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银屑病关节炎(PsA)是一种累及皮肤、关节、肌腱等多个组织的慢性炎症性疾病，严重限制患者的活动能力，并降低其生活质量与工作效率。传统改善病情抗风湿药(DMARDs)对部分患者效果有限，而现有传统单克隆抗体(mAb)生物制剂则因分子量过大(约150kDa)、组织穿透性差，难以有效分布于关节滑膜、肌腱等低血管化组织，导致滑膜液中药物浓度远低于血浆，无法充分发挥疗效。研究表明，仅约三分之一的患者在治疗6个月内能达到最小疾病活动度(MDA)。此外，PsA的发病与IL-17细胞因子家族密切相关，IL-17A和IL-17F在病灶组织中过度表达并形成同源/异源二聚体共同驱动炎症，仅抑制单一因子难以实现最佳治疗效果。因此，开发兼具双靶点抑制能力与高组织穿透性的新型抗体疗法，成为突破当前PsA治疗瓶颈的关键。

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.