niacinamide has been researched along with Granulocytic Leukemia, Chronic in 46 studies
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.
| Excerpt | Relevance | Reference |
|---|---|---|
| " The underlying mechanism of these adverse cardiac effects is largely unknown." | 5.51 | Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies. ( Becker, JR; Force, T; Galindo, CL; Glennon, MS; Gupte, M; Lal, H; Singh, AP; Umbarkar, P; Zhang, Q, 2019) |
| " This study aimed to describe pharmacokinetic (PK) properties of asciminib and to identify clinically relevant covariates impacting its exposure." | 3.11 | Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases. ( Combes, FP; Ho, YY; Hoch, M; Li, YF; Lorenzo, S; Sy, SKB, 2022) |
| "Sorafenib is used for the treatment of acute myeloid leukemia patients carrying internal tandem duplication of fms-like tyrosine kinase 3 (FLT3-ITD) mutation." | 2.52 | A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology. ( Mihaila, RG, 2015) |
| " Second, the binding of asciminib decreases the binding free energies of nilotinib by ∼3 and ∼7 kcal/mol for the wildtype and T315I-mutated protein, respectively, suggesting the possibility of reducing nilotinib dosage and lowering risk of developing resistance in the treatment of CML." | 1.72 | Allosteric enhancement of the BCR-Abl1 kinase inhibition activity of nilotinib by cobinding of asciminib. ( Amiri, W; Friedman, R; Lindahl, E; Oruganti, B; Rahimullah, R; Yang, J, 2022) |
| " Thus, this study aimed to observe the potential cardiovascular-related side effect after co-exposure to ASC and PON using zebrafish as an animal model." | 1.72 | Investigating Potential Cardiovascular Toxicity of Two Anti-Leukemia Drugs of Asciminib and Ponatinib in Zebrafish Embryos. ( Alos, HC; Audira, G; Aventurado, CA; Hsiao, CD; Lai, YH; Lim, KH; Lin, HC; Roldan, MJM; Saputra, F; Tsai, GJ; Vasquez, RD, 2022) |
| " The underlying mechanism of these adverse cardiac effects is largely unknown." | 1.51 | Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies. ( Becker, JR; Force, T; Galindo, CL; Glennon, MS; Gupte, M; Lal, H; Singh, AP; Umbarkar, P; Zhang, Q, 2019) |
| "Ponatinib (AP24534) is a multikinase inhibitor with in vitro and clinical activity in tyrosine kinase inhibitor (TKI)-resistant chronic myeloid leukemia, irrespective of BCR-ABL KD mutation." | 1.39 | Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD. ( Damon, LE; Lasater, EA; Lin, KC; Salerno, S; Shah, NP; Smith, CC; Stewart, WK; Zhu, X, 2013) |
| "A classic example is chronic myeloid leukemia (CML) caused by BCR-ABL fusion protein, wherein a BCR-ABL kinase inhibitor, imatinib (IM), was highly successful in the early chronic phase of the disease, but failed in the advanced stages due to amplification of oncogene or point mutations in the drug-binding site of kinase domain." | 1.38 | Rationally designed aberrant kinase-targeted endogenous protein nanomedicine against oncogene mutated/amplified refractory chronic myeloid leukemia. ( Hanumanthu, PL; Keechilat, P; Koyakutty, M; Malarvizhi, GL; Menon, D; Menon, K; Mony, U; Nair, S; Prabhu, R; Retnakumari, AP; Sidharthan, N; Thampi, MV, 2012) |
