The animal experiments were approved by the Institutional Animal Care and Use Committee of The Fifth Medical Center (former name: The 302nd Hospital of Chinese PLA), General Hospital of Chinese People's Liberation Army (the ID of certification: IACUC‐2019‐001, Figure S1 ). All the animal studies were conducted in accordance with the UK Animals (Scientific Procedures) Act of 1986 and the associated guidelines. AML cells or MHCC97‐H cells were cultured and resuspended in physiological saline. Next, cell suspensions or cell suspensions containing 2% Poloxamer 407 were subcutaneously injected into nude mice. The concentration of cells in the cell suspension was 107 cells/mL. About 0.2 mL cell suspension per site was injected subcutaneously into nude mice at various sites. Three to four days’ after injection, the mice received 1, 0.5, 0.2 or 0.1 mg/kg lenvatinib by oral administration. The mice received lenvatinib treatment once per 2 days. After 10 treatments (about 20‐21 days), the mice were harvested and the volumes or weights of subcutaneous tumor tissues were examined. The tumor volumes of subcutaneous tumor tissues were calculated as tumor length × tumor width × tumor width/2.13 , 14 The inhibition rates of lenvatinib on the subcutaneous growth of AML cells were calculated as [(control group tumor volumes)−(lenvatinib group tumor volumes)]/(control group tumor volumes) × 100%; [(control group tumor weights)−(lenvatinib group tumor weights)]/(control group tumor weights) × 100%.
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Lenvatinib
Lenvatinib
Lenvatinib is a multikinase inhibitor used in the treatment of certain types of cancer, including thyroid, kidney, and liver cancer.
This medication works by targeting and inhibiting several key enzymes involved in tumor growth and blood vessel formation, effectively slowing or stopping cancer progression.
Lenvatinib has demonstrated promising results in clinical trials, offering improved outcomes for patients with advanced or metastatic disease.
Researchers are continouously exploring the potential of this medication, investigating optimal dosing, combination therapies, and expanding its applications to other malignancies.
This medication works by targeting and inhibiting several key enzymes involved in tumor growth and blood vessel formation, effectively slowing or stopping cancer progression.
Lenvatinib has demonstrated promising results in clinical trials, offering improved outcomes for patients with advanced or metastatic disease.
Researchers are continouously exploring the potential of this medication, investigating optimal dosing, combination therapies, and expanding its applications to other malignancies.
Most cited protocols related to «Lenvatinib»
Administration, Oral
Animals
Cells
Chinese
Institutional Animal Care and Use Committees
lenvatinib
Mice, Nude
Mus
Neoplasms
physiology
Poloxamer 407
Psychological Inhibition
Saline Solution
Subcutaneous Tissue
Study 116 is an ongoing phase Ib multicenter open-label study of lenvatinib plus pembrolizumab in patients with uHCC. The study consists of 2 phases: a dose-limiting toxicity (DLT) phase and an expansion phase. Patients received lenvatinib 12 mg (if bodyweight ≥ 60 kg) or 8 mg (if bodyweight < 60 kg) orally once daily and pembrolizumab 200 mg intravenously on day 1 of a 21-day treatment cycle (for up to 2 years after cycle 1 day 1). If no DLTs were reported in the DLT phase, the expansion phase would be initiated using the recommended dose from the DLT phase. Treatment was continued until disease progression, development of unacceptable toxicity, or withdrawal of consent. Additional details regarding continued pembrolizumab treatment are provided in the Appendix (online only).
