We are analyzing https://link.springer.com/article/10.1007/s40262-018-0679-9.

Title:
Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib | Clinical Pharmacokinetics
Description:
Proteasome inhibitors disrupt multiple pathways in cells and the bone marrow microenvironment, resulting in apoptosis and inhibition of cell-cycle progression, angiogenesis, and proliferation. Bortezomib is a first-in-class proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma after one prior therapy. It is also effective in other plasma cell disorders and non-Hodgkin lymphomas. The main mechanism of action of bortezomib is to inhibit the chymotrypsin-like site of the 20S proteolytic core within the 26S proteasome, thereby inducing cell-cycle arrest and apoptosis. The pharmacokinetic profile of intravenous bortezomib is characterized by a two-compartment model with a rapid initial distribution phase followed by a longer elimination phase and a large volume of distribution. Bortezomib is available for subcutaneous and intravenous administration. Pharmacokinetic studies comparing subcutaneous and intravenous bortezomib demonstrated that systemic exposure was equivalent for both routes; pharmacodynamic parameters of 20S proteasome inhibition were also similar. Renal impairment does not influence the intrinsic pharmacokinetics of bortezomib. However, moderate or severe hepatic impairment causes an increase in plasma concentrations of bortezomib. Therefore, patients with moderate or severe hepatic impairment should start at a reduced dose. Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. This article critically reviews and summarizes the clinical pharmacokinetics and pharmacodynamics of bortezomib at various dosing levels and routes of administration as well as in specific patient subsets. In addition, we discuss the clinical efficacy and safety of bortezomib.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Health & Fitness
Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

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

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

Based on our best estimate, this website will receive around 7,734,772 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

article, google, scholar, pubmed, cas, bortezomib, myeloma, patients, multiple, clin, cancer, proteasome, phase, drug, study, pharmacokinetics, oncol, clinical, inhibitor, therapy, trial, cell, van, blood, dexamethasone, relapsed, httpsdoiorgjco, lymphoma, richardson, httpsdoiorgblood, central, treatment, adams, res, med, advanced, content, research, inhibitors, pharmacokinetic, intravenous, systemic, metabolism, cytochrome, safety, randomized, httpsdoiorg, pharmacol, httpsdoiorgs, amyloidosis,

Topics {✒️}

month download article/chapter tnf-alpha-induced apoptosis autologous stem-cell transplant prolonged progression-free survival san miguel jf relapsed/refractory clonal disease inducing cell-cycle arrest cancer therapy-induced apoptosis androgen-independent prostate cancer national cancer institute potential drug-drug interactions relapsed/refractory multiple myeloma full article pdf transplant-eligible myeloma patients article critically reviews model-based support bortezomib exposure–response relationships related subjects privacy choices/manage cookies pediatric leukemia patients cytochrome p450 reaction received research support population pharmacokinetic analysis saif abdul-majeed van de velde dipeptidyl boronic acids cytochrome p450 enzymes proteasome inhibitor ps-341 cell-cycle progression bortezomib-based therapy drug metab rev drug–drug interactions drug-drug interactions refractory hematologic malignancies european economic area bone marrow microenvironment intracellular protein degradation van der holt potential drug interactions mantle cell lymphoma adverse drug reactions computerised drug database proteasome inhibitor ps341 natl cancer inst randomized controlled trials newly diagnosed myeloma cell cycle control cyp3a inhibitor ketoconazole complete hematologic response de la rubia

