vorinostat has been researched along with Acute Myelogenous Leukemia in 58 studies
Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.
vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).
| Excerpt | Relevance | Reference |
|---|---|---|
| "To evaluate the safety and efficacy of the combination of the histone deacetylase inhibitor vorinostat with idarubicin and ara-C (cytarabine) in patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS)." | 9.16 | Phase II trial of vorinostat with idarubicin and cytarabine for patients with newly diagnosed acute myelogenous leukemia or myelodysplastic syndrome. ( Bekele, NB; Borthakur, G; Brandt, M; Cortes, JE; de Lima, M; Faderl, S; Garcia-Manero, G; Hu, Y; Jabbour, E; Kadia, TM; Kantarjian, HM; Konopleva, MY; McCue, D; Newsome, WM; Pierce, SR; Ravandi, F; Tambaro, FP; Yang, H, 2012) |
| " Interactions between resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in human acute myelogenous leukemia (AML) cells." | 7.78 | Resveratrol sensitizes acute myelogenous leukemia cells to histone deacetylase inhibitors through reactive oxygen species-mediated activation of the extrinsic apoptotic pathway. ( Chen, S; Dai, Y; Dent, P; Grant, S; Hock, S; Rosato, R; Yaseen, A, 2012) |
| "Vorinostat is an epigenetic targeted drug belonging to the histone deacetylase (HDAC) inhibitors family." | 6.47 | Vorinostat in acute myeloid leukemia and myelodysplastic syndromes. ( Prebet, T; Vey, N, 2011) |
| "To evaluate the safety and efficacy of the combination of the histone deacetylase inhibitor vorinostat with idarubicin and ara-C (cytarabine) in patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS)." | 5.16 | Phase II trial of vorinostat with idarubicin and cytarabine for patients with newly diagnosed acute myelogenous leukemia or myelodysplastic syndrome. ( Bekele, NB; Borthakur, G; Brandt, M; Cortes, JE; de Lima, M; Faderl, S; Garcia-Manero, G; Hu, Y; Jabbour, E; Kadia, TM; Kantarjian, HM; Konopleva, MY; McCue, D; Newsome, WM; Pierce, SR; Ravandi, F; Tambaro, FP; Yang, H, 2012) |
| " Interactions between resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in human acute myelogenous leukemia (AML) cells." | 3.78 | Resveratrol sensitizes acute myelogenous leukemia cells to histone deacetylase inhibitors through reactive oxygen species-mediated activation of the extrinsic apoptotic pathway. ( Chen, S; Dai, Y; Dent, P; Grant, S; Hock, S; Rosato, R; Yaseen, A, 2012) |
| "We determined the effects of vorinostat (suberoylanalide hydroxamic acid) and/or MK-0457 (VX-680), an Aurora kinase inhibitor on the cultured human (HL-60, OCI-AML3, and K562) and primary acute myelogenous leukemia (AML) and chronic myelogenous leukemia (CML), as well as on the murine pro-B BaF3 cells with ectopic expression of the unmutated and mutant forms of Bcr-Abl." | 3.74 | Cotreatment with vorinostat enhances activity of MK-0457 (VX-680) against acute and chronic myelogenous leukemia cells. ( Balusu, R; Bhalla, K; Buser, CA; Chen, J; Eaton, K; Fiskus, W; Jillella, A; Joshi, R; Kolhe, R; Lee, P; Peiper, S; Rao, R; Ustun, C; Wang, Y; Yang, Y, 2008) |
| "Older adults with acute myeloid leukemia (AML) are commonly considered for investigational therapies, which often only benefit subsets of patients." | 2.79 | Mcl-1 dependence predicts response to vorinostat and gemtuzumab ozogamicin in acute myeloid leukemia. ( Blake, N; Cardone, MH; Doykan, C; Elashoff, M; Lena, RJ; Medeiros, BC; Pierceall, WE; Walter, RB, 2014) |
| "To determine the maximum-tolerated dose (MTD) of the histone deacetylase inhibitor vorinostat combined with fixed doses of cytarabine (ara-C or cytosine arabinoside) and etoposide in patients with poor-risk or advanced acute leukemia, to obtain preliminary efficacy data, describe pharmacokinetics, and in vivo pharmacodynamic effects of vorinostat in leukemia blasts." | 2.78 | Translational phase I trial of vorinostat (suberoylanilide hydroxamic acid) combined with cytarabine and etoposide in patients with relapsed, refractory, or high-risk acute myeloid leukemia. ( Anyang, BN; Baer, MR; Beumer, JH; Carrier, F; Espinoza-Delgado, I; Fang, HB; Gojo, I; Lapidus, R; Ross, DD; Sadowska, M; Srivastava, RK; Tan, M, 2013) |
