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Afatinib

Afatinib is a tyrosine kinase inhibitor used in the treatment of non-small cell lung cancer.
It targets the epidermal growth factor receptor (EGFR) and is approved for patients with specific EGFR mutations.
Afatinib has been shown to improve progression-free survival compared to standard chemotherapy in these patient populations.
Researchers can leverage PubCompare.ai, an AI-driven platform, to optimize their Afatinib studies by easily locating protocols from literature, preprints, and patents, while utilizing AI-powered comparisons to identify the best protocols and products.
This can enhance reproducibility and accuracy in Afatinib research, taking studies to new heights.

Most cited protocols related to «Afatinib»

1
KRAS and NRAS Silencing and Antibody Validation
Cited 7 times
Reagents, including siRNA catalogue numbers, and the performance of all experimental procedures were all as described in references [1 (link)–4 (link)]. Afatinib was purchased from Selleckchem (Houston, TX). Neratinib was supplied by Puma Biotechnology Inc. (Los Angeles, CA). Cell culture materials were purchased from GIBCOBRL (GIBCOBRL Life Technologies, Grand Island, NY). Established cell lines were purchased from the ATCC. The GFP and RFP tagged K-RAS V12 plasmids were provided by Dr. John Hancock (Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston TX, USA). PDX isolates of human head and neck cancer were kindly provided by Dr. John Lee (Chan Soon-Shiong Institute of Molecular Medicine, Culver City, CA, USA). Commercially available validated short hairpin RNA molecules to knock down RNA / protein levels were validated in house and purchased from Qiagen (Valencia, CA) (Supplemental Figure 12). Antibodies directed against RAS proteins: Thermo-Fisher (Waltham MA) N-RAS PA5–14833; K-RAS PA5–44339. Based on data from Waters et al, we used two validated siRNA tools to knock down K-RAS or N-RAS for antibody validation purposes; custom made NRAS-5 CCUGAGUACUGACCUAAGAdTdT and K-RAS Silencer s7940 [52 ]. Knock down of K-RAS or N- RAS reduced fluorescent staining by ~80%. Methods of approach were as described [1 (link)–4 (link)] (see supplemental Methods section).
Dent P., Booth L., Roberts J.L., Liu J., Poklepovic A., Lalani A.S., Tuveson D., Martinez J, & Hancock J.F. (2019). Neratinib inhibits Hippo/YAP signaling, reduces mutant K-RAS expression, ONCOGENE and kills pancreatic and blood cancer cells. Oncogene, 38(30), 5890-5904.
Publication 2019
Afatinib Antibodies Cancer of Head and Neck Cell Culture Techniques Cell Lines Homo sapiens Immunoglobulins Lanugo neratinib NRAS protein, human Plasmids Proteins Puma ras Proteins RNA, Small Interfering Short Hairpin RNA
2
Culturing and Engineered Cell Lines
Cited 6 times
Human mammary epithelial cells (HMLE) were obtained from Sendurai A. Mani (MD Anderson Cancer Center, Houston TX) and NMuMG and BT474 cells were purchased from the ATCC (Manassas, VA, USA). The HMLE cells were cultured in DMEM:F12 supplemented with insulin (10 μg/ml), EGF (10 ng/ml), and hydrocortisone (250 μg/ml), this media was mixed 1:1 with Mammary Epithelial Cell Growth Medium (MEGM) purchased from Lonza (Allendale, NJ, USA). Bioluminescent HMLE cells were engineered to stably express firefly luciferase via lentiviral transduction under the selection of Blasticidin. Her2 and Twist expressing HMLE cells and Twist expressing NMuMG cells were constructed via stable transduction using pBabe viral particles and selected for using puromycin. NMuMG, Her2 transformed HMLE and BT474 cells were cultured in DMEM supplemented with 10% FBS, 1% Pen/Strep, and 10 μg/mL of insulin. Plasmids encoding eGFP, FGFR1-α-IIIc (NM_023110.2) or FGFR1-β-IIIc (NM_023105.2) were purchased from Cyagen Biosciences (Santa Clara, CA, USA). These constructs were used to construct lentiviral particles, and stable transduction was selected for under Hygromycin selection. TGF-β1 and basic FGF (FGF2) were purchased from R&D systems (Minneapolis, MN). BGJ-398, Lapatinib, Afatinib, Trametinib, VX11e, AZD-6244, and Idelalisib were purchased from Selleckchem (Houston, TX), solubilized in DMSO and used at the indicated concentrations. FIIN-2 and FIIN-4 were synthesized as previously described and similarly solubilized in DMSO [15 (link), 18 (link)].