Key inclusion criteria comprised the following: histologically or cytologically confirmed HCC (excluding fibrolamellar, sarcomatoid, and mixed cholangio-HCC tumors) or clinically confirmed HCC according to the American Association for the Study of Liver Diseases criteria; stage B (not suitable for transarterial chemoembolization) or C categorization based on the Barcelona Clinic Liver Cancer (BCLC) staging system; at least 1 measurable target lesion according to mRECIST per investigator assessment; Child-Pugh class A (score, 5-6); and Eastern Cooperative Oncology Group performance status (ECOG PS) of 0 or 1. Patients were excluded if they had clear invasion of the bile duct (classified clinically as a cholestatic type of HCC in which a patient’s initial manifestation is obstructive jaundice resulting from tumor thrombosis/compression/diffuse infiltration into the biliary tract); portal vein invasion with Vp426 (link); prior blood-enhancing treatment (including blood transfusion, blood products, or agents that stimulate blood cell production [eg, granulocyte colony-stimulating factor]) within 28 days before first dose of study drugs; prior treatment with lenvatinib or any anti–PD-1, anti–PD-L1, or anti–PD-L2 agent; and imaging findings with HCC having ≥ 50% liver occupation. Additionally, patients were excluded from the expansion phase if they had received prior systemic therapy for uHCC.
Written informed consent was provided by all patients before undergoing any study-specific procedures. The study protocol was approved by the relevant institutional review boards/independent ethics committees, and the study was conducted in accordance with the principles of the Declaration of Helsinki and Good Clinical Practice guidelines.
Key inclusion criteria comprised the following: histologically or cytologically confirmed HCC (excluding fibrolamellar, sarcomatoid, and mixed cholangio-HCC tumors) or clinically confirmed HCC according to the American Association for the Study of Liver Diseases criteria; stage B (not suitable for transarterial chemoembolization) or C categorization based on the Barcelona Clinic Liver Cancer (BCLC) staging system; at least 1 measurable target lesion according to mRECIST per investigator assessment; Child-Pugh class A (score, 5-6); and Eastern Cooperative Oncology Group performance status (ECOG PS) of 0 or 1. Patients were excluded if they had clear invasion of the bile duct (classified clinically as a cholestatic type of HCC in which a patient’s initial manifestation is obstructive jaundice resulting from tumor thrombosis/compression/diffuse infiltration into the biliary tract); portal vein invasion with Vp426 (link); prior blood-enhancing treatment (including blood transfusion, blood products, or agents that stimulate blood cell production [eg, granulocyte colony-stimulating factor]) within 28 days before first dose of study drugs; prior treatment with lenvatinib or any anti–PD-1, anti–PD-L1, or anti–PD-L2 agent; and imaging findings with HCC having ≥ 50% liver occupation. Additionally, patients were excluded from the expansion phase if they had received prior systemic therapy for uHCC.
Written informed consent was provided by all patients before undergoing any study-specific procedures. The study protocol was approved by the relevant institutional review boards/independent ethics committees, and the study was conducted in accordance with the principles of the Declaration of Helsinki and Good Clinical Practice guidelines.
BLOOD
Blood Cells
Blood Transfusion
Body Weight
CD274 protein, human
Child
Cholestasis
Disease Progression
Duct, Bile
Ethics Committees, Research
Granulocyte Colony-Stimulating Factor
Jaundice, Obstructive
lenvatinib
Liver
Liver Function Tests
Mixed Salivary Gland Tumor
Neoplasms
Patients
pembrolizumab
Portal System
Sarcoma
System, Biliary
Therapeutics
Thrombosis
Veins, Portal
For this retrospective study, we identified patients with unresectable HCC who were treated with sorafenib or lenvatinib between August 2009 and January 2019 at the Hokkaido University Hospital. Patients who met the diagnostic criteria for advanced HCC according to the American Association for the Study of Liver Diseases guidelines13 were treated for more than 2 months after treatment initiation, underwent response evaluation using dynamic computed tomography (CT) at baseline and at 2–3‐month intervals, and had adequate clinical data and baseline preserved serum samples for evaluation of serum biomarkers were included. Patients were excluded if they received sorafenib or lenvatinib in conjunction with other treatment, including transarterial chemoembolization (TACE), hepatic arterial infusion chemotherapy (HAIC), and other antitumor agents; were followed up for less than 2 months; had decompensated liver cirrhosis; had insufficient clinical data or no baseline preserved serum samples; and were not evaluated for treatment response using dynamic CT.
