Canonical NF-κB signaling is mechanistically related to UM cell survival, proliferation, and migration, as shown by pharmacologic inhibition like BAY11-7082, and niclosamide and genetic modulation like microRNA-9. NF-κB signaling, particularly the canonical branch, is required for UM malignancy, while noncanonical signaling is linked with high-risk features. Branch-specific genetic manipulations and clinically relevant models should be employed in future research to maximize therapeutic strategies.

To investigate the involvement of the NF-κB signaling pathway, HCT116 cells were treated with the NF-κB inhibitor Bay 11-7082...Mechanistically, TFPI-2 knockdown inhibited ferroptosis by promoting NF-κB pathway activity. This study reveals that TFPI-2 suppresses CRC progression by inducing ferroptosis through NF-κB signaling, providing new insights for future CRC therapy.

This mechanism can be effectively inhibited by silencing CXCR2 or by employing the NF-κB inhibitor BAY 11-7082...Additionally, in EC tissue samples, CXCL1 and CXCR2 expression, as well as the extent of macrophage infiltration, exhibited a significant positive relationship with disease progression, suggesting an unfavorable prognosis. In conclusion, targeting the CXCL1/CXCR2 axis is a potential therapeutic approach for EC treatment.

GSDME functions as a tumor suppressor by enhancing radiosensitivity and inhibiting proliferation and migration in ESCC, through the suppression of the NF-κB signaling pathway. These findings nominate GSDME as a promising biomarker and the NF-κB signaling pathway as a therapeutic target for overcoming radioresistance in ESCC.

P1, N=105, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

Instead, tranilast seems to indirectly suppress channel activation by reducing reactive oxygen species (ROS). This refined understanding of how tranilast modulates TRPV2 has important implications for the interpretation of prior and future pharmacological studies targeting TRPV2.

In this study, we propose a Gas-Metal Synergy Strategy, which integrates immune activation and biosafety, by engineering a pH-responsive manganese-based zeolitic imidazolate framework (named MRPH) nanoplatform co-loaded with the nitric oxide (NO) donor RRX-001...Both in vitro and in vivo studies demonstrate that MRPH significantly enhances gas-amplified metalloimmunotherapy. This work pioneers a low-toxicity paradigm that integrates gas therapy and metal-based immunotherapy, offering a transformative approach to solid tumor immunotherapy.

P2, N=80, Active, not recruiting, NodThera Limited | Recruiting --> Active, not recruiting

P2, N=50, Recruiting, Halia Therapeutics, Inc. | Not yet recruiting --> Recruiting | Initiation date: Sep 2025 --> Jan 2026

P2, N=37, Active, not recruiting, Halia Therapeutics, Inc. | Trial primary completion date: Oct 2025 --> Mar 2026

Furthermore, dapansutrile exhibits synergistic effects when combined with agents such as lonafarnib or immune checkpoint inhibitors, enhancing anti-inflammatory and anti-tumor responses. This review consolidates evidence on dapansutrile's molecular mechanisms, therapeutic applications, and biosafety, highlighting its potential as a novel, well-tolerated, and versatile anti-inflammatory agent. Future research should focus on optimizing its delivery, particularly to the central nervous system, and leveraging artificial intelligence to predict effective drug combinations.

Differentiated adipocytes were used for (1) treatment with 0, 5, 10, or 15 ng/mL of GH for 8 h, or 15 ng/mL of GH for 0, 4, 8 or 12 h; (2) co-treatment with 15 ng/mL GH and 0.1 ng/mL tumor necrosis factor α (TNF-α); (3) pretreatment with 10 μM BAY 11-7082, a nuclear factor kappa B (NF-κB) inhibitor, and then treatment with 15 ng/mL GH...Furthermore, TNF-α exacerbated GH-induced lipolysis and inflammation, whereas inhibition of NF-κB signaling pathway partially reverses these metabolic alterations of GH-treated adipocytes. These findings suggested that GH promote lipolysis in bovine adipocytes by activating inflammatory pathways.