Brown W.S., Akhand S.S, & Wendt M.K. (2016). FGFR signaling maintains a drug persistent cell population following epithelial-mesenchymal transition. Oncotarget, 7(50), 83424-83436.
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Publication 2016
Afatinib AZD 6244 BGJ398 Breast Cells Culture Media Epithelial Cells ERBB2 protein, human FGFR1 protein, human Fibroblast Growth Factor 2 Homo sapiens Hydrocortisone hygromycin A idelalisib Insulin Lapatinib Luciferases, Firefly Malignant Neoplasms Plasmids Puromycin Streptococcal Infections Sulfoxide, Dimethyl TGF-beta1 trametinib Virion
3
Targeted Exome Sequencing of Tumor and Normal Samples
Cited 6 times
DNA was extracted from patient’s tumor, early passage tumorgrafts developed from liver metastases, normal samples (adjacent non-cancerous liver or peripheral blood), and from normal tissue of the same mouse strain as those used to grow the xenografts using the Qiagen DNA FFPE tissue kit or Qiagen DNA blood mini kit (Qiagen, CA). Additional analyses were performed for CRC334 after afatinib anti-EGFR therapy and tumorgraft regrowth (indicated in footnote of Supplementary Table 4). Genomic DNA from tumor and normal samples were fragmented and used for Illumina TruSeq library construction (Illumina, San Diego, CA) according to the manufacturer’s instructions or as previously described33 (link). Exonic or targeted regions were captured in solution using the Agilent SureSelect v.4 kit or a custom targeted panel according to the manufacturer’s instructions (Agilent, Santa Clara, CA) (Supplementary Table 9). The captured library was then purified with a Qiagen MinElute column purification kit and eluted in 17 μl of 70°C EB to obtain 15 μl of captured DNA library. The captured DNA library was amplified in the following way: Eight 30uL PCR reactions each containing 19 μl of H2O, 6 μl of 5 × Phusion HF buffer, 0.6 μl of 10 mM dNTP, 1.5 μl of DMSO, 0.30 μl of Illumina PE primer #1, 0.30μl of Illumina PE primer #2, 0.30 μl of Hotstart Phusion polymerase, and 2 μl of captured exome library were set up. The PCR program used was: 98°C for 30 seconds; 14 cycles (exome) or 16 cycles (targeted) of 98°C for 10 seconds, 65°C for 30 seconds, 72°C for 30 seconds; and 72°C for 5 min. To purify PCR products, a NucleoSpin Extract II purification kit (Macherey-Nagel, PA) was used following the manufacturer’s instructions. Paired-end sequencing, resulting in 100 bases from each end of the fragments for exome libraries and 100 or 150 bases from each end of the fragment for targeted libraries, was performed using Illumina HiSeq 2000/2500 and Illumina MiSeq instrumentation (Illumina, San Diego, CA).
Bertotti A., Papp E., Jones S., Adleff V., Anagnostou V., Lupo B., Sausen M., Phallen J., Hruban C.A., Tokheim C., Niknafs N., Nesselbush M., Lytle K., Sassi F., Cottino F., Migliardi G., Zanella E.R., Ribero D., Russolillo N., Mellano A., Muratore A., Paraluppi G., Salizzoni M., Marsoni S., Kragh M., Lantto J., Cassingena A., Li Q.K., Karchin R., Scharpf R., Sartore-Bianchi A., Siena S., Diaz LA J.r., Trusolino L, & Velculescu V.E. (2015). The Genomic Landscape of Response to EGFR Blockade in Colorectal Cancer. Nature, 526(7572), 263-267.