We collected data on gender, age, etiology of HCC, blood cell counts, laboratory data, tumor makers (alpha‐fetoprotein [AFP] and des‐gamma‐carboxyprothrombin), Barcelona Clinic Liver Cancer (BCLC) stage, presence of extrahepatic metastases, and Child‐Pugh score at baseline. In addition, we evaluated the baseline levels of the candidate serum biomarkers, including fibroblast growth factor (FGF) 19 and 21, angiopoietin 2 (ANG2), hepatocellular growth factor (HGF), and vascular endothelial cell growth factor (VEGF). Serum FGF19, FGF21, ANG2, HGF, and VEGF levels were estimated using commercial ELISA according to the manufacturer's protocols (FGF19: R&D Systems, Minneapolis, MN, USA; FGF21: Merck Millipore, Darmstadt, Germany; ANG2: R&D Systems, Minneapolis, MN, USA; HGF: R&D Systems, Minneapolis, MN, USA; and VEGF: R&D Systems, Minneapolis, MN, USA).
Patients were routinely assessed using laboratory tests and physical findings every 2 weeks and enhanced CT every 2–3 months after treatment initiation.
We collected data on gender, age, etiology of HCC, blood cell counts, laboratory data, tumor makers (alpha‐fetoprotein [AFP] and des‐gamma‐carboxyprothrombin), Barcelona Clinic Liver Cancer (BCLC) stage, presence of extrahepatic metastases, and Child‐Pugh score at baseline. In addition, we evaluated the baseline levels of the candidate serum biomarkers, including fibroblast growth factor (FGF) 19 and 21, angiopoietin 2 (ANG2), hepatocellular growth factor (HGF), and vascular endothelial cell growth factor (VEGF). Serum FGF19, FGF21, ANG2, HGF, and VEGF levels were estimated using commercial ELISA according to the manufacturer's protocols (FGF19: R&D Systems, Minneapolis, MN, USA; FGF21: Merck Millipore, Darmstadt, Germany; ANG2: R&D Systems, Minneapolis, MN, USA; HGF: R&D Systems, Minneapolis, MN, USA; and VEGF: R&D Systems, Minneapolis, MN, USA).
Patients were routinely assessed using laboratory tests and physical findings every 2 weeks and enhanced CT every 2–3 months after treatment initiation.
acarboxy prothrombin
Aftercare
alpha-Fetoproteins
Angiopoietin-2
Antineoplastic Agents
Blood Cell Count
Blood Vessel
Cells
Child
Diagnosis
Enzyme-Linked Immunosorbent Assay
Fibroblast Growth Factor
fibroblast growth factor 21
Gender
Growth Factor
Hepatic Artery
lenvatinib
Liver
Liver Cirrhosis
Liver Diseases
Neoplasm Metastasis
Neoplasms
Patients
Pharmacotherapy
Physical Examination
Serum
Sorafenib
Staging, Cancer
Vascular Endothelial Growth Factors
X-Ray Computed Tomography
Animal experiments were performed in accordance with the guidelines approved by the Institutional Animal Care and Use Committee of Eisai Co., Ltd., Shanghai ChemPartner Co., Ltd., or Crown Bioscience Inc. Lenvatinib was dissolved in 3 mmol/L HCl. Sorafenib was dissolved in cremophor:ethanol (1:1) and then diluted fourfold with distilled water. HCC cells (2.5 × 106 to 5 × 106) in HBSS (for Hep3B2.1‐7 and SNU‐398) or culture medium (for PLC/PRF/5) were mixed with Matrigel [1:1] (Corning, Corning, NY) and then inoculated subcutaneously into the right flank of female BALB/c nude mice. When the tumors reached approximately 170–290 mm3, the mice were randomly allocated to treatment groups (Day 1). Lenvatinib, sorafenib, or the corresponding vehicle was given orally to individual mice once daily for the indicated doses and periods in each figure legend.
