entinostat has been researched along with Acute Myelogenous Leukemia in 15 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "Entinostat is a histone deacetylase inhibitor that has been combined with AZA with significant clinical activity in a previous phase I dose finding study." | 2.79 | Prolonged administration of azacitidine with or without entinostat for myelodysplastic syndrome and acute myeloid leukemia with myelodysplasia-related changes: results of the US Leukemia Intergroup trial E1905. ( Czader, M; Erba, HP; Figueroa, ME; Gabrilove, J; Gore, SD; Greenberg, PL; Herman, J; Juckett, M; Ketterling, R; Litzow, M; Malick, L; Melnick, A; Paietta, E; Prebet, T; Smith, MR; Sun, Z; Tallman, MS, 2014) |
| " The N-hydroxyl group of this motif is highly subject to sulfation/glucoronidation-based inactivation in humans; compounds containing this motif require much higher dosing in clinic to achieve therapeutic concentrations." | 1.43 | Development of Allosteric Hydrazide-Containing Class I Histone Deacetylase Inhibitors for Use in Acute Myeloid Leukemia. ( Chou, CJ; Inks, ES; Li, J; McClure, JJ; Peterson, YK; Zhang, C, 2016) |
| "The incidence of refractory acute myeloid leukemia (AML) is on the increase due in part to an aging population that fails to respond to traditional therapies." | 1.39 | Entinostat prevents leukemia maintenance in a collaborating oncogene-dependent model of cytogenetically normal acute myeloid leukemia. ( Austin, P; Bijl, JJ; Cellot, S; Dickson, GJ; Kettyle, LM; Krosl, J; Lappin, TR; Mayotte, N; Mills, KI; Mulgrew, NM; Ramsey, JM; Sauvageau, G; Sharpe, DJ; Thompson, A; Zhang, SD, 2013) |
| "We have recently established the MV4-11 acute myelogenous leukemia (AML) subline, designated as MV4-11 TP53 R248W, which possesses a missense mutation (CGG→TGG; R248W) in the TP53 gene, leading to inactivation of this transcription factor." | 1.37 | Simultaneous inhibition of DNA methyltransferase and histone deacetylase induces p53-independent apoptosis via down-regulation of Mcl-1 in acute myelogenous leukemia cells. ( Ikezoe, T; Nishioka, C; Udaka, K; Yang, J; Yokoyama, A, 2011) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 3 (20.00) | 29.6817 |
| 2010's | 10 (66.67) | 24.3611 |
| 2020's | 2 (13.33) | 2.80 |
| Authors | Studies |
|---|---|
| McClure, JJ | 1 |
| Zhang, C | 1 |
| Inks, ES | 2 |
| Peterson, YK | 2 |
| Li, J | 1 |
| Chou, CJ | 2 |
| Li, X | 1 |
| Jiang, Y | 2 |
| Xu, T | 1 |
| Himes, RA | 1 |
| Luo, X | 1 |
| Yin, G | 1 |
| Dolloff, N | 1 |
| Halene, S | 1 |
| Chan, SSL | 1 |
| Zeyen, P | 1 |
| Zeyn, Y | 1 |
| Herp, D | 1 |
| Mahmoudi, F | 1 |
| Yesiloglu, TZ | 1 |
| Erdmann, F | 1 |
| Schmidt, M | 1 |
| Robaa, D | 1 |
| Romier, C | 1 |
| Ridinger, J | 1 |
| Herbst-Gervasoni, CJ | 1 |
| Christianson, DW | 1 |
| Oehme, I | 1 |
| Jung, M | 1 |
| Krämer, OH | 1 |
| Sippl, W | 1 |
| Press, KR | 1 |
| Uy, N | 1 |
| Keefer, J | 1 |
| Gore, SD | 4 |
| Carraway, HE | 1 |
| Sakoian, S | 2 |