Publication 2015
Afatinib BLOOD Buffers DNA, Neoplasm DNA Library EGFR protein, human Exome Exons Genome Liver Malignant Neoplasms Mus Neoplasm Metastasis Neoplasms Oligonucleotide Primers Patients Strains Sulfoxide, Dimethyl Therapeutics Tissues Xenografting
4
EGFR Mutant Lung Adenocarcinoma Afatinib Response
Cited 5 times
Patients with stage IV lung adenocarcinoma diagnosed and treated between May 2014 and August 2016 in two Kaohsiung Medical University-affiliated hospitals (Kaohsiung Medical University Hospital and Kaohsiung Municipal Ta-Tung Hospital) in Taiwan were identified and followed until December 2016. The diagnosis of lung cancer was confirmed pathologically according to World Health Organization pathology classification, and tumor staging was made by a special committee including clinical pulmonologists, medical oncologists, chest surgeons, radiologists, pathologists and radiation oncologists, according to the seventh American Joint Committee on Cancer staging system. Patients were included if they: (1) had adequate tumor specimens for EGFR mutation examinations and had susceptible EGFR mutations including exon 19 deletions and exon 21 L858R point mutations; (2) were chemotherapy-naïve and treated with 30 mg or 40 mg daily of afatinib as the first-line treatment.
Baseline clinical characteristics were determined by retrospective chart review, including age at diagnosis, sex, Eastern Cooperative Oncology Group (ECOG) performance status at the beginning of first-line afatinib treatment, smoking history, and tumor histology. Glomerular filtration rate was estimated using the Modification of Diet in Renal Disease formula (eGFR-MDRD). Mutations in the EGFR gene were analyzed using an EGFR RGQ kit (Qiagen, UK) which utilized amplification refractory mutation specific (ARMS) polymerase chain reactions and Scorpion technology for detection and/or direct sequencing as in our previous report [12 (link)–16 (link)]. The initial treatment response was classified based on serial imaging studies using the revised Response Evaluation Criteria in Solid Tumors (RECIST 1.1) criteria. The PFS and OS with first-line treatment were defined as the duration from the start of the first treatment to the date of disease progression on imaging studies and the date of death, respectively. ADRs were recorded by physicians and graded according to the Common Terminology Criteria for Adverse Events (CTCAE) v4.0.
Yang C.J., Tsai M.J., Hung J.Y., Lee M.H., Tsai Y.M., Tsai Y.C., Hsu J.F., Liu T.C., Huang M.S, & Chong I.W. (2017). The clinical efficacy of Afatinib 30 mg daily as starting dose may not be inferior to Afatinib 40 mg daily in patients with stage IV lung Adenocarcinoma harboring exon 19 or exon 21 mutations. BMC Pharmacology & Toxicology, 18, 82.
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Publication 2017
Adenocarcinoma of Lung Afatinib Aleurites c-erbB-1 Proto-Oncogenes Chest Diagnosis Diet Disease Progression Drug Reaction, Adverse EGFR protein, human Exons Gene Deletion Glomerular Filtration Rate Joints Kidney Diseases Lung Cancer Mutation Neoplasms Oncologists Pathologists Patients Pharmacotherapy Physical Examination Physicians Point Mutation Polymerase Chain Reaction Pulmonologists Radiation Oncologists Radiologist Scorpions Surgeons
5
EGFR Mutant Protein Expression Analysis
Cited 5 times
293H cells were transiently transfected with various pcDNA3.1(−) vectors using Lipofectamine 2000 (Invitrogen) and 2 μg DNA per sample as previous described (43 (link)). The EGFR G719S, ex19ins, ex20ins, T790M, and L858R + T790M mutations were all generated via site-directed mutagenesis as described (43 (link)). Following 6 hour treatment with DMSO, afatinib, or increasing doses of erlotinib or CO-1686 at various concentrations, cells were lysed. Immunoblotting was performed using corresponding lysates with antibodies against phospho-EGFR (Santa Cruz, Dallas, TX) or total EGFR (BD Biosciences, San Diego, CA). Secondary anti-goat antibody was obtained from Santa Cruz (Dallas, TX), and secondary anti-mouse antibody was obtained from Cell Signaling (Danvers, MA).