| " HDACi have single-agent clinical activity in haematological malignancies and have synergistic anti-leukaemia activity when combined with anthracyclines in vitro." | 2.75 | A phase I study of vorinostat in combination with idarubicin in relapsed or refractory leukaemia. ( Egorin, MJ; Espinoza-Delgado, I; Ferrajoli, A; Garcia-Manero, G; Holleran, JL; Kadia, TM; Kantarjian, HM; Madden, TL; Maddipotti, S; Newsome, W; Ravandi, F; Sanchez-Gonzalez, B; Schroeder, C; Thomas, DA; Yang, H; Zwiebel, JA, 2010) |
| "Patients with relapsed or untreated acute myeloid leukemia who were not candidates for chemotherapy entered one of the two treatment arms." | 2.74 | A phase 2 study of vorinostat in acute myeloid leukemia. ( DiPersio, JF; Espinoza-Delgado, I; Gore, SD; Juckett, M; Laumann, K; Loaiza-Bonilla, A; Roy, V; Schaefer, EW; Slack, J; Wu, W, 2009) |
| "A number of new agents in acute myeloid leukemia (AML) have held much promise in recent years, but most have failed to change the therapeutic landscape." | 2.49 | New agents: great expectations not realized. ( Lancet, JE, 2013) |
| "Vorinostat is an epigenetic targeted drug belonging to the histone deacetylase (HDAC) inhibitors family." | 2.47 | Vorinostat in acute myeloid leukemia and myelodysplastic syndromes. ( Prebet, T; Vey, N, 2011) |
| "Cellular testing in acute myeloid leukemia (AML) cells showed only a weak effect, most probably because of the poor permeability of the inhibitors." | 1.56 | Design, synthesis, and biological evaluation of dual targeting inhibitors of histone deacetylase 6/8 and bromodomain BRPF1. ( Erdmann, F; Ghazy, E; Günther, S; Herp, D; Hügle, M; Jung, M; Morales, ER; Robaa, D; Romier, C; Schmidt, M; Schmidtkunz, K; Sippl, W; Zeyen, P, 2020) |
| " However, the efficacy and underlying toxicity of these hybrids in combination with other agents remain unclear." | 1.56 | Novel SAHA‑bendamustine hybrid NL‑101 in combination with daunorubicin synergistically suppresses acute myeloid leukemia. ( Guo, W; Huang, J; Huang, S; Huang, X; Jin, J; Li, F; Li, X; Ling, Q; Pan, J; Ye, W, 2020) |
| " 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) |
| "Vorinostat is a HDACi which has produced responses in these disorders." | 1.39 | Vorinostat induces apoptosis and differentiation in myeloid malignancies: genetic and molecular mechanisms. ( Almeida, AM; Belo, H; Cardoso, BA; Silva, G, 2013) |
| "Here we describe HA-HDI-resistant human acute myeloid leukemia (AML) HL-60 (HL-60/LR) cells that are resistant to LAQ824, vorinostat, LBH589, and sodium butyrate." | 1.35 | Molecular and biologic characterization and drug sensitivity of pan-histone deacetylase inhibitor-resistant acute myeloid leukemia cells. ( Atadja, P; Bhalla, K; Chen, J; Eaton, K; Fernandez, P; Fiskus, W; Herger, B; Joshi, R; Kolhe, R; Lee, P; Mandawat, A; Peiper, S; Rao, R; Wang, Y; Yang, Y, 2008) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 7 (12.07) | 29.6817 |
| 2010's | 43 (74.14) | 24.3611 |
| 2020's | 8 (13.79) | 2.80 |
| Authors | Studies |
|---|---|
| Liao, Y | 1 |
| Niu, X | 1 |
| Chen, B | 1 |
| Edwards, H | 1 |
| Xu, L | 2 |
| Xie, C | 1 |
| Lin, H | 2 |
| Polin, L | 1 |
| Taub, JW | 1 |
| Ge, Y | 1 |
| Qin, Z | 1 |
| McClure, JJ | 1 |
| Zhang, C | 1 |
| Inks, ES | 2 |
| Peterson, YK | 2 |
| Li, J | 1 |
| Chou, CJ | 2 |
| Huang, Y | 1 |
| Dong, G | 1 |
| Li, H | 1 |
| Liu, N | 2 |
| Zhang, W | 1 |
| Sheng, C | 1 |
| Li, X | 2 |
| Jiang, Y | 1 |
| Xu, T | 1 |
| Himes, RA | 1 |
| Luo, X | 1 |
| Yin, G | 1 |
| Dolloff, N | 1 |
| Halene, S | 1 |
| Chan, SSL | 1 |
| Ghazy, E | 1 |
| Zeyen, P | 1 |
| Herp, D | 1 |
| Hügle, M | 1 |
| Schmidtkunz, K | 1 |
| Erdmann, F | 1 |
| Robaa, D | 1 |
| Schmidt, M | 1 |
| Morales, ER | 1 |
| Romier, C | 1 |
| Günther, S | 1 |
| Jung, M | 1 |
| Sippl, W | 1 |
| Reßing, N | 1 |
| Schliehe-Diecks, J | 1 |
| Watson, PR | 1 |
| Sönnichsen, M | 1 |
| Cragin, AD | 1 |
| Schöler, A | 1 |
| Yang, J | 1 |
| Schäker-Hübner, L | 1 |
| Borkhardt, A | 1 |
| Christianson, DW | 1 |
| Bhatia, S | 1 |
| Hansen, FK | 1 |
| Pommert, L | 2 |
| Schafer, ES | 2 |
| Malvar, J | 1 |
| Gossai, N | 1 |
| Florendo, E | 1 |
| Pulakanti, K | 1 |
| Heimbruch, K | 1 |
| Stelloh, C | 1 |
| Chi, YY | 1 |
| Sposto, R | 1 |
| Rao, S | 1 |
| Huynh, VT | 1 |
| Brown, P | 1 |
| Chang, BH | 1 |
| Colace, SI | 2 |
| Hermiston, ML | 1 |
| Heym, K | 1 |
| Hutchinson, RJ | 1 |
| Kaplan, JA | 2 |
| Mody, R | 1 |
| O'Brien, TA | 1 |
| Place, AE | 1 |
| Shaw, PH | 1 |
| Ziegler, DS | 1 |
| Wayne, A | 1 |
| Bhojwani, D | 2 |
| Burke, MJ | 3 |
| Alatrash, G | 1 |
| Saberian, C | 1 |
| Bassett, R | 1 |
