Panitumumab (anti-EGFR)
(Synonyms: 帕尼单抗 (anti-EGFR)) 目录号 : GC66333
Panitumumab (anti-EGFR) 是一种全人源 IgG2 抗 EGFR 单克隆抗体，具有抗肿瘤活性。Panitumumab (anti-EGFR) 抑制肿瘤细胞增殖、存活和血管生成。Panitumumab (anti-EGFR) 可用于癌症研究，例如结肠癌。
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Panitumumab (anti-EGFR) is a fully human IgG2 anti-EGFR monoclonal antibody with anti-tumor activity. Panitumumab (anti-EGFR) inhibits tumor cell proliferation, survival and angiogenesis. Panitumumab (anti-EGFR) can be used in the research of cancers, such as colon cancer[1][2][4].
Panitumumab (2 nM-2 μM, 3 h) (anti-EGFR) inhibits ligand-dependent autophosphorylation in EGFR-expressing NCI-H1975 cells, NCI-H1650 cells and CHO cells[3].
Panitumumab (0-200 μg/mL, 48 h) (anti-EGFR) inhibits the proliferation of DLD-1 cells[4].
Panitumumab (80 μg/mL, 24 h) (anti-EGFR) increase beclin-1 (a marker of autophagy) levels in Caco-2 cells and DLD-1 cells[4].
Western Blot Analysis[3]
| Cell Line: | EGFR-expressing NCI-H1975 cells, NCI-H1650 cells and CHO cells |
| Concentration: | 2, 20, 200, 2000 nM |
| Incubation Time: | 3 h |
| Result: | Inhibited ligand-induced autophosphorylation of EGFR. |
Panitumumab (25, 100, or 500 μg/mouse, i.p., twice a week) (anti-EGFR) inhibits tumor growth in NCI-H1975 and NCI-H1650 xenografts, compared with control (P < 0.0003)[1].
| Animal Model: | NCI-H1975 and NCI-H1650 xenografts[3] |
| Dosage: | 25, 100, or 500 μg/mouse |
| Administration: | Intraperitoneal injection (i.p.), twice a week |
| Result: | Inhibited ligand-induced EGFR phosphorylation, tumor growth, and markers of proliferation. Decreased Ki-67 and phospho- mitogen-activated protein kinase (pMAPK) staining in both xenografts. |
| Cas No. | SDF | Download SDF | |
| 别名 | 帕尼单抗 (anti-EGFR) | ||
| 分子式 | 分子量 | ||
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Implementing anti-epidermal growth factor receptor (EGFR) therapy in metastatic colorectal cancer: challenges and future perspectives
Ann Oncol 2020 Jan;31(1):30-40.PMID:31912793DOI:10.1016/j.annonc.2019.10.007.
Epidermal growth factor receptor (EGFR) inhibitors are valuable therapeutics in metastatic colorectal cancer (mCRC). anti-EGFR monoclonal antibodies (MoAbs), such as cetuximab or Panitumumab, in combination with chemotherapy are effective treatment options for patients with RAS and BRAF wild-type mCRC. Nevertheless, several issues are still open concerning the optimal use of anti-EGFR drugs in the continuum of care of mCRC. Novel approaches for increasing the efficacy of anti-EGFR therapies include better molecular selection of EGFR-dependent mCRC, intensification of chemotherapy, combination of anti-EGFR MoAbs and immune checkpoint inhibitors, and reintroduction of EGFR blockade or 'rechallenge' in selected patients who have previously responded to anti-EGFR MoAb therapy. An extensive translational research program was conducted in the Cetuximab After Progression in KRAS wIld-type colorectal cancer patients-Gruppo Oncologico dell' Italia Meridionale (CAPRI-GOIM) study with the aims of determining which subgroups of patients could benefit from the continuous inhibition of EGFR, from evaluating the role of liquid biopsy-based and its concordance with tissue-based molecular testing, and from investigating novel potential mechanisms of resistance to anti-EGFR therapies. In this review, we summarize the translational and clinical findings of the CAPRI-GOIM program in the context of the current knowledge of therapeutic strategies and of ongoing research on more appropriate uses of anti-EGFR therapies in RAS and BRAF wild-type mCRC patients.
Brigatinib combined with anti-EGFR antibody overcomes osimertinib resistance in EGFR-mutated non-small-cell lung cancer
Nat Commun 2017 Mar 13;8:14768.PMID:28287083DOI:10.1038/ncomms14768.