Walter A.O., Sjin R.T., Haringsma H.J., Ohashi K., Sun J., Lee K., Dubrovskiy A., Labenski M., Zhu Z., Wang Z., Sheets M., Martin T.S., Karp R., van Kalken D., Chaturvedi P., Niu D., Nacht M., Petter R.C., Westlin W., Lin K., Jaw-Tsai S., Raponi M., Dyke T.V., Etter J., Weaver Z., Pao W., Singh J., Simmons A.D., Harding T.C, & Allen A. (2013). Discovery of a mutant-selective covalent inhibitor of EGFR that overcomes T790M-mediated resistance in NSCLC. Cancer discovery, 3(12), 1404-1415.
Publication 2013
Afatinib Antibodies Antibodies, Anti-Idiotypic Cells Cloning Vectors CO-1686 EGFR protein, human Erlotinib Goat lipofectamine 2000 Mus Mutagenesis, Site-Directed Mutation Sulfoxide, Dimethyl

Most recents protocols related to «Afatinib»

1
Evaluating CNS Response to Afatinib in NSCLC
CNS ORR, CNS disease control rate (DCR), CNS duration of response (DoR), CNS PFS, CNS time to response (TTR), cumulative incidence of CNS failure and best percentage change from baseline in TL size were recorded to evaluate the CNS response. CNS ORR was defined as the percentage of patients who achieved a best CNS response of complete response (CR) or partial response (PR). CNS DCR was defined as the proportion of patients with a CR or PR or stable disease (SD) in brain lesions. CNS DoR was defined as the time from first documentation of intracranial CR or PR until the time of progression (including intracranial progressive disease [PD] or extracranial PD) or death of any reason, whichever came first. CNS PFS was defined as the time from the first dose of afatinib until the time of progression (including intracranial PD or extracranial PD) or death of any reason, whichever came first. And CNS TTR was defined as the time from the first dose of afatinib to the time when the intracranial CR or PR to afatinib was first evaluated. The ORR and DCR were calculated with exact Clopper-Pearson 95% confidence intervals (CIs) based on the exact binomial distribution, and compared by chi-square test or Fisher’s exact test. CNS DoR, PFS, and TTR were estimated by the Kaplan-Meier method with corresponding 95% CIs, and compared by log-rank test. Besides, a Cox proportional hazards model was applied to estimate HRs and 95% CIs with significance set at p <0.05 level. A competing risk analysis estimating the cumulative incidence for the event of interest (CNS progression) in the presence of competing risk event (non-CNS progression) was performed using a semiparametric Fine–Gray regression model. All the p values reported in the analysis were two-sided, and a p <0.05 level was considered statistically significant in the tests. And all statistical analyses were calculated using SPSS (version 26.0) except for the competing risks analysis, which were calculated with R software (version 4.1.2), and plots were executed using R software (version 4.1.2).
Kang L., Mai J., Liang W., Zou Q., Huang C., Lin Y, & Liang Y. (2023). CNS efficacy of afatinib as first-line treatment in advanced non-small cell lung cancer patients with EGFR mutations. Frontiers in Oncology, 13, 1094195.
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Publication 2023
Afatinib Brain Diseases Disease Progression Patients
2
Afatinib for EGFR-Mutant NSCLC with Brain Metastases
EGFR-mutant NSCLC patients with BMs who received afatinib (30 mg or 40 mg, orally, once daily) as first-line treatment at Sun Yat-Sen University Cancer Center between March 2018 and January 2022 were retrospectively reviewed in this study. Patients received contrast computed tomography (CT) scans and contrast magnetic resonance imaging (MRI) at baseline and reviewed every 8 weeks from the start of afatinib until treatment discontinuation. Clinical and imaging data of eligible patients were extracted from the electronic medical records for response evaluation. This retrospective study was approved by the Institutional Review Board of Sun Yat-Sen University Cancer Center and conducted in accordance with the Declaration of Helsinki.
Kang L., Mai J., Liang W., Zou Q., Huang C., Lin Y, & Liang Y. (2023). CNS efficacy of afatinib as first-line treatment in advanced non-small cell lung cancer patients with EGFR mutations. Frontiers in Oncology, 13, 1094195.
