Lumakras (sotorasib) / Amgen 
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  • ||||||||||  JAB-3312 / Jacobio Pharma
    Enrollment open, Metastases:  JAB-3312 Based Combination Therapy in Adult Patients With Advanced Solid Tumors (clinicaltrials.gov) -  Mar 28, 2021   
    P1/2,  N=136, Recruiting, 
    The model developed in this paper may help understand the mechanism of anticancer drug resistance in KRAS-mutated lung cancer and help develop new targeted therapies to treat patients with this disease. Not yet recruiting --> Recruiting
  • ||||||||||  sotorasib (AMG 510) / Amgen
    Clinical, Journal:  The Prevalence and Concurrent Pathogenic Mutations of KRAS in Northeast Chinese Non-small-cell Lung Cancer Patients. (Pubmed Central) -  Mar 25, 2021   
    KRAS mutation is one of important driver genes in non-small-cell lung cancer (NSCLC) and the patients with KRAS mutations benefit from the inhibitor AMG510...KRAS mutation was the only isoforms of RAS family, of these 43.5% harbored the KRAS subtype in northeastern Chinese NSCLC patients. KRAS is associated with age, pathological stage and smoking status, more commonly harbored TP53/PTEN mutations, and providing more genome profile for targeted therapy in local clinical practice.
  • ||||||||||  MRTX1257 / Mirati, Lumakras (sotorasib) / Amgen, Xpovio (selinexor) / Ono Pharma, Karyopharm, Antengene
    [VIRTUAL] Inhibition of nuclear transport protein XPO1 potentiates the effect of KRAS G12C inhibitors () -  Mar 13, 2021 - Abstract #AACR2021AACR_4520;    
    Cell growth inhibition was determined by MTT assay. In conclusion, we have demonstrated that the inhibitor of nuclear transport protein XPO1 has the ability to potentiate the anticancer activity of KRASG12C inhibitors in in vitro preclinical models of PDAC and NSCLC.
  • ||||||||||  ASTX029 / Otsuka
    [VIRTUAL] Immune modulation by the dual-mechanism ERK inhibitor, ASTX029, in MAPK-activated tumor models () -  Mar 13, 2021 - Abstract #AACR2021AACR_4307;    
    P1/2
    Similar preclinical results were recently reported for a KRASG12C inhibitor, AMG 510, where treatment of in vivo models led to an increase in tumor infiltrating lymphocytes, macrophages, dendritic cells and an increase in active immune gene signatures leading to tumor immunity...Our results were consistent with increased immune activation, including increased interferon signaling and a change in the immune cell composition of the TME. These data demonstrate that treatment with ASTX029 leads to modulation of the TME and we hypothesize that to optimize therapeutic activity, ASTX029 could be partnered either with an immunomodulatory or tumor-directed agent.
  • ||||||||||  Mekinist (trametinib) / Novartis, Vectibix (panitumumab) / Amgen, Takeda, Lumakras (sotorasib) / Amgen
    [VIRTUAL] Oncogenic KRASG12C dependency in colorectal cancer () -  Mar 11, 2021 - Abstract #AACR2021AACR_3727;    
    Treatment of sotorasib in KRASG12C PDX-CRC cell lines showed that EGFR may not be the primary mediator of adaptive resistance in all models. However, inactivation of KRASG12C can be maintained through combinations targeting the kinases involved in the feedback mechanisms.
  • ||||||||||  adagrasib (MRTX849) / Mirati, Lumakras (sotorasib) / Amgen
    [VIRTUAL] Mechanisms of acquired resistance to KRAS G12C inhibition in cancer (Channel 07) -  Mar 11, 2021 - Abstract #AACR2021AACR_1482;    
    Diverse genomic and histologic mechanisms impart resistance to covalent KRASG12C inhibitors in patients with cancer. Acquired genomic mutations, amplifications, and rearrangements may be potentially targetable by combining KRASG12C inhibition with available kinase inhibitors or SHP2 inhibitors.
