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A Study to Evaluate the Safety, Tolerability, and Activity of TAK-931 in Participants With Metastatic Pancreatic Cancer, Metastatic Colorectal Cancer, and Other Advanced Solid Tumors

ABSTRACT: The purpose of this study is to confirm the safety and tolerability of TAK-931 in a cohort of Western participants with metastatic solid tumors and to evaluate the anti-tumor activity of TAK-931 in participants with metastatic pancreatic cancer, colorectal cancer (CRC), squamous esophageal cancer (sqEC), and squamous non-small-cell lung cancer (sqNSCLC).

DISEASE(S): Esophageal Neoplasms,Metastatic Pancreatic Cancer,Colorectal Cancer,Colorectal Neoplasms,Carcinoma, Non-small-cell Lung,Pancreatic Neoplasms

PROVIDER: 2252731 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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TAK-981

Project description:TAK-981

| PRJNA723842 | ENA

SUMOylation inhibitor TAK-981 potentiates rituximab activity by Type I IFN-dependent macrophage and NK cell stimulation

Project description:SUMOylation is a reversible post-translational modification that has been implicated in the regulation of various cellular processes including inflammatory responses and expression of Type I interferons (IFN1). In this report, we have explored the activity of the selective small molecule SUMOylation inhibitor TAK-981 in promoting antitumor innate immune responses. We demonstrate that treatment with TAK-981 results in IFN1-dependent macrophage and NK cell activation, promoting macrophage phagocytosis and NK cell cytotoxicity in ex vivo assays. Furthermore, pre-treatment with TAK-981 enhanced macrophage phagocytosis or NK cell cytotoxicity against CD20-positive target cells in combination with the anti-CD20 antibody rituximab. In vivo studies demonstrated synergistic antitumor activity of TAK-981 and rituximab in CD20-positive lymphoma xenograft models. TAK-981 is currently being studied in phase 1 clinical trials (NCT03648372, NCT04074330, NCT04776018, and NCT04381650) for the treatment of patients with lymphomas and solid tumors.

2024-04-24 | GSE185841 | GEO

The SUMOylation inhibitor TAK-981 induces a transcriptional reprogramming in human Natural Killer cells [RNA-seq]

Project description:SUMOylation, a post-translational modification of the ubiquitin family plays a critical role in the regulation of proteins function and fate. TAK-981 (Subasumstat) is a first-in-class inhibitor of the SUMO-activating enzyme used in various phase I/II clinical trials for solid tumors and lymphomas. In addition to its direct cytotoxic effect on cancer cells, TAK-981 activates anti-tumor immune response. We show here that TAK-981 activates human natural killer cells. TAK-981 mostly regulates genes involved in inflammation and immune response, in particular those related to the type-I and type-II interferon pathway.

2024-02-28 | GSE255279 | GEO

Marchantia polymorpha subsp. ruderalis cultivar:Tak-1 + Tak-2

Project description:Marchantia polymorpha subsp. ruderalis cultivar:Tak-1 + Tak-2 Genome sequencing and assembly

| PRJNA310693 | ENA

Marchantia polymorpha subsp. ruderalis strain:Tak-1 and Tak-2

Project description:Marchantia polymorpha whole-genome sequencing for strains Tak-1 and Tak-2

| PRJDB16711 | ENA

A Study of TAK-186 (Also Known as MVC-101) in Adults With Advanced or Metastatic Cancer

Project description:The main aim of this study is to check for side effects and tolerability of TAK-186 (also known as MVC-101) in adults with unremovable advanced or metastatic cancer. Another aim is to characterize and evaluate the activity of TAK-186 (MVC-101). Participants may receive treatment throughout the study for a maximum of 13 months and will be followed up at 30 days and then every 12 weeks for up to 48 weeks after the last treatment.

| 2374243 | ecrin-mdr-crc

A genome-wide CRISPR/Cas9 screen in acute myeloid leukemia cells identifies regulators of TAK-243 sensitivity

Project description:TAK-243 is a first-in-class inhibitor of ubiquitin-like modifier activating enzyme 1 (UBA1) that catalyzes ubiquitin activation, the first step in the ubiquitylation cascade. Based on its preclinical efficacy and tolerability, TAK-243 has been advanced to phase 1 clinical trials in advanced malignancies. Nonetheless, the determinants of TAK-243 sensitivity remain largely unknown. Here, we conducted a genome-wide CRISPR/Cas9 knockout screen in acute myeloid leukemia (AML) cells in the presence of TAK-243 to identify genes essential for TAK-243 action. We identified BEN domain-containing protein 3 (BEND3), a transcriptional repressor and a regulator of chromatin organization, as the top gene whose knockout confers resistance to TAK-243

2021-01-13 | GSE164639 | GEO

SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence [ChIP-Seq, ATAC-Seq]

Project description:We analyzed ChIP-seq, chromatin accessibility and RNA-seq across mouse esophageal squamous organoids and human esophageal squamous cell cancer

2021-03-17 | GSE167366 | GEO

SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence [RNA-Seq]

Project description:We analyzed ChIP-seq, chromatin accessibility and RNA-seq across mouse esophageal squamous organoids and human esophageal squamous cell cancer

2021-03-17 | GSE167365 | GEO

Comparative hepatic transcriptome analyses revealed possible pathogenic mechanisms of fasiglifam (TAK-875)-induced acute liver injury in mice

Project description:Fasiglifam (TAK-875), a G protein-coupled receptor 40 (GPR40) agonist, was a drug candidate for type 2 diabetes. However, its development was terminated in phase 3 trials due to liver safety concerns. Although TAK-875 was reported to inhibit hepatobiliary transporters and disturb bile acid disposition, pathogenic mechanisms of TAK-875-induced liver injury are not fully understood. In this study, we sought to identify the mechanisms with a hepatic genome-wide transcriptomic analysis in a murine model. We demonstrated that, among the three GPR40 agonists, TAK-875, AMG-837 and TUG-770, only TAK-875 induced acute liver injury in mice. Transcriptome profiles of TAK-875-exposed liver was compared with those of non-hepatotoxic analogues AMG-837 and TUG-770 as negative controls and those of classical hepatotoxicants concanavalin A and carbon tetrachloride as positive controls. The comparative hepatic transcriptome analyses revealed the enrichment of genes involved in inflammation, endoplasmic reticulum (ER) stress, apoptosis, and hepatic lipid accumulation, suggesting that these events play pathophysiologic roles in the development of TAK-875-induced liver injury. These results were validated by quantitative PCR with significant changes in chemokines, danger signals, ER stress mediators, proapoptotic factors, and hepatic steatosis markers only in TAK-875-exposed liver. Pretreatment of TAK-875-administered mice with an ER stress inhibitor 4-phenylbutyric acid (4-PBA) alleviated the liver injury. Consistent with the in vivo study, pretreatment of HepG2 cells with 4-PBA significantly improved the decrease of cell viability induced by TAK-875. In conclusion, by a comprehensive transcriptomic analysis of GPR40 agonists, we found multiple possible processes that contribute to TAK-875-induced acute liver injury in mice.

2018-10-10 | GSE112140 | GEO

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