Comparison of the efficacy and applicable patients of mobosetinib (Anvili) and osimertinib

Mobocertinib and Osimertinib (Osimertinib) are both EGFR targeted drugs, but there are significant differences in their molecular mechanisms of action, applicable populations, and clinical efficacy. Osimertinib is a third-generation EGFR-TKI that mainly targets common EGFR sensitive mutations (such as exon 19 deletions and pan>L858R point mutation) and drug resistance-related T790M mutations, have become the first-line standard treatment for advanced EGFR mutated non-small cell lung cancer. Mobosetinib is a drug targeting EGFR exon 20 insertion mutation (EGFR The first oral small molecule inhibitor of ex20ins), this type of mutation accounts for a relatively low proportion of all EGFR mutations (about 4% to 12%), and traditional EGFR-TKI has limited efficacy, so the emergence of moboxetinib has filled the clinical treatment gap.

In terms of efficacy, osimertinib not only performs well in controlling lung lesions due to its good blood-brain barrier permeability and strong inhibitory activity, but also significantly improves the prognosis of patients with brain metastases. A large amount of clinical trial data shows that the median progression-free survival (PFS) of patients with EGFR mutated advanced non-small cell lung cancer as a first-line treatment with osimertinib can reach 18.9 pan> months, and the overall survival (OS) exceeds 38 months, which is much higher than the first and second generation EGFR-TKI. At the same time, osimertinib also shows unique advantages in patients with drug-resistant mutation T790M positive, making it a globally recognized standard regimen. In contrast, mobosetinib mainly targets patients with EGFR ex20ins mutations who have lacked effective treatment options in the past. In its pivotal clinical trials, the objective response rate (ORR) of patients treated with mobosetinib ranged from 28% to 35% , the median progression-free survival is about 7 months, and the overall survival can reach about 24 months, showing good efficacy, especially for the second-line or later-line treatment population.

From a safety comparison, the adverse reactions of osimertinib are generally controllable. The most common are rash, diarrhea and mild blood changes, most of which are grade 1 to 2, and can be maintained through symptomatic treatment. The adverse reactions of mobosetinib are more specific and obvious, among which diarrhea is the most common. Some patients may have severe diarrhea of u200bu200bgrade 3 or above, which requires drug reduction or short-term drug withdrawal to alleviate the problem. In addition, moboxetinib may also cause prolongation of the QT interval, abnormal renal function indicators, and loss of appetite, which requires closer monitoring during its use. Therefore, although mobosetinib provides new treatment opportunities for patients with EGFR ex20ins mutations, its tolerability and adverse reaction management are more difficult than osimertinib.

In terms of patient selection, osimertinib is suitable for the vast majority of patients with common sensitive mutations in EGFR, including newly diagnosed late-stage patients and relapsed patients with T790M resistance mutations. Its clinical status has been very stable and has been widely included in international and domestic guidelines. The application population of mobosetinib is even more niche, mainly targeting patients with EGFR ex20ins mutation-positive non-small cell lung cancer. Such patients often have limited efficacy after receiving standard chemotherapy or immunotherapy, and urgently need the intervention of precise targeted drugs. With the popularization of molecular detection technology, the detection rate of EGFR ex20ins mutations has gradually increased, and the clinical application prospects of moboxetinib have also gradually expanded. Taken together, the efficacy and safety of osimertinib in common EGFR mutated lung cancer are more established, while mobosetinib has shown unique value in rare mutation populations. The two complement each other and jointly promote the development of personalized treatment for EGFR mutated lung cancer.

Reference materials:https://www.drugs.com/