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Regorafenib

Regorafenib is a multi-kinase inhibitor medication used to treat various types of cancer, including colorectal, gastrointestinal stromal, and hepatocellular carcinomas.
It works by blocking the activity of several proteins involved in tumor growth, angiogenesis, and metastasis.
Regorafenib has been shown to improve progression-free survival and overall survival in patients with advanced or metastatic cancers.
However, optimizing Regorafenib research can be challenging, requiring careful protocol selection and data analysis.
PubComapre.ai's AI-driven platform helps researchers enhance the reproducibility and accuracy of their Regorafenib studies by identifying the best protocols from literature, pre-prints, and patents through intelligent comparisons.
This powerful tool can improve the quality and impact of your Regorafenib research.

Most cited protocols related to «Regorafenib»

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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
OSU-03012, sildenafil, regorafenib, pazopanib, sorafenib tosylate were purchased from Selleckchem (Houston, TX). OSU-03012 (AR-12) and AR-13 were kindly provided by Arno Therapeutics (Flemington NJ). Cells were purchased from the ATCC and were not further validated beyond that claimed by ATCC. Cells were re-purchased every ∼6 months. Primary human glioblastoma (GBM) cells, developed by Dr. C.D. James when at the Mayo Clinic (Rochester, MN) has been described previously [6 (link)–9 (link)]. ADOR non-small cell lung cancer cells are personal a donation from the patient to the Dent laboratory. De novo cisplatin resistant “Spiky” ovarian cancer cells, a patient derived explant (PDX) model, were kindly provided by Dr. Karen Paz (Champions Oncology, NJ). The plasmid to express GRP78 was kindly provided to the Dent laboratory by Dr. A.S. Lee (University of Southern California Los Angeles, CA). The plasmids to express thioredoxin (TRX) and mutant thioredoxin (mTRX) were a kind gift from Dr. David Gius (Radiobiology Branch, National Cancer Institute, Bethesda, MD). The plasmids to express HSP27, eIF2α S51A, kinase-inactive PERK and all others listed in this manuscript were purchased from Addgene (Cambridge, MA). Commercially available validated short hairpin RNA molecules to knock down RNA/protein levels were from Qiagen (Valencia, CA) or were supplied by collaborators [12 (link), 13 (link)].
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Publication 2016
AR-12 compound Cells Cisplatin Glioblastoma Glucose Regulated Protein 78 kDa Homo sapiens HSPB1 protein, human Neoplasms Non-Small Cell Lung Carcinoma OSU 03012 Ovarian Cancer Patients pazopanib Phosphotransferases Plasmids Proteins regorafenib Short Hairpin RNA Sildenafil Sorafenib Therapeutics TXN protein, human
The human CRC cell lines (Table S1), including HCT116, RKO, DLD1, LoVo, Lim1215, Lim2405, SW480, SNU-C2B, LS411N, SW48, SW1463, SW837 and HCT-8 were obtained from the American Type Culture Collection (Manassas, VA). CCK-81, DiFi and NCI-H508 cells were obtained from Dr. Alberto Bardelli at University of Torino in Italy. Isogenic p53-KO, FBW7-KO, KRAS-KO (WT or G13D mutant allele), PIK3CA-KO (WT or H1047R or E545K mutant allele) HCT116 or DLD1 cell lines, as well as BRAF-KO (WT or V600E mutant allele) RKO and VACO432 cells, were obtained either from Dr. Bert Vogelstein at Johns Hopkins, or from Horizon Discovery (Cambridge, UK). The cell lines were last tested and authenticated for genotypes, drug response, morphology, and absence of mycoplasma in Feb, 2016. Loss of expression of targeted proteins was confirmed by western blotting and Mycoplasma testing was performed routinely by PCR. Regorafenib-resistant cell lines were generated by exposing regorafenib-sensitive HCT116, DLD1, RKO, SW480, Lim1215 and Lim2405 cells to 40 µM regorafenib for 3 days, followed by recovery for 5 days, and then repeated treatment/recovery for a total of 4 cycles.
All cell lines were maintained at 37°C in 5% CO2 and cultured in McCoy's 5A modified media (Invitrogen) supplemented with 10% defined FBS (HyClone), 100 units/ml penicillin, and 100 μg/ml streptomycin (Invitrogen). For drug treatment, cells were plated in 12-well plates at 20% to 30% density 24 hr before treatment. The DMSO (Sigma) stocks of agents used, including regorafenib, sorafenib, TW-37, ABT-737, UCN-01, YM-155, roscovitine, sunitinib, crizotinib, VX680, etoposide, temsirolimus, and sulindac (Selleck Chemicals), were diluted to appropriate concentrations with the cell culture medium. TRAIL (XcessBio, San Diego, CA) was diluted with distilled water.
Publication 2016
ABT-737 Alleles BRAF protein, human Cell Culture Techniques Cell Lines Cells Crizotinib Culture Media Etoposide Genotype Homo sapiens K-ras Genes Mycoplasma Penicillins Pharmaceutical Preparations PIK3CA protein, human regorafenib Roscovitine Sorafenib Streptomycin Sulfoxide, Dimethyl Sulindac Sunitinib temsirolimus TNFSF10 protein, human UCN 01 VX680 YM-155