| Thall, PF | 1 |
| Ledesma, C | 1 |
| Lu, Y | 1 |
| Daher, M | 1 |
| Valdez, BC | 1 |
| Kawedia, J | 1 |
| Popat, U | 1 |
| Mehta, R | 1 |
| Oran, B | 1 |
| Nieto, Y | 1 |
| Olson, A | 1 |
| Anderlini, P | 1 |
| Marin, D | 1 |
| Hosing, C | 1 |
| Alousi, AM | 1 |
| Shpall, EJ | 1 |
| Rondon, G | 1 |
| Chen, J | 3 |
| Qazilbash, M | 1 |
| Champlin, RE | 1 |
| Kebriaei, P | 1 |
| Chao, K | 1 |
| Stevens, AM | 1 |
| Jo, E | 1 |
| Hilsenbeck, SG | 1 |
| Gossai, NP | 1 |
| Doan, A | 1 |
| Guinipero, T | 1 |
| Otterson, D | 1 |
| Hinson, A | 1 |
| Wayne, AS | 1 |
| Alcitepe, İ | 1 |
| Salcin, H | 1 |
| Karatekin, İ | 1 |
| Kaymaz, BT | 1 |
| Abou Najem, S | 1 |
| Khawaja, G | 1 |
| Hodroj, MH | 1 |
| Babikian, P | 1 |
| Rizk, S | 1 |
| Jin, J | 2 |
| Guo, W | 1 |
| Li, F | 1 |
| Huang, J | 1 |
| Huang, X | 1 |
| Pan, J | 1 |
| Huang, S | 1 |
| Ye, W | 1 |
| Ling, Q | 1 |
| Glasser, CL | 1 |
| Lee, A | 1 |
| Eslin, D | 1 |
| Marks, L | 1 |
| Modak, S | 1 |
| Glade Bender, JL | 1 |
| Di Costanzo, A | 1 |
| Del Gaudio, N | 1 |
| Conte, L | 1 |
| Dell'Aversana, C | 2 |
| Vermeulen, M | 1 |
| de Thé, H | 1 |
| Migliaccio, A | 1 |
| Nebbioso, A | 2 |
| Altucci, L | 2 |
| Becktell, K | 1 |
| Houser, K | 1 |
| Saika, M | 1 |
| Inoue, D | 1 |
| Nagase, R | 1 |
| Sato, N | 1 |
| Tsuchiya, A | 1 |
| Yabushita, T | 1 |
| Kitamura, T | 1 |
| Goyama, S | 1 |
| Sayar, H | 1 |
| Cripe, LD | 1 |
| Saliba, AN | 1 |
| Abu Zaid, M | 1 |
| Konig, H | 1 |
| Boswell, HS | 1 |
| Ge, W | 1 |
| Liu, Z | 1 |
| Sun, Y | 1 |
| Wang, T | 1 |
| Guo, H | 1 |
| Chen, X | 2 |
| Li, S | 1 |
| Wang, M | 1 |
| Chen, Y | 1 |
| Ding, Y | 1 |
| Zhang, Q | 1 |
| Kubasch, AS | 1 |
| Platzbecker, U | 1 |
| Gojo, I | 2 |
| Tan, M | 1 |
| Fang, HB | 1 |
| Sadowska, M | 1 |
| Lapidus, R | 1 |
| Baer, MR | 1 |
| Carrier, F | 1 |
| Beumer, JH | 1 |
| Anyang, BN | 1 |
| Srivastava, RK | 1 |
| Espinoza-Delgado, I | 4 |
| Ross, DD | 1 |
| Warlick, ED | 1 |
| Cao, Q | 1 |
| Miller, J | 1 |
| Petruccelli, LA | 2 |
| Pettersson, F | 2 |
| Del Rincón, SV | 1 |
| Guilbert, C | 1 |
| Licht, JD | 1 |
| Miller, WH | 2 |
| Kruczynski, A | 1 |
| Pillon, A | 1 |
| Créancier, L | 1 |
| Vandenberghe, I | 1 |
| Gomes, B | 1 |
| Brel, V | 1 |
| Fournier, E | 1 |
| Annereau, JP | 1 |
| Currie, E | 1 |
| Guminski, Y | 1 |
| Bonnet, D | 1 |
| Bailly, C | 1 |
| Guilbaud, N | 1 |
| Cao, H | 1 |
| Cheng, Y | 1 |
| You, L | 1 |
| Qian, J | 1 |
| Qian, W | 1 |
| Torgersen, ML | 1 |
| Engedal, N | 1 |
| Bøe, SO | 1 |
| Hokland, P | 1 |
| Simonsen, A | 1 |
| Chandran, P | 1 |
| Kavalakatt, A | 1 |
| Malarvizhi, GL | 1 |
| Vasanthakumari, DR | 1 |
| Retnakumari, AP | 1 |
| Sidharthan, N | 1 |
| Pavithran, K | 1 |
| Nair, S | 1 |
| Koyakutty, M | 1 |
| Walter, RB | 3 |
| Medeiros, BC | 3 |
| Gardner, KM | 1 |
| Orlowski, KF | 1 |
| Gallegos, L | 1 |
| Scott, BL | 1 |
| Hendrie, PC | 1 |
| Estey, EH | 2 |
| Lancet, JE | 1 |
| Lepore, I | 1 |
| Pilyugin, M | 1 |
| Conte, M | 1 |
| De Bellis, F | 1 |
| Tambaro, FP | 2 |
| Izzo, T | 1 |
| Garcia-Manero, G | 5 |
| Ferrara, F | 1 |
| Irminger-Finger, I | 1 |
| Radany, EH | 1 |
| Wong, P | 1 |
| Ma, S | 1 |
| Wu, K | 1 |
| Wang, B | 1 |
| Wong, JY | 1 |
| Lin, WH | 1 |
| Yeh, TK | 1 |
| Jiaang, WT | 1 |
| Yen, KJ | 1 |
| Chen, CH | 1 |
| Huang, CT | 1 |
| Yen, SC | 1 |
| Hsieh, SY | 1 |
| Chou, LH | 1 |
| Chen, CP | 1 |
| Chiu, CH | 1 |
| Kao, LC | 1 |
| Chao, YS | 1 |
| Chen, CT | 1 |
| Hsu, JT | 1 |
| Pierceall, WE | 1 |
| Lena, RJ | 1 |
| Blake, N | 1 |
| Doykan, C | 1 |
| Elashoff, M | 1 |
| Cardone, MH | 1 |
| Rich, A | 1 |
| Sun, J | 1 |
| Aldayel, AS | 1 |
| Yin, CC | 1 |
| Medeiros, LJ | 1 |
| Konoplev, S | 1 |
| Kirschbaum, M | 1 |
| Goldberg, SL | 1 |
| Bredeson, C | 1 |
| Kujawski, LA | 1 |
| Yang, A | 1 |
| Marks, P | 1 |
| Frankel, P | 1 |
| Sun, X | 1 |
| Tosolini, A | 1 |
| Eid, JE | 1 |
| Lubiniecki, GM | 1 |
| Issa, JP | 1 |
| Zhou, L | 1 |
| Zhang, Y | 1 |
| Chen, S | 2 |
| Kmieciak, M | 1 |
| Leng, Y | 1 |
| Rizzo, KA | 1 |
| Dumur, CI | 1 |
| Ferreira-Gonzalez, A | 1 |
| Dai, Y | 2 |
| Grant, S | 3 |
| Ornstein, MC | 1 |
| Mukherjee, S | 1 |
| Sekeres, MA | 1 |
| How, J | 1 |
| Minden, MD | 1 |
| Brian, L | 1 |
| Chen, EX | 1 |
| Brandwein, J | 1 |
| Schuh, AC | 1 |
| Schimmer, AD | 1 |
| Gupta, V | 1 |
| Webster, S | 1 |
| Degelder, T | 1 |
| Haines, P | 1 |
| Stayner, LA | 1 |
| McGill, S | 1 |
| Wang, L | 1 |
| Piekarz, R | 1 |
| Wong, T | 1 |
