Herein, we elucidate the photodegradation pathway of A-D-A-type non-fullerene acceptors for organic photovoltaics. Using IT-4F as a benchmark example, we isolated the photoproducts and proved them isomers of IT-4F formed by a 6-e electrocyclic reaction between the dicyanomethylene unit and the thiophene ring, followed by a 1,5-sigmatropic hydride shift. This photoisomerization was accelerated under inert conditions, as explained by DFT calculations predicting a triplet-mediated reaction path (quenchable by oxygen). Adding controlled amounts of the photoproduct P1 to PM6:IT-4F bulk heterojunction cells led to a progressive decrease in photocurrent and fill factor attributed to its poor absorption and charge transport properties. The reaction is a general photodegradation pathway for a series of A-D-A molecules with 1,1-dicyanomethylene-3-indanone termini, and its rate varies with the structure of the donor and acceptor moiety.

Planarity is essential for many organic electronic materials as it maximizes the intramolecular p-orbital overlap and enables efficient intermolecular interactions through pstacking. We propose as tatistical way of quantifying the planarity of awide range of conjugated systems.The quantification takes into account all torsional conformations and their relative contribution to the overall structural disorder,through ap lanarity index hcos 2 fi.T he propensity for planarization and the effect of rotational disorder were examined for aseries of commonly used building blocks.T he application of the analysis to extended conjugated systems and the correlations between the gas-phase hcos 2 fi and crystallographically observed planarity in the solid state were explored. Our calculations also reveal ap reviously unrecognized effect of increasing band gap upon planarization for conjugated systems coupling strong electron donor and acceptor units.

Caking of powder materials is undesired in various industries, and for thousands of years people are fighting against caking. Herein, the principle of caking is employed to create macroscopic plastic supramolecular films through a cold sintering process. A nanometer-sized, irregular coordinating cluster is first generated with a bulky head surfactant and multifunctional ligand, and the addition of metal ions immediately leads to amorphous white precipitates. Upon adsorbing moisture, a rearrangement of the molecules in the precipitates results in cold sintering, so that the particles in the precipitates grow into a transparent macroscopic film. The mechanical strength of the film is comparable to plastics, but allows welding and molding with finger at ambient temperature in moist environment. Mechanical tests suggest the supramolecular plastic does not fatigue even after several tens circles' remolding, indicating their superior material engineering capability. This strategy can be extended to different chemistries to fabricate films with different mechanical strength. Various functional components can be doped into the resultant films, rendering them a platform toward multifunctional materials, such as luminescent devices or sensors for pollution gases. The current strategy opens up a new vista in material science is expected.

Background Chimeric antigen receptor (CAR) T-cell therapy using brexucabtagene autoleucel (BA) induces remission in many patients with mantle cell lymphoma (MCL), and BA is the only CAR T-cell therapy approved by the FDA for MCL. However, development of relapses to BA is recognized with poor patient outcomes. Multiple CAR T-cell therapies have been approved for other lymphomas and the resistance mechanisms have been investigated. However, the mechanisms underlying BA relapse in MCL have not been investigated and whether any previously reported resistance mechanisms apply to BA-relapsed patients with MCL is unknown. Methods To interrogate BA resistance mechanisms in MCL, we performed single-cell RNA sequencing on 39 longitudinally collected samples from 15 BA-treated patients, and multiplex cytokine profiling on 80 serial samples from 20 patients. Results We demonstrate that after BA relapse, the proportion of T cells, especially cytotoxic T cells (CTLs), decreased among non-tumor cells, while the proportion of myeloid cells correspondingly increased. TIGIT, LAG3, and CD96 were the predominant checkpoint molecules expressed on exhausted T cells and CTLs; only TIGIT was significantly increased after relapse. CTLs expanded during remission, and then contracted during relapse with upregulated TIGIT expression. Tumor cells also acquired TIGIT expression after relapse, leading to the enhanced interaction of tumor cell TIGIT with monocyte CD155/PVR. In myeloid cells, post-relapse HLA-II expression was reduced relative to pretreatment and during remission. Myeloid-derived suppressor cells (MDSCs) were enriched after relapse with elevated expression of activation markers, including CLU (clusterin) and VCAN (versican). Extracellular chemokines (CCL4, CXCL9, CXCL13), soluble checkpoint inhibitors (sPD-L1, sTIM3, s4-1BB), and soluble receptors (sIL-2R, sTNFRII) were decreased during remission but elevated after relapse. Conclusions Our data demonstrate that multiple tumor-intrinsic and -extrinsic factors are associated with T-cell suppression and BA relapse. Among these, TIGIT appears to be the central player given its elevated expression after BA relapse in not only CTLs but also MCL cells. The acquisition of TIGIT expression on tumor cells is MCL-specific and has not been reported in other CAR T-treated diseases. Together, our data suggest that co-targeting TIGIT may prevent CAR T relapses and thus promote long-term progression-free survival in MCL patients.