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Bortezomib

Bortezomib is a proteasome inhibitor used in the treatment of multiple myeloma and mantle cell lymphoma.
It works by blocking the activity of the proteasome, a large protein complex that plays a crucial role in the degradation of unwanted or damaged proteins within cells.
This disruption of protein homeostasis can lead to cell death, particularly in rapidly dividing cancer cells.
Bortezomib has demonstrated efficacy in improving overall survival and progression-free survival in patients with these hematological malignancies.
Reserchers can utilize the PubCompare.ai platforrm to streamline Bortezomib-related studies, optimizing their research approach through AI-powered comparisons of protocols from literature, preprints, and patents.

Most cited protocols related to «Bortezomib»

1
Reproducible Bioinformatics Analysis Pipeline
Cited 23 times
Annotated R code (in Sweave format) to reproduce all of the analysis in this paper is available from our website [57 ]. The CGP gene expression data are available from ArrayExpress under accession number E-MTAB-783. The IC50 data for the drugs is available from the CGP website [52 ]. The docetaxel data are available from GEO under accession numbers [GEO:GSE349] and [GEO:GSE350]. The cisplatin data are available from ArrayExpress under accession number E-GEOD-18864. The bortezomib data are available from GEO under accession number [GEO:GSE9782]. The erlotinib data are available from GEO under accession number [GEO:GSE33072]. Complete details and R code showing how to acquire and preprocess all of these data, as well as the associated clinical data are available in Sweave format on our website.
Geeleher P., Cox N.J, & Huang R.S. (2014). Clinical drug response can be predicted using baseline gene expression levels and in vitro drug sensitivity in cell lines. Genome Biology, 15(3), R47.
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Publication 2014
Bortezomib Cisplatin Docetaxel Erlotinib Gene Expression Pharmaceutical Preparations
2
Randomized Trial of Bortezomib for Pediatric AML
Cited 18 times
The AAML1031 study was an open-label multi-center randomized trial including patients aged 0 to 29.5 years with previously untreated primary AML. Exclusion criteria were: prior chemotherapy, acute promyelocytic leukemia [t(15;17)], juvenile myelomonocytic leukemia, bone marrow failure syndromes, or secondary AML. The National Cancer Institute’s central institutional review board (IRB) and IRB at each enrolling center approved the study; patients and families provided informed consent or assent as appropriate. The trial was conducted in accordance with the Declaration of Helsinki. The trial was registered at clinicaltrials.gov identifier: NCT01371981.
Patients were randomly assigned at enrollment to either standard AML treatment or standard treatment with bortezomib. Randomization was conducted in blocks of four. Bortezomib was administered at a dose of 1.3 mg/m2 once on days 1, 4, and 8 of each chemotherapy course.
Patients with high allelic ratio FLT3 ITD were offered enrollment on a phase I sorafenib treatment arm if that arm was open. Patients with HAR FLT3 ITD who declined enrollment in the sorafenib arm, or who enrolled while the arm was suspended, continued to receive treatment according to their initial randomization. These patients were included in safety analyses but were excluded from all efficacy analyses.
Patients were classified as low- or high-risk after Induction I. Low-risk patients received four courses of chemotherapy and high-risk patients received three courses of chemotherapy followed by allogeneic SCT. High-risk patients without an appropriate donor received four courses of chemotherapy.
The primary end point was EFS from study entry. EFS was defined as the time from study entry until death, refractory disease, or relapse of any type, whichever occurred first. The secondary end points were OS, remission rates, relapse risk, post induction disease-free survival (DFS), and treatment-related mortality (TRM). OS was defined as time from study entry until death. Relapse risk was defined as the time from the end of Induction II for patients in complete remission (CR) to relapse, where deaths without a relapse were considered competing events. DFS was defined as the time from end of Induction II for patients in CR until relapse or death. Refractory disease was defined as the persistence of central nervous system (CNS) disease after Induction I, or the presence of morphologic bone marrow blasts ≥5% or any extramedullary disease at the end of Induction II. Patients with refractory disease were removed from protocol therapy. TRM was defined as the time from either study entry, or from end of Induction II for patients in CR, to deaths without a relapse, with relapses considered as competing events. Patients without an event were censored at their date of last known contact. However, for TRM analyses, patients were censored 30 days post end of therapy or 200 days post SCT.
Aplenc R., Meshinchi S., Sung L., Alonzo T., Choi J., Fisher B., Gerbing R., Hirsch B., Horton T., Kahwash S., Levine J., Loken M., Brodersen L., Pollard J., Raimondi S., Kolb E.A, & Gamis A. (2020). Bortezomib with standard chemotherapy for children with acute myeloid leukemia does not improve treatment outcomes: a report from the Children’s Oncology Group. Haematologica, 105(7), 1879-1886.
Publication 2020
Acute Promyelocytic Leukemia Alleles Bone Marrow Bone Marrow Failure Disorders Bortezomib Central Nervous System Diseases Donors Ethics Committees, Research FLT3 protein, human Juvenile Myelomonocytic Leukemia Patients Pharmacotherapy Relapse Safety Sorafenib Therapeutics
3
Proteasome Purification and Activity Assays
Cited 17 times

