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Imatinib

Imatinib is a targeted cancer therapy medication used to treat certain types of blood cancers and solid tumors.
It works by blocking the activity of specific proteins involved in the growth and division of cancer cells.
Imatinib has been shown to be effective in treating chronic myelogenous leukemia, gastrointestinal stromal tumors, and other malignancies.
Researchers can use PubCompare.ai's AI-driven platform to easily locate and compare Imatinib-related protocols from literature, preprints, and patents, helping to improve reproducibility and accuracy in their Imatinib studies.
With cutting-edge comparison tools, scientists can identify the optimal protocols and products for their Imatinib research, enhancing the overall quality and impact of their work.

Most cited protocols related to «Imatinib»

1
Collapsing Microarray Gene Expression Data
Cited 22 times
The demonstration cases described below feature published microarray gene-expression data. They were converted to ranked lists by calculating t-test P-values between the relevant sample types (classes) for each probe, that were log10-transformed and signed to indicate direction of change (positive for increased in Class B, negative for increased in Class A or decreased in Class B). Probes were annotated with current mouse or human UniGene identifiers and homologs were identified using HomoloGene; only the probe with the highest absolute signed t-test P-value within those with matching UniGene identifiers was kept in the collapsing step. Data downloaded from Gene-expression Omnibus (GEO) (19 (link)): MPAKT prostate cancer mouse model, GSE1413; breast tumors with ER, PR and HER2 status, GSE2603; MMTV-HER2/neu mouse model, GSE2528; BCR-ABL transfected cell line, GSE10912; mammary stem cell, GSE3711; KRAS2 overexpression cell line, GSE3151; lung tumors with KRAS2 status, GSE3141; imatinib treatment in leukemia patients, GSE2535; dasatinib treatment in cell lines, GSE9633 and GSE6569; castration and testosterone treatment in mice, GSE5901; gedunin treatment in prostate cancer cell line, GSE5506. Data downloaded from Array Express (20 (link)): imatinib treatment in leukemia patients, E-MEXP-433 (21 (link)). Data downloaded from an individual lab website: KRAS2 lung tumors and mouse model (1 (link)), Cmap database (10 (link)). Data communicated by collaborators: PTEN knockout prostate cancer mouse model, Dr Shunyou Wang, laboratory of Dr Hong Wu, UCLA (22 (link)).
Plaisier S.B., Taschereau R., Wong J.A, & Graeber T.G. (2010). Rank–rank hypergeometric overlap: identification of statistically significant overlap between gene-expression signatures. Nucleic Acids Research, 38(17), e169.
Publication 2010
Breast Breast Neoplasm Castration Cell Lines Dasatinib erbb2 Gene ERBB2 protein, human gedunin Gene Expression Homo sapiens Imatinib KRAS protein, human Leukemia Lung Neoplasms Mice, Knockout Microarray Analysis Mouse mammary tumor virus Mus Patients Prostate Cancer PTEN protein, human Stem Cells Testosterone
2
Metastatic GIST: Imatinib and Sunitinib Failure
Cited 14 times