| "In contrast to BCR-ABL-positive chronic myelogenous leukemia, only few cases of imatinib resistance and mutations of the FP kinase domain have been described so far." | 1.37 | The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro. ( Aberg, E; Duyster, J; Engh, RA; Gorantla, SP; Oliveira, TM; Peschel, C; Thöne, S; von Bubnoff, N, 2011) |
| "In human chronic myelogenous leukemia cells, K562, which are relatively resistant to various inducers of apoptosis, the apoptosis was induced by picolinic acid and dipicolinic acid in about 50% of the cells 5-10 mM via the caspase pathway, but was not at 1 mM." | 1.31 | Apoptosis induced by niacin-related compounds in K562 cells but not in normal human lymphocytes. ( Fujita, H; Ogata, S; Okumura, K; Shibata, K; Taguchi, H; Takeuchi, M, 2000) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 4 (8.70) | 29.6817 |
| 2010's | 15 (32.61) | 24.3611 |
| 2020's | 27 (58.70) | 2.80 |
| Authors | Studies |
|---|---|
| İbiş, B | 1 |
| Tiribelli, M | 1 |
| Eşkazan, AE | 4 |
| Deeks, ED | 1 |
| Manley, PW | 3 |
| Huth, F | 1 |
| Moussaoui, S | 1 |
| Schoepfer, J | 3 |
| Yeung, DT | 1 |
| Shanmuganathan, N | 1 |
| Hughes, TP | 4 |
| García-Gutiérrez, V | 3 |
| Hernandez-Boluda, JC | 3 |
| Li, YF | 1 |
| Combes, FP | 1 |
| Hoch, M | 1 |
| Lorenzo, S | 1 |
| Sy, SKB | 1 |
| Ho, YY | 1 |
| Oruganti, B | 1 |
| Lindahl, E | 1 |
| Yang, J | 1 |
| Amiri, W | 1 |
| Rahimullah, R | 1 |
| Friedman, R | 2 |
| Luna, A | 2 |
| Pérez-Lamas, L | 1 |
| Boque, C | 2 |
| Giraldo, P | 2 |
| Xicoy, B | 3 |
| Ruiz Nuño, C | 1 |
| Vega, MM | 1 |
| Alvarez-Larrán, A | 2 |
| Salamanca, A | 1 |
| García-Noblejas, A | 1 |
| Vall-Llovera, F | 1 |
| Villalon, L | 1 |
| De Las Heras, N | 1 |
| Ramila, E | 1 |
| Pérez-Encinas, M | 1 |
| Cuevas, B | 2 |
| Perez-Lopez, R | 1 |
| Sanchez-Guijo, F | 2 |
| Jiménez-Velasco, A | 2 |
| Lakhwani, S | 2 |
| Casado, LF | 1 |
| Rosell, A | 2 |
| Escola, A | 1 |
| Fernández, MJ | 1 |
| Garcia-Hernandez, C | 2 |
| Cervero, C | 1 |
| Mora, E | 2 |
| Sagüés, M | 2 |
| Suarez-Varela, S | 2 |
| Vélez, P | 2 |
| Carrascosa Mastell, P | 1 |
| Bitaube, RF | 1 |
| Serrano, L | 2 |
| Cortes, M | 2 |
| Vera Goñi, JA | 1 |
| Steegmann, JL | 2 |
| de Soria, VGG | 1 |
| Alonso-Dominguez, JM | 2 |
| Araujo, MC | 1 |
| Coll, AP | 1 |
| Kockerols, CCB | 1 |
| Janssen, JJWM | 2 |
| Blijlevens, NMA | 1 |
| Klein, SK | 1 |
| Van Hussen-Daenen, LGM | 1 |
| Van Gorkom, GGY | 1 |
| Smit, WM | 1 |
| Van Balen, P | 1 |
| Biemond, BJ | 1 |
| Cruijsen, MJ | 1 |
| Corsten, MF | 1 |
| Te Boekhorst, PAW | 1 |
| Koene, HR | 1 |
| Van Sluis, GL | 1 |
| Cornelissen, JJ | 1 |
| Westerweel, PE | 1 |
| Lin, HC | 1 |
| Saputra, F | 1 |
| Audira, G | 1 |
| Lai, YH | 1 |
| Roldan, MJM | 1 |
| Alos, HC | 1 |
| Aventurado, CA | 1 |
| Vasquez, RD | 1 |
| Tsai, GJ | 1 |
| Lim, KH | 1 |
| Hsiao, CD | 1 |
| Fernando, F | 1 |
| Innes, AJ | 1 |
| Claudiani, S | 2 |
| Pryce, A | 1 |
| Hayden, C | 1 |
| Byrne, J | 1 |
| Gallipoli, P | 1 |
| Copland, M | 1 |
| Apperley, JF | 1 |