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Publication 2017
Cells Culture Media Immunofluorescence regorafenib
All animal experiments were approved by the University of Pittsburgh Institutional Animal Care and Use Committee. Female 5–6 week-old Nu/Nu mice (Charles River, Wilmington, MA) were housed in a sterile environment with micro isolator cages and allowed access to water and chow ad libitum. Mice were injected subcutaneously in both flanks with 4×106 WT or PUMA-KO HCT116 cells. After tumor growth for 7 days, mice were treated daily with regorafenib at 30 mg/kg by oral gavage for 10 consecutive days. For combination experiments, mice were treated with 15 mg/kg regorafenib daily by oral gavage, 25 mg/kg 5-FU (APP Pharmaceuticals, Schaumburg, IL) every other day by i.p. injection, or their combination for 10 consecutive days. Regorafenib was dissolved in Cremephor EL/95% ethanol (50:50) as a 4× stock solution (24 (link)), and 5-FU was supplied as a stock solution. Both drugs were diluted to the final concentration with sterile water before use. Tumor growth was monitored by calipers, and tumor volumes were calculated according to the formula ½ × length × width2. Mice were euthanized when tumors reached ~1.0 cm3 in size. Tumors were dissected and fixed in 10% formalin and embedded in paraffin. Terminal deoxynucleotidyl transferase mediated dUTP Nick End Labeling (TUNEL; Millipore), active caspase 3 (Cell Signaling), CD31 (Spring Bioscience, Pleasanton, CA), and Carbonic Anhydrase 9 (CA9; Santa Cruz) immunostaining was performed on 5 μM paraffin-embedded tumor sections as previously described (25 (link)), by using an AlexaFluor 488- or AlexaFluor 594-conjugated secondary antibody (Invitrogen) for detection.
Publication 2014
CA9 protein, human Caspase 3 deoxyuridine triphosphate DNA Nucleotidylexotransferase Ethanol Formalin HCT116 Cells Immunoglobulins In Situ Nick-End Labeling Institutional Animal Care and Use Committees Mice, Nude Mus Neoplasms Paraffin Embedding Pharmaceutical Preparations Puma regorafenib Rivers Sterility, Reproductive Tube Feeding Woman

Most recents protocols related to «Regorafenib»

The sh-circDCAF8 vector was constructed by designing and synthesizing shRNA that targets human circDCAF8. The Lv-circDCAF8 vector was created by constructing lentiviral vectors that also include human circDCAF8. The lentiviral vectors mentioned above were designed by GenePharma (Shanghai, China). Target cells were transfected using lentiviral vectors, and the stable transfected cells were chosen using puromycin and confirmed with qRT-PCR. The shRNA target sequences are listed in Table S1, and the full sequence of circDCAF8 is listed in Table S2. The mimic and inhibitor of miR-217 and their negative controls were obtained from GenePharma (Shanghai, China). The cells were cultured in 6-well plates and transfected plasmid or inhibitor using Lipofectamine 2000 (Invitrogen, USA). Hep-G2 and Hep-3B cells were chosen to be induced regorafenib resistant HCC cells. Regorafenib was purchased from MCE (MedChemExpress, NJ, USA). Regorafenib resistant HCC cells were established by long-term exposure to regorafenib. Specifically, HCC cells were first treated with a modest dosage of regorafenib (0.625 µM) for 2 weeks and then the medium containing regorafenib was exchanged with fresh complete medium for an additional 2 weeks. Afterwards, the regorafenib dose was progressively raised while the culture pattern was maintained. This process continued until the regorafenib dose reached 10 µM, the maximum clinically tolerated dose, and the remaining cells were regorafenib-resistant HCC cells.
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Publication 2024

Example 3

Analysis of Lung Function Regulatory Effect of Regorafenib in Animal Model with Chronic Obstructive Pulmonary Disease

In addition, the present inventors performed an experiment to determine whether regorafenib is able to restore lost function of damaged lungs in order to confirm whether regorafenib is able to treat chronic obstructive pulmonary disease.