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Publication 2012
Disease Progression Eligibility Determination FLT1 protein, human Gastrointestinal Stromal Tumors Genetic Heterogeneity Heart Imatinib inhibitors Kidney Neoplasms Patients Sunitinib Therapeutics X-Ray Computed Tomography
3
Nude Mouse Xenograft Model of Chronic Myeloid Leukemia
Cited 13 times
Nude Balb/c mice were bred at the animal facility of Guangzhou Medical College. The mice were housed in barrier facilities with a 12-hour light/dark cycle, with food and water available ad libitum. A total of 3 × 107 of KBM5 or KBM5-T315I cells were inoculated subcutaneously on the flanks of 5-week-old male nude mice. After 72 hours of inoculation, mice were treated with vehicle (10% DMSO, 30% cremophor and 60% NaCl), gambogic acid (3 mg/kg/2 days, i.p.), imatinib (50 mg/kg/d, i.g.) and the combination of gambogic acid and imatinib for a total of 17 days. Tumors were measured and tumor volumes were calculated by the following formula: a2 × b × 0.4, where a is the smallest diameter and b is the diameter perpendicular to a. Tumor xenografts were removed, weighed, stored, and fixed. All animal studies were conducted with the approval of the Institutional Animal Care and Use Committee of Guangzhou Medical College.
Shi X., Chen X., Li X., Lan X., Zhao C., Liu S., Huang H., Liu N., Liao S., Song W., Zhou P., Wang S., Xu L., Wang X., Dou Q.P, & Liu J. (2013). Gambogic Acid Induces Apoptosis in Imatinib-Resistant Chronic Myeloid Leukemia Cells via Inducing Proteasome Inhibition and Caspase-Dependent Bcr-Abl Downregulation. Clinical cancer research : an official journal of the American Association for Cancer Research, 20(1), 151-163.
Publication 2013
Animals Cells cremophor Food gambogic acid Heterografts Imatinib Institutional Animal Care and Use Committees Males Mice, Inbred BALB C Mice, Nude Mus Neoplasms Sodium Chloride Sulfoxide, Dimethyl Vaccination
4
Autophagy Induction and Inhibition Assays
Cited 12 times
To induce autophagy, HeLa, HEK293, and OVCAR8 cells were treated with PP242 (2 to 20 μM) for 0 to 24 h. K562 cells were incubated with imatinib (either 1 or 2 μM) or PP242 (10 μM) for 0 to 22 h. To induce autophagy by starvation, K562 or HEK293 cells were washed 3 times with PBS (137 mM NaCl, 2.7 mM KCl, 10 mM Na2HPO4, 1.8 mM KH2PO4) and incubated in Earle's Balanced Salt Solution (Life Technologies Corporation, 14155063) for various time points. To block autophagy flux, cells were incubated with chloroquine (2.5 to 20 μM) for 0.5 to 6 h.
Guo S., Liang Y., Murphy S.F., Huang A., Shen H., Kelly D.F., Sobrado P, & Sheng Z. (2015). A rapid and high content assay that measures cyto-ID-stained autophagic compartments and estimates autophagy flux with potential clinical applications. Autophagy, 11(3), 560-572.
Publication 2015
Autophagy Cardiac Arrest Cells Chloroquine HEK293 Cells HeLa Cells Imatinib K562 Cells PP242 Sodium Chloride
5
Modeling Apo-Closed and Inward-Facing ABCG2 Conformations
Cited 9 times
In order to model the apo-closed conformation, the high-resolution structure of human ABCG2 bound to the 5D3 Fab and MZ29 inhibitor (PDBid 6ETI) was used as an initial template for model building and refinement. The 5D3 Fab and all ligands were removed from the structure, leaving just the ABCG2 TM and NBD domains. TM5 was manually shifted and rotated to match the proper helical character and sequence register observed in the closed conformation map. Similarly, the unraveled portion of TM2 was manually adjusted in COOT to fit the apo-closed conformation map. The model was then iteratively adjusted manually in COOT and refined in real-space with phenix.real_space_refine.
The structure of human ABCG2 bound to the 5D3 Fab and MZ29 inhibitor (PDBid 6ETI) was also used as an initial template for model building and refinement for inward facing ABCG2 structures. The 5D3 Fab and all ligands were removed from the structure, leaving just the ABCG2 TM and NBD domains. The resulting model was rigid body fit in UCSF Chimera48 (link) into the inward facing conformation map of ABCG2 bound to imatinib, MXN, or SN38 and then refined by iterative rounds of manual adjustment in COOT49 (link), with manual placement and real-space refinement of ligands, followed by real-space refinement in phenix.real_space_refine50 (link). Chemical descriptions and refinement restraints for MXN and imatinib were obtained from the CCP451 (link) monomer library and phenix.ready_set. A molecule of SN38 was manually built in JLigand52 (link), and refinement restraints were generated in phenix.ready_set. Final calculation of map vs model FSC was performed by first simulating a map from the refined atomic models to Nyquist frequency using UCSF Chimera, and then using this simulated map to calculate FSC with the final map from Relion autorefine.
Orlando B.J, & Liao M. (2020). ABCG2 transports anticancer drugs via a closed-to-open switch. Nature Communications, 11, 2264.
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Publication 2020
Character Chimera DNA Library Helix (Snails) Homo sapiens Human Body Imatinib Ligands Muscle Rigidity

Most recents protocols related to «Imatinib»

1
Monitoring Signaling Pathways in CML Cell Lines
Not available on PMC !

Example 7

In order to provide a more readily available and reproducible cell system (and to avoid the problems seen with existing methods), experimental systems based on tissue culture cell lines may be utilized to monitor the impact of drugs on signaling pathways.

Flow cytometric methods using tissue culture cells have been routinely used for investigating the effects of drugs, for example, inhibitors of Bcr/Abl kinase that are useful in the therapy of chronic myeloid leukemia (CML). CML is associated with the Philadelphia chromosome, a genetic translocation that fuses the Abl1 gene on chromosome 9 with part of the BCR gene on chromosome 22. The resulting fusion protein contains a receptor tyrosine kinase that constitutively activates several downstream signaling pathways, including P-STAT5, P-Crkl, P-mTOR, and P—HSF. The Abl kinase is the target of several therapeutics currently used clinically, including imatinib (GLEEVEC™), nilotinib, and dasatinib. These compounds act by inhibiting the tyrosine kinase activity at the receptor level, and also concomitantly inhibit all downstream signaling pathways.

