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

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==Clinical trials==
 
==Clinical trials==
 
*[http://www.syndax.com/dev-clinical.aspx List of Entinostat clinical trials]
 
*[http://www.syndax.com/dev-clinical.aspx List of Entinostat clinical trials]
*Breast cancer
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*[[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 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]
 
**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]
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==References==
 
==References==
 
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[[Category:HDAC inhibitors]]
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[[Category:Breast cancer medications]]
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[[Category:Investigational]]

Revision as of 23:31, 23 November 2014

In clinical trials. Also known as MS-275, SNDX-275.

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.

Clinical trials

Patient drug information

No information available.

References