| Milojkovic, D | 2 |
| Yılmaz, R | 1 |
| Pan, S | 1 |
| Leng, J | 1 |
| Deng, X | 1 |
| Ruan, H | 1 |
| Zhou, L | 1 |
| Jamal, M | 1 |
| Xiao, R | 1 |
| Xiong, J | 1 |
| Yin, Q | 1 |
| Wu, Y | 1 |
| Wang, M | 1 |
| Yuan, W | 1 |
| Shao, L | 1 |
| Zhang, Q | 2 |
| Eide, CA | 1 |
| Zabriskie, MS | 2 |
| Savage Stevens, SL | 1 |
| Antelope, O | 2 |
| Vellore, NA | 2 |
| Than, H | 1 |
| Schultz, AR | 1 |
| Clair, P | 1 |
| Bowler, AD | 1 |
| Pomicter, AD | 2 |
| Yan, D | 1 |
| Senina, AV | 1 |
| Qiang, W | 2 |
| Kelley, TW | 2 |
| Szankasi, P | 2 |
| Heinrich, MC | 2 |
| Tyner, JW | 1 |
| Rea, D | 3 |
| Cayuela, JM | 2 |
| Kim, DW | 2 |
| Tognon, CE | 1 |
| O'Hare, T | 2 |
| Druker, BJ | 2 |
| Deininger, MW | 2 |
| Mauro, MJ | 2 |
| Cortes, JE | 1 |
| Minami, H | 1 |
| DeAngelo, DJ | 1 |
| Breccia, M | 1 |
| Goh, YT | 1 |
| Talpaz, M | 1 |
| Hochhaus, A | 1 |
| le Coutre, P | 1 |
| Ottmann, O | 1 |
| Deininger, MWN | 1 |
| Mahon, FX | 1 |
| Minami, Y | 1 |
| Yeung, D | 1 |
| Ross, DM | 2 |
| Tallman, MS | 1 |
| Park, JH | 1 |
| Hynds, D | 1 |
| Duan, Y | 1 |
| Meille, C | 1 |
| Hourcade-Potelleret, F | 1 |
| Vanasse, KG | 2 |
| Lang, F | 2 |
| Romero, D | 1 |
| Özgür Yurttaş, N | 1 |
| Sahin, I | 1 |
| Reagan, JL | 1 |
| G Lindström, HJ | 1 |
| Nesr, G | 1 |
| Laffan, M | 1 |
| Innes, A | 1 |
| Apperley, J | 1 |
| Barys, L | 1 |
| Cowan-Jacob, SW | 3 |
| Estrada, N | 1 |
| Angona, A | 1 |
| Ramírez, MJ | 1 |
| Colorado Araujo, M | 1 |
| Encinas, MP | 1 |
| Casado Montero, LF | 1 |
| Moreno Vega, M | 1 |
| Gomez, V | 1 |
| Paz Coll, A | 1 |
| de Paz, R | 1 |
| Fernandez-Ruiz, A | 1 |
| Perez Lopez, R | 1 |
| Ortiz-Fernández, A | 1 |
| Steegmann-Olmedillas, JL | 1 |
| Cortes, J | 2 |
| Hall, KH | 1 |
| Brooks, A | 1 |
| Waller, EK | 1 |
| Wylie, AA | 2 |
| Jahnke, W | 2 |
| Loo, A | 2 |
| Furet, P | 2 |
| Marzinzik, AL | 2 |
| Pelle, X | 2 |
| Donovan, J | 1 |
| Zhu, W | 1 |
| Buonamici, S | 2 |
| Hassan, AQ | 2 |
| Lombardo, F | 2 |
| Iyer, V | 2 |
| Palmer, M | 1 |
| Berellini, G | 2 |
| Dodd, S | 2 |
| Thohan, S | 1 |
| Bitter, H | 1 |
| Branford, S | 1 |
| Petruzzelli, L | 1 |
| Warmuth, M | 2 |
| Hofmann, F | 1 |
| Keen, NJ | 1 |
| Sellers, WR | 1 |
| Sarosiek, K | 1 |
| Larocque, EA | 1 |
| Naganna, N | 1 |
| Opoku-Temeng, C | 1 |
| Lambrecht, AM | 1 |
| Sintim, HO | 1 |
| Cotesta, S | 1 |
| Drueckes, P | 1 |
| Fabbro, D | 1 |
| Gabriel, T | 1 |
| Groell, JM | 1 |
| Grotzfeld, RM | 1 |
| Henry, C | 1 |
| Jones, D | 1 |
| Rummel, G | 1 |
| Salem, B | 1 |
| Zoller, T | 1 |
| Singh, AP | 1 |
| Glennon, MS | 1 |
| Umbarkar, P | 1 |
| Gupte, M | 1 |
| Galindo, CL | 1 |
| Force, T | 1 |
| Becker, JR | 1 |
| Lal, H | 1 |
| El Rashedy, AA | 1 |
| Appiah-Kubi, P | 1 |
| Soliman, MES | 1 |
| Zamora, L | 1 |
| Smith, CC | 1 |
| Lasater, EA | 1 |
| Zhu, X | 1 |
| Lin, KC | 1 |
| Stewart, WK | 1 |
| Damon, LE | 1 |
| Salerno, S | 1 |
| Shah, NP | 1 |
| Czarnecka, AM | 1 |
| Oborska, S | 1 |
| Rzepecki, P | 1 |
| Szczylik, C | 1 |
| Mihaila, RG | 1 |
| Halbach, S | 1 |
| Hu, Z | 1 |
| Gretzmeier, C | 1 |
| Ellermann, J | 1 |
| Wöhrle, FU | 1 |