| Prebet, T | 3 |
| Ramsey, JM | 1 |
| Kettyle, LM | 1 |
| Sharpe, DJ | 1 |
| Mulgrew, NM | 1 |
| Dickson, GJ | 1 |
| Bijl, JJ | 1 |
| Austin, P | 1 |
| Mayotte, N | 1 |
| Cellot, S | 1 |
| Lappin, TR | 1 |
| Zhang, SD | 1 |
| Mills, KI | 1 |
| Krosl, J | 1 |
| Sauvageau, G | 1 |
| Thompson, A | 1 |
| Blagitko-Dorfs, N | 1 |
| Duque-Afonso, J | 1 |
| Hiller, J | 1 |
| Yalcin, A | 1 |
| Greve, G | 1 |
| Abdelkarim, M | 1 |
| Hackanson, B | 1 |
| Lübbert, M | 1 |
| Sun, Z | 2 |
| Figueroa, ME | 1 |
| Ketterling, R | 1 |
| Melnick, A | 1 |
| Greenberg, PL | 1 |
| Herman, J | 2 |
| Juckett, M | 2 |
| Smith, MR | 2 |
| Malick, L | 2 |
| Paietta, E | 2 |
| Czader, M | 2 |
| Litzow, M | 2 |
| Gabrilove, J | 2 |
| Erba, HP | 2 |
| Tallman, MS | 2 |
| Ketterling, RP | 1 |
| Zeidan, A | 1 |
| Greenberg, P | 1 |
| Figueroa, M | 1 |
| Robert, C | 1 |
| Nagaria, PK | 1 |
| Pawar, N | 1 |
| Adewuyi, A | 1 |
| Gojo, I | 1 |
| Meyers, DJ | 1 |
| Cole, PA | 1 |
| Rassool, FV | 1 |
| Norsworthy, KJ | 1 |
| Cho, E | 1 |
| Arora, J | 1 |
| Kowalski, J | 1 |
| Tsai, HL | 1 |
| Warlick, E | 1 |
| Showel, M | 1 |
| Pratz, KW | 1 |
| Sutherland, LA | 1 |
| Ferguson, A | 1 |
| Greer, J | 1 |
| Espinoza-Delgado, I | 1 |
| Jones, RJ | 1 |
| Matsui, WH | 1 |
| Smith, BD | 1 |
| Nishioka, C | 4 |
| Ikezoe, T | 4 |
| Yang, J | 4 |
| Koeffler, HP | 3 |
| Yokoyama, A | 4 |
| Udaka, K | 1 |
| Zhou, L | 1 |
| Ruvolo, VR | 1 |
| McQueen, T | 1 |
| Chen, W | 1 |
| Samudio, IJ | 1 |
| Conneely, O | 1 |
| Konopleva, M | 1 |
| Andreeff, M | 1 |
| Takeuchi, S | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Dose-Finding Trial of the Histone Deacetylase Inhibitor MS-275 (NSC 706995) in Combination With 5-Azacitidine (5AC, NSC 102816) in Patients With Myelodysplastic Syndromes (MDS), Chronic Myelomonocytic Leukemia (CMMoL) and Acute Myeloid Leukemia (AML)[NCT00101179] | Phase 1 | 63 participants (Actual) | Interventional | 2004-11-03 | Completed | ||
| A Randomized Phase II Trial of Azacitidine With or Without the Histone Deacetylase Inhibitor Entinostat for the Treatment of Myelodysplastic Syndrome, Chronic Myelomonocytic Leukemia (Dysplastic Type), and Acute Myeloid Leukemia With Multilineage Dysplasi[NCT00313586] | Phase 2 | 197 participants (Actual) | Interventional | 2006-08-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
"Clinical response is defined as a complete response (CR), partial response (PR) or trilineage response (TR) graded according to the following criteria:~World Health Organization classification of the acute leukemias and myelodysplastic syndrome (by Bennett)~Myelodysplastic syndromes standardized response criteria: further definition (by Cheson et al.)~Report of an international working group to standardize response criteria for myelodysplastic syndromes (by Cheson et al.)" (NCT00313586)
Timeframe: Assessed every 3 months if patient is < 2 years from study entry, every 6 months if patient is 2 - 5 years from study entry.
