Trichostatin A (VTR-297)
Relapsed or Refractory Hematologic Malignancies
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Catalyst Info & Data Links
TITLE: Trichostatin A (VTR-297) for Relapsed or Refractory Hematologic Malignancies
ClinicalTrial.gov (NCT03838926): Tolerability Study of Trichostatin A In Subjects With Relapsed or Refractory Hematologic Malignancies
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MECHANISM OF ACTION / RATIONALE
Acetylation and deacetylation of histones play an important role in transcription regulation of eukaryotic cells (Lehrmann et al., 2002; Mai et al., 2005). The acetylation status of histones and non-histone proteins is determined by histone deacetylases (HDACs) and histone acetyl-transferases (HATs). HATs add acetyl groups to lysine residues, while HDACs remove the acetyl groups. In general, acetylation of histone promotes a more relaxed chromatin structure, allowing transcriptional activation. HDACs can act as transcription repressors, due to histone deacetylation, and consequently promote chromatin condensation. HDAC inhibitors (HDACi) selectively alter gene transcription, in part, by chromatin remodeling and by changes in the structure of proteins in transcription factor complexes (Gui et al., 2004). Further, the HDACs have many non-histone proteins substrates such as hormone receptors, chaperone proteins and cytoskeleton proteins, which regulate cell proliferation and cell death (Table 1). Thus, HDACi-induced transformed cell death involves transcription-dependent and transcription-independent mechanisms (Learn more).
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#VNDA, #Trichostatin_A, #VTR-297, #Hematologic_Malignancies
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