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Publication 2009
26S proteasome Amino Acids Anabolism Apoptosis Biological Assay Bortezomib Cells Cell Survival Centrifugation Dietary Supplements inhibitors isolation Multicatalytic Endopeptidase Complex Muscle Tissue MV-151 phosphine Polypeptides Promega Protein Subunits Rabbits Sepharose Streptavidin Sulfoxide, Dimethyl
4
Measuring Protein Synthesis in Cells
Cited 13 times
For in vitro analysis 103-104 bone marrow or sorted cells were plated in 100 μl of methionine free Dulbecco’s Modified Eagle’s Medium (Sigma) supplemented with 200 μM L-cysteine (Sigma), 50 μM 2-mercaptoethanol (Sigma), 1mM L-glutamine (Gibco) and 0.1% bovine serum albumin (BSA; Sigma). For analysis of HPG and AHA incorporation, cells were pre-cultured for 45 minutes to deplete endogenous methionine. For OP-Puro, the medium was supplemented with 1mM L-methionine (Sigma). HPG (Life Technologies; 1mM final concentration), AHA (Life Technologies; 1mM final concentration) or OP-Puro (Medchem Source; 50 μM final concentration) were added to the culture medium for 1 hour (HPG and OP-Puro) or 2.5 hours (AHA), then cells were removed from wells and washed twice in Ca2+ and Mg2+ free phosphate buffered saline (PBS). Cells were fixed in 0.5ml of 1% paraformaldehyde (Affymetrix) in PBS for 15 minutes on ice. Cells were washed in PBS, then permeabilized in 200 μl PBS supplemented with 3% fetal bovine serum (Sigma) and 0.1% saponin (Sigma) for 5 minutes at room temperature. The azide-alkyne cycloaddition was performed using the Click-iT Cell Reaction Buffer Kit (Life Technologies) and azide conjugated to Alexa Fluor 488 or Alexa Fluor 555 (Life Technologies) at 5μM final concentration. After the 30 minute reaction, the cells were washed twice in PBS supplemented with 3% fetal bovine serum and 0.1% saponin, then resuspended in PBS supplemented with 4’,6-diamidino-2-phenylindole (DAPI; 4 μg/ml final concentration) and analyzed by flow cytometry. To inhibit OP-Puro, HPG or AHA incorporation, cycloheximide (Sigma) was added 30 minutes prior to OP-Puro or HPG at a final concentration of 100 μg/ml. All cultures were incubated at 37°C in 6.5% CO2 and constant humidity.
For in vivo analysis, OP-Puro (50mg/kg body mass; pH 6.4–6.6 in PBS) was injected intraperitoneally. One hour later mice were euthanized, unless indicated otherwise. Bone marrow was harvested, and 3×106 cells were stained with combinations of antibodies against cell surface markers as described below. After washing, the cells were fixed, permeabilized, and the azide-alkyne cycloaddition was performed as described above. “Relative rates of protein synthesis” were calculated by normalizing OP-Puro signals to whole bone marrow after subtracting autofluorescence background. “Mean OP-Puro fluorescence” reflected absolute fluorescence values for each cell population from multiple independent experiments.