| Siu, LL | 1 |
| Holleran, JL | 2 |
| Egorin, MJ | 2 |
| Yee, KW | 1 |
| Zhu, X | 1 |
| Liu, X | 1 |
| Cheng, Z | 1 |
| Zhu, J | 1 |
| Wang, F | 1 |
| Qi, W | 1 |
| Yan, J | 1 |
| Sun, Z | 1 |
| Liu, H | 1 |
| Peng, X | 1 |
| Hao, Y | 1 |
| Zheng, N | 1 |
| Wu, Q | 1 |
| Romanski, A | 2 |
| Bug, G | 2 |
| Fiskus, W | 2 |
| Rao, R | 2 |
| Fernandez, P | 1 |
| Herger, B | 1 |
| Yang, Y | 2 |
| Kolhe, R | 2 |
| Mandawat, A | 1 |
| Wang, Y | 2 |
| Joshi, R | 2 |
| Eaton, K | 2 |
| Lee, P | 2 |
| Atadja, P | 1 |
| Peiper, S | 2 |
| Bhalla, K | 2 |
| Balusu, R | 1 |
| Ustun, C | 1 |
| Jillella, A | 1 |
| Buser, CA | 1 |
| Miller, CP | 1 |
| Rudra, S | 1 |
| Keating, MJ | 1 |
| Wierda, WG | 1 |
| Palladino, M | 1 |
| Chandra, J | 1 |
| Schaefer, EW | 1 |
| Loaiza-Bonilla, A | 1 |
| Juckett, M | 1 |
| DiPersio, JF | 1 |
| Roy, V | 1 |
| Slack, J | 1 |
| Wu, W | 1 |
| Laumann, K | 1 |
| Gore, SD | 1 |
| Kadia, TM | 2 |
| Yang, H | 3 |
| Ferrajoli, A | 1 |
| Maddipotti, S | 1 |
| Schroeder, C | 1 |
| Madden, TL | 1 |
| Ravandi, F | 2 |
| Thomas, DA | 1 |
| Newsome, W | 1 |
| Sanchez-Gonzalez, B | 1 |
| Zwiebel, JA | 1 |
| Kantarjian, HM | 2 |
| Wei, Y | 1 |
| Kadia, T | 1 |
| Tong, W | 1 |
| Zhang, M | 1 |
| Jia, Y | 1 |
| Hu, Y | 2 |
| Viallet, J | 1 |
| O'Brien, S | 1 |
| Green, SR | 1 |
| Choudhary, AK | 1 |
| Fleming, IN | 1 |
| Prebet, T | 1 |
| Vey, N | 1 |
| Dupéré-Richer, D | 1 |
| Retrouvey, H | 1 |
| Skoulikas, S | 1 |
| Powell, BL | 1 |
| Schiffer, CA | 1 |
| Appelbaum, FR | 1 |
| Bekele, NB | 1 |
| Jabbour, E | 1 |
| Borthakur, G | 1 |
| Konopleva, MY | 1 |
| Faderl, S | 1 |
| Cortes, JE | 1 |
| Brandt, M | 1 |
| McCue, D | 1 |
| Newsome, WM | 1 |
| Pierce, SR | 1 |
| de Lima, M | 1 |
| Schwarz, K | 1 |
| Keller, M | 1 |
| Wietbrauk, S | 1 |
| Vogel, A | 1 |
| Roos, J | 1 |
| Oancea, C | 1 |
| Brill, B | 1 |
| Krämer, OH | 1 |
| Serve, H | 1 |
| Ruthardt, M | 1 |
| Yaseen, A | 1 |
| Hock, S | 1 |
| Rosato, R | 1 |
| Dent, P | 2 |
| Silva, G | 1 |
| Cardoso, BA | 1 |
| Belo, H | 1 |
| Almeida, AM | 1 |
| Barbetti, V | 1 |
| Gozzini, A | 1 |
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| Marzi, I | 1 |
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| Santini, V | 1 |
| Dello Sbarba, P | 1 |
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| Grisolano, JL | 1 |
| O'Neal, J | 1 |
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| Tomasson, MH | 1 |
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| Almenara, JA | 1 |
| Kolla, SS | 1 |
| Maggio, SC | 1 |
| Coe, S | 1 |
| Giménez, MS | 1 |
| Desmond, JC | 1 |
| Raynaud, S | 1 |
| Tung, E | 1 |
| Hofmann, WK | 1 |
| Haferlach, T | 1 |
| Koeffler, HP | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Epigenetic Reprogramming in Relapse AML: A Phase 1 Study of Decitabine and Vorinostat Followed by Fludarabine, Cytarabine and G-CSF (FLAG) in Children and Young Adults With Relapsed/Refractory AML[NCT02412475] | Phase 1 | 3 participants (Actual) | Interventional | 2015-02-21 | Terminated (stopped due to We opened a competing study with the TACL consortium) | ||
| A Phase 1/2 Study of Vorinostat (Zolinza®) in Combination With Gemtuzumab Ozogamicin (Mylotarg®) and Azacitidine (Vidaza®) in Patients 50 Years of Age and Older With Relapsed/Refractory Non-APL Acute Myeloid Leukemia (AML)[NCT00895934] | Phase 1/Phase 2 | 52 participants (Actual) | Interventional | 2009-05-31 | Completed | ||
| A Phase I Clinical Trial of Vorinostat in Combination With Decitabine in Patients With Acute Myelogenous Leukemia or Myelodysplastic Syndrome[NCT00479232] | Phase 1 | 71 participants (Actual) | Interventional | 2007-06-30 | Completed | ||
| A Phase 2 Study of Suberoylanilide Hydroxamic Acid (SAHA) in Acute Myeloid Leukemia (AML)[NCT00305773] | Phase 2 | 37 participants (Actual) | Interventional | 2006-01-31 | Completed | ||
| Phase II Trial of Vorinostat (Suberoylanilide Hydroxamic Acid or SAHA; Zolinza™) in Combination With Gemtuzumab Ozogamicin (Mylotarg™) as Induction and Post-Remission Therapy in Older Patients With Previously Untreated Non-M3 Acute Myeloid Leukemia[NCT00673153] | Phase 2 | 31 participants (Actual) | Interventional | 2008-03-31 | Terminated | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
(NCT00895934)
Timeframe: up to 2 years
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 2/Selected Dose | 5 |
