Boosting oxygen evolution reaction activity with Mo incorporated NiFe-LDH electrocatalyst for efficient water electrolysis.

This work demonstrates a simple and scalable methodology for the binder-free direct growth of Mo-doped NiFe-layered double hydroxides on a nickel substrate via an electrodeposition route at room temperature. A three-dimensional (3D) nanosheet array morphology of the electrocatalyst provides immense electrochemical surface area as well as abundant catalytically active sites. Mo incorporation in the NiFe-LDH plays a crucial role in regulating the catalytic activity of oxygen evolution reaction (OER). The prepared electrocatalyst exhibited low overpotential (i.e., 230 mV) at 30 mA cm-2 for OER in an alkaline electrolyte (i.e., 1 M KOH). Furthermore, the optimized Mo-doped NiFe-LDH electrode was used as an anode in a laboratory-scale in situ single cell test system for alkaline water electrolysis at 80 °C with a continuous flow of 30 wt% KOH, and it shows the efficient electrochemical performance with a lower cell voltage of 1.80 V at a current density of 400 mA cm-2. In addition, an admirable long-term cell durability is also demonstrated by the cell for 24 h. This work encourages new designs and further development of electrode material for alkaline water electrolysis on a commercial scale.

Targeting RAF Isoforms and Tumor Microenvironments in RAS or BRAF Mutant Colorectal Cancers with SJ-C1044 for Anti-Tumor Activity.

Colorectal cancer (CRC) is a significant global health issue characterized by a high prevalence of KRAS gene mutations. The RAS/MAPK pathway, involving KRAS, plays a crucial role in CRC progression. Although some RAS inhibitors have been approved, their efficacy in CRC is limited. To overcome these limitations, pan-RAF inhibitors targeting A-Raf, B-Raf, and C-Raf have emerged as promising therapeutic strategies. However, resistance to RAF inhibition and the presence of an immunosuppressive tumor microenvironment (TME) pose additional obstacles to effective therapy. Here, we evaluated the potential of a novel pan-RAF inhibitor, SJ-C1044, for targeting mutant KRAS-mediated signaling and inhibiting CRC cell proliferation. Notably, SJ-C1044 also exhibited inhibitory effects on immunokinases, specifically, CSF1R, VEGFR2, and TIE2, which play crucial roles in immune suppression. SJ-C1044 demonstrated potent antitumor activity in xenograft models of CRC harboring KRAS or BRAF mutations. Importantly, treatment with SJ-C1044 resulted in increased infiltration of T cells and reduced presence of tumor-associated macrophages and regulatory T cells within the TME. Thus, SJ-C1044 shows immunomodulatory potential and the ability to enhance antitumor responses. The study underscores the therapeutic potential of SJ-C1044 as a novel pan-RAF inhibitor capable of targeting oncogenic signaling pathways and overcoming immune suppression in CRC.