Synthesis of PCDTBT-Based Fluorinated Polymers for High Open-Circuit Voltage in Organic Photovoltaics: Towards an Understanding of Relationships between Polymer Energy Levels Engineering and Ideal Morphology Control

The introduction of fluorine (F) atoms onto conjugated polymer backbone has verified to be an effective way to enhance the overall performance of polymer-based bulk-heterojunction (BHJ) solar cells, but the underlying working principles are not yet fully uncovered. As our attempt to further understand the impact of F, herein we have reported two novel fluorinated analogues of PCDTBT, namely, <b>PCDTFBT</b> (1F) and <b>PCDT2FBT</b> (2F), through inclusion of either one or two F atoms into the benzothiadiazole (BT) unit of the polymer backbone and the characterization of their physical properties, especially their performance in solar cells. Together with a profound effect of fluorination on the optical property, nature of charge transport, and molecular organization, F atoms are effective in lowering both the HOMO and LUMO levels of the polymers without a large change in the energy bandgaps. <b>PCDTFBT</b>-based BHJ solar cell shows a power conversion efficiency (PCE) of 3.96 % with high open-circuit voltage (<i>V</i>_OC) of 0.95 V, mainly due to the deep HOMO level (−5.54 eV). To the best of our knowledge, the resulting <i>V</i>_OC is comparable to the record <i>V</i>_OC values in single junction devices. Furthermore, to our delight, the best <b>PCDTFBT</b>-based device, prepared using 2 % v/v diphenyl ether (DPE) additive, reaches the PCE of 4.29 %. On the other hand, doubly-fluorinated polymer <b>PCDT2FBT</b> shows the only moderate PCE of 2.07 % with a decrease in <i>V</i>_OC (0.88 V), in spite of the further lowering of the HOMO level (−5.67 eV) with raising the number of F atoms. Thus, our results highlight that an improvement in efficiency by tuning the energy levels of the polymers by means of molecular design can be expected only if their truly optimized morphologies with fullerene in BHJ systems are materialized

Additional file 2 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 2. Table S2. PFS association statistics for clinical variables and molecular features e.g. p-value, HR ratio, median PFS

Additional file 5 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 5. Table S5. Summary of oncogenic events in paired PDtumors. Endocrine therapy: endocrine therapy in combination with Palbo treatment

Additional file 1 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 1. Table S1. Sample-levelannotation including patient clinical attributes, tumor characteristics andgenomic/molecular features

Additional file 3 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 3. Table S3. PFS associationstatistics for gene signatures (GSVA scores)

Additional file 4 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 4. Table S4. Comparison of genomic alteration prevalence at BL vs. PD

Additional file 6 of Longitudinal multi-omics study of palbociclib resistance in HR-positive/HER2-negative metastatic breast cancer

Additional file 6. Fig. S1. Kaplan-Meier plots of poor prognostic biomarkers. Fig. S2. Characteristics of the HRD-high cluster. Fig. S3. Characteristics of HRD-high tumors co-occurring with TP53 mutation. Fig. S4. Kaplan-Meier plots of expression-based prognosis markers. Fig. S5. Proliferative cluster enriched in poor prognostic markers. Fig. S6. Integrative analysis identified distinct prognostic clusters. Fig. S7. Molecular characteristics of integrative clusters. Fig. S8. Subtype switching driven by changes in PAM50 score composition. Fig. S9. Increased tumor growth and proliferation at PD. Fig. S10. IHC analysis of cell cycle markers. Fig. S11. Landscape of PD-specific genomic alterations. Fig. S12. RB1 LOF associated with increased APOBEC signature at PD. Fig. S13. APOBEC signature enriched in PD-specific tumor subclones