Syndax Pharma 
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  • ||||||||||  cisplatin / Generic mfg.
    [VIRTUAL] Cisplatin chemoresistance and chromatin dynamics in oral carcinoma: opportunities for epi-drugs administration in solid tumors? () -  May 30, 2021 - Abstract #EACR2021EACR_1851;    
    Xenograft model demonstrated that cisplatin as a monotherapy increased the growth of chemoresistant tumors and epi-drugs in combination with cisplatin decreased tumor growth, but entinostat and vorinostat administered as monotherapy were more efficient to decrease tumor growth. Conclusion In summary, cisplatin alters epigenetic machinery, which promotes CSC accumulation and aceletares tumor growth and the administration of epi-drugs as monotherapy reverses the effects of chemoresistance.
  • ||||||||||  cisplatin / Generic mfg.
    [VIRTUAL] Cisplatin chemoresistance and chromatin dynamics in oral carcinoma: opportunities for epi-drugs administration in solid tumors? () -  May 30, 2021 - Abstract #EACR2021EACR_1850;    
    Xenograft model demonstrated that cisplatin as a monotherapy increased the growth of chemoresistant tumors and epi-drugs in combination with cisplatin decreased tumor growth, but entinostat and vorinostat administered as monotherapy were more efficient to decrease tumor growth. Conclusion In summary, cisplatin alters epigenetic machinery, which promotes CSC accumulation and aceletares tumor growth and the administration of epi-drugs as monotherapy reverses the effects of chemoresistance.
  • ||||||||||  cisplatin / Generic mfg.
    [VIRTUAL] Cisplatin chemoresistance and chromatin dynamics in oral carcinoma: opportunities for epi-drugs administration in solid tumors? () -  May 30, 2021 - Abstract #EACR2021EACR_1849;    
    Xenograft model demonstrated that cisplatin as a monotherapy increased the growth of chemoresistant tumors and epi-drugs in combination with cisplatin decreased tumor growth, but entinostat and vorinostat administered as monotherapy were more efficient to decrease tumor growth. Conclusion In summary, cisplatin alters epigenetic machinery, which promotes CSC accumulation and aceletares tumor growth and the administration of epi-drugs as monotherapy reverses the effects of chemoresistance.
  • ||||||||||  cisplatin / Generic mfg.
    [VIRTUAL] Cisplatin chemoresistance and chromatin dynamics in oral carcinoma: opportunities for epi-drugs administration in solid tumors? () -  May 30, 2021 - Abstract #EACR2021EACR_1848;    
    Xenograft model demonstrated that cisplatin as a monotherapy increased the growth of chemoresistant tumors and epi-drugs in combination with cisplatin decreased tumor growth, but entinostat and vorinostat administered as monotherapy were more efficient to decrease tumor growth. Conclusion In summary, cisplatin alters epigenetic machinery, which promotes CSC accumulation and aceletares tumor growth and the administration of epi-drugs as monotherapy reverses the effects of chemoresistance.
  • ||||||||||  Epidaza (chidamide) / Chipscreen, Meiji Seika, Eisai, HUYA Bioscience, entinostat (SNDX-275) / Kyowa Kirin, Syndax Pharma
    Journal:  CAP rigidification of MS-275 and chidamide leads to enhanced antiproliferative effects mediated through HDAC1, 2 and tubulin polymerization inhibition. (Pubmed Central) -  May 27, 2021   
    In pursuit of extracting the benefits of evidenced microtubule-destabilizing activity of the anilide 7, it was further evaluated against non-small-cell lung cancer cell lines as well as the multiple-drug resistant uterine cancer cell line (MES-SA/Dx5) and overwhelmingly positive results in context of inhibitory effects were attained. Furthermore, molecular modelling studies were performed and some key interactions of the anilide 7 with the amino acid residues of the active site of HDAC1 isoform and tubulin were figured out.
  • ||||||||||  Epidaza (chidamide) / Chipscreen, Meiji Seika, Eisai, HUYA Bioscience
    Journal, Epigenetic controller:  In situ exploring Chidamide, a histone deacetylase inhibitor, induces molecular changes of leukemic T-lymphocyte apoptosis using Raman spectroscopy. (Pubmed Central) -  May 15, 2021   
    Importantly, our research is the first to demonstrate that the action site of HDAC inhibitors on Jurkat cell is located in the DNA minor groove. Most importantly, the application of Raman spectrum in exploring in-situ molecular changes information, histone acetylation modification in epigenetics, drug action sites and cell cycle affected by HDAC inhibitors will supply new idea and reference for the design and modification of HDAC inhibitors.