| Intervention | Proportion of patients (Number) |
|---|---|
| Arm A (Azacitidine; Non-treatment-induced Cohort) | 0.32 |
| Arm B (Azacitidine + Entinostat; Non-treatment-induced Cohort) | 0.27 |
| Arm A (Azacitidine; Treatment-induced Cohort) | 0.46 |
| Arm B (Azacitidine + Entinostat; Treatment-induced Cohort) | 0.17 |
3 trials available for entinostat and Acute Myelogenous Leukemia
| Article | Year |
|---|---|
Prolonged administration of azacitidine with or without entinostat for myelodysplastic syndrome and acute myeloid leukemia with myelodysplasia-related changes: results of the US Leukemia Intergroup trial E1905.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherap | 2014 |
Azacitidine with or without Entinostat for the treatment of therapy-related myeloid neoplasm: further results of the E1905 North American Leukemia Intergroup study.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherap | 2016 |
Azacitidine with or without Entinostat for the treatment of therapy-related myeloid neoplasm: further results of the E1905 North American Leukemia Intergroup study.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherap | 2016 |
Azacitidine with or without Entinostat for the treatment of therapy-related myeloid neoplasm: further results of the E1905 North American Leukemia Intergroup study.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherap | 2016 |
Azacitidine with or without Entinostat for the treatment of therapy-related myeloid neoplasm: further results of the E1905 North American Leukemia Intergroup study.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherap | 2016 |
Differentiation therapy in poor risk myeloid malignancies: Results of companion phase II studies.
Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Benzamides; Bexarotene; Female; Granulocyte-Macropha | 2016 |
12 other studies available for entinostat and Acute Myelogenous Leukemia
| Article | Year |
|---|---|
Development of Allosteric Hydrazide-Containing Class I Histone Deacetylase Inhibitors for Use in Acute Myeloid Leukemia.
Topics: Allosteric Regulation; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; HEK293 Cel | 2016 |
Design of Hydrazide-Bearing HDACIs Based on Panobinostat and Their p53 and FLT3-ITD Dependency in Antileukemia Activity.
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Drug Design; fms-Like Tyrosine Kinase 3; Histone D | 2020 |
Identification of histone deacetylase 10 (HDAC10) inhibitors that modulate autophagy in transformed cells.
Topics: Apoptosis; Autophagy; Histone Deacetylase 1; Histone Deacetylase 6; Histone Deacetylase Inhibitors; | 2022 |
Clinical evaluation of combined azacitidine and entinostat on the induction of fetal hemoglobin in patients with acute myeloid leukemias and myelodysplastic syndromes.
Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Azacitidine; Benzamides; Clinical Trials, Phas | 2018 |
Entinostat prevents leukemia maintenance in a collaborating oncogene-dependent model of cytogenetically normal acute myeloid leukemia.
Topics: Animals; Benzamides; Gene Expression Profiling; Gene Expression Regulation, Leukemic; Histone Deacet | 2013 |
Epigenetic priming of AML blasts for all-trans retinoic acid-induced differentiation by the HDAC class-I selective inhibitor entinostat.
Topics: Adult; Aged; Antineoplastic Agents; Benzamides; Cell Differentiation; Cell Line; DNA Methylation; Dr | 2013 |
Histone deacetylase inhibitors decrease NHEJ both by acetylation of repair factors and trapping of PARP1 at DNA double-strand breaks in chromatin.
Topics: Acetylation; Benzamides; Chromatin; DNA Breaks, Double-Stranded; DNA End-Joining Repair; Histone Dea | 2016 |
Blockade of mTOR signaling potentiates the ability of histone deacetylase inhibitor to induce growth arrest and differentiation of acute myelogenous leukemia cells.
Topics: Acetylation; Animals; Apoptosis; Benzamides; CCAAT-Enhancer-Binding Proteins; Cell Differentiation; | 2008 |
Simultaneous inhibition of DNA methyltransferase and histone deacetylase induces p53-independent apoptosis via down-regulation of Mcl-1 in acute myelogenous leukemia cells.
Topics: Apoptosis; Azacitidine; Benzamides; Blotting, Western; Cell Cycle; Cell Proliferation; Cyclin-Depend | 2011 |
HDAC inhibition by SNDX-275 (Entinostat) restores expression of silenced leukemia-associated transcription factors Nur77 and Nor1 and of key pro-apoptotic proteins in AML.
Topics: Antineoplastic Agents; Apoptosis; Base Sequence; Benzamides; Blotting, Western; DNA Primers; Flow Cy | 2013 |
Inhibition of MEK/ERK signaling synergistically potentiates histone deacetylase inhibitor-induced growth arrest, apoptosis and acetylation of histone H3 on p21waf1 promoter in acute myelogenous leukemia cell.
Topics: Acetylation; Apoptosis; Benzamides; Benzimidazoles; Cyclin-Dependent Kinase Inhibitor p21; Drug Syne | 2008 |
MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells.
Topics: Acetylation; Benzamides; Blotting, Western; Cell Cycle; Cell Proliferation; Enzyme Inhibitors; Femal | 2008 |