Specifically, 6-week-old C57BL/6 mice were purchased and acclimatized for one week, after which the acclimatized 7-week-old mice (average 25 g) were subjected to nasal administration with saline and PPE [elastase from porcine pancreas] (EPC, EC134) at a concentration of 5 U. Two weeks after administration, the mice were orally administered with 200 μl of regorafenib (SelleckChem, BAY 73-4506) at a concentration of 5 mg/kg for one week. Then, the mice were anesthetized using 300 μl of anesthetic on week 3, after which the lung function of each mouse was measured using a flexiVent (system for measuring the function of lungs) and quantified by subtracting the error value therefrom.

As shown in FIG. 3, it could be confirmed that various lung function indicators lost in mice with chronic obstructive pulmonary disease induced by PPE administration were restored through treatment with regorafenib.

Based on the aforementioned results, the present inventors confirmed that regorafenib is capable of inhibiting increased immune response caused by chronic obstructive pulmonary disease, and of improving and restoring damaged and changed lung structure and lung function, whereby regorafenib can be used as a novel therapeutic agent for chronic obstructive pulmonary diseases including emphysema, chronic bronchitis, asthma, and pneumonia.

As is apparent from the above description, regorafenib according to the present invention is capable of inhibiting increased immune response, which is a symptom of chronic obstructive pulmonary disease, and of improving and restoring changed lung structure and damaged lung function, and can be effectively used for the manufacture of a medicament for the prevention, amelioration, or treatment of chronic obstructive pulmonary disease.

Although preferable exemplary embodiments of the present invention have been disclosed in detail above, it will be obvious to those skilled in the art that the present invention may be implemented in a modified form without departing from the essential characteristics of the present invention. Therefore, the disclosed embodiments are to be considered in an illustrative rather than a restrictive way. The scope of the present invention is indicated in the claims rather than the foregoing description, and all differences within the scope equivalent thereto should be construed as being included in the present invention.

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Patent 2024

Example 1

Analysis of Immune Response Inhibitory Effect Through Treatment with Regorafenib in Animal Model with Chronic Obstructive Pulmonary Disease

The present inventors performed an experiment to determine whether regorafenib has activity capable of treating chronic obstructive pulmonary disease. The initial response induced by PPE (porcine pancreatic elastase) representatively includes immune responses that occur in damaged lung tissue. The activated immune response promotes the proliferation of various immune cells and the secretion of various inflammatory mediators. Specifically, the overall number of immune cells increases with an increase in individual immune cells involved in the immune response. In particular, an increase in the numbers of macrophages, lymphocytes, eosinophils, and neutrophils is observed. The increase in the number of these cells can be confirmed through a bronchoalveolar lavage (BAL) fluid test.

Therefore, in the present invention, mice with chronic obstructive pulmonary disease, particularly emphysema, in which alveolar damage was induced by reducing elastin content using PPE, were prepared and then treated with regorafenib to thus analyze whether chronic obstructive pulmonary disease was ameliorated. Specifically, 6-week-old C57BL/6 mice were purchased and acclimatized for one week. Thereafter, the acclimatized 7-week-old mice (average 25 g) were orally administered with 200 μl of regorafenib (SelleckChem, BAY 73-4506) at a concentration of 5 mg/kg. The next day, that is, on day 1, each mouse's status was observed, followed by nasal administration of PPE [elastase from porcine pancreas] (EPC, EC134) at a concentration of 5 U. Then, each mouse's status was observed on days 2 and 3, followed by oral administration of 200 μl of regorafenib at a concentration of 5 mg/kg. On day 4, the mice were anesthetized using 200 μl of anesthetic (Zoletil to rompun to saline at a ratio of 1:1:8), after which the neck of each mouse was incised to thus expose the airway, which was then cut in half and a catheter was inserted therein. Thereafter, 1 ml of HBSS [Hanks' balanced salt solution] (Sigma Aldrich, H6648) was placed in a syringe, which was then connected to the catheter, after which procedures of injection and then extraction were performed three times to collect the BAL fluid. The BAL fluid thus obtained was centrifuged to collect cells, and the collected cells were suspended in HBSS, treated with a red blood cell lysis buffer (Sigma Aldrich, 11814389001) at 1:1, allowed to react at room temperature for 2 minutes, further added with HBSS, and then centrifuged. In this procedure, red blood cells are removed. The centrifuged cells were diluted and centrifuged using a Cytospin (Hanil Science), and then attached to a slide. The attached cells were stained using a NovaUltr™ Hema-Diff Stain Kit (IHCWORLD, IW-3017) according to the manufacturer's instructions. The stained slide was analyzed and quantified using a microscope.