Efficacy Defined as Best Response Achieved During Study Treatment Measured by Complete Remission (CR) Rate (NCT00895934)
Timeframe: up to 3 years
| Intervention | Participants (Count of Participants) |
|---|---|
| Phase 2/Selected Dose | 18 |
(NCT00895934)
Timeframe: 42 days
| Intervention | participants (Number) |
|---|---|
| Dose 1 | 0 |
| Dose 2 | 0 |
| Dose 3 | 0 |
| Dose 4 | 1 |
(NCT00895934)
Timeframe: Up to 3 years
| Intervention | participants (Number) |
|---|---|
| Phase 1 Dose-Finding Cohorts 1-3 | 4 |
| Phase 2/Selected Dose | 18 |
Participants who received at least one dose of vorinostat in combination with decitabine intravenous (IV) at a dose of 20 mg/m^2 daily for 5 days along with oral vorinostat 400 mg once daily for 7 to 14 days in a 28-day cycle concurrently or sequentially, were evaluated to determine the maximum tolerable dose (MTD) determined by the number of participants experiencing dose limiting toxicity (DLT) events defined as any Grade 3 or 4 non-hematological toxicity (reported adverse event) and/or myelosuppression lasting >42 days. (NCT00479232)
Timeframe: Day 1 to 28 of Cycle 1
| Intervention | participants (Number) |
|---|---|
| Concurrent, Vorinostat 400mg qd x 7d/4wk + Decitabine | 0 |
| Concurrent, Vorinostat 400mg qd x 7d/2wk + Decitabine | 0 |
| Concurrent, Vorinostat 400mg qd x 14d/4wk + Decitabine (MTD) | 0 |
| Sequential, Vorinostat 400mg qd x 7d/4wk + Decitabine | 0 |
| Sequential, Vorinostat 400mg qd x 10d/4wk + Decitabine | 0 |
| Sequential, Vorinostat 400mg qd x 14d/4wk + Decitabine (MTD) | 1 |
Objective Response Rate was measured in participants with intermediate-high risk MDS or untreated AML who were treated with vorinostat and decitabine either on a concurrent or sequential regimen. The Objective response was defined as any confirmed complete remission or any confirmed partial remission for AML participants and complete remission, confirmed partial remission or confirmed hematologic improvement for MDS participants. (NCT00479232)
Timeframe: Approximately 6 months
| Intervention | percentage of participants (Number) |
|---|---|
| Untreated AML or Intermediate, Concurrent | 35.0 |
| Untreated AML or Intermediate, Sequential | 13.6 |
Objective Response Rate was measured in participants with refractory or relapse AML (acute myelogenous leukemia) in combination with Decitabine who were treated with vorinostat and decitabine on either a concurrent or sequential regimen. The Objective response was defined as any confirmed complete remission or any confirmed partial remission for AML participants and complete remission, confirmed partial remission or confirmed hematologic improvement for Myelodysplastic Syndrome (MDS) participants. (NCT00479232)
Timeframe: Approximately 6 months
| Intervention | percentage of participants (Number) |
|---|---|
| Refractory or Relapsed AML, Concurrent | 7.1 |
| Refractory or Relapsed AML, Sequential | 0.0 |
"The confirmed complete response rate was estimated by the number of participants with CR divided by the total number of evaluable participants.~According to the International Working Group (IWG) Criteria for response in AML, to be considered a CR, the following must be met for at least 4 weeks: ANC > 1500/mL, platelets > 100000/mL, no circulating blasts, bone marrow cellularity >20% (biopsy), trilineage maturation, < 5% bone marrow blasts, no auer rods and no extramedullary disease." (NCT00305773)
Timeframe: Up to 2 years
| Intervention | percentage of participants (Number) |
|---|---|
| Arm A (Once Daily Vorinostat) | 0 |
| Arm B (Thrice Daily Vorinostat) | 4.5 |
"Adverse events were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 3.~Description of Grades:~Grade 1: Mild Grade 2: Moderate Grade 3: Severe Grade 4: Life-threatening Grade 5: Death" (NCT00305773)
Timeframe: Duration of study (up to 2 years)
| Intervention | participants (Number) |
|---|---|
| Arm A (Once Daily Vorinostat) | 10 |
| Arm B (Thrice Daily Vorinostat) | 17 |
Overall survival (OS) was defined as the time from registration to death of any cause. Surviving patients were censored at the date of last follow-up. The median OS with 95% CI was estimated using the Kaplan Meier method. (NCT00305773)
Timeframe: Duration of study (up to 2 years)
| Intervention | days (Median) |
|---|---|
| Arm A (Once Daily Vorinostat) | 105 |
| Arm B (Thrice Daily Vorinostat) | 153 |
