Data from the National Health Commission of China in 2024 shows that the overweight and obesity rates among Chinese adults have reached 34.3% and 16.4%, respectively, meaning more than half of the adult population is overweight. Obesity is a significant risk factor for diabetes, cardiovascular diseases, various cancers, and metabolic syndrome. It is projected that by 2050, over half of the global adult population will be overweight or obese. Faced with the limited effectiveness of current lifestyle interventions and the side effects of existing medications, the development of novel, safe, and effective anti-obesity strategies is urgently needed.

Psoriatic arthritis (PsA) is a chronic inflammatory disease affecting multiple tissues, including the skin, joints, and entheses, severely restricting patients' mobility and diminishing their quality of life and work productivity. Conventional disease-modifying antirheumatic drugs (DMARDs) show limited efficacy in some patients. Existing traditional monoclonal antibody (mAb) biologics face challenges due to their large molecular size (approximately 150 kDa) and poor tissue penetration, hindering effective distribution to poorly vascularized tissues like the synovium and entheses. This results in significantly lower drug concentrations in synovial fluid compared to plasma, limiting their therapeutic potential. Studies indicate that only about one-third of patients achieve minimal disease activity (MDA) within six months of initiating biologic or targeted synthetic DMARDs. Furthermore, PsA pathogenesis is closely linked to the interleukin-17 (IL-17) cytokine family. Both IL-17A and IL-17F are overexpressed in lesional tissues and form homodimers and heterodimers that collectively drive inflammation. Inhibiting only a single cytokine is often insufficient for optimal therapeutic outcomes. Therefore, developing novel antibody therapies that combine dual-target inhibition with enhanced tissue penetration is crucial for overcoming current treatment bottlenecks in PsA.

T-cell malignancies are a group of highly aggressive hematologic tumors with high relapse rates and generally poor patient prognosis. A significant challenge arises because CD5, a characteristic marker of malignant T-cells, is also expressed on almost all normal T-cells. This makes CD5-targeting CAR-T therapies unable to distinguish friend from foe, leading them to attack normal T-cells and potentially cause immune function failure. Natural Killer (NK) cells, as key effector cells of the immune system, can recognize and eliminate tumor cells without prior antigen sensitization. Furthermore, their surface lacks CD5 expression, making them ideal effector cells for targeting CD5⁺ tumor cells.

The tumor suppressor protein p16^INK4a (p16) plays a critical role in cell cycle regulation by inhibiting CDK4/6 kinase activity, thereby preventing abnormal cell proliferation and acting as a natural "cancer guardian." However, in many cancers, the p16 gene is frequently inactivated by mutations. Missense mutations, in particular, lead to protein structural instability, making p16 prone to degradation or misfolding, and consequently, loss of its tumor-suppressive function. It is estimated that over half of familial melanomas and many sporadic tumors harbor p16 mutations. Traditional gene therapies or small-molecule drugs struggle to directly "fix" such structurally unstable proteins. Therefore, finding molecular chaperones that can stabilize mutant p16 has emerged as a new therapeutic direction.