To assess the effect of proteasome activity on OP-Puro incorporation mice were administered an intravenous injection of bortezomib (Cell Signaling; 1mg/kg body mass) 1 hour before OP-Puro administration. OP-Puro incorporation was assessed as described above 1 hour later unless indicated otherwise.
Signer R.A., Magee J.A., Salic A, & Morrison S.J. (2014). Haematopoietic stem cells require a highly regulated protein synthesis rate. Nature, 509(7498), 49-54.
Publication 2014
2-Mercaptoethanol alexa fluor 488 Alexa Fluor 555 Alkynes Antibodies Azides Bone Marrow Bortezomib Cardiac Arrest Cells Culture Media Cycloaddition Reaction Cycloheximide Cysteine DAPI Eagle Fetal Bovine Serum Flow Cytometry Fluorescence Glutamine Human Body Humidity Methionine Multicatalytic Endopeptidase Complex Mus O-propargyl-puromycin paraform Phosphates Protein Biosynthesis Saline Solution Saponin Serum Albumin, Bovine
5
Multi-Omics Data Integration for CLL
Cited 9 times
The data were taken from (Dietrich et al, 2018), where details on the data generation and processing can be found. Briefly, this data set consists of somatic mutations (combination of targeted and whole exome sequencing), RNA expression (RNA‐Seq), DNA methylation (Illumina arrays) and ex vivo drug response screens (ATP‐based CellTiter‐Glo assay). For the training of MOFA, we included 62 drug response measurements (excluding NSC 74859 and bortezomib due to bad quality) at five concentrations each (D = 310) with a threshold at 1.1 to remove outliers. Mutations were considered if present in at least three samples (D = 69). Low counts from RNA‐Seq data were filtered out and the data were normalized using the estimateSizeFactors and varianceStabilizingTransformation function of DESeq2 (Love et al, 2014). For training, we considered the top D = 5,000 most variable mRNAs after exclusion of genes from the Y chromosome. Methylation data were transformed to M‐values, and we extracted the top 1% most variable CpG sites excluding sex chromosomes (D = 4,248). We included patients diagnosed with CLL and having data in at least two views into the MOFA model leading to a total of N = 200 samples.
Argelaguet R., Velten B., Arnol D., Dietrich S., Zenz T., Marioni J.C., Buettner F., Huber W, & Stegle O. (2018). Multi‐Omics Factor Analysis—a framework for unsupervised integration of multi‐omics data sets. Molecular Systems Biology, 14(6), e8124.
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Publication 2018
Biological Assay Bortezomib Diploid Cell DNA Methylation Genes Love Methylation Mutation NSC 74859 Patients Pharmaceutical Preparations RNA, Messenger RNA-Seq Sex Chromosomes Substance Abuse Detection Transcription, Genetic Y Chromosome