  • ||||||||||  AsiDNA (etidaligide) / Onxeo
    [VIRTUAL] Acquired resistance to KRASG12C inhibitors evolves from drug tolerant cells vulnerable to AsiDNA () -  Mar 11, 2021 - Abstract #AACR2021AACR_572;    
    We used continuous treatment protocols, to select resistance to KRASG12Ci Sotorasib and MRTX849 and assessed the impact of AsiDNA addition on resistance prevention and abrogation. Our results provide the evidence that resistance to KRASG12Ci can evolve from DTC, and point to the therapeutic opportunity of combining AsiDNA and KRASG12Ci to overcome tumor progression or relapse.
  • ||||||||||  BI 1823911 / Boehringer Ingelheim
    [VIRTUAL] In vitro and in vivo characterization of BI 1823911 - a novel KRASG12C selective small molecule inhibitor () -  Mar 11, 2021 - Abstract #AACR2021AACR_475;    
    Among other MAPK and PI3K pathway inhibitors, a SOS1::KRAS inhibitor was confirmed as promising combination partner. We will show results from in vitro and in vivo combination studies in NSCLC and CRC tumor models that show deep and durable responses upon combination of BI 1823911 with SOS1::KRAS inhibitor BI 1701963 providing a strong rationale for clinical investigation of this combination.
  • ||||||||||  VS-6766 / Verastem
    [VIRTUAL] Dual RAF/MEK inhibitor VS-6766 enhances antitumor efficacy of KRAS-G12C inhibitors through a vertical pathway inhibition strategy () -  Mar 11, 2021 - Abstract #AACR2021AACR_467;    
    In 3D proliferation assays in vitro, VS-6766 was synergistic with both sotorasib and adagrasib in reducing viability of a panel of KRAS G12C mt NSCLC and colorectal cancer cell lines...In KRAS G12C mt NSCLC xenograft models in vivo, combination with VS-6766 (0.3 mg/kg QD) augmented tumor growth inhibition by sotorasib (30 mg/kg QD) in the H2122 KRAS G12C mt NSCLC model, whereas trametinib (0.3 mg/kg QD) was much less effective in augmenting sotorasib efficacy...Similarly, in the H358 KRAS G12C mt NSCLC model, triple combination of VS-6766, sotorasib and a FAK inhibitor induced >35% tumor regression in 10/10 mice following 21 days of treatment. These results support the clinical evaluation of VS-6766 ± defactinib in combination with a G12C inhibitor for treatment of KRAS G12C mt solid tumors.
  • ||||||||||  ETS-001 / Etern Biopharma
    [VIRTUAL] Discovery of ETS-001, a highly potent allosteric SHP2 inhibitor to treat RTK/RAS-driven cancers () -  Mar 11, 2021 - Abstract #AACR2021AACR_401;    
    In addition, combinational benefit of ETS-001 and ribociclib was observed in esophageal cancer models, which exhibited high frequency of concurrent oncogenic alterations in RTKs and cell cycle pathway. Taken together, our findings provide preclinical evidence that ETS-001 as a potent SHP2 inhibitor, alone or in combination with other targeted-therapy agents, can effectively inhibit MAPK activation and treat cancers with diverse oncogenic mutations in the RAS/MAPK pathway.
  • ||||||||||  Lumakras (sotorasib) / Amgen
    Enrollment change, Trial primary completion date, Monotherapy, IO biomarker:  CodeBreak101: Sotorasib Activity in Subjects With Advanced Solid Tumors With KRAS p.G12C Mutation (CodeBreak 101) (clinicaltrials.gov) -  Feb 21, 2021   
    P1b,  N=1003, Recruiting, 
    Taken together, our findings provide preclinical evidence that ETS-001 as a potent SHP2 inhibitor, alone or in combination with other targeted-therapy agents, can effectively inhibit MAPK activation and treat cancers with diverse oncogenic mutations in the RAS/MAPK pathway. N=520 --> 1003 | Trial primary completion date: Jul 2027 --> May 2023