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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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We are analyzing https://link.springer.com/article/10.1186/1756-8722-7-9.

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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
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What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

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Topics {✒️}

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Schema {🗺️}

WebPage:
      mainEntity:
         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
         pageStart:1
         pageEnd:13
         license:https://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/1756-8722-7-9
         keywords:
            Phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway
            BENC-511
            S14161
            Multiple myeloma
            Drug discovery
            Oncology
            Hematology
            Cancer Research
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                        name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                        type:PostalAddress
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                        name:Department of Pharmacology, School of Pharmacy, Soochow University, Suzhou, China
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ScholarlyArticle:
      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
      pageStart:1
      pageEnd:13
      license:https://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/1756-8722-7-9
      keywords:
         Phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway
         BENC-511
         S14161
         Multiple myeloma
         Drug discovery
         Oncology
         Hematology
         Cancer Research
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         name:BioMed Central
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            type:ImageObject
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      author:
            name:Kunkun Han
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                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Xin Xu
            affiliation:
                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
                  type:Organization
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            name:Guodong Chen
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                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
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            name:Yuanying Zeng
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                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
                  type:Organization
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            name:Jingyu Zhu
            affiliation:
                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
                  type:Organization
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            name:Xiaolin Du
            affiliation:
                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
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                  name:Soochow University
                  address:
                     name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
                     type:PostalAddress
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                  address:
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                     type:PostalAddress
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            name:Zhaopeng Liu
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                  name:Shandong University
                  address:
                     name:Department of Organic Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan, China
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      address:
         name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
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         name:Department of Organic Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan, China
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            name:Soochow University
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               name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
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      name:Zubin Zhang
      affiliation:
            name:Soochow University
            address:
               name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      name:Biyin Cao
      affiliation:
            name:Soochow University
            address:
               name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
               type:PostalAddress
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      name:Zhaopeng Liu
      affiliation:
            name:Shandong University
            address:
               name:Department of Organic Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan, China
               type:PostalAddress
            type:Organization
      name:Xinliang Mao
      affiliation:
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            address:
               name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Department of Pharmacology, School of Pharmacy, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Department of Organic Chemistry, Key Laboratory of Chemical Biology (Ministry of Education), School of Pharmaceutical Sciences, Shandong University, Jinan, China
      name:Cyrus Tang Hematology Center, Soochow University, Suzhou, China
      name:Department of Pharmacology, School of Pharmacy, Soochow University, Suzhou, China

External Links {🔗}(183)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.53s.