The LIXC‐012 xenograft study was performed at Shanghai ChemPartner Co., Ltd. (Shanghai, China). LIXC‐012 cells (2 × 106) in serum‐free medium mixed with Matrigel [1:1] (Corning) were inoculated subcutaneously into the right flank of female nu/nu mice. When the tumors reached approximately 80–300 mm3, the mice were randomly allocated to treatment groups (Day 1); mice then orally received lenvatinib, sorafenib, or the corresponding vehicle once daily for 14 days. Multiple mice in each vehicle control group were removed from the study because of excess tumor volume or cachexia‐induced body weight loss (BWL) after Day 11.
Patient‐derived xenograft (PDX; LI0050 and LI0334) studies were performed at Crown Bioscience Inc. (Taicang, China). Each tumor fragment (diameter, 2–3 mm) was inoculated subcutaneously into the right flank of female BALB/c nude mice. When the tumors reached approximately 130–150 mm3 (Day 1), the mice were randomly allocated to treatment groups; mice then orally received lenvatinib, sorafenib, or vehicle (3 mmol/L HCl only) once daily for 28 days. In the PDX studies, when BWL was ≥20% for any individual mouse, that mouse was given dosing holiday(s) until its body weight recovered to baseline (BWL, ≤10%).
Tumor dimensions were measured two or three times weekly with a caliper, and tumor volume was calculated as ½ × length × width2. Relative body weight (RBW) was calculated by dividing the daily body weight by that of the same mouse on Day 1.
The LIXC‐012 xenograft study was performed at Shanghai ChemPartner Co., Ltd. (Shanghai, China). LIXC‐012 cells (2 × 106) in serum‐free medium mixed with Matrigel [1:1] (Corning) were inoculated subcutaneously into the right flank of female nu/nu mice. When the tumors reached approximately 80–300 mm3, the mice were randomly allocated to treatment groups (Day 1); mice then orally received lenvatinib, sorafenib, or the corresponding vehicle once daily for 14 days. Multiple mice in each vehicle control group were removed from the study because of excess tumor volume or cachexia‐induced body weight loss (BWL) after Day 11.
Patient‐derived xenograft (PDX; LI0050 and LI0334) studies were performed at Crown Bioscience Inc. (Taicang, China). Each tumor fragment (diameter, 2–3 mm) was inoculated subcutaneously into the right flank of female BALB/c nude mice. When the tumors reached approximately 130–150 mm3 (Day 1), the mice were randomly allocated to treatment groups; mice then orally received lenvatinib, sorafenib, or vehicle (3 mmol/L HCl only) once daily for 28 days. In the PDX studies, when BWL was ≥20% for any individual mouse, that mouse was given dosing holiday(s) until its body weight recovered to baseline (BWL, ≤10%).
Tumor dimensions were measured two or three times weekly with a caliper, and tumor volume was calculated as ½ × length × width2. Relative body weight (RBW) was calculated by dividing the daily body weight by that of the same mouse on Day 1.
Body Weight
Cachexia
Cells
cremophor
Ethanol
Hemoglobin, Sickle
Heterografts
Human Body
Institutional Animal Care and Use Committees
lenvatinib
matrigel
Mice, Inbred BALB C
Mice, Nude
Mus
Neoplasms
Patients
Serum
Sorafenib
Woman
On the basis of the phase Ib dose-finding results,25 patients were administered lenvatinib 20 mg once daily orally and pembrolizumab 200 mg intravenously once every 3 weeks in 3-week cycles (maximum of 35 pembrolizumab treatments).