  • ||||||||||  axatilimab (SNDX-6352) / Syndax Pharma, Incyte
    Enrollment closed, Trial completion date, Trial primary completion date:  SNDX-6352-0503: A Phase 1/2 Study to Evaluate SNDX- 6352 in Participants With Active cGVHD (clinicaltrials.gov) -  May 14, 2021   
    P1/2,  N=37, Active, not recruiting, 
    Most importantly, the application of Raman spectrum in exploring in-situ molecular changes information, histone acetylation modification in epigenetics, drug action sites and cell cycle affected by HDAC inhibitors will supply new idea and reference for the design and modification of HDAC inhibitors. Recruiting --> Active, not recruiting | Trial completion date: Jun 2021 --> May 2022 | Trial primary completion date: Dec 2020 --> Nov 2021
  • ||||||||||  Zarzio (filgrastim biosimilar) / Novartis
    [VIRTUAL] NUP98/NSD1-POSITIVE AML IS ADDICTED TO A FUNCTIONAL MENIN-MLL INTERACTION () -  May 13, 2021 - Abstract #EHA2021EHA_898;    
    Notably, we found that and its potential target gene FLT3 are uniformly downregulated in a dose dependent manner suggesting an impact of this drug on a secondary leukaemic driver. Conclusion This study demonstrates the relevance of the Menin-MLL interaction for NUP98/NSD1-driven leukemogenesis in primary patient cells and highlights the pharmacologic inhibition of this interaction as a promising therapeutic option for this poor prognosis AML.
  • ||||||||||  Venclexta (venetoclax) / Roche, AbbVie, Zarzio (filgrastim biosimilar) / Novartis
    [VIRTUAL] MENIN INHIBITION DECREASES BCL-2 AND SYNERGIZES WITH VENETOCLAX IN NPM1/FLT3-MUTATED AML () -  May 13, 2021 - Abstract #EHA2021EHA_895;    
    Aims To investigate the anti-leukemic activity and potential synergism and mechanisms of the combination of the menin-MLL1 inhibitor SDNX-50469, an equipotent surrogate of the clinical compound SNDX-5613 and venetoclax in vivo in an NPM1c/FLT3-ITD/TKD patient-derived xenograft (PDX) model...Conclusion Our study further validated menin as a therapeutic target and demonstrated that its inhibition synergizes with venetoclax in NPM1/FLT3-mutated AML, which warrants further clinical evaluation. Inhibition of FLT3 may further enhance the therapeutic efficacy of menin and Bcl-2 co-targeting in NPM1 and FLT3 mutated AML.
  • ||||||||||  Desferal (deferoxamine) / Kermanshah University of Medical Sciences, Novartis, entinostat (SNDX-275) / Kyowa Kirin, Syndax Pharma
    Journal:  Effects of Environmental Conditions on Nephron Number: Modeling Maternal Disease and Epigenetic Regulation in Renal Development. (Pubmed Central) -  May 13, 2021   
    Among the selected epigenetic inhibitors, various compounds elicited an effect on renal growth, such as HDAC (entinostat, TH39), histone demethylase (deferasirox, deferoxamine) and histone methyltransferase (cyproheptadine) inhibitors. Thus, metanephric organ cultures provide a valuable system for studying metabolic conditions and a tool for screening for epigenetic modifiers in renal development.
  • ||||||||||  Keytruda (pembrolizumab) / Merck (MSD), Jingzhuda (entinostat) / EOC Pharma, EddingPharm
    Trial primary completion date, Metastases:  An Exploratory Study of Pembrolizumab Plus Entinostat in Non-Inflamed Stage III/IV Melanoma (clinicaltrials.gov) -  May 11, 2021   
    P2,  N=14, Recruiting, 
    Class 1 HDACs may be considered as targets for the macrophage-initiated pulmonary inflammation in ALI in a preclinical setting. Trial primary completion date: Dec 2020 --> Dec 2022
  • ||||||||||  entinostat (SNDX-275) / Kyowa Hakko Kirin, Syndax Pharma
    Journal:  Protein acetylation derepresses Serotonin Synthesis to potentiate Pancreatic Beta-Cell Function through HDAC1-PKA-Tph1 signaling. (Pubmed Central) -  May 4, 2021   
    Specifically, inhibition of HDAC1 and HDAC3 by MS-275 strongly promoted Tph1 expression and endogenous serotonin synthesis in rat islets, concomitantly with enhanced insulin secretory capacity in vivo and ex vivo...HDAC1 inhibition exerted a synergistic effect with cAMP/PKA signal on Tph1 expression. The present findings highlight a novel role of HDAC1-PKA-Tph1 signaling in governing β-cell functional compensation by derepressing serotonin synthesis.
