entinostat has been researched along with Metastase in 10 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "This study identified the MTD of the entinostat, lapatinib, and trastuzumab combination that provided acceptable tolerability and anti-tumour activity in heavily pre-treated patients with HER2+ metastatic breast cancer, supporting a confirmatory trial." | 9.30 | A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment. ( Alvarez, R; Barcenas, CH; Booser, DJ; Brewster, AM; Brown, PH; Davis, DW; Giordano, SH; Ibrahim, NK; Iwase, T; Jackson, SA; Lee, J; Lim, B; Moscow, JA; Moulder, SL; Murthy, RK; Piekarz, R; Shen, Y; Tripathy, D; Ueno, NT; Valero, V; Willey, JS; Wu, J, 2019) |
| "Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to hormonal therapies in estrogen receptor-positive (ER+) breast cancer." | 9.17 | Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata ( Cruickshank, S; Ismail-Khan, RR; Klein, PM; Lee, MJ; Lichinitser, M; Melichar, B; Miller, KD; Munster, PN; Trepel, JB; Yardley, DA, 2013) |
| "This study identified the MTD of the entinostat, lapatinib, and trastuzumab combination that provided acceptable tolerability and anti-tumour activity in heavily pre-treated patients with HER2+ metastatic breast cancer, supporting a confirmatory trial." | 5.30 | A phase Ib study of entinostat plus lapatinib with or without trastuzumab in patients with HER2-positive metastatic breast cancer that progressed during trastuzumab treatment. ( Alvarez, R; Barcenas, CH; Booser, DJ; Brewster, AM; Brown, PH; Davis, DW; Giordano, SH; Ibrahim, NK; Iwase, T; Jackson, SA; Lee, J; Lim, B; Moscow, JA; Moulder, SL; Murthy, RK; Piekarz, R; Shen, Y; Tripathy, D; Ueno, NT; Valero, V; Willey, JS; Wu, J, 2019) |
| "Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to hormonal therapies in estrogen receptor-positive (ER+) breast cancer." | 5.17 | Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromata ( Cruickshank, S; Ismail-Khan, RR; Klein, PM; Lee, MJ; Lichinitser, M; Melichar, B; Miller, KD; Munster, PN; Trepel, JB; Yardley, DA, 2013) |
| "Oxidative stress attenuates melanoma metastasis, and melanoma cells must reduce oxidative stress to metastasize." | 1.51 | Class I HDAC inhibitors enhance YB-1 acetylation and oxidative stress to block sarcoma metastasis. ( Cheng, H; Colborne, S; Cran, J; Delaidelli, A; Delattre, O; El-Naggar, AM; Gleave, M; Hughes, CS; Huntsman, DG; Kedersha, N; Mandinova, A; Morin, GB; Negri, GL; Pan, M; Rafn, B; Somasekharan, SP; Sorensen, PH; Surdez, D; Wang, XQ; Wang, Y; Zhang, F; Zhang, H, 2019) |
| "Entinostat treatment was able to reduce the CD44(high)/CD24(low) cell population, ALDH-1 activity, as well as protein and mRNA expression of known TIC markers such as Bmi-1, Nanog, and Oct-4." | 1.42 | Histone Deacetylase Inhibitor Entinostat Inhibits Tumor-Initiating Cells in Triple-Negative Breast Cancer Cells. ( Kazi, A; Sabnis, G; Schech, A; Shah, P; Yu, S, 2015) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (10.00) | 29.6817 |
| 2010's | 7 (70.00) | 24.3611 |
| 2020's | 2 (20.00) | 2.80 |
| Authors | Studies |
|---|---|
| El-Naggar, AM | 1 |
| Somasekharan, SP | 1 |
| Wang, Y | 4 |
| Cheng, H | 1 |
| Negri, GL | 1 |
| Pan, M | 1 |
| Wang, XQ | 1 |
| Delaidelli, A | 1 |
| Rafn, B | 1 |
| Cran, J | 1 |
| Zhang, F | 1 |
| Zhang, H | 2 |
| Colborne, S | 1 |
| Gleave, M | 1 |
| Mandinova, A | 1 |
| Kedersha, N | 1 |
| Hughes, CS | 1 |
| Surdez, D | 1 |
| Delattre, O | 1 |
| Huntsman, DG | 1 |
| Morin, GB | 1 |
| Sorensen, PH | 1 |
| Kiweler, N | 1 |
| Wünsch, D | 1 |
| Wirth, M | 1 |
| Mahendrarajah, N | 1 |
| Schneider, G | 1 |
| Stauber, RH | 1 |
| Brenner, W | 1 |
| Butter, F | 1 |
| Krämer, OH | 1 |
| Lu, Z | 1 |
| Zou, J | 1 |
| Li, S | 1 |
| Topper, MJ | 1 |
| Tao, Y | 1 |