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Publication 2023
Afatinib EGFR protein, human Ethics Committees, Research Malignant Neoplasms Non-Small Cell Lung Carcinoma Patients Radionuclide Imaging Venous Catheter, Central X-Ray Computed Tomography
3
Cytotoxicity Evaluation of Cancer Drugs
For lung cancer cell lines, cells were seeded in 96‐well plates and incubated at 37 °C for 24 h. Then cells were incubated with 200 µL of medium containing increasing doses of the drugs gefitinib (Selleckchem Houston, TX), erlotinib (Selleckchem Houston, TX), afatinib (Selleckchem Houston, TX), crizotinib (Selleckchem Houston, TX), or cisplatin (Sigma‐Aldrich, St Louis, MO) for 72 h. To detect and calculate the half maximal inhibitory concentration (IC50), 5 mg mL−1 of (MTT) (Sigma‐Aldrich, St Louis, MO) was added and the mixture was incubated at 37 °C for 4 h. The absorbance was determined at 570 nm. For organoids assays, organoids were dissociated by mechanical shearing, strained through a 70 µm filter, resuspended using LOM medium containing 5% GFR‐BME, and finally 30 µL of suspension were seeded into 384‐well plate. Organoids were treated with increasing concentrations of drugs for 5 days. Cell viability was detected by Cell titer–Glo 2.0 assay kit (Promega) and luminescence were measured by a multifunctional reader. The drug response curve was plotted and IC50 was calculated using nonlinear regression model by GraphPad Prism 7.0.
Wang S., Chen J., Jiang Y., Lei Z., Ruan Y.C., Pan Y., Yam J.W., Wong M.P, & Xiao Z. (2023). Targeting GSTP1 as Therapeutic Strategy against Lung Adenocarcinoma Stemness and Resistance to Tyrosine Kinase Inhibitors. Advanced Science, 10(7), 2205262.
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Publication 2023
Afatinib Biological Assay Cell Lines Cells Cell Survival Cisplatin Crizotinib Erlotinib Gefitinib Luminescence Lung Cancer Organoids Pharmaceutical Preparations prisma Promega Psychological Inhibition
4
Pharmacovigilance Analysis of Anti-HER2 Therapy ADRs

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Publication 2023
Ado-Trastuzumab Emtansine Afatinib Antineoplastic Agents Capecitabine dacomitinib Disabled Persons Drug Reaction, Adverse ERBB2 protein, human Ethics Committees, Research Health Care Professionals Hospitalization Lapatinib Malignant Neoplasms margetuximab mobocertinib Monoclonal Antibodies neratinib Patients pertuzumab Pharmaceutical Preparations Pharmacotherapy poziotinib pyrotinib Trastuzumab Treatment Protocols tucatinib
5
Afatinib and Chemotherapy for GBC
The study is designed as a randomised, open-label and multicentre clinical trial with a combined regimen of afatinib and chemotherapy drugs compared with chemotherapy drugs alone in patients with GBC with ErbB pathway mutation who underwent surgical removal (see figure 1 for an overview of the study design). A minimum of 102 patients will be enrolled from national four top-ranked hospitals in Shanghai, China (Renji Hospital, Ruijin Hospital and Xinhua Hospital, all affiliated to Shanghai Jiao Tong University School of Medicine, and Zhongshan Hospital Affiliated to Fudan University). The study has started on 1 June 2020 and the recruitment is expected to last 36 months. Medical records and biological samples including ctDNA detection will be collected and evaluated during the 3-year follow-up after diagnosis (see online supplemental appendix 1 for a detailed time schedule of study). Disease-free survival (DFS) and overall survival (OS) will also be evaluated.
Yang M., Zhao Y., Li Y., Cui X., Liu F., Wu W., Wang X.A., Li M., Liu Y, & Liu Y. (2023). Afatinib in combination with GEMOX chemotherapy as the adjuvant treatment in patients with ErbB pathway mutated, resectable gallbladder cancer: study protocol for a ctDNA-based, multicentre, open-label, randomised, controlled, phase II trial. BMJ Open, 13(2), e061892.