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib
         description:Proteasome inhibitors disrupt multiple pathways in cells and the bone marrow microenvironment, resulting in apoptosis and inhibition of cell-cycle progression, angiogenesis, and proliferation. Bortezomib is a first-in-class proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma after one prior therapy. It is also effective in other plasma cell disorders and non-Hodgkin lymphomas. The main mechanism of action of bortezomib is to inhibit the chymotrypsin-like site of the 20S proteolytic core within the 26S proteasome, thereby inducing cell-cycle arrest and apoptosis. The pharmacokinetic profile of intravenous bortezomib is characterized by a two-compartment model with a rapid initial distribution phase followed by a longer elimination phase and a large volume of distribution. Bortezomib is available for subcutaneous and intravenous administration. Pharmacokinetic studies comparing subcutaneous and intravenous bortezomib demonstrated that systemic exposure was equivalent for both routes; pharmacodynamic parameters of 20S proteasome inhibition were also similar. Renal impairment does not influence the intrinsic pharmacokinetics of bortezomib. However, moderate or severe hepatic impairment causes an increase in plasma concentrations of bortezomib. Therefore, patients with moderate or severe hepatic impairment should start at a reduced dose. Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. This article critically reviews and summarizes the clinical pharmacokinetics and pharmacodynamics of bortezomib at various dosing levels and routes of administration as well as in specific patient subsets. In addition, we discuss the clinical efficacy and safety of bortezomib.
         datePublished:2018-05-26T00:00:00Z
         dateModified:2018-05-26T00:00:00Z
         pageStart:157
         pageEnd:168
         sameAs:https://doi.org/10.1007/s40262-018-0679-9
         keywords:
            Pharmacotherapy
            Pharmacology/Toxicology
            Internal Medicine
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs40262-018-0679-9/MediaObjects/40262_2018_679_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs40262-018-0679-9/MediaObjects/40262_2018_679_Fig2_HTML.png
         isPartOf:
            name:Clinical Pharmacokinetics
            issn:
               1179-1926
               0312-5963
            volumeNumber:58
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer International Publishing
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Carlyn Rose C. Tan
               affiliation:
                     name:Fox Chase Cancer Center
                     address:
                        name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Saif Abdul-Majeed
               affiliation:
                     name:Fox Chase Cancer Center
                     address:
                        name:Office of Clinical Research, Fox Chase Cancer Center, Philadelphia, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Brittany Cael
               affiliation:
                     name:Jeanes Hospital
                     address:
                        name:Department of Pharmacy, Bone Marrow Transplant Program, Jeanes Hospital, Philadelphia, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Stefan K. Barta
               affiliation:
                     name:Fox Chase Cancer Center
                     address:
                        name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Clinical Pharmacokinetics and Pharmacodynamics of Bortezomib
      description:Proteasome inhibitors disrupt multiple pathways in cells and the bone marrow microenvironment, resulting in apoptosis and inhibition of cell-cycle progression, angiogenesis, and proliferation. Bortezomib is a first-in-class proteasome inhibitor approved for the treatment of multiple myeloma and mantle cell lymphoma after one prior therapy. It is also effective in other plasma cell disorders and non-Hodgkin lymphomas. The main mechanism of action of bortezomib is to inhibit the chymotrypsin-like site of the 20S proteolytic core within the 26S proteasome, thereby inducing cell-cycle arrest and apoptosis. The pharmacokinetic profile of intravenous bortezomib is characterized by a two-compartment model with a rapid initial distribution phase followed by a longer elimination phase and a large volume of distribution. Bortezomib is available for subcutaneous and intravenous administration. Pharmacokinetic studies comparing subcutaneous and intravenous bortezomib demonstrated that systemic exposure was equivalent for both routes; pharmacodynamic parameters of 20S proteasome inhibition were also similar. Renal impairment does not influence the intrinsic pharmacokinetics of bortezomib. However, moderate or severe hepatic impairment causes an increase in plasma concentrations of bortezomib. Therefore, patients with moderate or severe hepatic impairment should start at a reduced dose. Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. This article critically reviews and summarizes the clinical pharmacokinetics and pharmacodynamics of bortezomib at various dosing levels and routes of administration as well as in specific patient subsets. In addition, we discuss the clinical efficacy and safety of bortezomib.
      datePublished:2018-05-26T00:00:00Z
      dateModified:2018-05-26T00:00:00Z
      pageStart:157
      pageEnd:168
      sameAs:https://doi.org/10.1007/s40262-018-0679-9
      keywords:
         Pharmacotherapy
         Pharmacology/Toxicology
         Internal Medicine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs40262-018-0679-9/MediaObjects/40262_2018_679_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs40262-018-0679-9/MediaObjects/40262_2018_679_Fig2_HTML.png
      isPartOf:
         name:Clinical Pharmacokinetics
         issn:
            1179-1926
            0312-5963
         volumeNumber:58
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer International Publishing
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Carlyn Rose C. Tan
            affiliation:
                  name:Fox Chase Cancer Center
                  address:
                     name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Saif Abdul-Majeed
            affiliation:
                  name:Fox Chase Cancer Center
                  address:
                     name:Office of Clinical Research, Fox Chase Cancer Center, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Brittany Cael
            affiliation:
                  name:Jeanes Hospital
                  address:
                     name:Department of Pharmacy, Bone Marrow Transplant Program, Jeanes Hospital, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Stefan K. Barta
            affiliation:
                  name:Fox Chase Cancer Center
                  address:
                     name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Clinical Pharmacokinetics
      issn:
         1179-1926
         0312-5963
      volumeNumber:58
Organization:
      name:Springer International Publishing
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Fox Chase Cancer Center
      address:
         name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
         type:PostalAddress
      name:Fox Chase Cancer Center
      address:
         name:Office of Clinical Research, Fox Chase Cancer Center, Philadelphia, USA
         type:PostalAddress
      name:Jeanes Hospital
      address:
         name:Department of Pharmacy, Bone Marrow Transplant Program, Jeanes Hospital, Philadelphia, USA
         type:PostalAddress
      name:Fox Chase Cancer Center
      address:
         name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Carlyn Rose C. Tan
      affiliation:
            name:Fox Chase Cancer Center
            address:
               name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
               type:PostalAddress
            type:Organization
      name:Saif Abdul-Majeed
      affiliation:
            name:Fox Chase Cancer Center
            address:
               name:Office of Clinical Research, Fox Chase Cancer Center, Philadelphia, USA
               type:PostalAddress
            type:Organization
      name:Brittany Cael
      affiliation:
            name:Jeanes Hospital
            address:
               name:Department of Pharmacy, Bone Marrow Transplant Program, Jeanes Hospital, Philadelphia, USA
               type:PostalAddress
            type:Organization
      name:Stefan K. Barta
      affiliation:
            name:Fox Chase Cancer Center
            address:
               name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
      name:Office of Clinical Research, Fox Chase Cancer Center, Philadelphia, USA
      name:Department of Pharmacy, Bone Marrow Transplant Program, Jeanes Hospital, Philadelphia, USA
      name:Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(320)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.57s.

LINK . SPRINGER . COM {}