-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
*Only for medical professionals to read and refer to the results of the post-mortem analysis of the Volitinib Phase II study.
The predictive value of ctDNA in the treatment of METex14+NSCLC is worth looking forward to.
MET gene abnormality accounts for about 3% of non-small cell lung cancer (NSCLC).
It is not only primary carcinogenic, but also can be an important mechanism for driving drug resistance after other gene-targeted therapies.
MET 14 exon skipping mutation (METex14+) is the most prominent type of MET abnormality.
Patients with this mutation are not sensitive to chemotherapy and have a poor prognosis.
Pulmonary sarcomatoid carcinoma (PSC) is a rare type of lung cancer with a very poor prognosis.
Nearly 1/3 of PSC patients have METex14 mutations.
In recent years, the development of targeted drugs for abnormal MET has progressed rapidly.
Among them, the local highly selective MET tyrosine kinase inhibitor Volitinib has performed outstandingly.
In the phase II clinical trial (NCT028997479) of Volitinib for the treatment of METex14+PSC or other NSCLC subtypes, the objective response rate (ORR) of all treated patients reached 47.
5%, and the disease control rate (DCR) was as high as 93.
4%, and it was safe Controllable.
On April 10, 2021, local time, at the American Association for Cancer Research (AACR) annual meeting, the Volitinib Phase II clinical study announced the ctDNA analysis in the METex14+NSCLC circulating tumor DNA (ctDNA).
savolitinib phase II study in Non-Small Cell Lung Cancer patients harboring MET exon 14 skipping alterations, abstract number CT158).What is the predictive value of ctDNA in the treatment of METex14+NSCLC? Let us take a look! Patients who were undetectable at baseline or had ctDNA cleared after treatment survived longer.
Volitinib Phase II study included patients with METex14+ unresectable or metastatic PSC or other types of NSCLC.
70 patients received Volitinib treatment, of which 25 The example is PSC (35.
7%).
Collect plasma samples before administration and during tumor assessment return visits until the disease progresses or the treatment ends.
Detect MET and other somatic genetic changes in ctDNA samples by next-generation sequencing (425 panel, Geneseeq).
A total of 66 patients provided baseline plasma samples, of which 46 (70%) had METex14 ctDNA detected at baseline.
Of these patients, 19 had PSC (19/22, 86%), and 27 had other NSCLC (27/44, 61%).
Table 1 The results of the analysis of baseline characteristics of patients showed that compared with patients with METex14 ctDNA detected at baseline, patients with no METex14 ctDNA at baseline had a longer progression-free survival (PFS) and overall survival (OS).
Figure 1 Baseline METex14 ctDNA status and clinical outcome.
Among 46 patients with METex14 ctDNA detected at baseline, 24 patients had evaluable clearance rates, of which 14 patients had ctDNA clearance (undetectable), with a median clearance time of 1.
4 months.
After treatment with Volitinib, the median PFS and median OS of patients with ctDNA clearance were significantly longer than those with ctDNA detected.
Figure 2 METex14 ctDNA clearance rate and clinical outcome Some patients have other gene mutations, which may be related to volitinib treatment resistance.
Previous studies have shown that METex14+NSCLC patients often have other mutations, which may be related to treatment resistance.
In this study, the researchers also explored the genetic changes that occurred at the same time as METex14.
The results showed that of the 21 samples that could be analyzed for ctDNA at baseline and disease progression, 12 (57%) patients also observed other genetic changes, such as KRAS, NRAS, BRAF, PIK3CA, and secondary MET mutations and FGF19 amplification.
These mutations may be related to volitinib resistance.
Figure 3 Summary of mutations that may be related to volitinib resistance: ctDNA is a free genomic fragment released by only tumor cells that carries tumor-specific genetic changes.
It can reveal the comprehensive genetic information of the tumor and more accurately reflect the tumor tissue Heterogeneity and tumor burden.
Due to the convenience of sampling, ctDNA has been widely used in tumor diagnosis, efficacy evaluation, real-time monitoring, individualized medication, and recurrence prediction.
The post-hoc analysis of ctDNA in the phase II study of Volitinib reported in this conference showed that among METex14+NSCLC patients, patients who were undetectable at baseline or who had cleared ctDNA after treatment with Volitinib had a longer survival time.
In addition, the study found that some patients also have KRAS, NRAS, BRAF and other mutations, which may be related to volitinib resistance.