Most recents protocols related to «Bortezomib»

1
Mitochondrial Motility Regulation by Delta-2 Tubulin and Bortezomib
Not available on PMC !

EXAMPLE 4

To determine the effect bortezomib and delta-2 tubulin accumulation have on mitochondrial motility, DRG neurons were transduced with lentivirus to express wild-type tubulin or delta-2 tubulin. As shown in FIGS. 15A and B, DRG neurons that expressed delta-2 tubulin showed a significant reduction in the motility of the mitochondria in the neurons as compared to control neurons or neurons that expressed wild-type tubulin. Expression of delta-2 tubulin affected every state of mitochondrial movement analyzed except for the stationary state (STA) (FIG. 15C). The effect of CCP1 knockdown on mitochondrial movement in the presence of bortezomib was also analyzed. As shown in FIG. 15D, treatment with bortezomib greatly affected the movement of mitochondria in DRG neurons. However, the knockdown of CCP1 activity rescued the effects bortezomib had on the motility of the mitochondria (FIG. 15D-F).

US11874284B2. Delta-2-tubulin as a biomarker and therapeutic target for peripheral neuropathy (2024-01-16). THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK [US], UNIVERSITÀ DEGLI STUDI DI MILANO-BICOCCA [IT]. Inventors: Francesca Bartolini [US], Maria Elena Pero [US], Guido Cavaletti [IT].
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Patent 2024
Bortezomib delta-Tubulin Lentivirus Mitochondria Mitochondrial Inheritance Motility, Cell Motor Neurons Movement Neurons Tubulin
2
CCP1 Regulates Delta-2 Tubulin in Peripheral Neuropathy
Not available on PMC !

EXAMPLE 3

CCP1 is a tubulin enzyme that participates in the generation of delta-2 tubulin (FIG. 9). To determine the importance of CCP1 in neuropathy upon treatment with a chemotherapy agent, DRGs were treated with 200 mM bortezomib in vitro for 24 hrs. DRGs were also treated with a short hairpin RNA targeting CCP1. As shown in FIG. 10 and FIG. 14, the knockdown of CCP1 activity prevented accumulation of delta-2 tubulin and prevented DRG axonopathy that occurs upon treatment with bortezomib. These data are supportive of a pathogenic role of delta-2 tubulin in chemotherapy-induced peripheral neuropathy and the important role CCP1 plays in generating delta-2 tubulin.

US11874284B2. Delta-2-tubulin as a biomarker and therapeutic target for peripheral neuropathy (2024-01-16). THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK [US], UNIVERSITÀ DEGLI STUDI DI MILANO-BICOCCA [IT]. Inventors: Francesca Bartolini [US], Maria Elena Pero [US], Guido Cavaletti [IT].
Full text: Click here
Patent 2024
Bortezomib delta-Tubulin Enzymes pathogenesis Peripheral Nervous System Diseases Pharmacotherapy Short Hairpin RNA Tubulin
3
Asymmetric Synthesis of Bortezomib Prodrug
Not available on PMC !

Example 8

The asymmetric synthesis of bortezomib-prodrug (FIG. 13) may involve the preparation of intermediate-1 (N-sulfinyl α-amino boron pinacolato complex) by following published methods. Selective removal of the N-sufinyl group under mild acidic conditions may produce the amine hydrochloride (intermediate 2), which may then be coupled with N-Boc-L-phenylalanine by a TBTU/DIPEA mediated reaction protocol. Intermediate-3 (amine hydrochloride) may then undergo coupling with the commercially available 3-am inopyrazine-2-carboxylic acid to produce the pinacol boronate of bortezomib. This may subsequently be hydrolyzed under biphasic conditions utilizing iso-butylboronic acid as a pinacol sequestering agent. Finally the intermediate-4 may undergo a sodium cyanoborohydride mediated reductive amination with ALDO (PC) in presence of catalytic amounts of TFA to produce bortezomib prodrug.

