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  • ||||||||||  Review, Journal:  The Emerging Therapeutic Landscape of ALK Inhibitors in Non-Small Cell Lung Cancer. (Pubmed Central) -  Dec 30, 2020   
    The discovery of the EML4-ALK fusion gene in a limited subset of patients affected by NSCLC and the subsequent clinical development of crizotinib in 2011 has been an impressive milestone in lung cancer research...Afterward, modern tyrosine kinase inhibitors (TKIs), such as ceritinib, alectinib, brigatinib, and lorlatinib, have been approved by the Food and Drug Administration (FDA) for the management of anaplastic lymphoma kinase (ALK)-positive NSCLCs...In this review, we provide a comprehensive overview of the state-of-the-art targeted therapy options in ALK-positive NSCLCs. Resistance, potential therapeutic strategies to overcome drug resistance, and future perspectives for this subset of patients are critically analyzed and summarized.
  • ||||||||||  Ensacove (ensartinib) / Xcovery
    Trial completion date, Trial primary completion date:  eXalt3: Study Comparing X-396 (Ensartinib) to Crizotinib in ALK Positive Non-Small Cell Lung Cancer (NSCLC) Patients (clinicaltrials.gov) -  Aug 27, 2020   
    P3,  N=290, Active, not recruiting, 
    A significant improvement in event-free survival across all models, and particularly when combined with chemotherapy in an ALK-mutant PDX model, provides preclinical rationale for further exploration of TPX-0005 in ALK-mutant pediatric tumors. Trial completion date: Dec 2020 --> Mar 2021 | Trial primary completion date: Dec 2020 --> Mar 2021
  • ||||||||||  ensartinib (X-396) / Xcovery
    [VIRTUAL] eXalt3 Findings Support Ensartinib as a First-Line Treatment Option in ALK-positive NSCLC () -  Aug 8, 2020 - Abstract #IASLCWCLCI2020IASLC-WCLC-I_17;    
    During her discussion of eXalt3, Christine Lovely, MD, of Vanderbilt University Medical Center and Vanderbilt Ingram Cancer Center, wondered how thoracic oncologists can continue to improve care for patients with ALK mutations. She offered suggestions as to next steps in terms of “thinking about combinations in the first-line that extend the benefit, … combinations in the second-line that overcome resistance, … incorporating dynamic monitoring of ctDNA into our prospective trials to be nimble in adjusting therapy, [and] consideration of comutations…, which can affect response to TKI therapy.” The final eXalt3 findings are anticipated late this year and will hopefully shed light on whether ensartinib offers a survival advantage over crizotinib.
  • ||||||||||  ensartinib (X-396) / Xcovery, Xalkori (crizotinib) / Pfizer
    [VIRTUAL] Phase 3 Randomized Study of Ensartinib vs Crizotinib in Anaplastic Lymphoma Kinase (ALK)–Positive NSCLC Patients: eXalt3 () -  Jul 29, 2020 - Abstract #IASLCWCLCI2020IASLC-WCLC-I_7;    
    P3
    She offered suggestions as to next steps in terms of “thinking about combinations in the first-line that extend the benefit, … combinations in the second-line that overcome resistance, … incorporating dynamic monitoring of ctDNA into our prospective trials to be nimble in adjusting therapy, [and] consideration of comutations…, which can affect response to TKI therapy.” The final eXalt3 findings are anticipated late this year and will hopefully shed light on whether ensartinib offers a survival advantage over crizotinib. In patients with ALK+ NSCLC, ensartinib significantly prolonged PFS over crizotinib with a favorable safety profile, representing a new option in the first-line setting.
  • ||||||||||  ensartinib (X-396) / Xcovery
    Journal:  Effects and mechanism of ensartinib (X-396) on the adhesion and metastasis of non-small cell lung cancer cells. (Pubmed Central) -  Jul 16, 2020   
    It also downregulated the expression of MMP-2 and MMP-9 in H460 and A549 cells, and inhibited the expression of Ras, p-c-Raf, p-ERK 1/2 and p-Akt upstream in a concentration- and time-dependent manner. Ensartinib inhibits the adhesion, invasion and migration of NSCLC cells, and such effect is related to downregulation of MMP-2 and MMP-9 expression, inhibition of ERK signaling pathway and p-Akt expression.