PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34176264-0 2021 Development of Alectinib-Based PROTACs as Novel Potent Degraders of Anaplastic Lymphoma Kinase (ALK). alectinib 15-24 anaplastic lymphoma kinase Mus musculus 68-94 34176264-1 2021 A series of novel anaplastic lymphoma kinase (ALK) degraders were designed and synthesized based on proteolysis-targeting chimera (PROTAC) technology by linking two alectinib analogs (36 and 37) with pomalidomide through linkers of different lengths and types. alectinib 165-174 anaplastic lymphoma kinase Mus musculus 18-44 34176264-1 2021 A series of novel anaplastic lymphoma kinase (ALK) degraders were designed and synthesized based on proteolysis-targeting chimera (PROTAC) technology by linking two alectinib analogs (36 and 37) with pomalidomide through linkers of different lengths and types. alectinib 165-174 anaplastic lymphoma kinase Mus musculus 46-49 34176264-6 2021 Taken together, our findings suggest that alectinib-based PROTACs associated with the degradation of ALK may have promising beneficial effects for treating ALK-driven malignancies. alectinib 42-51 anaplastic lymphoma kinase Mus musculus 101-104 34176264-6 2021 Taken together, our findings suggest that alectinib-based PROTACs associated with the degradation of ALK may have promising beneficial effects for treating ALK-driven malignancies. alectinib 42-51 anaplastic lymphoma kinase Mus musculus 156-159 34176264-0 2021 Development of Alectinib-Based PROTACs as Novel Potent Degraders of Anaplastic Lymphoma Kinase (ALK). alectinib 15-24 anaplastic lymphoma kinase Mus musculus 96-99 33758275-8 2021 The combination of YHO-1701 with alectinib resulted in significantly greater antitumor activity without exhibiting body weight loss in an NCI-H2228 [echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion] xenograft mouse model. alectinib 33-42 anaplastic lymphoma kinase Mus musculus 205-208 34520436-0 2022 Sensitivity of eight types of ALK fusion variant to alectinib in ALK-transformed cells. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 30-33 34520436-0 2022 Sensitivity of eight types of ALK fusion variant to alectinib in ALK-transformed cells. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 65-68 34520436-1 2022 Tyrosine kinase inhibitors of anaplastic lymphoma kinase (ALK-TKIs) including alectinib have been the standard therapy against ALK fusion gene-positive non-small cell lung cancers (NSCLCs). alectinib 78-87 anaplastic lymphoma kinase Mus musculus 58-61 34520436-1 2022 Tyrosine kinase inhibitors of anaplastic lymphoma kinase (ALK-TKIs) including alectinib have been the standard therapy against ALK fusion gene-positive non-small cell lung cancers (NSCLCs). alectinib 78-87 anaplastic lymphoma kinase Mus musculus 127-130 34520436-4 2022 To examine the influence of ALK variants on the efficacy of ALK-TKIs, we analyzed the sensitivity to alectinib of eight types of ALK variant: three major variants (V1, V2 and V3a) and five less common variants (V4; kinesin family member 5-ALK; kinesin light chain 1-ALK; striatin, calmodulin-binding protein-ALK; and tropomyosin-receptor kinase fused gene-ALK). alectinib 101-110 anaplastic lymphoma kinase Mus musculus 129-132 34520436-7 2022 Intracellular ALK phosphorylation levels and its downstream signaling mediators, STAT3 and ERK, were suppressed by alectinib in each ALK variant-expressing Ba/F3 cell. alectinib 115-124 anaplastic lymphoma kinase Mus musculus 14-17 33728771-9 2021 These results suggested that treatment with the second-generation ALK inhibitors, alectinib and ceritinib, might serve as potent therapeutic strategies against GBM. alectinib 82-91 anaplastic lymphoma kinase Mus musculus 66-69 31972351-3 2020 METHODS: We induced alectinib-resistance in an LMC mouse model with ALK-rearranged NSCLC cell line, A925LPE3, by continuous oral alectinib treatment, established A925L/AR