| Dengjel, J | 1 |
| Brummer, T | 1 |
| Kurosu, T | 1 |
| Ohki, M | 1 |
| Wu, N | 1 |
| Kagechika, H | 1 |
| Miura, O | 1 |
| von Bubnoff, N | 1 |
| Gorantla, SP | 1 |
| Engh, RA | 1 |
| Oliveira, TM | 1 |
| Thöne, S | 1 |
| Aberg, E | 1 |
| Peschel, C | 1 |
| Duyster, J | 1 |
| Retnakumari, AP | 1 |
| Hanumanthu, PL | 1 |
| Malarvizhi, GL | 1 |
| Prabhu, R | 1 |
| Sidharthan, N | 1 |
| Thampi, MV | 1 |
| Menon, D | 1 |
| Mony, U | 1 |
| Menon, K | 1 |
| Keechilat, P | 1 |
| Nair, S | 1 |
| Koyakutty, M | 1 |
| Rahmani, M | 1 |
| Nguyen, TK | 1 |
| Dent, P | 2 |
| Grant, S | 2 |
| Dasmahapatra, G | 1 |
| Yerram, N | 1 |
| Dai, Y | 1 |
| Ogata, S | 1 |
| Takeuchi, M | 1 |
| Fujita, H | 1 |
| Shibata, K | 1 |
| Okumura, K | 1 |
| Taguchi, H | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase 3, Multi-center, Open-label, Randomized Study of Oral ABL001 Versus Bosutinib in Patients With Chronic Myelogenous Leukemia in Chronic Phase (CML-CP), Previously Treated With 2 or More Tyrosine Kinase Inhibitors[NCT03106779] | Phase 3 | 233 participants (Actual) | Interventional | 2017-10-26 | Active, not recruiting | ||
| A Phase I, Multicenter, Open-label Study of Oral ABL001 in Patients With Chronic Myelogenous Leukemia (CML) or Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia (Ph+ ALL)[NCT02081378] | Phase 1 | 326 participants (Actual) | Interventional | 2014-04-24 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
MMR was defined as a ≥ 3.0 log reduction in BCR-ABL1 transcripts compared to the standardized baseline equivalent to ≤ 0.1% BCR-ABL1/ABL% by IS as measured by RQ-PCR. (NCT03106779)
Timeframe: 24 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| Asciminib | 40 |
| Bosutinib | 10 |
6 reviews available for niacinamide and Granulocytic Leukemia, Chronic
| Article | Year |
|---|---|
Asciminib: First Approval.
Topics: Antineoplastic Agents; Clinical Trials as Topic; Cytochrome P-450 CYP3A; Cytochrome P-450 CYP3A Inhi | 2022 |
An evaluation of asciminib for patients with chronic myeloid leukemia previously treated with ≥2 tyrosine kinase inhibitors.
Topics: Drug Resistance, Neoplasm; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Pr | 2022 |
Novel therapeutic approaches in chronic myeloid leukemia.
Topics: Antineoplastic Agents; Clinical Trials as Topic; Drug Resistance, Neoplasm; Everolimus; Fusion Prote | 2020 |
The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase.
Topics: Binding Sites; Cell Proliferation; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Humans; Leuk | 2020 |
Third-line therapy for chronic myeloid leukemia: current status and future directions.
Topics: Aniline Compounds; Animals; Antineoplastic Agents; Clinical Trials as Topic; Fusion Proteins, bcr-ab | 2021 |
A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology.
Topics: Amiloride; Antineoplastic Agents; Apoptosis; Cation Transport Proteins; Cell Line, Tumor; DNA Damage | 2015 |
3 trials available for niacinamide and Granulocytic Leukemia, Chronic
| Article | Year |
|---|---|
Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases.
