava Viacount assay, on apoptosis ...

Mutations in the catalytic subunit of the phosphatidylinositol 3-kinase (PI3K, encoded by PIK3CA) are common in breast cancer. Drugs inhibiting PI3K show efficacy in a small proportion of patients; some tumors are intrinsically resistant, whereas others become resistant. Le et al. found that another kinase, proviral insertion site in murine leukemia virus (PIM), maintains the activity of downstream effectors of the PI3K pathway and that cotargeting PIM may be effective in patients that show resistance to PI3K inhibitors. A large gain-of-function screen in cultured PI3K-mutant, luminal A-type breast cancer cells identified genes encoding isoforms of PIM as promoting resistance to the PI3K inhibitor BYL719. Overexpression of PIM1 (more so than that of PIM2 or PIM3) decreased the potency of BYL719 and other PI3K pathway inhibitors in various types of breast cancer cells. Cultures of PI3K-mutant breast cancer cells that were resistant to BYL719 had greater abundance of all three PIM isoforms than ...

NVP-BGT226 | PI3K/mTOR inhibitor | BGT 226 | NVP-BGT226 | BGT226 | CAS [1245537-68-1] - [915020-55-2] | Axon 2029 | Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of life science reagents for your research

PF 04691502 | PI3K/mTOR inhibitor | PF04691502 | CAS [1013101-36-4] | Axon 1855 | Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of life science reagents for your research

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SF1126 is a water soluble, small-molecule prodrug containing the pan-PI3K/mTOR inhibitor LY294002/SF1101 conjugated to the RGD-containing tetra-peptide SF1174 with potential antineoplastic and antiangiogenic activities. The targeting peptide SF1174 moiety of pan-PI3K/mTOR inhibitor SF1126 selectively binds to cell surface integrins and, upon cell entry, the agent is hydrolyzed to the active drug SF1101; SF1101 selectively inhibits all isoforms of phosphoinositide-3-kinase (PI3K) and other members of the PI3K superfamily, such as the mammalian target of rapamycin (mTOR) and DNA-PK.

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Dysregulation of the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling has been found in several types of human cancer, including hepatocellular carcinoma (HCC). NVP-BEZ235 is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against HCC in preclinical models. Autophagy is a cellular lysosomal degradation pathway essential for the regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mTOR signaling and often counteracts the efficacy of certain cancer therapeutic agents. In this study, we explored the role of autophagy in apoptosis induced by NVP-BEZ235 in two HCC cell lines, Hep3B and PLC/PRF/5, and identified the mechanism of combinatorial treatment. NVP-BEZ235 was effective in inhibiting the growth of the two HCC cell lines possibly though induction of apoptosis. NVP-BEZ235 also potently increased the expression of LC3-II and decreased the expression of p62, indicating ...

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This study is the first to provide evidence for the efficacy of the novel dual PI3K/mTOR inhibitor NVP-BEZ235 in preclinical models of ovarian cancer. We demonstrate that NVP-BEZ235 effectively blocked PI3K/Akt/mTOR pathway signaling, decreased cell proliferation, and sensitized cells to cisplatin treatment. In immunocompetent mice with established ovarian tumor disease, oral administration of NVP-BEZ235 decreased pAkt, p4E-BP1, and Ki67 in tumor tissue, and resulted in significantly longer survival compared to control animals. Importantly, NVP-BEZ235 was effective in both platinum-sensitive and platinum-resistant cell models.. Targeting the PI3K/Akt/mTOR pathway in cancer disease has been a focus of drug development recently, but the optimal therapeutic strategy has yet to be identified. Prior studies including studies from our laboratory in preclinical models of ovarian cancer have mainly investigated the effects of either PI3K or mTOR inhibition alone (8, 33-40). For example, the mTOR ...

PURPOSE: Nelfinavir, a PI3K pathway inhibitor, is a radiosensitizer that increases tumor blood flow in preclinical models. We conducted an early-phase study to demonstrate the safety of nelfinavir combined with hypofractionated radiotherapy (RT) and to develop biomarkers of tumor perfusion and radiosensitization for this combinatorial approach. EXPERIMENTAL DESIGN: Ten patients with T3-4 N0-2 M1 rectal cancer received 7 days of oral nelfinavir (1,250 mg b.i.d.) and a further 7 days of nelfinavir during pelvic RT (25 Gy/5 fractions/7 days). Perfusion CT (p-CT) and DCE-MRI scans were performed pretreatment, after 7 days of nelfinavir and prior to the last fraction of RT. Biopsies taken pretreatment and 7 days after the last fraction of RT were analyzed for tumor cell density (TCD). RESULTS: There were 3 drug-related grade 3 adverse events: diarrhea, rash, and lymphopenia. On DCE-MRI, there was a mean 42% increase in medianKtrans, and a corresponding median 30% increase in mean blood flow on p-CT during RT

BEZ235 (NVP-BEZ235) is a potent dual PI3K and mTOR inhibitor of p110α, p110γ, p110δ and p110β with IC50 of 4 nM, 5 nM, 7 nM and 75 nM, respectively. Buy PI3K inhibitor BEZ235 (NVP-BEZ235, Dactolisib) from AbMole BioScience.

Exelixis, Inc. (Nasdaq: EXEL) reported interim data from a phase 1 dose-escalation trial of XL765, a novel small molecule inhibitor of phosphoinositide-3 kinase (PI3K) and mTOR, which are

Gedatolisib (PKI-587) is a highly potent dual inhibitor of PI3Kα, PI3Kγ, and mTOR with IC50s of 0.4 nM, 5.4 nM and 1.6 nM, respectively. PKI-587 is equally effective in both complexes of mTOR, mTORC1 and mTORC2. - Mechanism of Action & Protocol.

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MSC2360844 is a potent, orally active and selective PI3Kδ inhibitor, with an IC50 of 145 nM. MSC2360844 shows highly selective against a panel of 278 additional kinases. - Mechanism of Action & Protocol.