As a representative model of CML, human K562 cell line, which expresses the Bcr/Abl fusion protein and constitutively phosphorylates the downstream STAT5 target (Cytometry 54A; 75-88, 2003), was used in the following experiment. As shown in FIG. 10, treatment of K562 cells for 30 min with 2 μM GLEEVEC™ (imatinib, or STI571) results in >95% inhibition of the phosphorylation of the downstream STAT5 target. Also, as shown in FIG. 10, although the phosphorylation of STAT5 is inhibited after 30 min imatinib exposure, there is no change in the cell cycle, as measured by DNA content.

Phosphorylated STAT5 (P-STAT5) acts as a transcriptional activator of several target proteins, including Cyclin D. Constitutive expression of Cyclin D (induced by P-STAT5) maintains K562 cells in cell cycle. It was found that exposure to imatinib for 24 hr decreases S-phase (as a marker of cell proliferation) by ˜50%, and further exposure to imatinib for an additional 24 hr decreases S-phase by an additional 50-70% (data not shown).

US11867690B2. Identification of functional cell states (2024-01-09). ASEDASCIENCES AG [CH]. Inventors: Bartlomiej Rajwa [US], Vincent T Shankey [US].
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Patent 2024
Cell Culture Techniques Cell Cycle Cell Lines Cell Proliferation Cells Chromosomes, Human, Pair 9 Chromosomes, Human, Pair 22 CRKL protein Cyclin D Cyclins Dasatinib Flow Cytometry FRAP1 protein, human Fusion Proteins, bcr-abl Genes Gleevec Homo sapiens Imatinib inhibitors K562 Cells Leukemias, Chronic Granulocytic nilotinib Pharmaceutical Preparations Philadelphia Chromosome Phosphorylation Phosphotransferases Proteins Protein Targeting, Cellular Psychological Inhibition Receptor Protein-Tyrosine Kinases SERPINA3 protein, human Signal Transduction Pathways Staphylococcal Protein A STAT5A protein, human STI571 Tissues Transcription, Genetic Translocation, Chromosomal Vision
2
Intensive Chemotherapy Regimens for Relapsed/Refractory ALL
As described in our previous studies, induction chemotherapy was started with a modified regimen of fractionated cyclophosphamide, vincristine, doxorubicin, dexamethasone (hyper-CVAD), and alternating high-dose cytarabine and mitoxantrone.22 (link)–25 (link, link, link) Patients who failed to achieve CR or relapsed after CR received intensified salvage chemotherapy using an MEC regimen consisting of cytarabine (2 g/m2, every 12 h, days 1–4), mitoxantrone (12 mg/m2, days 1–4), and etoposide (100 mg/m2, days 5–7). Patients with Ph-positive ALL also received tyrosine kinase inhibitors (imatinib or dasatinib).24 (link)–28 (link, link, link, link) In patients who revealed minimal residual disease (MRD) at 3 months post-transplant, we applied preemptive tyrosine kinase inhibitors. Since 2016, blinatumomab was used as a monotherapy for all above indications instead of MEC regimen in the same way of our previous study.21 (link) Before application of blinatumomab, all patients received prephase dexamethasone to reduce leukemic burden and cytokine release syndrome (CRS). During the first cycle, blinatumomab was continuously infused for 4 weeks (9 μg/day for the first 7 days and 28 μg/day thereafter). After a 2-week treatment-free interval, a second 4-week cycle was initiated at a dosage of 28 μg/day from day 1 to day 28. Even after 2016, we applied the MEC regimen to some patients who failed to blinatumomab, while some others were treated with inotuzumab ozogamicin (INO) as it became available for R/R Ph-negative ALL since late 2019.29 ,30 (link) Doses of INO were administered at 0.8 mg on day 1 of the first cycle (0.5 mg on the day of the second cycle) and 0.5 mg on days 8 and 15. The interval of the first cycle was 28 days, and up to two cycles were approved.
Yoon J.H., Kwag D., Lee J.H., Min G.J., Park S.S., Park S., Lee S.E., Cho B.S., Eom K.S., Kim Y.J., Kim H.J., Min C.K., Cho S.G., Wook Lee J, & Lee S. (2023). Superior survival outcome of blinatumomab compared with conventional chemotherapy for adult patients with relapsed or refractory B-cell precursor acute lymphoblastic leukemia: a propensity score–matched cohort analysis. Therapeutic Advances in Hematology, 14, 20406207231154713.
Publication 2023
blinatumomab Cyclophosphamide Cytarabine Cytokine Release Syndrome Dasatinib Dexamethasone Doxorubicin Etoposide Grafts Imatinib Induction Chemotherapy Inotuzumab Ozogamicin MAV protocol Mitoxantrone Neoplasm, Residual Patients Pharmacotherapy Treatment Protocols Vincristine
3
COVID-19 Infection Severity and Outcomes
Cited 1 time