The primary end point in this study was ORR at week 24 (ORRWK24). Responses were confirmed by a second assessment ≥ 4 weeks after initial response. Secondary end points included ORR, duration of response (DOR), PFS, overall survival (OS), disease control rate (DCR; defined as the proportion of patients with a best overall response of complete response [CR], partial response [PR], or stable disease), and clinical benefit rate (CBR; defined as the proportion of patients with CR, PR, or durable stable disease [defined as stable disease ≥ 23 weeks]). Tumor responses for primary and secondary end points were assessed by the investigator per irRECIST.27 (link)Prespecified exploratory end points included tumor responses per irRECIST27 (link) and RECIST version 1.120 (link) by IIR (assessed by BioTel Research, BioTelemetry), and antitumor activity according to PD-L1 status. Activity by tumor histology and MSI status were post hoc exploratory analyses. Adverse events (AEs) were assessed according to Common Terminology Criteria for Adverse Events version 4.03.
For all patients, tumor assessments (investigator assessment and IIR) were completed at baseline, every 6 weeks for the first 24 weeks, and every 9 weeks thereafter. PD-L1 status was determined using an investigational version of the PD-L1 immunochemistry 22C3pharmDx28 (link) and a provisional combined positive score (defined as the number of staining tumor and immune cells relative to total tumor cells) cutoff of 1. Central testing to determine MSI was conducted using the MSI Analysis System, and central testing for mismatch repair (MMR) status was conducted using the Ventana MMR Immunohistochemical Assay. Available data regarding known MSI/MMR status based on local testing per institutional guidelines was also collected.
Toxicity was managed by supportive medications, treatment interruption, dose reduction (lenvatinib only; re-escalation was not allowed), and/or treatment discontinuation in accordance with predefined dose-modification guidelines. Information regarding treatment discontinuation of either lenvatinib or pembrolizumab and patient assessments during the follow-up period of this study can be found in the Data Supplement.
The primary end point in this study was ORR at week 24 (ORRWK24). Responses were confirmed by a second assessment ≥ 4 weeks after initial response. Secondary end points included ORR, duration of response (DOR), PFS, overall survival (OS), disease control rate (DCR; defined as the proportion of patients with a best overall response of complete response [CR], partial response [PR], or stable disease), and clinical benefit rate (CBR; defined as the proportion of patients with CR, PR, or durable stable disease [defined as stable disease ≥ 23 weeks]). Tumor responses for primary and secondary end points were assessed by the investigator per irRECIST.27 (link)Prespecified exploratory end points included tumor responses per irRECIST27 (link) and RECIST version 1.120 (link) by IIR (assessed by BioTel Research, BioTelemetry), and antitumor activity according to PD-L1 status. Activity by tumor histology and MSI status were post hoc exploratory analyses. Adverse events (AEs) were assessed according to Common Terminology Criteria for Adverse Events version 4.03.
For all patients, tumor assessments (investigator assessment and IIR) were completed at baseline, every 6 weeks for the first 24 weeks, and every 9 weeks thereafter. PD-L1 status was determined using an investigational version of the PD-L1 immunochemistry 22C3pharmDx28 (link) and a provisional combined positive score (defined as the number of staining tumor and immune cells relative to total tumor cells) cutoff of 1. Central testing to determine MSI was conducted using the MSI Analysis System, and central testing for mismatch repair (MMR) status was conducted using the Ventana MMR Immunohistochemical Assay. Available data regarding known MSI/MMR status based on local testing per institutional guidelines was also collected.
Toxicity was managed by supportive medications, treatment interruption, dose reduction (lenvatinib only; re-escalation was not allowed), and/or treatment discontinuation in accordance with predefined dose-modification guidelines. Information regarding treatment discontinuation of either lenvatinib or pembrolizumab and patient assessments during the follow-up period of this study can be found in the Data Supplement.