We look forward to further verifying the predictive value of ctDNA in the treatment of METex14+NSCLC in an expanded population.
The predictive value of ctDNA in the treatment of METex14+NSCLC is worth looking forward to.
MET gene abnormality accounts for about 3% of non-small cell lung cancer (NSCLC).
It is not only primary carcinogenic, but also can be an important mechanism for driving drug resistance after other gene-targeted therapies.
MET 14 exon skipping mutation (METex14+) is the most prominent type of MET abnormality.
Patients with this mutation are not sensitive to chemotherapy and have a poor prognosis.
Pulmonary sarcomatoid carcinoma (PSC) is a rare type of lung cancer with a very poor prognosis.
Nearly 1/3 of PSC patients have METex14 mutations.
In recent years, the development of targeted drugs for abnormal MET has progressed rapidly.
Among them, the local highly selective MET tyrosine kinase inhibitor Volitinib has performed outstandingly.
In the phase II clinical trial (NCT028997479) of Volitinib for the treatment of METex14+PSC or other NSCLC subtypes, the objective response rate (ORR) of all treated patients reached 47.
5%, and the disease control rate (DCR) was as high as 93.
4%, and it was safe Controllable.
On April 10, 2021, local time, at the American Association for Cancer Research (AACR) annual meeting, the Volitinib Phase II clinical study announced the ctDNA analysis in the METex14+NSCLC circulating tumor DNA (ctDNA).
savolitinib phase II study in Non-Small Cell Lung Cancer patients harboring MET exon 14 skipping alterations, abstract number CT158).What is the predictive value of ctDNA in the treatment of METex14+NSCLC? Let us take a look! Patients who were undetectable at baseline or had ctDNA cleared after treatment survived longer.
Volitinib Phase II study included patients with METex14+ unresectable or metastatic PSC or other types of NSCLC.
70 patients received Volitinib treatment, of which 25 The example is PSC (35.
7%).
Collect plasma samples before administration and during tumor assessment return visits until the disease progresses or the treatment ends.
Detect MET and other somatic genetic changes in ctDNA samples by next-generation sequencing (425 panel, Geneseeq).
A total of 66 patients provided baseline plasma samples, of which 46 (70%) had METex14 ctDNA detected at baseline.
Of these patients, 19 had PSC (19/22, 86%), and 27 had other NSCLC (27/44, 61%).
Table 1 The results of the analysis of baseline characteristics of patients showed that compared with patients with METex14 ctDNA detected at baseline, patients with no METex14 ctDNA at baseline had a longer progression-free survival (PFS) and overall survival (OS).
Figure 1 Baseline METex14 ctDNA status and clinical outcome.
Among 46 patients with METex14 ctDNA detected at baseline, 24 patients had evaluable clearance rates, of which 14 patients had ctDNA clearance (undetectable), with a median clearance time of 1.
4 months.
After treatment with Volitinib, the median PFS and median OS of patients with ctDNA clearance were significantly longer than those with ctDNA detected.
Figure 2 METex14 ctDNA clearance rate and clinical outcome Some patients have other gene mutations, which may be related to volitinib treatment resistance.
Previous studies have shown that METex14+NSCLC patients often have other mutations, which may be related to treatment resistance.
In this study, the researchers also explored the genetic changes that occurred at the same time as METex14.
The results showed that of the 21 samples that could be analyzed for ctDNA at baseline and disease progression, 12 (57%) patients also observed other genetic changes, such as KRAS, NRAS, BRAF, PIK3CA, and secondary MET mutations and FGF19 amplification.
These mutations may be related to volitinib resistance.
Figure 3 Summary of mutations that may be related to volitinib resistance: ctDNA is a free genomic fragment released by only tumor cells that carries tumor-specific genetic changes.
It can reveal the comprehensive genetic information of the tumor and more accurately reflect the tumor tissue Heterogeneity and tumor burden.
Due to the convenience of sampling, ctDNA has been widely used in tumor diagnosis, efficacy evaluation, real-time monitoring, individualized medication, and recurrence prediction.
The post-hoc analysis of ctDNA in the phase II study of Volitinib reported in this conference showed that among METex14+NSCLC patients, patients who were undetectable at baseline or who had cleared ctDNA after treatment with Volitinib had a longer survival time.
In addition, the study found that some patients also have KRAS, NRAS, BRAF and other mutations, which may be related to volitinib resistance.
We look forward to further verifying the predictive value of ctDNA in the treatment of METex14+NSCLC in an expanded population.