Severity of infection was defined according to the WHO classification available at the time of enrolment [24 ]. The use of corticosteroids within the previous 30 days included therapy with prednisone or its equivalent at a dose > 0.5 mg/kg/day for at least 1 month. Prior infection and antibiotic therapy were defined as a diagnosis of infection and/or the receival of antibiotics in the 30 days prior to hospital admission, respectively. Status of haematological malignancy was defined as new diagnosis, remission, refractory/relapsing disease or yet to define, according to the guidelines of European Society for Medical Oncology [25 ]. Active malignancy was defined as patients with new diagnosis or refractory/relapsing disease [25 ]. Prior active treatment included the receival of chemotherapy or immunotherapy, or both, in the previous 90 days. Immunotherapy included the receival of monoclonal antibodies (rituximab, daratumumab and obinutuzumab) and tyrosine kinase inhibitors (imatinib, ibrutinib, ruxolitinib and venetoclax). Worsening of respiratory conditions was based on the change of PaO2/FiO2 and was defined as: (i) need of supplementary oxygen therapy or (ii) need of increasing oxygen therapy supplementation in a patient with SARS-CoV2 infection for reasons directly related to the infection, as it was already reported [8 (link)].
Time of viral shedding was defined as the number of days from the first viral detection by RT-PCR on nasopharyngeal specimen until the first negative result.
The study was approved by the local ethics committee (ID Prot. 109/2020).
Oliva A., Cogliati Dezza F., Petrucci F., Romani F.E., Morviducci M., Mirabelli F.M., Cancelli F., Valeriani E., Marcelli G., Pugliese F., Turriziani O., Ricci P., Venditti M., Palange P, & Mastroianni C.M. (2023). Outcome of COVID-19 patients with haematological malignancies after the introduction of vaccination and monoclonal antibodies: results from the HM-COV 2.0 study. Clinical and Experimental Medicine, 23(6), 2275-2285.
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Publication 2023
Adrenal Cortex Hormones Antibiotics COVID 19 daratumumab Diagnosis Europeans Hematologic Neoplasms ibrutinib Imatinib Immunotherapy Infection Malignant Neoplasms Monoclonal Antibodies Nasopharynx obinutuzumab Patients Pharmacotherapy Prednisone Regional Ethics Committees Respiration Disorders Reverse Transcriptase Polymerase Chain Reaction Rituximab ruxolitinib Therapies, Oxygen Inhalation venetoclax
4
COVID-19 Infection Severity and Outcomes
Severity of infection was defined according to the WHO classification available at the time of enrolment [24 ]. The use of corticosteroids within the previous 30 days included therapy with prednisone or its equivalent at a dose > 0.5 mg/kg/day for at least 1 month. Prior infection and antibiotic therapy were defined as a diagnosis of infection and/or the receival of antibiotics in the 30 days prior to hospital admission, respectively. Status of haematological malignancy was defined as new diagnosis, remission, refractory/relapsing disease or yet to define, according to the guidelines of European Society for Medical Oncology [25 ]. Active malignancy was defined as patients with new diagnosis or refractory/relapsing disease [25 ]. Prior active treatment included the receival of chemotherapy or immunotherapy, or both, in the previous 90 days. Immunotherapy included the receival of monoclonal antibodies (rituximab, daratumumab and obinutuzumab) and tyrosine kinase inhibitors (imatinib, ibrutinib, ruxolitinib and venetoclax). Worsening of respiratory conditions was based on the change of PaO2/FiO2 and was defined as: (i) need of supplementary oxygen therapy or (ii) need of increasing oxygen therapy supplementation in a patient with SARS-CoV2 infection for reasons directly related to the infection, as it was already reported [8 (link)].
Time of viral shedding was defined as the number of days from the first viral detection by RT-PCR on nasopharyngeal specimen until the first negative result.
The study was approved by the local ethics committee (ID Prot. 109/2020).
Oliva A., Cogliati Dezza F., Petrucci F., Romani F.E., Morviducci M., Mirabelli F.M., Cancelli F., Valeriani E., Marcelli G., Pugliese F., Turriziani O., Ricci P., Venditti M., Palange P, & Mastroianni C.M. (2023). Outcome of COVID-19 patients with haematological malignancies after the introduction of vaccination and monoclonal antibodies: results from the HM-COV 2.0 study. Clinical and Experimental Medicine, 23(6), 2275-2285.
Full text: Click here
Publication 2023
Adrenal Cortex Hormones Antibiotics COVID 19 daratumumab Diagnosis Europeans Hematologic Neoplasms ibrutinib Imatinib Immunotherapy Infection Malignant Neoplasms Monoclonal Antibodies Nasopharynx obinutuzumab Patients Pharmacotherapy Prednisone Regional Ethics Committees Respiration Disorders Reverse Transcriptase Polymerase Chain Reaction Rituximab ruxolitinib Therapies, Oxygen Inhalation venetoclax
5
Clinical Outcomes in Imatinib COVID-19 Treatment