Time to treatment failure (TTF) was defined as the time from registration to until the date of treatment discontinuation of any reason. Patients receiving treatment at the time of analysis were considered censored. The median TTF with 95% CI was estimated using the Kaplan Meier method. (NCT00305773)
Timeframe: Duration of treatment (up to 17 cycles)
| Intervention | days (Median) |
|---|---|
| Arm A (Once Daily Vorinostat) | 42 |
| Arm B (Thrice Daily Vorinostat) | 46 |
(NCT00673153)
Timeframe: after completion of induction therapy, administered every 21-42 days for up to two courses
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I | 6 |
(NCT00673153)
Timeframe: after completion of induction therapy, administered every 21-42 days for up to two courses
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I | 1 |
(NCT00673153)
Timeframe: At day 30
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I | 20 |
(NCT00673153)
Timeframe: At day 30
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I | 8 |
(NCT00673153)
Timeframe: At relapse
| Intervention | Participants (Count of Participants) |
|---|---|
| Arm I | 7 |
5 reviews available for vorinostat and Acute Myelogenous Leukemia
| Article | Year |
|---|---|
New agents: great expectations not realized.
Topics: Aminoglycosides; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Arabinonucleosides; Benzo | 2013 |
Myelomastocytic leukemia with aberrant CD25 expression: case report and review of the literature.
Topics: Adenocarcinoma; Antigens, Neoplasm; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumo | 2014 |
More is better: combination therapies for myelodysplastic syndromes.
Topics: Antineoplastic Agents; Azacitidine; Benzamides; Clinical Trials as Topic; Decitabine; Disease Progre | 2015 |
Vorinostat in acute myeloid leukemia and myelodysplastic syndromes.
Topics: Antineoplastic Agents; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; Leukemia, Myeloid, | 2011 |
Can we improve outcomes in patients with acute myelogenous leukemia? Incorporating HDAC inhibitors into front-line therapy.
Topics: Antibiotics, Antineoplastic; Antimetabolites, Antineoplastic; Clinical Trials, Phase I as Topic; Cyt | 2012 |
12 trials available for vorinostat and Acute Myelogenous Leukemia
| Article | Year |
|---|---|
Decitabine and vorinostat with FLAG chemotherapy in pediatric relapsed/refractory AML: Report from the therapeutic advances in childhood leukemia and lymphoma (TACL) consortium.
Topics: Antineoplastic Combined Chemotherapy Protocols; Child; Cytarabine; Decitabine; Humans; Leukemia, Mye | 2022 |
Vorinostat Combined with Busulfan, Fludarabine, and Clofarabine Conditioning Regimen for Allogeneic Hematopoietic Stem Cell Transplantation in Patients with Acute Leukemia: Long-Term Study Outcomes.
Topics: Acute Disease; Busulfan; Clofarabine; Drug Therapy, Combination; Graft vs Host Disease; Hematopoieti | 2022 |
Real-world experience in treating pediatric relapsed/refractory or therapy-related myeloid malignancies with decitabine, vorinostat, and FLAG therapy based on a phase 1 study run by the TACL consortium.
Topics: Antineoplastic Combined Chemotherapy Protocols; Child; Cytarabine; Decitabine; Granulocyte Colony-St | 2022 |
Translational phase I trial of vorinostat (suberoylanilide hydroxamic acid) combined with cytarabine and etoposide in patients with relapsed, refractory, or high-risk acute myeloid leukemia.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; ATP Binding Cassette Transporter, Subfa | 2013 |
Gemtuzumab ozogamicin in combination with vorinostat and azacitidine in older patients with relapsed or refractory acute myeloid leukemia: a phase I/II study.
Topics: Age Factors; Aged; Aminoglycosides; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemo | 2014 |
Mcl-1 dependence predicts response to vorinostat and gemtuzumab ozogamicin in acute myeloid leukemia.
Topics: Aged; Aged, 80 and over; Aminoglycosides; Antibodies, Monoclonal, Humanized; Antineoplastic Combined | 2014 |
A phase 1 clinical trial of vorinostat in combination with decitabine in patients with acute myeloid leukaemia or myelodysplastic syndrome.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Azacitid | 2014 |
A phase I trial of two sequence-specific schedules of decitabine and vorinostat in patients with acute myeloid leukemia.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Azacitidine; Decitab | 2015 |
A phase 2 study of vorinostat in acute myeloid leukemia.
