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Title:
Identification of a promising PI3K inhibitor for the treatment of multiple myeloma through the structural optimization | Journal of Hematology & Oncology
Description:
Background We previously reported a PI3K inhibitor S14161 which displays a promising preclinical activity against multiple myeloma (MM) and leukemia, but the chiral structure and poor solubility prevent its further application. Methods Six S14161 analogs were designed based on the structure–activity relationship; activity of the compounds in terms of cell death and inhibition of PI3K were analyzed by flow cytometry and Western blotting, respectively; anti-myeloma activity in vivo was performed on two independent xenograft models. Results Among the six analogs, BENC-511 was one of the most potent compounds which significantly inhibited PI3K activity and induced MM cell apoptosis. BENC-511 was able to inactivate PI3K and its downstream signals AKT, mTOR, p70S6K, and 4E-BP1 at 1 μM but had no effects on their total protein expression. Consistent with its effects on PI3K activity, BENC-511 induced MM cell apoptosis which was evidenced by the cleavage of Caspase-3 and PARP. Notably, addition of insulin-like growth factor 1 and interleukin-6, two important triggers for PI3K activation in MM cells, partly blocked BENC-511-induced MM cell death, which further demonstrated that PI3K signaling pathway was critical for the anti-myeloma activity of BENC-511. Moreover, BENC-511 also showed potent oral activity against myeloma in vivo. Oral administration of BENC-511 decreased tumor growth up to 80% within 3 weeks in two independent MM xenograft models at a dose of 50 mg/kg body weight, but presented minimal toxicity. Suppression of BENC-511 on MM tumor growth was associated with decreased PI3K/AKT activity and increased cell apoptosis. Conclusions Because of its potent anti-MM activity, low toxicity (LD50 oral >1.5 g/kg), and easy synthesis, BENC-511 could be developed as a promising agent for the treatment of MM via suppressing the PI3K/AKT signaling pathway.
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Keywords {🔍}
benc, cell, cells, akt, pubmed, article, pik, figure, google, scholar, activation, cas, signaling, pikakt, myeloma, opm, pathway, treated, activity, apoptosis, hours, igf, growth, effects, rpmi, analysis, tumor, cancer, blood, phosphorylation, inhibitor, multiple, mtor, treatment, parp, potent, group, central, signals, psk, total, protein, lines, demonstrated, inhibitors, measured, authors, inhibition, models, ebp,
Topics {✒️}
domino oxa-michael-henry reactions pi3k/akt/mtor-addicted lymphomas 6-bromo-8-ethoxy-3-nitro-2h-chromene anti-myeloma drug discovery full size image regulating pro-tumoural signalling igf-1/pi3k/akt signaling pathway pi3k/akt/mtor pathway inhibitors article download pdf electron-donating methoxy substituent 50 mg/kg body weight 8-ethoxy-3-nitro-2h-chromene serine/threonine protein kinase extra-terminal protein inhibitor pi3k/akt confers chemoresistance activate pi3k/akt pathway electron-withdrawing cyano group annexin v-fluorescein isothiocyanate pi3k/akt signaling pathway cancer drug discovery pten/akt/pi3k signaling regulates pi3k/akt signals pi3k/pkb signaling module multiple myeloma progression] open access license mast-cell-mediated diseases suppress pi3k/akt activation induced gsk-3β activation potent anti-mm activity pi3k/akt/mtor pathway author information authors decreased pi3k/akt activity pi3k inhibitor nvp-bkm120 xinliang mao promising preclinical activity pi3k/akt signaling found enhances cell invasion study structure-activity relationships pi3k/akt inhibition leads related subjects privacy choices/manage cookies downstream signals akt mm cell lines full access authors’ original file mm cell death myeloma xenograft models potently suppresses akt 3-nitro-2h-chromene attenuates pathway signaling
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headline:Identification of a promising PI3K inhibitor for the treatment of multiple myeloma through the structural optimization