Biological Assay
CD274 protein, human
Cells
Dietary Supplements
Drug Tapering
lenvatinib
Mismatch Repair
Neoplasms
Patients
pembrolizumab
Pharmaceutical Preparations
Most recents protocols related to «Lenvatinib»
Lenvatinib therapy should be conducted as follows: patients in the TACE-LEN were already taking lenvatinib after enrollment. Before recommending TACE plus lenvatinib, patients should fully understand the efficacy, adverse reactions that may occur during treatment, and costs of the drug. Lenvatinib was given within 3 days of the first TACE treatment if the patient agreed with the doctor‘s advice on medication. Lenvatinib was given once a day, and the specific dosage depended on the body weight. The dosages of lenvatinib were 12 mg (weight ≥60 kg) and 8 mg (weight <60 kg). The patient should stop taking lenvatinib for 3 days before each TACE treatment, and clinical observation is required after TACE. If adverse event (AE) induction (such as fever, nausea, and vomiting) did not occur, the patient could resume taking lenvatinib after TACE treatment. If the adverse reaction caused by TACE was serious, patients should stop taking lenvatinib until their adverse reaction was relieved. According to the guidelines, it was permissible to interrupt the dose of lenvatinib to reduce the toxicity associated with lenvatinib (to 8 mg and 4 mg daily or 4 mg every other day). Patients taking lenvatinib did not take other antitumor drugs.
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The recommended dosage of lenvatinib is 8 mg once daily for patients with a body weight less than 60 kg and 12 mg once daily for patients with a body weight of 60 kg or greater.
Patients received 12 mg/day (for bodyweight ≥ 60 kg) or 8 mg/day (for bodyweight < 60 kg) oral lenvatinib daily. The lenvatinib dose was interrupted and subsequently reduced to 8 mg and 4 mg/day or 4 mg every other day when grade 3 or greater adverse events according to the common terminology criteria for adverse events version 5.0 occurred. When lenvatinib treatment was discontinued due to adverse event or progressive disease, another systemic therapy such as sorafenib, regorafenib, cabozantinib, and ramucirumab, was administered if applicable.
Oncologically unresectable tumors classi ed as a partial response (PR) or stable disease (SD) based on RECIST ver1.1 or mRECIST that were maintained for at least 8 weeks or technically unresectable tumors that became resectable due to the response to lenvatinib treatment were considered amenable to curative resection, and the patient was considered a candidate for surgical intervention with a few exceptions. If patients had manageable extrahepatic metastases, noncurative surgery leaving the extrahepatic metastases in situ was performed if surgery was considered to contribute to prolonged survival or lenvatinib therapy could not be continued due to adverse effects. The indication for surgery was nally determined at the multidisciplinary tumor board conference based on tumor location, distribution, and response to lenvatinib. Ablation therapy for intrahepatic tumors and pulmonary metastases was also utilized if indicated. Major hepatectomy was de ned as resection of four or more liver segments.
Top products related to «Lenvatinib»
Sourced in United States, Italy
Lenvatinib is a chemical compound used in laboratory research settings. It is a tyrosine kinase inhibitor that targets multiple receptor tyrosine kinases involved in angiogenesis and tumor growth. The core function of Lenvatinib is to serve as a research tool for investigating cellular signaling pathways and their potential therapeutic implications.
Sourced in Japan
Lenvatinib is a small-molecule tyrosine kinase inhibitor. It targets multiple receptor tyrosine kinases involved in angiogenesis and tumor proliferation.
Sourced in Japan
Lenvima is a pharmaceutical product developed by Eisai. It is a multi-kinase inhibitor that targets several receptor tyrosine kinases involved in tumor angiogenesis and tumor growth signaling pathways.
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.
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.
Sourced in United States, Austria, Canada, Belgium, United Kingdom, Germany, China, Japan, Poland, Israel, Switzerland, New Zealand, Australia, Spain, Sweden
Prism 8 is a data analysis and graphing software developed by GraphPad. It is designed for researchers to visualize, analyze, and present scientific data.
Sourced in Japan, United States, China, Germany, United Kingdom
The Cell Counting Kit-8 is a colorimetric assay for the determination of cell viability and cytotoxicity. It utilizes a water-soluble tetrazolium salt that produces a water-soluble formazan dye upon reduction in the presence of an electron carrier. The amount of the formazan dye generated is directly proportional to the number of living cells.