Topics: Antineoplastic Agents; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Pos | 2022 |
Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases.
Topics: Antineoplastic Agents; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Pos | 2022 |
Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases.
Topics: Antineoplastic Agents; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Pos | 2022 |
Population Pharmacokinetics of Asciminib in Tyrosine Kinase Inhibitor-Treated Patients with Philadelphia Chromosome-Positive Chronic Myeloid Leukemia in Chronic and Acute Phases.
Topics: Antineoplastic Agents; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Pos | 2022 |
Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Dose-Response Relationship, Drug; Drug Resist | 2019 |
Mechanisms of resistance to the BCR-ABL1 allosteric inhibitor asciminib.
Topics: Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Humans; K | 2017 |
37 other studies available for niacinamide and Granulocytic Leukemia, Chronic
| Article | Year |
|---|---|
Asciminib as a new option in the treatment of chronic myeloid leukemia.
Topics: Antineoplastic Combined Chemotherapy Protocols; Drug Resistance, Neoplasm; Humans; Leukemia, Myeloge | 2021 |
A kinase inhibitor which specifically targets the ABL myristate pocket (STAMP), but unlike asciminib crosses the blood-brain barrier.
Topics: Animals; Antineoplastic Agents; Blood-Brain Barrier; Cell Line; Dogs; Dose-Response Relationship, Dr | 2022 |
Asciminib: a new therapeutic option in chronic-phase CML with treatment failure.
Topics: Antineoplastic Agents; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelog | 2022 |
Allosteric enhancement of the BCR-Abl1 kinase inhibition activity of nilotinib by cobinding of asciminib.
Topics: Adenosine Triphosphate; Antineoplastic Agents; Cell Line, Tumor; Dasatinib; Drug Resistance, Neoplas | 2022 |
Real-life analysis on safety and efficacy of asciminib for ponatinib pretreated patients with chronic myeloid leukemia.
Topics: Antineoplastic Agents; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Humans; Imidazoles; Leuk | 2022 |
Treatment patterns and clinical outcomes of asciminib in a real-world multiresistant chronic myeloid leukemia patient population.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Niacinamide; Protein Ki | 2023 |
Investigating Potential Cardiovascular Toxicity of Two Anti-Leukemia Drugs of Asciminib and Ponatinib in Zebrafish Embryos.
Topics: Animals; Antineoplastic Agents; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Imidazoles; Leu | 2022 |
The outcome of post-transplant asciminib in patients with chronic myeloid leukaemia.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukemia, Myeloid; Niacinamide; Protein Ki | 2023 |
Breaking the mold: asciminib as a standard-of-care of the therapeutic armamentarium of chronic myeloid leukemia in the upfront setting.
Topics: Chronic Disease; Drug Resistance, Neoplasm; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, | 2023 |
Asciminib (Scemblix) for chronic myeloid leukemia.
Topics: Antineoplastic Agents; Chronic Disease; Drug Resistance, Neoplasm; Humans; Leukemia, Myelogenous, Ch | 2023 |
Nicotinamide increases the sensitivity of chronic myeloid leukemia cells to doxorubicin via the inhibition of SIRT1.
Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Biomarkers, Tumor; Cell Proliferation; Doxorubicin; | 2020 |
Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants.
Topics: Allosteric Regulation; Animals; Antineoplastic Combined Chemotherapy Protocols; Binding Sites; Cell | 2019 |
Initial results with asciminib in CML.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Protein Kinase Inhibitors; Py | 2020 |
Asciminib in Relapsed Chronic Myeloid Leukemia.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Protein Kinase Inhibitors; Py | 2020 |
Asciminib in Relapsed Chronic Myeloid Leukemia. Reply.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Pyrazoles | 2020 |
The effects of combination treatments on drug resistance in chronic myeloid leukaemia: an evaluation of the tyrosine kinase inhibitors axitinib and asciminib.
Topics: Antineoplastic Combined Chemotherapy Protocols; Axitinib; Cell Line, Tumor; Computer Simulation; Das | 2020 |
Platelet function in patients with chronic myeloid leukemia treated with asciminib.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Pyrazoles | 2020 |
Safety and efficacy of asciminib treatment in chronic myeloid leukemia patients in real-life clinical practice.
Topics: Adult; Aged; Aged, 80 and over; Female; Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chr | 2021 |
Asciminib in chronic myeloid leukemia: many questions still remain to be answered.