| Jiao, X | 1 |
| Xie, W | 1 |
| Kong, X | 1 |
| Vaz, M | 1 |
| Li, H | 1 |
| Cai, Y | 1 |
| Xia, L | 1 |
| Huang, P | 1 |
| Rodgers, K | 1 |
| Lee, B | 1 |
| Riemer, JB | 1 |
| Day, CP | 1 |
| Yen, RC | 1 |
| Cui, Y | 1 |
| Zhang, W | 1 |
| Easwaran, H | 1 |
| Hulbert, A | 1 |
| Kim, K | 2 |
| Juergens, RA | 1 |
| Yang, SC | 1 |
| Battafarano, RJ | 1 |
| Bush, EL | 1 |
| Broderick, SR | 1 |
| Cattaneo, SM | 1 |
| Brahmer, JR | 1 |
| Rudin, CM | 1 |
| Wrangle, J | 1 |
| Mei, Y | 1 |
| Kim, YJ | 1 |
| Zhang, B | 1 |
| Wang, KK | 1 |
| Forde, PM | 1 |
| Margolick, JB | 1 |
| Nelkin, BD | 1 |
| Zahnow, CA | 1 |
| Pardoll, DM | 1 |
| Housseau, F | 1 |
| Baylin, SB | 1 |
| Shen, L | 1 |
| Brock, MV | 1 |
| Lim, B | 1 |
| Murthy, RK | 1 |
| Lee, J | 1 |
| Jackson, SA | 1 |
| Iwase, T | 1 |
| Davis, DW | 1 |
| Willey, JS | 1 |
| Wu, J | 1 |
| Shen, Y | 1 |
| Tripathy, D | 1 |
| Alvarez, R | 1 |
| Ibrahim, NK | 1 |
| Brewster, AM | 1 |
| Barcenas, CH | 1 |
| Brown, PH | 1 |
| Giordano, SH | 1 |
| Moulder, SL | 1 |
| Booser, DJ | 1 |
| Moscow, JA | 1 |
| Piekarz, R | 1 |
| Valero, V | 1 |
| Ueno, NT | 1 |
| Yardley, DA | 1 |
| Ismail-Khan, RR | 1 |
| Melichar, B | 1 |
| Lichinitser, M | 1 |
| Munster, PN | 1 |
| Klein, PM | 1 |
| Cruickshank, S | 1 |
| Miller, KD | 1 |
| Lee, MJ | 1 |
| Trepel, JB | 1 |
| Skora, AD | 1 |
| Li, Z | 1 |
| Liu, Q | 1 |
| Tam, AJ | 1 |
| Blosser, RL | 1 |
| Diaz, LA | 1 |
| Papadopoulos, N | 1 |
| Kinzler, KW | 1 |
| Vogelstein, B | 1 |
| Zhou, S | 1 |
| Schech, A | 1 |
| Kazi, A | 1 |
| Yu, S | 1 |
| Shah, P | 1 |
| Sabnis, G | 1 |
| Hiroshima, Y | 1 |
| Maawy, A | 1 |
| Zhang, Y | 1 |
| Zhang, N | 1 |
| Murakami, T | 1 |
| Chishima, T | 1 |
| Tanaka, K | 1 |
| Ichikawa, Y | 1 |
| Bouvet, M | 1 |
| Endo, I | 1 |
| Hoffman, RM | 1 |
| Srivastava, RK | 1 |
| Kurzrock, R | 1 |
| Shankar, S | 1 |
| Hölsken, A | 1 |
| Eyüpoglu, IY | 1 |
| Lueders, M | 1 |
| Tränkle, C | 1 |
| Dieckmann, D | 1 |
| Buslei, R | 1 |
| Hahnen, E | 1 |
| Blümcke, I | 1 |
| Siebzehnrübl, FA | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase 2, Randomized, Double-Blind, Multicenter Study of Exemestane With and Without SNDX-275 in Postmenopausal Women With Locally Recurrent or Metastatic Estrogen Receptor-Positive Breast Cancer, Progressing on Treatment With a Non-Steroidal Aromatase I[NCT00676663] | Phase 2 | 130 participants (Actual) | Interventional | 2008-06-13 | Completed | ||
| A Phase I Study of Entinostat in Combination With Enzalutamide for Treatment of Patients With Castration-Resistant Prostate Cancer[NCT03829930] | Phase 1 | 6 participants (Actual) | Interventional | 2019-05-01 | Terminated (stopped due to Sponsor discontinued the drug) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
CBR is defined as the percentage of participants with overall response (CR + PR) plus stable disease (SD) for 6 months as assessed by the investigator based on RECIST, version 1.0. CR is defined as the disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or intolerable AE up to primary completion date (Median follow-up 6 months)
| Intervention | percentage of participants (Number) |
|---|---|
| Exemestane 25 mg + Placebo | 25.8 |
| Exemestane 25 mg + Entinostat 5 mg | 26.6 |
ORR is defined as the percentage of participants with response during treatment classified as complete response (CR) or partial response (PR), as assessed by the investigator based on Response Evaluation Criteria in Solid Tumors (RECIST), version 1.0. CR is defined as the disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or intolerable Adverse Event (AE) up to primary completion date (Median follow-up 6 months)
| Intervention | percentage of participants (Number) |
|---|---|
| Exemestane 25 mg + Placebo | 4.6 |
| Exemestane 25 mg + Entinostat 5 mg | 4.7 |