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Publication 2023
Aman Cell Respiration Imatinib Medical Devices Nasal Cannula Noninvasive Ventilation Oxygen Oxygen Saturation Patients Renal Replacement Therapy Saturation of Peripheral Oxygen Tissue, Membrane Vasoconstrictor Agents

Top products related to «Imatinib»

1
Imatinib by Selleck Chemicals
Sourced in United States, Germany, United Kingdom, China, France
Imatinib is a tyrosine kinase inhibitor. It is a laboratory reagent used in research applications.
2
Imatinib by Merck Group
Sourced in United States, Germany, China, Italy
Imatinib is a lab equipment product manufactured by Merck Group. It is a tyrosine kinase inhibitor that functions by blocking the activity of certain enzymes involved in cellular processes.
3
Imatinib by Novartis
Sourced in Switzerland, United States, China
Imatinib is a laboratory product manufactured by Novartis. It is a small-molecule tyrosine kinase inhibitor.
4
Imatinib by LC Laboratories
Sourced in United States, China
Imatinib is a small molecule inhibitor. It is used as a laboratory reagent for research purposes.
5
Fetal bovine serum (fbs) by Thermo Fisher Scientific
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
6
Dasatinib by Selleck Chemicals
Sourced in United States, Germany, China, United Kingdom
Dasatinib is a laboratory reagent used in research applications. It is a tyrosine kinase inhibitor that can be used to study cellular signaling pathways.
7
Dimethyl sulfoxide (dmso) by Merck Group
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Rpmi 1640 by Thermo Fisher Scientific
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RPMI 1640 is a common cell culture medium used for the in vitro cultivation of a variety of cells, including human and animal cells. It provides a balanced salt solution and a source of essential nutrients and growth factors to support cell growth and proliferation.
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Nilotinib by Selleck Chemicals
Sourced in United States, Germany, France
Nilotinib is a synthetic chemical compound that functions as a tyrosine kinase inhibitor. It is primarily used in research and laboratory settings to study cellular signaling pathways and biochemical processes.
10
Imatinib by Cayman Chemical
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Imatinib is a laboratory chemical product manufactured by Cayman Chemical. It is a tyrosine kinase inhibitor.

More about "Imatinib"

Imatinib, also known as Gleevec or STI-571, is a potent and selective tyrosine kinase inhibitor (TKI) used in the treatment of certain types of blood cancers and solid tumors.
It works by blocking the activity of the BCR-ABL fusion protein, which is a driver of uncontrolled cell growth in chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GISTs).
Imatinib has been extensively studied and has revolutionized the treatment of CML, transforming it from a fatal disease to a manageable condition for many patients.
It has also demonstrated efficacy in the treatment of other malignancies, such as Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) and certain types of myelodysplastic syndromes.
In addition to its therapeutic applications, Imatinib is a valuable tool for researchers investigating the underlying mechanisms of cancer and developing new targeted therapies.
PubCompare.ai's AI-driven platform can assist researchers by providing easy access to Imatinib-related protocols from literature, preprints, and patents, helping to improve the reproducibility and accuracy of their studies.
Researchers can utilize PubCompare.ai's cutting-edge comparison tools to identify the optimal protocols and products for their Imatinib research, enhancing the overall quality and impact of their work.
This includes comparing the use of Imatinib with other TKIs, such as Dasatinib and Nilotinib, as well as the use of common cell culture reagents like FBS and RPMI 1640 medium, and the solvent DMSO.
By leveraging the insights and resources available through PubCompare.ai, researchers can accelerate their Imatinib-related studies, leading to more robust and impactful findings that contribute to the ongoing advancements in cancer treatment and understanding.