LCL161

01/01/2020 - "In this study, we found that the potency of LCL161 is not affected by the expression of ABCB1 in KB-TAX50, KB-VIN10, and NTU0.017 cancer cells. "
10/01/2014 - "This first-in-human dose-escalation study assessed the maximum-tolerated dose (MTD), safety, pharmacokinetics, and pharmacodynamics of LCL161 in patients with advanced solid tumors. "
01/01/2023 - "We describe the structural mechanism for targeting of BIRC2BIR3 by a potent but biochemically uncharacterized small molecule inhibitor LCL161 and demonstrate that LCL161 disrupts the association of endogenous BIRC2 with H3 and stimulates cell death in cancer cells. "
01/01/2023 - "LCL161 enhances expansion and survival of engineered anti-tumor T cells but is restricted by death signaling."
01/01/2020 - "In conclusion, LCL161 has the potential for use in the management of cancer patients with ABCB1 and BIRC5-related drug resistance. "

11/25/2020 - "Combination treatment with necroptosis-inducing small molecules, including a SMAC mimetic (LCL161) and a pan-BCL2 inhibitor (ABT-263), showed therapeutic efficacy in YARS-overexpressing breast cancer cells. "
01/01/2020 - "Cell culture experiments showed that LCL161 in combination with CI can significantly promote the apoptosis of breast cancer drug-resistant cells. "
01/01/2020 - "Cell culture experiments were carried out to explore the effect of LCL161 combined with CI on the proliferation of breast cancer drug-resistant cells. "
01/01/2020 - "Our results show that LCL161 combined with CI can promote the apoptosis of drug-resistant breast cancer cells by down-regulation of RRM2, CDK4, and ITGB1 expression through Cancer pathways, p53 or PI3K-AKT signaling pathway. "
01/01/2019 - "These findings support the hypothesis that LCL161 combined with caspase inhibition can induce a necroptosis effect on MCF-7/DDP cells, suggesting that it has potential to be an effective treatment for breast cancer."

10/01/2021 - "Resected lung metastases from treated and untreated mice remained sensitive to LCL161 in combination with TNFα ex vivo. "
01/01/2021 - "Functional analyses confirmed target inhibition and apoptosis induction in the LCL161 sensitive PDOs from the recurrent metastases. "
10/01/2021 - "The smac mimetic LCL161 targets established pulmonary osteosarcoma metastases in mice."
01/01/2021 - "Increased sensitivity to SMAC mimetic LCL161 identified by longitudinal ex vivo pharmacogenomics of recurrent, KRAS mutated rectal cancer liver metastases."
01/01/2021 - "Exploratory analyses of a drug screen library of 33 investigational anticancer agents showed the strongest ex vivo sensitivity to the SMAC mimetic LCL161 in PDOs of recurrent disease compared to those of the initial metastasis. "

04/01/2012 - "LCL161 showed a median relative IC(50) value of >10 µM, being more potent against several leukemia and lymphoma lines. "
12/01/2010 - "In addition, LCL161 synergized in vivo with nilotinib to reduce leukemia burden significantly below the baseline level suppression exhibited by a moderate-to-high dose of nilotinib. "
07/26/2018 - "Preliminary cellular studies in various models of leukemia, multiple myeloma, and pancreatic cancers suggest that the derived agents possess a potentially intriguing pattern of activity, especially for cell lines that are resistant to the pan-IAP antagonist and clinical candidate LCL161."

10/01/2021 - "This sensitivity has also been demonstrated in vivo using the Smac mimetic LCL161, which inhibited the growth of subcutaneous and intramuscular osteosarcomas. "
10/01/2021 - "This suggested that there was little to no acquired resistance to LCL161 treatment in surviving osteosarcoma cells and implied that tumor microenvironmental factors underlie the observed variation in responses to LCL161."
10/01/2021 - "The smac mimetic LCL161 targets established pulmonary osteosarcoma metastases in mice."
09/14/2019 - "Treatment with GDC-0152 or LCL161 suppressed the growth of subcutaneously or intramuscularly implanted osteosarcomas. "
09/14/2019 - "Previous work revealed that cells from murine osteosarcomas were efficiently sensitized by physiologically achievable concentrations of some Smac mimetics (including GDC-0152 and LCL161) to killing by the inflammatory cytokine TNFα in vitro, but survived exposure to Smac mimetics as sole agents. "