description:We previously reported a PI3K inhibitor S14161 which displays a promising preclinical activity against multiple myeloma (MM) and leukemia, but the chiral structure and poor solubility prevent its further application. Six S14161 analogs were designed based on the structure–activity relationship; activity of the compounds in terms of cell death and inhibition of PI3K were analyzed by flow cytometry and Western blotting, respectively; anti-myeloma activity in vivo was performed on two independent xenograft models. Among the six analogs, BENC-511 was one of the most potent compounds which significantly inhibited PI3K activity and induced MM cell apoptosis. BENC-511 was able to inactivate PI3K and its downstream signals AKT, mTOR, p70S6K, and 4E-BP1 at 1 μM but had no effects on their total protein expression. Consistent with its effects on PI3K activity, BENC-511 induced MM cell apoptosis which was evidenced by the cleavage of Caspase-3 and PARP. Notably, addition of insulin-like growth factor 1 and interleukin-6, two important triggers for PI3K activation in MM cells, partly blocked BENC-511-induced MM cell death, which further demonstrated that PI3K signaling pathway was critical for the anti-myeloma activity of BENC-511. Moreover, BENC-511 also showed potent oral activity against myeloma in vivo. Oral administration of BENC-511 decreased tumor growth up to 80% within 3 weeks in two independent MM xenograft models at a dose of 50 mg/kg body weight, but presented minimal toxicity. Suppression of BENC-511 on MM tumor growth was associated with decreased PI3K/AKT activity and increased cell apoptosis. Because of its potent anti-MM activity, low toxicity (LD50 oral >1.5 g/kg), and easy synthesis, BENC-511 could be developed as a promising agent for the treatment of MM via suppressing the PI3K/AKT signaling pathway.
datePublished:2014-01-15T00:00:00Z
dateModified:2014-01-15T00:00:00Z
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Phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway
BENC-511
S14161
Multiple myeloma
Drug discovery
Oncology
Hematology
Cancer Research
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headline:Identification of a promising PI3K inhibitor for the treatment of multiple myeloma through the structural optimization
description:We previously reported a PI3K inhibitor S14161 which displays a promising preclinical activity against multiple myeloma (MM) and leukemia, but the chiral structure and poor solubility prevent its further application. Six S14161 analogs were designed based on the structure–activity relationship; activity of the compounds in terms of cell death and inhibition of PI3K were analyzed by flow cytometry and Western blotting, respectively; anti-myeloma activity in vivo was performed on two independent xenograft models. Among the six analogs, BENC-511 was one of the most potent compounds which significantly inhibited PI3K activity and induced MM cell apoptosis. BENC-511 was able to inactivate PI3K and its downstream signals AKT, mTOR, p70S6K, and 4E-BP1 at 1 μM but had no effects on their total protein expression. Consistent with its effects on PI3K activity, BENC-511 induced MM cell apoptosis which was evidenced by the cleavage of Caspase-3 and PARP. Notably, addition of insulin-like growth factor 1 and interleukin-6, two important triggers for PI3K activation in MM cells, partly blocked BENC-511-induced MM cell death, which further demonstrated that PI3K signaling pathway was critical for the anti-myeloma activity of BENC-511. Moreover, BENC-511 also showed potent oral activity against myeloma in vivo. Oral administration of BENC-511 decreased tumor growth up to 80% within 3 weeks in two independent MM xenograft models at a dose of 50 mg/kg body weight, but presented minimal toxicity. Suppression of BENC-511 on MM tumor growth was associated with decreased PI3K/AKT activity and increased cell apoptosis. Because of its potent anti-MM activity, low toxicity (LD50 oral >1.5 g/kg), and easy synthesis, BENC-511 could be developed as a promising agent for the treatment of MM via suppressing the PI3K/AKT signaling pathway.
datePublished:2014-01-15T00:00:00Z
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Phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway
BENC-511
S14161
Multiple myeloma
Drug discovery
Oncology
Hematology
Cancer Research
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