Osimertinib has been demonstrated to overcome the epidermal growth factor receptor (EGFR)-T790M, the most relevant acquired resistance to first-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs). However, the C797S mutation, which impairs the covalent binding between the cysteine residue at position 797 of EGFR and osimertinib, induces resistance to osimertinib. Currently, there are no effective therapeutic strategies to overcome the C797S/T790M/activating-mutation (triple-mutation)-mediated EGFR-TKI resistance. In the present study, we identify brigatinib to be effective against triple-mutation-harbouring cells in vitro and in vivo. Our original computational simulation demonstrates that brigatinib fits into the ATP-binding pocket of triple-mutant EGFR. The structure-activity relationship analysis reveals the key component in brigatinib to inhibit the triple-mutant EGFR. The efficacy of brigatinib is enhanced markedly by combination with anti-EGFR antibody because of the decrease of surface and total EGFR expression. Thus, the combination therapy of brigatinib with anti-EGFR antibody is a powerful candidate to overcome triple-mutant EGFR.
anti-EGFR monoclonal antibody Panitumumab for the treatment of patients with metastatic colorectal cancer: an overview of current practice and future perspectives
Expert Opin Biol Ther 2017 Oct;17(10):1297-1308.PMID:28752777DOI:10.1080/14712598.2017.1356815.
Targeted agents alone or in combination with chemotherapy are current standard of treatment for metastatic colorectal cancer (mCRC). Panitumumab is a fully human monoclonal antibody which inhibits the epidermal growth factor receptor (EGFR). It is currently approved in combination with chemotherapy in first- and second-line and as a monotherapy in chemorefractory patients. RAS gene mutations confer resistance to anti-EGFR agents; thus, Panitumumab is restricted to the treatment of RAS wild-type (WT) tumors. Areas covered: This review explores the available data on Panitumumab and presents new perspectives on predictive markers of anti-EGFR efficacy including primary tumor sidedness and BRAF mutations. Other details covered include Panitumumab's mechanism of action, pharmacokinetics, pharmacodynamics and safety aspects of the therapy as well as mechanisms of secondary resistance and future prospects of treatment in different settings. Expert opinion: Panitumumab has significantly added to the treatment armamentarium for RAS WT mCRC. The effort spent in identifying predictive biomarkers of Panitumumab efficacy has been of pivotal importance to development of the molecular selection of patients with mCRC. Primary and secondary resistance, however, still represent important issues. Novel strategies to overcome those issues are currently underway with promising results which highlight the potential use of Panitumumab in combination with other targeted agents in the future.
anti-EGFR therapy in metastatic colorectal cancer: mechanisms and potential regimens of drug resistance
Gastroenterol Rep (Oxf) 2020 Jun 23;8(3):179-191.PMID:32665850DOI:10.1093/gastro/goaa026.
Cetuximab and Panitumumab, as the highly effective antibodies targeting epidermal growth factor receptor (EGFR), have clinical activity in the patients with metastatic colorectal cancer (mCRC). These agents have good curative efficacy, but drug resistance also exists at the same time. The effects of KRAS, NRAS, and BRAF mutations and HER2 amplification on the treatment of refractory mCRC have been elucidated and the corresponding countermeasures have been put forward. However, the changes in EGFR and its ligands, the mutations or amplifications of PIK3CA, PTEN, TP53, MET, HER3, IRS2, FGFR1, and MAP2K1, the overexpression of insulin growth factor-1, the low expression of Bcl-2-interacting mediator of cell death, mismatch repair-deficient, and epigenetic instability may also lead to drug resistance in mCRC. Although the emergence of drug resistance has genetic or epigenetic heterogeneity, most of these molecular changes relating to it are focused on the key signaling pathways, such as the RAS/RAF/mitogen-activated protein kinase or phosphatidylinositol 3-kinase/Akt/mammalian target of the rapamycin pathway. Accordingly, numerous efforts to target these signaling pathways and develop the novel therapeutic regimens have been carried out. Herein, we have reviewed the underlying mechanisms of the resistance to anti-EGFR therapy and the possible implications in clinical practice.
KRAS, NRAS, BRAF, HER2 and microsatellite instability in metastatic colorectal cancer - practical implications for the clinician
Radiol Oncol 2019 Sep 24;53(3):265-274.PMID:31553708DOI:10.2478/raon-2019-0033.
Background Colorectal cancer is a successful model of genetic biomarker development in oncology. Currently, several predictive or prognostic genetic alterations have been identified and are used in clinical practice. The RAS gene family, which includes KRAS and NRAS act as predictors for anti-epithelial growth factor receptor treatment (anti-EGFR), and it has been suggested that NRAS mutations also play a role in prognosis: patients harboring NRAS alterations have a significantly shorter survival compared to those with wild type tumours. BRAF V600E mutations are rare and occur mostly in tumors located in the ascending colon in elderly female patients. BRAF is instrumental in establishing prognosis: survival is shorter by 10-16 months in BRAF-mutant patients, and BRAF may be a negative prognostic factor for patients who undergo hepatic or pulmonary metastasectomy. Moreover, this mutation is used as a negative predictive factor for anti-EGFR therapies. Two new biomarkers have recently been added to the metastatic colorectal cancer panel: HER2 and microsatellite instability. While HER2 is still being investigated in different prospective studies in order to validate its prognostic role, microsatellite instability already guides clinical decisions in substituted with advanced colorectal cancer. Conclusions There are current evidences that support using above mentioned genetic biomarkers to better identify the right medicine that is supposed to be used in the right patient. This approach contributes to a more individualized patient-oriented treatment in daily clinical practice.