An experimental and theoretical study of exciplex-forming compounds containing trifluorobiphenyl and 3,6-di-tert-butylcarbazole units and their performances in OLEDs

Derivatives of trifluorobiphenyl and 3,6-di-tert-butylcarbazole were synthesised as potential components of emitting layers of OLEDs. Molecular design of the compounds was performed taking into consideration the hydrogen bonding ability of the fluorine atom and electron-donating ability of the carbazole moiety. Their toluene solutions exhibited very high triplet-energy values of 3.03 eV and 3.06 eV. Ionisation energies of the compounds in the solid-state were found to be in the range from 5.98 to 6.17 eV. Density functional theory (DFT) calculations using the ωB97XD functional, with the ω parameter tuned in the presence of the solvent, uncovered singlet–triplet energy splitting in good agreement with the experimental results. The materials were tested in the emissive layers of OLEDs, showing the ability to form exciplexes with complementary electron-accepting 2,4,6-tris[3-(diphenylphosphinyl)phenyl]-1,3,5-triazine. Using the synthesised compounds as exciplex-forming materials, highly efficient exciplex emission-based OLEDs were developed. In the best case, a high maximum current efficiency of 24.8 cd A−1, and power and external quantum efficiencies of 12.2 lm W−1 and 7.8%, respectively, were achieved

Macrophage-released pyrimidines inhibit gemcitabine therapy in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDA) is characterized by abundant infiltration of tumor-associated macrophages (TAMs). TAMs have been reported to drive resistance to gemcitabine, a frontline chemotherapy in PDA, though the mechanism of this resistance remains unclear. Profiling metabolite exchange, we demonstrate that macrophages programmed by PDA cells release a spectrum of pyrimidine species. These include deoxycytidine, which inhibits gemcitabine through molecular competition at the level of drug uptake and metabolism. Accordingly, genetic or pharmacological depletion of TAMs in murine models of PDA sensitizes these tumors to gemcitabine. Consistent with this, patients with low macrophage burden demonstrate superior response to gemcitabine treatment. Together, these findings provide insights into the role of macrophages in pancreatic cancer therapy and have potential to inform the design of future treatments. Additionally, we report that pyrimidine release is a general function of alternatively activated macrophage cells, suggesting an unknown physiological role of pyrimidine exchange by immune cells