Topics: Adult; Aged; Aged, 80 and over; Female; Humans; Hydroxamic Acids; Leukemia, Myeloid, Acute; Male; Mi | 2009 |
A phase I study of vorinostat in combination with idarubicin in relapsed or refractory leukaemia.
Topics: Acetylation; Acute Disease; Adult; Aged; Aged, 80 and over; Antigens, Neoplasm; Antineoplastic Combi | 2010 |
Phase II trial of vorinostat and gemtuzumab ozogamicin as induction and post-remission therapy in older adults with previously untreated acute myeloid leukemia.
Topics: Aged; Aged, 80 and over; Aminoglycosides; Antibodies, Monoclonal, Humanized; Antineoplastic Combined | 2012 |
Phase II trial of vorinostat with idarubicin and cytarabine for patients with newly diagnosed acute myelogenous leukemia or myelodysplastic syndrome.
Topics: Adolescent; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Disease-Free Survival; Fema | 2012 |
41 other studies available for vorinostat and Acute Myelogenous Leukemia
| Article | Year |
|---|---|
Synthesis and Antileukemic Activities of Piperlongumine and HDAC Inhibitor Hybrids against Acute Myeloid Leukemia Cells.
Topics: Antineoplastic Agents; Apoptosis Regulatory Proteins; Cell Line, Tumor; Dioxolanes; DNA Repair; Drug | 2016 |
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 |
Discovery of Janus Kinase 2 (JAK2) and Histone Deacetylase (HDAC) Dual Inhibitors as a Novel Strategy for the Combinational Treatment of Leukemia and Invasive Fungal Infections.
Topics: Animals; Apoptosis; Candida albicans; Cell Cycle; Cell Line, Tumor; Histone Deacetylase 6; Histone D | 2018 |
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 |
Design, synthesis, and biological evaluation of dual targeting inhibitors of histone deacetylase 6/8 and bromodomain BRPF1.
Topics: Acetylation; Adaptor Proteins, Signal Transducing; Antineoplastic Agents; Cell Line, Tumor; DNA-Bind | 2020 |
Development of Fluorinated Peptoid-Based Histone Deacetylase (HDAC) Inhibitors for Therapy-Resistant Acute Leukemia.
Topics: Antineoplastic Agents; Cell Line, Tumor; Decitabine; Histone Deacetylase 1; Histone Deacetylase 6; H | 2022 |
HDAC inhibitor Vorinostat and BET inhibitor Plx51107 epigenetic agents' combined treatments exert a therapeutic approach upon acute myeloid leukemia cell model.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Epigenesis, Genetic; Histone | 2022 |
Adjuvant Epigenetic Therapy of Decitabine and Suberoylanilide Hydroxamic Acid Exerts Anti-Neoplastic Effects in Acute Myeloid Leukemia Cells.
Topics: Adjuvants, Pharmaceutic; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regula | 2019 |
Novel SAHA‑bendamustine hybrid NL‑101 in combination with daunorubicin synergistically suppresses acute myeloid leukemia.
Topics: Animals; Bendamustine Hydrochloride; Cell Line, Tumor; Cell Proliferation; Cell Survival; Daunorubic | 2020 |
Epigenetic Combination Therapy for Children With Secondary Myelodysplastic Syndrome (MDS)/Acute Myeloid Leukemia (AML) and Concurrent Solid Tumor Relapse.
Topics: Adolescent; Antineoplastic Agents; Azacitidine; Decitabine; Drug Therapy, Combination; Epigenesis, G | 2017 |
The HDAC inhibitor SAHA regulates CBX2 stability via a SUMO-triggered ubiquitin-mediated pathway in leukemia.
Topics: Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Neoplastic; Histone Deacetylase In | 2018 |
Epigenetic Therapy in a Patient With Down Syndrome and Refractory Acute Myeloid Leukemia.
Topics: Antineoplastic Combined Chemotherapy Protocols; Cytarabine; Decitabine; Down Syndrome; Granulocyte C | 2019 |
ASXL1 and SETBP1 mutations promote leukaemogenesis by repressing TGFβ pathway genes through histone deacetylation.
Topics: Acetylation; Animals; Carrier Proteins; Cell Line, Tumor; Cell Survival; Disease Models, Animal; His | 2018 |
Combination of sorafenib, vorinostat and bortezomib for the treatment of poor-risk AML: report of two consecutive clinical trials.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Bortezomib; Clinical Trials, Phase I as | 2019 |
Design and synthesis of parthenolide-SAHA hybrids for intervention of drug-resistant acute myeloid leukemia.
Topics: Antineoplastic Agents; Apoptosis; Cell Proliferation; Dose-Response Relationship, Drug; Drug Design; | 2019 |
The wolf of hypomethylating agent failure: what comes next?
Topics: Animals; Azacitidine; Leukemia, Myeloid, Acute; Myelodysplastic Syndromes; Vorinostat; Wolves | 2019 |
Bortezomib and vorinostat in refractory acute myelogenous leukemia and high-risk myelodysplastic syndromes: produces stable disease but at the cost of high toxicity.
Topics: Antineoplastic Agents; Boronic Acids; Bortezomib; Histone Deacetylase Inhibitors; Humans; Hydroxamic | 2013 |
Expression of leukemia-associated fusion proteins increases sensitivity to histone deacetylase inhibitor-induced DNA damage and apoptosis.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; DNA Damage; DNA Repair; Drug Resistance, Neoplas | 2013 |
F14512, a polyamine-vectorized anti-cancer drug, currently in clinical trials exhibits a marked preclinical anti-leukemic activity.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blotting, Western; Boronic Acids | 2013 |
Homoharringtonine and SAHA synergistically enhance apoptosis in human acute myeloid leukemia cells through upregulation of TRAIL and death receptors.