According to the method described above, a mouse animal model of chronic obstructive pulmonary disease was prepared by administering the mouse lungs with 5 U of PPE, and in order to verify whether the immune response was modulated, one day before administration of PPE and on days 2 and 3 after administration of PPE, regorafenib (5 mg/kg) was administered thereto, and on day 4, bronchoalveolar lavage fluid was obtained and the immune cells therein were stained to thus quantitatively analyze the type of immune cells and the number of individual cells. Here, mice administered only with saline were used as a control group, and 5 mice were placed in each group.

Based on the results of analysis, the number of immune cells increased significantly in the PPE treatment group compared to the control group, whereas in the regorafenib treatment group, the number of immune cells increased due to PPE decreased by about 50% (FIGS. 1B and 1C). Among the types of immune cells that increased in number, the number of macrophages was found to have increased the most, and the number of macrophages was decreased from about 6×104 to 4×104 through treatment with regorafenib (FIG. 1D). In addition, it was confirmed that the number of lymphocytes was increased to 6×103 but was decreased to about 2.5×103 by regorafenib. In addition, it was confirmed that the numbers of eosinophils and neutrophils were significantly decreased through treatment with regorafenib.

Based on these results, the present inventors have found that regorafenib of the present invention is capable of inhibiting or reducing the increase in the initial immune response, which is a symptom of chronic obstructive pulmonary disease.

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Patent 2024
Not available on PMC !

Example 2

Analysis of Improvement Effect of Changes in Lung Structure Through Treatment with Regorafenib in Animal Model with Chronic Obstructive Pulmonary Disease

One of the pathological indicators of chronic obstructive pulmonary disease is changed alveolar size. Changes in the alveolar size can be analyzed by quantifying the mean linear intercept (Lm) value, representing the average distance between the alveolar walls, in a microscopic field of view. When chronic obstructive pulmonary disease is induced, this value increases, indicating an increase in the alveolar size.

Therefore, the present inventors analyzed whether it is possible to alleviate changes in lung structure by measuring the change in Lm value due to treatment with regorafenib in a mouse animal model with emphysema, a chronic obstructive pulmonary disease, prepared over three weeks through administration of PPE (FIG. 2A).

Specifically, 6-week-old C57BL/6 mice were acclimatized for one week, after which the acclimatized 7-week-old mice (average 25 g) were subjected to nasal administration with saline and PPE [elastase from porcine pancreas] (EPC, EC134) at a concentration of 5 U. Two weeks after administration, the mice were orally administered with 200 μl of regorafenib (SelleckChem, BAY 73-4506) at a concentration of 5 mg/kg for one week, and on week 3, the lungs were extracted from each mouse, placed in a cassette, immersed in 10% NBF, and stored for one day, after which a parafilm block was prepared using a tissue processor. The prepared block was cut using a sectioning machine, attached to a slide, subjected to H&E staining, and then quantified by measuring the Lm value based on microscopic images.

Based on the results of analysis, as shown in FIGS. 2B and 2C, the Lm value significantly increased in the PPE treatment group compared to the control group, whereas in the regorafenib treatment group, the Lm value decreased by about 50% compared to the PPE treatment group. Through these results, the present inventors confirmed that chronic obstructive pulmonary disease was normally induced in mice due to PPE administration in this experiment, and also that the changed lung structure in the induced chronic obstructive pulmonary disease was reversed and restored so as to be comparable to the normal state by regorafenib.

Therefore, it has been found that regorafenib has activity capable of improving and regulating structural changes in alveoli accompanying chronic obstructive pulmonary disease.