US11872313B2. Prodrug compositions, prodrug nanoparticles, and methods of use thereof (2024-01-16). Washington University [US]. Inventors: Gregory M. Lanza [US], Dipanjan Pan [US].
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Patent 2024
Acids Amination Amines Anabolism Boron Bortezomib Carboxylic Acids Catalysis DIPEA n-butylboronic acid Phenylalanine pinacol Prodrugs Sequestering Agents sodium cyanoborohydride
4
Apoptosis Induction in Mast Cells
After 24 h exposure to bortezomib (10 nM), carfilzomib (5 nM), ixazomib (50 nM), alisertib, volasertib (500 nM) and avapritinib (250 nM) alone or in combination with bortezomib or alisertib, apoptotic cell death was assessed in HMC-1 and ROSAKIT D816V cells by using the Annexin-V-FLUOS Staining Kit by Roche Applied Science, according manufacturer instructions and measuring the uptake of fluorescinated Annexin V and propidium iodide (both from Roche). A FACSCanto II flow cytometer (Beckton Dickinson) set at 488 nm excitation and 530 nm wavelength bandpass filter for fluorescein detection or 580 nm for PI detection and a dedicated software (DIVA, Beckton Dickinson) were used for analysis.
Mancini M., Monaldi C., De Santis S., Papayannidis C., Rondoni M., Sartor C., Bruno S., Pagano L., Criscuolo M., Zanotti R., Bonifacio M., Tosi P., Arock M., Valent P., Cavo M, & Soverini S. (2023). SETD2 non genomic loss of function in advanced systemic mastocytosis is mediated by an Aurora kinase A/MDM2 axis and can be therapeutically targeted. Biomarker Research, 11, 29.
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Publication 2023
alisertib Annexin A5 Apoptosis avapritinib Bortezomib carfilzomib Cells Fluorescein FLUOS ixazomib Propidium Iodide volasertib
5
Proteasome Inhibitor Effects on Protein Regulation
HMC-1 and ROSAKIT D816V cells maintained in control medium or after 24 h-incubation with 10 nM bortezomib, 5 nM carfilzomib, 50 nM ixazomib and 5 µM SP141 were lysed to extract total cellular proteins. WB, co-immunoprecipitation and immunoblotting were performed as described in the Supplementary methods. The following primary antibodies were used for Co-IP/immunoblotting and WB: anti-SETD2 (goat polyclonal antibody, cat. PAB7385, Abnova), anti-H3K36Me3 (rabbit monoclonal antibody, clone D5A7 cat. 4909) anti-p53 (rabbit monoclonal antibody, clone 7F5 cat.2527), anti-Mdm2 (rabbit monoclonal antibody, cloneD1V2Z, cat. 86,934), anti-ubiquitin (rabbit monoclonal antibody, clone E6K4Y, cat. 20,326), anti-Aurora kinase A (rabbit monoclonal antibody, clone D3V7T, cod. 91,590, anti-phospho-Aurora kinase A(T288) (rabbit monoclonal antibody, clone C39D8, cod. 3079), anti-Plk1 (rabbit monoclonal antibody, clone208G4, cod. 4513), anti phospho-Plk1(T210) (rabbit polyclonal antibody, cat. 5472), anti-phospho-Ser/Thr (rabbit polyclonal antibody, cat. 9631)(all from Cell Signaling Technology). Beta-actin (mouse monoclonal antibody, clone AC-15, cod. SC-69879 Santa Cruz biotechnology) or beta-tubulin (rabbit monoclonal antibody, clone 3F7, cod. 2128 Cell Signaling Technology) were used as loading control. Immunoreactive proteins were visualized by probing with horseradish peroxidase-conjugated secondary antibodies and then by enhanced chemiluminescence (ECL, Thermo Fisher Scientific). Signal intensities in single blots obtained from three individual experiments were quantified with the ImageJ software, which attributes a numerical value to signals of chemiluminescent substrates, thereby allowing a comparative analysis of protein levels across different samples.
Mancini M., Monaldi C., De Santis S., Papayannidis C., Rondoni M., Sartor C., Bruno S., Pagano L., Criscuolo M., Zanotti R., Bonifacio M., Tosi P., Arock M., Valent P., Cavo M, & Soverini S. (2023). SETD2 non genomic loss of function in advanced systemic mastocytosis is mediated by an Aurora kinase A/MDM2 axis and can be therapeutically targeted. Biomarker Research, 11, 29.
Full text: Click here
Publication 2023
Antibodies Aurora Kinase A beta-Actin beta-Tubulin Bortezomib carfilzomib Cells Chemiluminescence Clone Cells Co-Immunoprecipitation Goat Horseradish Peroxidase hSet2 protein, human Immunoglobulins ixazomib MDM2 protein, human Monoclonal Antibodies Mus PLK1 protein, human Proteins Rabbits Staphylococcal Protein A Ubiquitin

Top products related to «Bortezomib»