  • ||||||||||  entinostat (SNDX-275) / Kyowa Hakko Kirin, Syndax Pharma
    Journal:  Reduced chromatin binding of MYC is a key effect of HDAC inhibition in MYC amplified medulloblastoma. (Pubmed Central) -  Apr 28, 2021   
    The substantial weight loss suggests a potential adverse metabolic interaction between these drugs. Our data elucidates the molecular interaction of MYC and HDAC2 and support a model in which inhibition of class I HDACs directly targets MYC´s trans-activating and trans-repressing function.
  • ||||||||||  Keytruda (pembrolizumab) / Merck (MSD), Jingzhuda (entinostat) / EOC Pharma, EddingPharm
    Trial completion date, Trial primary completion date, Combination therapy:  Combination Therapy With Entinostat and Pembrolizumab in Relapsed and Refractory Lymphomas (clinicaltrials.gov) -  Apr 22, 2021   
    P2,  N=47, Recruiting, 
    Our data elucidates the molecular interaction of MYC and HDAC2 and support a model in which inhibition of class I HDACs directly targets MYC´s trans-activating and trans-repressing function. Trial completion date: Jun 2021 --> Jun 2022 | Trial primary completion date: Jun 2021 --> Jun 2022
  • ||||||||||  entinostat (SNDX-275) / Kyowa Hakko Kirin, Syndax Pharma
    Preclinical, Journal:  Differential effects of HDAC inhibitors on PPN oscillatory activity in vivo. (Pubmed Central) -  Mar 31, 2021   
    Rat pups were injected (acute, single dose) with TSA (4 or 20 mg/kg), MC1568 (4 or 20 mg/kg), or MS275 (20 or 100 mg/kg)...In conclusion, the present results in vivo validate our previous findings in vitro and further expand information on the effects of HDAC inhibition on PPN rhythmicity. PPN neurons require normal activity of HDAC class IIa in order to oscillate at gamma band.
  • ||||||||||  entinostat (SNDX-275) / Kyowa Hakko Kirin, Syndax Pharma
    Journal:  Synthesis and biological study of class I selective HDAC inhibitors with NO releasing activity. (Pubmed Central) -  Mar 30, 2021   
    It is worth noting that compounds 7c, 7d and 7e exhibited more potent in vitro antiproliferative activities than MS275 against all four tested solid tumor cell lines. The promising in vivo antitumor potency of 7c was demonstrated in a HCT116 xenograft model.
  • ||||||||||  Jingzhuda (entinostat) / EOC Pharma, EddingPharm
    Enrollment change, Trial termination:  Window of Opportunity Trial of Entinostat in Patients With Newly Diagnosed Stage I-IIIC,TNBC (clinicaltrials.gov) -  Mar 25, 2021   
    P1,  N=5, Terminated, 
    The promising in vivo antitumor potency of 7c was demonstrated in a HCT116 xenograft model. N=20 --> 5 | Active, not recruiting --> Terminated; Funding withdrawn.
  • ||||||||||  entinostat (SNDX-275) / Kyowa Hakko Kirin, Syndax Pharma
    Journal:  High salt intake induces collecting duct HDAC1-dependent NO signaling. (Pubmed Central) -  Mar 23, 2021   
    Ex vivo treatment of dissociated IM from HS-fed mice with a selective HDAC1 inhibitor (MS-275) decreased NO production with no change in ET-1 peptide or mRNA levels...Moreover, flow-induced increases in mIMCD-3 cell NO production were blunted by HDAC1 or calcium inhibition. Taken together, these findings indicate that HS intake induces HDAC1-dependent activation of the ETR/NO pathway contributing to the natriuretic response.
  • ||||||||||  temozolomide / Generic mfg.
    [VIRTUAL] Response to novel imipridone combination therapies targeting H3K27M mutant diffuse midline glioma (DMG) () -  Mar 13, 2021 - Abstract #AACR2021AACR_4371;    
    We sought to identify synergy between ONC201 or second generation impridones (ONC206 and ONC212), and other chemotherapeutics with known promising pre-clinical activity against DMGs.Seven patient derived H3K27M mutant DIPG cell lines (SU-DIPG-IV, SU-DIPG-13, SU-DIPG-25, SUDIPG-27, SU-DIPG-29, SU-DIPG-36, SF8628) were grown in culture and exposed to ONC201, ONC206, or ONC212 either as monotherapy or in combination with other FDA approved chemotherapeutics (histone de-acetylase inhibitors [HDACi], marizomib, etoposide, and temozolomide)...We identified strong synergy between ONC201 and HDAC inhibitors: Panobinostat (CI 0.01) and Romidepsin (CI 0.08), with lesser synergy detected with Entinostat (CI 0.59)...Our results suggest an increased sensitivity of H3K27M DIPG cell lines to second generation imipridones as compared to ONC201. Additionally, we have shown promising synergism between imipridones with Panobinostat or Romidepsin, which should be considered for clinical translation.