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Patent 2024
Administration, Intranasal Animal Model BAY 73-4506 Chronic Obstructive Airway Disease Figs Inventors Lung Mice, Inbred C57BL Microscopy Mus Pancreatic Elastase Pigs Pulmonary Emphysema regorafenib Saline Solution Tissues Tooth Socket
Group 1 consists of SK-Hep-1 and HCC-LM3 cells that were treated with different concentrations of Regorafenib (0, 5, 10, 15, 30, 60 µM) for 24 h to assess the anti-tumor activity of Regorafenib (S86421, Shyuanye, China) [14 (link)]. Group 2 consists of three subgroups: Control, vehicle, and Regorafenib. The two cells were cultured under normal conditions. In the vehicle group, 0.5 µL of DMSO was added to the culture medium of the two cells. In the Regorafenib group, the two cells were exposed to a concentration of 10 µM Regorafenib for 24 h. Group 3 consists of four subgroups: sh-NC, sh-METTL14, oe-NC, and oe-METTL14. In each subgroup of the two cells, transfection was performed with sh-NC, sh-METTL14, oe-NC, and oe-METTL14, respectively. Group 4 consists of four subgroups: vehicle + oe-NC, vehicle + oe-METTL14, Regorafenib + oe-NC, and Regorafenib + oe-METTL14. Group 5 consists of four subgroups: vehicle + sh-NC, vehicle + sh-CHOP, Regorafenib + sh-NC, and Regorafenib + sh-CHOP. Group 5 consists of four subgroups: Regorafenib + Control, Regorafenib + sh-NC, Regorafenib + sh-CHOP, Regorafenib + oe-NC, Regorafenib + oe-CHOP. Group 5 consists of four subgroups: Regorafenib + oe-NC + oe-NC, Regorafenib + oe-NC + oe-CHOP, Regorafenib + oe-METTL14 + oe-NC, Regorafenib + oe-METTL14 + oe-CHOP.
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Publication 2024

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Regorafenib is a multi-kinase inhibitor used in laboratory research. It functions by inhibiting multiple protein kinases involved in tumor angiogenesis, oncogenesis, and tumor microenvironment.
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Regorafenib is a small-molecule multi-kinase inhibitor developed by Bayer for use in laboratory research. It functions by blocking the activity of several enzymes involved in processes such as angiogenesis, oncogenesis, and tumor microenvironment interactions. Regorafenib is commonly used in studies investigating cellular signaling pathways and their modulation.
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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.
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Sorafenib is a laboratory reagent that functions as a multi-kinase inhibitor. It is commonly used in research settings to study cellular signaling pathways and their modulation.
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Lipofectamine 2000 is a cationic lipid-based transfection reagent designed for efficient and reliable delivery of nucleic acids, such as plasmid DNA and small interfering RNA (siRNA), into a wide range of eukaryotic cell types. It facilitates the formation of complexes between the nucleic acid and the lipid components, which can then be introduced into cells to enable gene expression or gene silencing studies.
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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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Streptomycin is a broad-spectrum antibiotic used in laboratory settings. It functions as a protein synthesis inhibitor, targeting the 30S subunit of bacterial ribosomes, which plays a crucial role in the translation of genetic information into proteins. Streptomycin is commonly used in microbiological research and applications that require selective inhibition of bacterial growth.
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Regorafenib is a multi-kinase inhibitor that targets various signaling pathways involved in tumor growth and angiogenesis. It is used as a research tool to study the effects of inhibiting these pathways in cell-based and animal models.

More about "Regorafenib"

Regorafenib is a multi-kinase inhibitor medication used to treat various types of cancer, including colorectal, gastrointestinal stromal, and hepatocellular carcinomas.
It works by blocking the activity of several proteins involved in tumor growth, angiogenesis, and metastasis.
Regorafenib has been shown to improve progression-free survival and overall survival in patients with advanced or metastatic cancers.
However, optimizing Regorafenib research can be challenging, requiring careful protocol selection and data analysis.
PubCompare.ai's AI-driven platform helps researchers enhance the reproducibility and accuracy of their Regorafenib studies by identifying the best protocols from literature, pre-prints, and patents through intelligent comparisons.
This powerful tool can improve the quality and impact of your Regorafenib research.
Regorafenib, also known as Stivarga, is a multi-kinase inhibitor that targets various proteins involved in cancer progression, such as VEGFR, PDGFR, and FGFR.
It has been approved for the treatment of colorectal cancer, gastrointestinal stromal tumors (GIST), and hepatocellular carcinoma (HCC).
Researchers may use Regorafenib in combination with other anti-cancer agents, such as Sorafenib, to enhance its efficacy.
When conducting Regorafenib studies, researchers often use cell lines, such as HCT116 (colorectal cancer) and GIST-T1 (GIST), and perform experiments using techniques like MTT assay, Western blotting, and cell migration assays.
These experiments may require the use of FBS (Fetal Bovine Serum) as a cell culture supplement, GraphPad Prism 5 for data analysis, and reagents like Lipofectamine 2000 for transfection, DMSO as a solvent, and antibiotics like Penicillin and Streptomycin to prevent bacterial contamination.
By utilizing PubCompare.ai's advanced AI-driven platform, researchers can optimize their Regorafenib studies, enhance reproducibility, and improve the overall quality and impact of their research findings.
This can lead to a better understanding of Regorafenib's mechanisms of action, its potential combination therapies, and its clinical applications in the treatment of various cancers.