Sourced in United States, China, Japan, Germany, United Kingdom, Canada, France, Italy, Australia, Spain, Switzerland, Netherlands, Belgium, Lithuania, Denmark, Singapore, New Zealand, India, Brazil, Argentina, Sweden, Norway, Austria, Poland, Finland, Israel, Hong Kong, Cameroon, Sao Tome and Principe, Macao, Taiwan, Province of China, Thailand
TRIzol reagent is a monophasic solution of phenol, guanidine isothiocyanate, and other proprietary components designed for the isolation of total RNA, DNA, and proteins from a variety of biological samples. The reagent maintains the integrity of the RNA while disrupting cells and dissolving cell components.
Sourced in United States, China, United Kingdom, Germany, France, Australia, Canada, Japan, Italy, Switzerland, Belgium, Austria, Spain, Israel, New Zealand, Ireland, Denmark, India, Poland, Sweden, Argentina, Netherlands, Brazil, Macao, Singapore, Sao Tome and Principe, Cameroon, Hong Kong, Portugal, Morocco, Hungary, Finland, Puerto Rico, Holy See (Vatican City State), Gabon, Bulgaria, Norway, Jamaica
DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
More about "Lenvatinib"
Lenvatinib, also known as Lenvima, is a potent multi-kinase inhibitor medication used in the treatment of various types of cancer, including thyroid, kidney, and liver cancer.
This innovative therapeutic agent works by targeting and inhibiting several critical enzymes involved in the growth and development of tumors, as well as the formation of new blood vessels that support cancer progression.
Lenvatinib has demonstrated promising results in clinical trials, offering improved outcomes for patients with advanced or metastatic disease.
Researchers are continuously exploring the potential of this medication, investigating optimal dosing, combination therapies, and expanding its applications to other malignancies.
The use of Lenvatinib often involves the use of cell culture techniques, such as the use of fetal bovine serum (FBS) and Penicillin/streptomycin antibiotics to maintain and support cell growth.
Additionally, researchers may utilize tools like the Prism 8 statistical software and the Cell Counting Kit-8 assay to analyze and quantify the effects of Lenvatinib on cancer cells.
The TRIzol reagent may also be employed to extract and purify RNA from cells for gene expression analysis.
By leveraging the power of PubCompare.ai, an AI-driven platform, researchers can optimize their Lenvatinib studies by comparing data from literature, pre-prints, and patents.
This cutting-edge tool helps enhance the reproducibility and accuracy of research protocols, unlocking the full potential of Lenvatinib studies and contributing to the advancement of cancer treatment.
This innovative therapeutic agent works by targeting and inhibiting several critical enzymes involved in the growth and development of tumors, as well as the formation of new blood vessels that support cancer progression.
Lenvatinib has demonstrated promising results in clinical trials, offering improved outcomes for patients with advanced or metastatic disease.
Researchers are continuously exploring the potential of this medication, investigating optimal dosing, combination therapies, and expanding its applications to other malignancies.
The use of Lenvatinib often involves the use of cell culture techniques, such as the use of fetal bovine serum (FBS) and Penicillin/streptomycin antibiotics to maintain and support cell growth.
Additionally, researchers may utilize tools like the Prism 8 statistical software and the Cell Counting Kit-8 assay to analyze and quantify the effects of Lenvatinib on cancer cells.
The TRIzol reagent may also be employed to extract and purify RNA from cells for gene expression analysis.
By leveraging the power of PubCompare.ai, an AI-driven platform, researchers can optimize their Lenvatinib studies by comparing data from literature, pre-prints, and patents.
This cutting-edge tool helps enhance the reproducibility and accuracy of research protocols, unlocking the full potential of Lenvatinib studies and contributing to the advancement of cancer treatment.