Publication 2023
Afatinib Biopharmaceuticals Diagnosis Genes, erbB Mutation Operative Surgical Procedures Patients Pharmaceutical Preparations Pharmacotherapy Treatment Protocols

Top products related to «Afatinib»

1
Afatinib by Selleck Chemicals
Sourced in United States, China, Germany
Afatinib is a chemical compound used in laboratory research. It functions as a tyrosine kinase inhibitor, targeting specific receptors involved in cellular signaling pathways.
2
Erlotinib by Selleck Chemicals
Sourced in United States, China, Germany, Australia
Erlotinib is a laboratory reagent used in research applications. It is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor (EGFR). Erlotinib is commonly used in cell-based assays and in vitro studies to investigate EGFR signaling pathways.
3
Gefitinib by Selleck Chemicals
Sourced in United States, Germany, China, France
Gefitinib is a tyrosine kinase inhibitor used in laboratory research. It functions by inhibiting the epidermal growth factor receptor (EGFR) tyrosine kinase.
4
Osimertinib by Selleck Chemicals
Sourced in United States, China, United Kingdom
Osimertinib is a chemical compound used in laboratory research. It is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor (EGFR). Osimertinib is commonly used in studies related to cancer research and drug development.
5
Afatinib by LC Laboratories
Sourced in United States
Afatinib is a small-molecule tyrosine kinase inhibitor that targets the epidermal growth factor receptor (EGFR) family, including EGFR (ErbB1), HER2 (ErbB2), ErbB3, and ErbB4. It is used for research purposes in various biological and biochemical applications.
6
Lapatinib by Selleck Chemicals
Sourced in United States, China, Germany
Lapatinib is a synthetic organic compound used as a laboratory reagent. It functions as a tyrosine kinase inhibitor, specifically targeting the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) proteins.
7
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.
8
Crizotinib by Selleck Chemicals
Sourced in United States, Germany
Crizotinib is a tyrosine kinase inhibitor used in laboratory research. It functions by inhibiting the activity of certain enzymes, such as ALK and c-MET, which are involved in cellular signaling pathways.
9
Dimethyl sulfoxide (dmso) by Merck Group
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
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.
10
Dacomitinib by Selleck Chemicals
Sourced in United States
Dacomitinib is a tyrosine kinase inhibitor used as a chemical reagent in laboratory research. It functions by inhibiting the activity of the epidermal growth factor receptor (EGFR) protein.

More about "Afatinib"

Afatinib is a potent and selective tyrosine kinase inhibitor (TKI) that has been approved for the treatment of non-small cell lung cancer (NSCLC).
It specifically targets the epidermal growth factor receptor (EGFR), a key driver of tumor growth and survival in certain NSCLC patients.
Afatinib has been shown to significantly improve progression-free survival compared to standard chemotherapy in NSCLC patients with specific EGFR mutations, such as deletions in exon 19 or the L858R mutation in exon 21.
Researchers can leverage the power of AI-driven platforms like PubCompare.ai to optimize their Afatinib studies.
PubCompare.ai allows researchers to easily locate relevant protocols from the scientific literature, preprints, and patents, while utilizing AI-powered comparisons to identify the best protocols and products.
This can enhance the reproducibility and accuracy of Afatinib research, taking studies to new heights.
In addition to Afatinib, other EGFR-targeting TKIs, such as Erlotinib, Gefitinib, Osimertinib, and Lapatinib, have also been studied for the treatment of NSCLC.
These agents have different mechanisms of action, binding profiles, and resistance profiles, which can be important considerations in the management of NSCLC.
Researchers may also utilize various cell culture techniques, including the use of fetal bovine serum (FBS) and dimethyl sulfoxide (DMSO), to assess the efficacy and mechanisms of action of Afatinib and other EGFR-targeting TKIs.
Additionally, the ALK inhibitor Crizotinib has been investigated in NSCLC patients with specific genetic alterations, highlighting the importance of personalized approaches in cancer treatment.
By leveraging the insights and capabilities of AI-driven platforms like PubCompare.ai, researchers can optimize their Afatinib studies, leading to enhanced reproducibility, accuracy, and ultimately, improved patient outcomes in the treatment of non-small cell lung cancer.