ML-T7, a powerful inhibitor of Tim-3, effectively disrupts its interactions with PtdSer and CEACAM1. This compound enhances the antitumor activity of adoptive transfer therapy involving cytotoxic T lymphocytes (CTLs) and CAR T cells, while also boosting T cell effector functions. Additionally, ML-T7 augments the killing activity of NK cells against tumor cells and improves the antigen-presenting capacity of dendritic cells (DCs). Demonstrating antitumor efficacy in preclinical models, ML-T7 shows potential either as a standalone treatment or in combination with Nivolumab for tumor immunotherapy research [1].

ML-T7 (10 μM, 0-6 days) 通过Tim-3增强TCR/STAT5信号通路，促进CD8+细胞抗肿瘤活性 [1]; (10 μM, 24 h) 通过Tim-3和Tim-4促进DC的成熟和功能，增强DC抗原呈递能力 [1]; (10 μM, 24 h) 增强CTL激活和细胞因子产生，减少CTLs的凋亡 [1]; (10 μM, 48 h) 显著增强人NK细胞系NK92细胞中IFN-γ、TNF-α、CD107a和granzyme B的产生 [1]。Western Blot Analysis [1]: Cell Line: CD8+ cell; Concentration: 10 μM; Incubation Time: 0-6 days; Result: Increased the phosphorylation of phospholipase C–γ1 (PLC-γ1), ZAP70, LCK, ERK1/2, and STAT5 upon anti-CD3/CD28 stimulation. Cell Invasion Assay [1]: Cell Line: Bone Marrow Cells; Concentration: 10 μM; Incubation Time: 24 h; Result: Increased the expression of DC maturation markers.

ML-T7（10-50 mg/kg；腹腔注射；每隔2天，10次）可抑制肿瘤生长并延长小鼠生存期，对小鼠体重无不良影响[1]。ML-T7（20 mg/kg；腹腔注射；每隔2天，10次）与Nivolumab联合使用可增强Nivolumab的抗肿瘤效果，并显著提高HCC小鼠的存活率[1]。ML-T7（50 mg/kg，腹腔注射；每隔2天，共3周）在小鼠中表现出良好的安全性[1]。动物模型：10周龄自发性原位HCC小鼠[1]。剂量：10-50 mg/kg，给药方式：腹腔注射（i.p.），每隔2天，共10次，结果：肿瘤和脾内CD8+ T细胞增加，T细胞衰竭减少，增强CTLs、NK细胞和DCs功能。动物模型：10周龄原位Akt/c-Myc HCC小鼠[1]。剂量：20 mg/kg，给药方式：腹腔注射（i.p.），每隔2天，10次，结果：ML-T7与Nivolumab联合用药显示出更强的抗肿瘤活性，组合疗法活化NK细胞，抑制MDSCs和Tregs积累。