Difference between revisions of "Entinostat (SNDX-275)"

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'''In clinical trials.'''  Also known as MS-275, SNDX-275.
 
 
 
==General information==
 
==General information==
 
Class/mechanism: Histone deacetylase (HDAC) inhibitor.  Entinostat inhibits class I histone deacetylases, which regulate gene expression by affecting chromatin structure.  HDACs normally catalyze removal of acetyl groups from acetylated lysine residues in histones and non-histone proteins, which helps to regulate gene expression.  Inhibition of histone deacetylases results in hyperacetylation of histones and modulates gene expression by creating an open chromatin state that leads to expression of previously silenced genes.  Although the mechanism of action is not fully understood, inhibiting HDACs has been observed to result in cell cycle arrest and apoptosis of cancer cells.<ref>[http://www.syndax.com/dev-entinostat.aspx Entinostat manufacturer's website]</ref>
 
Class/mechanism: Histone deacetylase (HDAC) inhibitor.  Entinostat inhibits class I histone deacetylases, which regulate gene expression by affecting chromatin structure.  HDACs normally catalyze removal of acetyl groups from acetylated lysine residues in histones and non-histone proteins, which helps to regulate gene expression.  Inhibition of histone deacetylases results in hyperacetylation of histones and modulates gene expression by creating an open chromatin state that leads to expression of previously silenced genes.  Although the mechanism of action is not fully understood, inhibiting HDACs has been observed to result in cell cycle arrest and apoptosis of cancer cells.<ref>[http://www.syndax.com/dev-entinostat.aspx Entinostat manufacturer's website]</ref>
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For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as [http://www.thomsonhc.com/home/dispatch Micromedex], [http://online.lexi.com/ Lexicomp], [http://www.utdol.com/online/content/search.do UpToDate (courtesy of Lexicomp)], or the prescribing information.
 
For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as [http://www.thomsonhc.com/home/dispatch Micromedex], [http://online.lexi.com/ Lexicomp], [http://www.utdol.com/online/content/search.do UpToDate (courtesy of Lexicomp)], or the prescribing information.
 
==Clinical trials==
 
*[http://www.syndax.com/dev-clinical.aspx List of Entinostat clinical trials]
 
*[[Breast cancer]]
 
**ENCORE 303: [http://www.clinicaltrials.gov/ct2/show/NCT00828854 A Phase 2, Multicenter Study of the Effect of the Addition of SNDX-275 to Continued Aromatase Inhibitor (AI) Therapy in Postmenopausal Women With ER+ Breast Cancer Whose Disease is Progressing]
 
**ENCORE 301: [http://www.clinicaltrials.gov/ct2/show/NCT00676663 Study to Evaluate Exemestane With and Without SNDX-275 in Treatment of Postmenopausal Women With Advanced Breast Cancer]
 
**NCI 8597: [http://clinicaltrials.gov/ct2/show/NCT01234532 Entinostat and Anastrozole or Tamoxifen in Treating Women With Triple-Negative Breast Cancer That Can Be Removed by Surgery]
 
**NCI 8822: [http://clinicaltrials.gov/ct2/show/NCT01349959 Azacitidine and Entinostat in Treating Patients With Advanced Breast Cancer]
 
*Lung cancer
 
**ENCORE 401: [http://www.clinicaltrials.gov/ct2/show/NCT00602030 Study to Evaluate Erlotinib With or Without SNDX-275 in the Treatment of Patients With Advanced Non-Small Cell Lung Cancer (NSCLC)]
 
**NCI 7759: [http://www.clinicaltrials.gov/ct2/show/NCT00387465 Azacitidine and MS-275 in Treating Patients With Recurrent Advanced Non-Small Cell Lung Cancer]
 
**NCI 8311: [http://clinicaltrials.gov/ct2/show/NCT01207726 Trial of Adjuvant Combined Epigenetic Therapy With 5-azacitidine and Entinostat in Resected Stage I Non-small Cell Lung Cancer Versus Standard Care (J1037)]
 
*ENCORE 501: [http://www.clinicaltrials.gov/ct2/show/NCT00866333 A Phase 2 Multi-Center Study of Entinostat (SNDX-275) in Patient With Relapsed or Refractory Hodgkin's Lymphoma]
 
*NCI 7870: [http://clinicaltrials.gov/ct2/show/NCT01038778 Interleukin 2, Aldesleukin and Entinostat for Kidney Cancer]
 
*NCI 8298: [http://clinicaltrials.gov/ct2/show/NCT01132573 Entinostat and Clofarabine in Treating Patients With Newly Diagnosed, Relapsed, or Refractory Poor-Risk Acute Lymphoblastic Leukemia or Bilineage/Biphenotypic Leukemia]
 
*NCI 8272: [http://clinicaltrials.gov/ct2/show/NCT01159301 Entinostat and Sorafenib Tosylate in Treating Patients With Advanced or Metastatic Solid Tumors or Refractory or Relapsed Acute Myeloid Leukemia]
 
*NCI 8341: [http://clinicaltrials.gov/ct2/show/NCT01105377 Azacitidine and Entinostat in Treating Patients With Metastatic Colorectal Cancer]
 
  
 
==Patient drug information==
 
==Patient drug information==
 
No information available.
 
No information available.
  
 +
==Also known as==
 +
*'''Code names:''' MS-275, SNDX-275
 
==References==
 
==References==
 
<references/>
 
<references/>
  
 
[[Category:Drug index]]
 
[[Category:Drug index]]
[[Category:Chemotherapy]]
 
 
[[Category:Oral medications]]
 
[[Category:Oral medications]]
  

Revision as of 02:27, 30 April 2018

General information

Class/mechanism: Histone deacetylase (HDAC) inhibitor. Entinostat inhibits class I histone deacetylases, which regulate gene expression by affecting chromatin structure. HDACs normally catalyze removal of acetyl groups from acetylated lysine residues in histones and non-histone proteins, which helps to regulate gene expression. Inhibition of histone deacetylases results in hyperacetylation of histones and modulates gene expression by creating an open chromatin state that leads to expression of previously silenced genes. Although the mechanism of action is not fully understood, inhibiting HDACs has been observed to result in cell cycle arrest and apoptosis of cancer cells.[1]
Route: PO
Extravasation: n/a

For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the prescribing information.

Patient drug information

No information available.

Also known as

  • Code names: MS-275, SNDX-275

References