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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s40262-018-0703-0, but it redirected us to https://link.springer.com/article/10.1007/s40262-018-0703-0. The analysis below is for the second page.

Title[redir]:
Clinical Pharmacokinetics and Pharmacodynamics of Dabrafenib | Clinical Pharmacokinetics
Description:
Dabrafenib is a potent and selective inhibitor of BRAF-mutant kinase that is approved, as monotherapy or in combination with trametinib (mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor), for unresectable or metastatic BRAF-mutated melanoma, advanced non-small cell lung cancer and anaplastic thyroid cancer harbouring the BRAFV600E mutation. The recommended dose of dabrafenib is 150 mg twice daily (bid) under fasted conditions. After single oral administration of the recommended dose, the absolute oral bioavailability (F) of dabrafenib is 95%. Dabrafenib shows a time-dependent increase in apparent clearance (CL/F) following multiple doses, which is likely due to induction of its own metabolism through cytochrome P450 (CYP) 3A4. Therefore, steady state is reached only after 14 days of daily dose administration. Moreover, the extent of this auto-induction process is dependent on the dose, which explains why dabrafenib systemic exposure at steady state increases less than dose proportionally over the dose range of 75–300 mg bid. The main elimination route of dabrafenib is the oxidative metabolism via CYP3A4/2C8 and biliary excretion. Among the three major metabolites identified, hydroxy-dabrafenib appears to contribute to the pharmacological activity. Age, sex and body weight did not have any clinically significant influence on plasma exposure to dabrafenib. No dose adjustment is needed for patients with mild renal or hepatic impairment, whereas the impacts of severe impairment on dabrafenib pharmacokinetics remain unknown. Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug–drug interactions are expected with dabrafenib. The relationship between clinical outcomes and plasma exposure to dabrafenib and hydroxy-dabrafenib should be investigated more deeply.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,904,851 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, article, google, scholar, dabrafenib, cas, melanoma, braf, central, cancer, patients, trametinib, metastatic, clin, pharmacokinetics, phase, drug, oncol, inhibitor, clinical, cell, long, dose, trial, lancet, inhibitors, france, combination, audrey, raf, paris, benoit, blanchet, kinase, med, pharmacol, mek, access, therapy, treatment, accessed, multicentre, openlabel, flaherty, combined, ther, engl, brain, toulouse, privacy,

Topics {✒️}

eu/docs/en_gb/document_library/epar_-_product_information/human/002604/wc500149671 eu/docs/en_gb/document_library/epar_-_public_assessment_report/human/002604/wc500149673 threonine-protein kinase b-raf braf-mutated high-grade glioma month download article/chapter gov/downloads/drugs/guidances/ucm070246 b-raf-driven tumors braf mutation-positive tumors val600 braf-mutant melanoma braf v600-mutant tumours p450-mediated ddi risk small-cell lung cancer carbon-carbon bond cleavage gov/drugsatfda_docs/nda/2013/202806orig1s000clinpharmr mitogen-activated protein kinase gov/ct2/show/nct02873650 metastatic braf-mutated melanoma braf-mutated metastatic melanoma cyp3a4/2b6/2c inducer benoit blanchet declare braf v600e mutation gov/drugsatfda_docs/label/2018/202806s010lbl trametinib combination therapy marie-noëlle paludetto drug–drug interactions audrey thomas-schoemann wild-type braf mapk-activated protein kinases braf-mutant kinase article puszkiel davies ma etienne chatelut full article pdf combination therapy braf v600 mutations privacy choices/manage cookies drug metab dispos therapeutic drug monitoring drug monitoring unit benoit blanchet dabrafenib-treated melanoma patients health-related quality braf-mutated melanoma raf inhibitors activate falchook gs untreated brain metastases braf inhibitors equal drug interaction potential mol cancer ther pharmacokinetic profile

Questions {❓}

  • Paradoxical oncogenesis: are all BRAF inhibitors equal?

Schema {🗺️}

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      headline:Clinical Pharmacokinetics and Pharmacodynamics of Dabrafenib
      description:Dabrafenib is a potent and selective inhibitor of BRAF-mutant kinase that is approved, as monotherapy or in combination with trametinib (mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor), for unresectable or metastatic BRAF-mutated melanoma, advanced non-small cell lung cancer and anaplastic thyroid cancer harbouring the BRAFV600E mutation. The recommended dose of dabrafenib is 150 mg twice daily (bid) under fasted conditions. After single oral administration of the recommended dose, the absolute oral bioavailability (F) of dabrafenib is 95%. Dabrafenib shows a time-dependent increase in apparent clearance (CL/F) following multiple doses, which is likely due to induction of its own metabolism through cytochrome P450 (CYP) 3A4. Therefore, steady state is reached only after 14 days of daily dose administration. Moreover, the extent of this auto-induction process is dependent on the dose, which explains why dabrafenib systemic exposure at steady state increases less than dose proportionally over the dose range of 75–300 mg bid. The main elimination route of dabrafenib is the oxidative metabolism via CYP3A4/2C8 and biliary excretion. Among the three major metabolites identified, hydroxy-dabrafenib appears to contribute to the pharmacological activity. Age, sex and body weight did not have any clinically significant influence on plasma exposure to dabrafenib. No dose adjustment is needed for patients with mild renal or hepatic impairment, whereas the impacts of severe impairment on dabrafenib pharmacokinetics remain unknown. Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug–drug interactions are expected with dabrafenib. The relationship between clinical outcomes and plasma exposure to dabrafenib and hydroxy-dabrafenib should be investigated more deeply.
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