Topics: Animals; Apoptosis; Caspase 8; Caspase 9; Cell Line, Tumor; Cell Proliferation; Drug Synergism; Drug | 2013 |
Targeting autophagy potentiates the apoptotic effect of histone deacetylase inhibitors in t(8;21) AML cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; Cell Line, Tumor; Chloroquine; | 2013 |
Epigenetics targeted protein-vorinostat nanomedicine inducing apoptosis in heterogeneous population of primary acute myeloid leukemia cells including refractory and relapsed cases.
Topics: Apoptosis; Computer Simulation; Epigenesis, Genetic; Histone Deacetylase Inhibitors; HL-60 Cells; Hu | 2014 |
HDAC inhibitors repress BARD1 isoform expression in acute myeloid leukemia cells via activation of miR-19a and/or b.
Topics: Epigenesis, Genetic; Gene Expression Regulation, Leukemic; Histone Deacetylase Inhibitors; HL-60 Cel | 2013 |
Suberoylanilide hydroxamic acid induces hypersensitivity to radiation therapy in acute myelogenous leukemia cells expressing constitutively active FLT3 mutants.
Topics: Cell Line, Tumor; DNA Damage; DNA Repair; Enzyme Activation; fms-Like Tyrosine Kinase 3; Gene Expres | 2013 |
Evaluation of the antitumor effects of BPR1J-340, a potent and selective FLT3 inhibitor, alone or in combination with an HDAC inhibitor, vorinostat, in AML cancer.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamide | 2014 |
A regimen combining the Wee1 inhibitor AZD1775 with HDAC inhibitors targets human acute myeloid leukemia cells harboring various genetic mutations.
Topics: Animals; Apoptosis; CDC2 Protein Kinase; Cell Cycle Checkpoints; Cell Cycle Proteins; Checkpoint Kin | 2015 |
Quantitative Analysis of Global Proteome and Lysine Acetylome Reveal the Differential Impacts of VPA and SAHA on HL60 Cells.
Topics: Acetylation; Amino Acid Motifs; Amino Acid Sequence; Cluster Analysis; Computational Biology; HL-60 | 2016 |
Establishment and Characterization of Long-Term Cultures Derived from Primary Acute Myeloid Leukemia Cells for HDAC Inhibitor Research.
Topics: Antigens, CD34; Apoptosis; Biomarkers, Tumor; Cell Culture Techniques; Cell Proliferation; Cell Sepa | 2017 |
Molecular and biologic characterization and drug sensitivity of pan-histone deacetylase inhibitor-resistant acute myeloid leukemia cells.
Topics: Acetylation; Animals; Antineoplastic Agents; Apoptosis; Azacitidine; Benzoquinones; Cell Differentia | 2008 |
Cotreatment with vorinostat enhances activity of MK-0457 (VX-680) against acute and chronic myelogenous leukemia cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Drug Synergism; Fusion Pr | 2008 |
Caspase-8 dependent histone acetylation by a novel proteasome inhibitor, NPI-0052: a mechanism for synergy in leukemia cells.
Topics: Acetylation; Antioxidants; Apoptosis; Boronic Acids; Bortezomib; Caspase 8; Drug Synergism; Drug The | 2009 |
The combination of a histone deacetylase inhibitor with the BH3-mimetic GX15-070 has synergistic antileukemia activity by activating both apoptosis and autophagy.
Topics: Apoptosis; Autophagy; Benzamides; BH3 Interacting Domain Death Agonist Protein; Cell Line, Tumor; Dr | 2010 |
Combination of sapacitabine and HDAC inhibitors stimulates cell death in AML and other tumour types.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Arabinonucleosides; Cell Death; Cell Line, | 2010 |
Vorinostat induces reactive oxygen species and DNA damage in acute myeloid leukemia cells.
Topics: Antineoplastic Agents; Antioxidants; Apoptosis; Cell Division; Cell Line, Tumor; Cell Proliferation; | 2011 |
Deacetylase inhibitors modulate proliferation and self-renewal properties of leukemic stem and progenitor cells.
Topics: Animals; Blotting, Western; Colony-Forming Units Assay; Core Binding Factor Alpha 2 Subunit; DNA Pri | 2012 |
Resveratrol sensitizes acute myelogenous leukemia cells to histone deacetylase inhibitors through reactive oxygen species-mediated activation of the extrinsic apoptotic pathway.
Topics: Acetylation; Apoptosis; Caspase 8; Cell Line, Tumor; DNA Damage; Drug Synergism; Histone Deacetylase | 2012 |
Vorinostat induces apoptosis and differentiation in myeloid malignancies: genetic and molecular mechanisms.
Topics: Antineoplastic Agents; Apoptosis; Base Sequence; Cell Cycle Checkpoints; Cell Differentiation; Cell | 2013 |
Time- and residue-specific differences in histone acetylation induced by VPA and SAHA in AML1/ETO-positive leukemia cells.
Topics: Acetylation; Apoptosis; Cell Differentiation; Core Binding Factor Alpha 2 Subunit; Gene Expression R | 2013 |
An activated receptor tyrosine kinase, TEL/PDGFbetaR, cooperates with AML1/ETO to induce acute myeloid leukemia in mice.
Topics: 3T3 Cells; Acetylation; Animals; Benzamides; Blotting, Southern; Bone Marrow Transplantation; Core B | 2003 |
Mechanism and functional role of XIAP and Mcl-1 down-regulation in flavopiridol/vorinostat antileukemic interactions.
Topics: Antineoplastic Agents; Apoptosis; Apoptosis Inducing Factor; Blast Crisis; Blotting, Western; Butyra | 2007 |
Discovery of epigenetically silenced genes in acute myeloid leukemias.
Topics: alpha Catenin; Azacitidine; Carrier Proteins; CpG Islands; Decitabine; DNA Methylation; Epigenesis, | 2007 |