APL-180

The end-capping group (EG) is the essential electron-withdrawing component of nonfullerene acceptors (NFAs) in bulk heterojunction (BHJ) organic solar cells (OSCs). To systematically probe the impact of two frequent EG functionalization strategies, π-extension and halogenation, in A-DAD-A type NFAs, we synthesized and characterized four such NFAs: BT-BIC, LIC, L4F, and BO-L4F. To assess the relative importance of these strategies, we contrast these NFAs with the baseline acceptors, Y5 and Y6. Up to 16.6% power conversion efficiency (PCE) in binary inverted OSCs with BT-BO-L4F combining π-extension and halogenation was achieved. When these two factors are combined, the effect on optical absorption is cumulative. Single-crystal π-π stacking distances are similar for the EG strategies of π-extension. Increasing the alkyl substituent length from BT-L4F to BT-BO-L4F significantly alters the packing motif and eliminates the EG core interactions of BT-L4F. Electronic structure computations reveal some of the largest NFA π-π electronic couplings observed to date, 103.8 meV in BT-L4F and 47.5 meV in BT-BO-L4F. Computed electronic reorganization energies, 132 and 133 meV for BT-L4F and BT-BO-L4F, respectively, are also lower than Y6 (150 meV). BHJ blends show preferential π-face-on orientation, and both fluorination and π-extension increase NFA crystallinity. Femto/nanosecond transient absorption spectroscopy (fs/nsTA) and integrated photocurrent device analysis (IPDA) indicate that π-extension modifies the phase separation to enhance film ordering and carrier mobility, while fluorination suppresses unimolecular recombination. This systematic study highlights the synergistic effects of NFA π-extension and fluorination in affording efficient OSCs and provides insights into designing next-generation materials.

Atherosclerosis is one of the world's most aggressive diseases, claiming over 17.5 million lives per year. This disease is usually caused by high amounts of lipoproteins circulating in the blood stream, which leads to plaque formation. Ultimately, these plaques can undergo thrombosis and lead to major heart damage. A major contributor to these vulnerable plaques is macrophage apoptosis. Development of nanovehicles that carry contrast and therapeutic agents to the mitochondria within these macrophages is attractive for the diagnosis and treatment of atherosclerosis. Here, we report the design and synthesis of a dual-targeted synthetic nanoparticle (NP) to perform the double duty of diagnosis and therapy in atherosclerosis treatment regime. A library of dual-targeted NPs with an encapsulated iron oxide NP, mito-magneto (MM), with a magnetic resonance imaging (MRI) contrast enhancement capability was elucidated. Relaxivity measurements revealed that there is a substantial enhancement in transverse relaxivities upon the encapsulation of MM inside the dual-targeted NPs, highlighting the MRI contrast-enhancing ability of these NPs. Successful in vivo imaging documenting the distribution of MM-encapsulated dual-targeted NPs in the heart and aorta in mice ensured the diagnostic potential. The presence of mannose receptor targeting ligands and the optimization of the NP composition facilitated its ability to perform therapeutic duty by targeting the macrophages at the plaque. These dual-targeted NPs with the encapsulated MM were able to show therapeutic potential and did not trigger any toxic immunogenic response.