1
Bortezomib by Selleck Chemicals
Sourced in United States, Germany, China, United Kingdom, Belgium
Bortezomib is a proteasome inhibitor used in research laboratory settings. It functions by blocking the proteasome, a complex of enzymes responsible for the degradation of unwanted or damaged proteins within cells.
2
Bortezomib by LC Laboratories
Sourced in United States
Bortezomib is a chemical compound produced by LC Laboratories. It is a proteasome inhibitor that is used in research applications.
3
Bortezomib by Merck Group
Sourced in United States, Germany, Sao Tome and Principe
Bortezomib is a proteasome inhibitor used in the manufacturing of pharmaceutical products. It is a key component in the production process for various medications.
4
Cycloheximide (chx) by Merck Group
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, Japan, Spain, Canada, Switzerland, India, Israel, Brazil, Poland, Portugal, Australia, Morocco, Sweden, Austria, Senegal, Belgium
Cycloheximide is a laboratory reagent commonly used as a protein synthesis inhibitor. It functions by blocking translational elongation in eukaryotic cells, thereby inhibiting the production of new proteins. This compound is often utilized in research applications to study cellular processes and mechanisms related to protein synthesis.
5
Mg132 by Merck Group
Sourced in United States, Germany, China, United Kingdom, Macao, Sao Tome and Principe, France, Canada, Italy, Switzerland, Morocco, Belgium, Japan, Sweden, Australia, Austria, Israel, Spain
MG132 is a proteasome inhibitor, a type of laboratory reagent used in research applications. It functions by blocking the activity of the proteasome, a complex of enzymes responsible for the degradation of proteins within cells. MG132 is commonly used in cell biology and biochemistry studies to investigate the role of the proteasome in various cellular processes.
6
Fetal bovine serum (fbs) by Thermo Fisher Scientific
Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal
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.
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.
8
Carfilzomib by Selleck Chemicals
Sourced in United States
Carfilzomib is a proteasome inhibitor, a type of lab equipment used in biochemical and pharmaceutical research. It functions by inhibiting the proteasome, a large protein complex responsible for the degradation of proteins within cells. This action can lead to the accumulation of proteins and subsequent cellular effects, making Carfilzomib a valuable tool for researchers studying protein regulation and cellular processes.
9
Penicillin streptomycin by Thermo Fisher Scientific
Sourced in United States, Germany, United Kingdom, China, Canada, France, Japan, Australia, Switzerland, Israel, Italy, Belgium, Austria, Spain, Gabon, Ireland, New Zealand, Sweden, Netherlands, Denmark, Brazil, Macao, India, Singapore, Poland, Argentina, Cameroon, Uruguay, Morocco, Panama, Colombia, Holy See (Vatican City State), Hungary, Norway, Portugal, Mexico, Thailand, Palestine, State of, Finland, Moldova, Republic of, Jamaica, Czechia
Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
10
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.

More about "Bortezomib"

Bortezomib, a proteasome inhibitor, has emerged as a groundbreaking therapeutic option for the treatment of multiple myeloma and mantle cell lymphoma.
This versatile drug works by blocking the activity of the proteasome, a crucial protein complex responsible for the degradation of unwanted or damaged proteins within cells.
By disrupting this delicate protein homeostasis, Bortezomib can induce cell death, particularly in rapidly dividing cancer cells.
The efficacy of Bortezomib in improving overall survival and progression-free survival in patients with these hematological malignancies has been well-documented.
Researchers can leverage the power of the PubCompare.ai platform to streamline their Bortezomib-related studies, optimizing their research approach through AI-powered comparisons of protocols from literature, preprints, and patents.
Bortezomib's mechanism of action is similar to that of other proteasome inhibitors, such as Cycloheximide and MG132.
These compounds share the ability to disrupt the delicate balance of protein degradation within cells, leading to cell death.
Researchers may also utilize cell culture media like RPMI 1640, along with supplements like FBS and Penicillin/streptomycin, to create the optimal environment for studying the effects of Bortezomib and related compounds.
Carfilzomib, another proteasome inhibitor, has also been explored as a potential treatment option for hematological malignancies.
Researchers can leverage the PubCompare.ai platform to compare and contrast the efficacy and safety profiles of Bortezomib and Carfilzomib, as well as investigate the potential synergistic effects of combining these therapies.
By harnessing the power of PubCompare.ai, researchers can streamline their Bortezomib-related studies, optimize their research approach, and uncover novel insights that can contribute to the advancement of personalized cancer treatments.
The platform's AI-driven comparisons of protocols from literature, preprints, and patents can provide invaluable guidance, helping researchers navigate the complex landscape of Bortezomib research and, ultimately, improve patient outcomes.