cells. alectinib 20-29 anaplastic lymphoma kinase Mus musculus 68-71 29048652-2 2017 Various ALK inhibitors are in clinical use for the treatment of ALK-NSCLC, including the first generation ALK inhibitor, crizotinib, and recently the more highly potent alectinib and ceritinib. alectinib 169-178 anaplastic lymphoma kinase Mus musculus 8-11 30149189-0 2018 Bioanalytical liquid chromatography-tandem mass spectrometric assay for the quantification of the ALK inhibitors alectinib, brigatinib and lorlatinib in plasma and mouse tissue homogenates. alectinib 113-122 anaplastic lymphoma kinase Mus musculus 98-101 31334113-5 2019 Employing neuroblastoma cell lines and mouse xenografts we show a clear and efficient inhibition of ALK activity by alectinib. alectinib 116-125 anaplastic lymphoma kinase Mus musculus 100-103 29048652-5 2017 Src signaling was identified as an alectinib resistance mechanism, and combination treatment with ALK and Src inhibitors was highly effective for inhibiting the growth of ALK inhibitor resistant cells in vitro and in mouse xenograft models. alectinib 35-44 anaplastic lymphoma kinase Mus musculus 98-101 29048652-5 2017 Src signaling was identified as an alectinib resistance mechanism, and combination treatment with ALK and Src inhibitors was highly effective for inhibiting the growth of ALK inhibitor resistant cells in vitro and in mouse xenograft models. alectinib 35-44 anaplastic lymphoma kinase Mus musculus 171-174 28455243-3 2017 In this study, we show that the novel ALK inhibitor alectinib effectively suppressed cell proliferation and induces apoptosis in NB cell lines with either wild-type ALK or mutated ALK (F1174L and D1091N) by blocking ALK-mediated PI3K/Akt/mTOR signaling. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 38-41 28455243-3 2017 In this study, we show that the novel ALK inhibitor alectinib effectively suppressed cell proliferation and induces apoptosis in NB cell lines with either wild-type ALK or mutated ALK (F1174L and D1091N) by blocking ALK-mediated PI3K/Akt/mTOR signaling. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 165-168 28455243-3 2017 In this study, we show that the novel ALK inhibitor alectinib effectively suppressed cell proliferation and induces apoptosis in NB cell lines with either wild-type ALK or mutated ALK (F1174L and D1091N) by blocking ALK-mediated PI3K/Akt/mTOR signaling. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 165-168 28455243-3 2017 In this study, we show that the novel ALK inhibitor alectinib effectively suppressed cell proliferation and induces apoptosis in NB cell lines with either wild-type ALK or mutated ALK (F1174L and D1091N) by blocking ALK-mediated PI3K/Akt/mTOR signaling. alectinib 52-61 anaplastic lymphoma kinase Mus musculus 165-168 26849637-2 2016 Although alectinib shows inhibitory activity against various crizotinib-resistant ALK mutations in studies using cell-free kinase assays and Ba/F3 cell-based assays, it has not been tested for efficacy against non-small cell lung cancer (NSCLC) with the ALK mutations. alectinib 9-18 anaplastic lymphoma kinase Mus musculus 82-85 26682573-9 2016 We found combination therapy targeting ALK and EGFR with alectinib and afatinib showed efficacy both in vitro and in a mouse xenograft model. alectinib 57-66 anaplastic lymphoma kinase Mus musculus 39-42 26019170-6 2015 Forced expression of EML4-ALK in Ba/F3 cells markedly increased PD-L1 expression, whereas endogenous PD-L1 expression in EML4-ALK-positive NSCLC cells was attenuated by treatment with the specific ALK inhibitor alectinib or by RNAi with ALK siRNAs. alectinib 211-220 anaplastic lymphoma kinase Mus musculus 26-29 25556163-3 2015 A recent in vitro study demonstrated significant antitumor activity of alectinib for brain metastases using mouse models of ALK-positive non-small-cell lung cancer. alectinib 71-80 anaplastic lymphoma kinase Mus musculus 124-127