BOLD-100

P1/2, N=52, Recruiting, Bold Therapeutics Inc. | N=38 --> 52

P1, N=32, Not yet recruiting, University Health Network, Toronto | Initiation date: Jun 2025 --> Mar 2026

Moreover, the UTMD technique enhanced the tumoral accumulation and penetration of nanobubbles, improving delivery specificity and minimizing off-target effects. This combined treatment strategy, including UTMD, provides a promising translational potential for ESCC therapy.

The ML potential approach takes electrostatic embedding and long-range electrostatics into account. We demonstrate the applicability of the workflow on the well-studied protein-ligand complex of myeloid cell leukemia 1 and the inhibitor 19G and on the anticancer drug NKP1339 acting on the glucose-regulated protein 78.

P1, N=32, Not yet recruiting, University Health Network, Toronto

BOLD-100 synergizes with AZD6738, an ATR inhibitor, to enhance anti-tumor efficacy compared to either agent alone in both in vitro and in vivo models. These findings suggest that BOLD-100, especially in combination with an ATR inhibitor, represents a promising therapeutic option for patients with PDAC.

Our aim is to investigate cellular responses of several PM cell lines to a regimen that includes BOLD-100 in addition to other commonly used treatments. BOLD-100 is a ruthenium-based anticancer therapeutic.

This was associated with increased cholesterol uptake/biosynthesis and decreased sensitivity to the ruthenium-based anticancer drug BOLD-100. Overall, the present study contributes to shedding light on the molecular pathways connecting mechanical cues, tumor metabolism and drug responsiveness.

P1/2, N=220, Recruiting, Bold Therapeutics, Inc. | Active, not recruiting --> Recruiting | Phase classification: P1b/2a --> P1/2 | N=117 --> 220 | Trial completion date: Sep 2024 --> Sep 2026 | Trial primary completion date: Dec 2023 --> Jun 2026

These results unveil possible novel therapeutic opportunity for BRAFMT CRC. Implications: BOLD-100 induces BRAFMT-dependent replication stress, and targeted strategies against replication stress (eg. by using ATR inhibitors) in combination with BOLD-100 may serve as a potential novel therapeutic strategy for clinically aggressive BRAFMT CRC.

Among ruthenium complexes studied as anticancer metallodrugs, NKP-1339, NAMI-A, RM175, and RAPTA-C have already entered clinical trials due to their potent antitumor activity demonstrated in preclinical studies and reduced toxicity in comparison with platinum drugs...Coumarin derivative 2a positively regulated the expression and activity of c-Myc and NPM1 in RKO colon carcinoma cells, while the Ru(II) half-sandwich complex 2cRu induced downregulation of AKT and ERK signaling in PANC-1 cells concomitant with reduced intracellular levels of reactive oxygen species. Altogether, our findings indicated that coumarin-modified half-sandwich Ru(II) complexes held potential as anticancer agents against gastrointestinal malignancies.

Summarizing, BOLD-100 is identified as epigenetically active substance acting via targeting several onco-metabolic pathways. Identification of the lipid metabolism as driver of acquired BOLD-100 resistance opens novel strategies to tackle therapy failure.