OS was defined as the number of months elapsed between the date of randomization and the date of death (whatever the cause). (NCT00676663)
Timeframe: First dose of study drug to end of study (Median follow-up 24 months in the EE arm and 26.4 months in the EP arm)
| Intervention | months (Median) |
|---|---|
| Exemestane 25 mg + Placebo (EP) | 19.84 |
| Exemestane 25 mg + Entinostat 5 mg (EE) | 28.13 |
PFS is defined as the number of months from the date of randomization to the earlier of progressive disease (PD) or death due to any cause. (NCT00676663)
Timeframe: From date of randomization to discontinuation due to disease progression or death up to primary completion date (Median follow-up 6 months)
| Intervention | months (Median) |
|---|---|
| Exemestane 25 mg + Placebo | 2.27 |
| Exemestane 25 mg + Entinostat 5 mg | 4.28 |
"An AE is defined as any untoward medical occurrence in a patient or clinical investigation patient administered a pharmaceutical product and that does not necessarily have a causal relationship with this treatment. Worsening of a pre-existing medical condition was considered an AE if there was either an increase in severity, frequency, or duration of the condition or an association with significantly worse outcomes. Abnormal clinical laboratory findings determined by the investigator to be clinically significant were recorded as AEs. A TEAE is an AE that starts after the administration of study drug.~A SAE is any AE that is fatal, life threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth effect or other significant medical hazard." (NCT00676663)
Timeframe: First dose to within 30 days of last dose of study drug (Up to Approximately 2 Years)
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| TEAE | SAE | |
| Exemestane 25 mg + Entinostat 5 mg | 60 | 10 |
| Exemestane 25 mg + Placebo | 56 | 8 |
2 trials available for entinostat and Metastase
8 other studies available for entinostat and Metastase
| Article | Year |
|---|---|
Class I HDAC inhibitors enhance YB-1 acetylation and oxidative stress to block sarcoma metastasis.
Topics: Acetylation; Animals; Antineoplastic Agents; Benzamides; Bone Neoplasms; Cell Line, Tumor; Cells, Cu | 2019 |
Histone deacetylase inhibitors dysregulate DNA repair proteins and antagonize metastasis-associated processes.
Topics: Animals; Benzamides; Cell Plasticity; Cisplatin; DNA Repair; DNA Repair Enzymes; DNA-Binding Protein | 2020 |
Epigenetic therapy inhibits metastases by disrupting premetastatic niches.
Topics: Animals; Azacitidine; Benzamides; Cell Differentiation; Cell Movement; Chemotherapy, Adjuvant; Disea | 2020 |
Eradication of metastatic mouse cancers resistant to immune checkpoint blockade by suppression of myeloid-derived cells.
Topics: Animals; Antibodies, Monoclonal; Azacitidine; Benzamides; Cell Line, Tumor; Colorectal Neoplasms; Co | 2014 |
Histone Deacetylase Inhibitor Entinostat Inhibits Tumor-Initiating Cells in Triple-Negative Breast Cancer Cells.
Topics: Animals; Antineoplastic Agents; Benzamides; Biomarkers; CD24 Antigen; Cell Line, Tumor; Disease Mode | 2015 |
Patient-derived mouse models of cancer need to be orthotopic in order to evaluate targeted anti-metastatic therapy.
Topics: Animals; Benzamides; Disease Models, Animal; Female; Humans; Mice; Neoplasm Metastasis; Precision Me | 2016 |
MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition in vivo.
Topics: Animals; Apoptosis; Benzamides; Breast Neoplasms; Caspase 3; Cell Line, Tumor; Cell Proliferation; D | 2010 |
Ex vivo therapy of malignant melanomas transplanted into organotypic brain slice cultures using inhibitors of histone deacetylases.
Topics: Animals; Benzamides; Blood-Brain Barrier; Brain; Brain Neoplasms; Cell Line, Tumor; Cell Proliferati | 2006 |