Topics: Antineoplastic Agents; Drug Resistance, Neoplasm; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Po | 2021 |
Overcoming TKI resistance in a patient with chronic myeloid leukemia using combination BCR-ABL inhibition with asciminib and bosutinib.
Topics: Adult; Aniline Compounds; Antineoplastic Combined Chemotherapy Protocols; Female; Humans; Leukemia, | 2021 |
Asciminib for the treatment of patients with chronic myeloid leukemia.
Topics: Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Niacinamide; Pyrazoles | 2021 |
The allosteric inhibitor ABL001 enables dual targeting of BCR-ABL1.
Topics: Allosteric Regulation; Allosteric Site; Animals; Catalytic Domain; Cell Proliferation; Dasatinib; Dr | 2017 |
Double trouble for CML.
Topics: Fusion Proteins, bcr-abl; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Neoplasm Recurre | 2017 |
Alkynylnicotinamide-Based Compounds as ABL1 Inhibitors with Potent Activities against Drug-Resistant CML Harboring ABL1(T315I) Mutant Kinase.
Topics: Alkynes; Animals; Antineoplastic Agents; Cell Line, Tumor; Humans; Imatinib Mesylate; Imidazoles; Is | 2018 |
Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1.
Topics: Allosteric Regulation; Animals; Dogs; Drug Discovery; Fusion Proteins, bcr-abl; Humans; Leukemia, My | 2018 |
Ponatinib-induced cardiotoxicity: delineating the signalling mechanisms and potential rescue strategies.
Topics: Animals; Animals, Genetically Modified; Antineoplastic Agents; Apoptosis; Cardiotoxicity; Cells, Cul | 2019 |
A Synergistic Combination Against Chronic Myeloid Leukemia: An Intra-molecular Mechanism of Communication in BCR-ABL1 Resistance.
Topics: Antineoplastic Combined Chemotherapy Protocols; Drug Resistance, Neoplasm; Drug Synergism; Fusion Pr | 2019 |
Current treatment of myeloproliferative neoplasias: three scenarios.
Topics: Antineoplastic Agents; Drug Resistance, Neoplasm; Humans; Imatinib Mesylate; Leukemia, Myelogenous, | 2020 |
Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.
Topics: Amino Acid Sequence; Amino Acid Substitution; Benzothiazoles; Cell Line, Tumor; Drug Resistance, Neo | 2013 |
Development of chronic myeloid leukaemia in patients treated with anti-VEGF therapies for clear cell renal cell cancer.
Topics: Adult; Aged; Bone Marrow Cells; Carcinoma, Renal Cell; Humans; Indoles; Leukemia, Myelogenous, Chron | 2015 |
Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cells.
Topics: Adaptor Proteins, Signal Transducing; Axitinib; Cell Line, Tumor; Drug Resistance, Neoplasm; Fusion | 2016 |
Sorafenib induces apoptosis specifically in cells expressing BCR/ABL by inhibiting its kinase activity to activate the intrinsic mitochondrial pathway.
Topics: Acetophenones; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamides; Benzenesulfona | 2009 |
The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro.
Topics: Amino Acid Sequence; Antineoplastic Agents; Benzamides; Benzenesulfonates; Blotting, Western; Cell L | 2011 |
Rationally designed aberrant kinase-targeted endogenous protein nanomedicine against oncogene mutated/amplified refractory chronic myeloid leukemia.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Blotting, Western; Cell Proliferation; Drug Carriers; | 2012 |
The multikinase inhibitor sorafenib induces apoptosis in highly imatinib mesylate-resistant bcr/abl+ human leukemia cells in association with signal transducer and activator of transcription 5 inhibition and myeloid cell leukemia-1 down-regulation.
Topics: Antineoplastic Agents; Apoptosis; Benzamides; Benzenesulfonates; Dose-Response Relationship, Drug; D | 2007 |
Synergistic interactions between vorinostat and sorafenib in chronic myelogenous leukemia cells involve Mcl-1 and p21CIP1 down-regulation.
Topics: Benzenesulfonates; Cell Line, Tumor; Cell Survival; Cyclin-Dependent Kinase Inhibitor p21; Drug Syne | 2007 |
Apoptosis induced by niacin-related compounds in K562 cells but not in normal human lymphocytes.
Topics: Antineoplastic Agents; Apoptosis; Humans; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positi | 2000 |