The lead drug product candidate (NBF-006) is a proprietary siRNA-based lipid nanoparticle (LNP) comprising GSTP siRNA (NDT-05-1040). Additionally, in a surgically implanted orthotopic lung tumor model, the survival rate of the NBF-006 treatment group was significantly prolonged (P <0.005) as compared to the vehicle control group. Together, these preclinical studies supported advancement of NBF-006 into clinical studies.

To highlight possible correlations of type 2 diabetes mellitus (T2DM) with microscopic / macroscopic characteristics of colorectal cancer tissues, along with the expression of Ten-Eleven Translocation 2 (TET2) and glutathione-S-transferase pi (GST-pi) proteins.

These changes increase the resistance of pancreatic cancer cells and xenograft tumors to IR. Our findings indicate that ferroptosis participates in irradiation-induced cell death and that GSTP1 prevents IR-induced death of pancreatic cancer cells by inhibiting ferroptosis.

Overall, furan induced liver injury, leading to the appearance of SOX9-positive hepatocytes, some of which were subjected to dedifferentiation in the inflammatory microenvironment of a cholangiocarcinoma-prone lobe. Thus, the appearance of SOX9-positive hepatocytes together with GST-P-positive hepatocytes could be initial events in furan-induced hepatocarcinogenesis via non-genotoxic mechanisms.

P1, N=49, Completed, Nitto BioPharma, Inc. | Active, not recruiting --> Completed | Trial completion date: Aug 2024 --> Mar 2024 | Trial primary completion date: Mar 2024 --> Nov 2023

Higher levels and a preferential nuclear localization of GSTP protein were also observed in HepG2 and Huh-7 hepatocarcinoma cells compared to HepaRG non-cancerous cells, along with increased basal and Ebselen-stimulated levels of free GSH and PSSG...Nrf2 nuclear translocation and β-TrCP expression also increased in HCC cells, whereas the GSTP transfection in HepaRG cells induced Nrf2 transcriptional activation. In conclusion, GSTP expression and subcellular distribution can contribute to the GSH-dependent redox reprogramming of HCC cells directly influencing the Nrf2/Keap1 system.

The current evidence is not sufficient to confirm or reject the intervention effect. Future research should consider gene-gene and gene-environment interactions, which could offer a more comprehensive understanding of the complex biology of melanoma.

Cell survival assays revealed that PRDX1 depletion substantially increased ovarian cancer cell sensitivity to cisplatin, docetaxel, and doxorubicin. Biochemical experiments showed that PRDX1 interacted with GSTP1 through Cysteine 83, which regulated GSTP1 activity as well as chemotherapy resistance in ovarian cancer cells. Our findings indicate that the molecular chaperone activity of PRDX1 is a promising new therapeutic target for ovarian cancer.

P1, N=44, Active, not recruiting, Nitto BioPharma, Inc. | Recruiting --> Active, not recruiting