Which generation of targeted drug is dabrafenib? What is the mechanism of action?

Dabrafenib(Dabrafenib) is a first-generation targeted drug that targets BRAF V600E or V600K, dabrafenib is indicated as a single agent for the treatment of patients with unresectable or metastatic melanoma who have a FDA-approved trial detecting a BRAF V600E mutation. Dabrafenib in combination with trametinib is indicated for the treatment of patients with unresectable or metastatic melanoma with BRAF V600E or V600K mutations tested in FDA-approved trials. Dabrafenib in combination with trametinib for the adjuvant treatment of patients with melanoma whose BRAF V600E or V600K mutations have been detected in an FDA-approved trial and who have lymph node involvement after complete resection. Dabrafenib in combination with trametinib is indicated for the treatment of patients with metastatic non-small cell lung cancer (NSCLC) with BRAF V600E mutations detected in an FDA-approved trial. Dabrafenib in combination with trametinib is indicated for the treatment of patients with BRAF V600E-mutated locally advanced or metastatic anaplastic thyroid cancer (ATC) who have no satisfactory locoregional treatment options. Dabrafenib in combination with trametinib is indicated for the treatment of adult and pediatric patients aged 1 year and older with BRAF V600E-mutated unresectable or metastatic solid tumors who have progressed on prior therapy and for whom no satisfactory alternative treatment options are available. Dabrafenib in combination with trametinib is indicated for the treatment of pediatric patients aged 1 year and older with BRAF V600E-mutated low-grade glioma (LGG) who require systemic therapy. Due to known inherent resistance to BRAF inhibition, dabrafenib is not suitable for the treatment of patients with colorectal cancer. Not suitable for the treatment of patients with wild-type BRAF solid tumors.

Dabrafenibis an inhibitor of certain mutant BRAFkinases with in vitro IC50BRAF V600E, BRAF V600K and BRAF The values for V600Denzyme were 0.65, 0.5 and 1.84nm respectively. Dabrafenib also inhibited IC wild-type BRAF and CRAFkinase 50 with values of 3.2 and 5.0, respectively. nM, as well as higher concentrations of other kinases such as SIK1, NEK11 and LIMK1. Some mutations in the BRAF gene, including those leading to BRAF V600E, can lead to constitutively activated BRAF kinase, thereby stimulating tumor cell growth. Dabrafenibinhibits cell growth in various BRAF V600 mutation-positive tumors in vitro and in vivo. Dabrafeniband trimatinib target two different kinases in the RAS/RAF/MEK/ERK pathway. The combination of dabrafenib and trimetinib resulted in greater in vitro growth inhibition of BRAF V600 mutation-positive tumor cell lines and prolonged inhibition of tumor growth in BRAF V600 mutation-positive tumor xenografts compared with either agent alone. In the context of BRAFmutated colorectal cancer, induction of EGFR-mediated reactivation of the MAPK pathway is considered to be an intrinsic resistance mechanism to BRAF inhibitors. Dabrafenib mesylate is a kinase inhibitor. The chemical name of dabrafenib mesylate isN-{ 3-[5-(2-Amino-4-pyrimidinyl)-2-(1, 1-Dimethylethyl)-1,3-thiazole-4-yl]-2-Fluorophenyl}-2, 6-Difluorobenzenesulfonamide, methanesulfonate. Its molecular formula is C23H20F3N5O2S2CH4O3The molecular weight is 615.68grams/moles. If you want to get more high-quality information, you can contact Yaode. Yade will do its best to learn more about high-quality overseas drugs for you.

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