2. Immunology/Inflammation PI3K/Akt/mTOR
  3. PD-1/PD-L1 mTOR
  4. PD-1/PD-L1-IN-62

PD-1/PD-L1-IN-62 是一种 PD-L1 抑制剂和 mTOR 调节剂。PD-1/PD-L1-IN-62 抑制 PD-L1 的 IC50 为 6.9 nM，并解除 PD-1/PD-L1 通路介导的免疫抑制。PD-1/PD-L1-IN-62 通过抑制 mTOR 磷酸化并下调下游靶点 SREBP1，显著降低胆固醇和甘油三酯水平以减少脂质蓄积。PD-1/PD-L1-IN-62 能够促进 CD3+CD8+ T 细胞向肿瘤组织浸润，进而有效抑制肿瘤生长。PD-1/PD-L1-IN-62 可用于肝细胞癌的研究。

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PD-1/PD-L1-IN-62

PD-1/PD-L1-IN-62 Chemical Structure

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PD-1/PD-L1-IN-62 相关抗体

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mTOR mTORC1 mTORC2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

PD-1/PD-L1-IN-62 is a PD-L1 inhibitor and mTOR modulator. PD-1/PD-L1-IN-62 inhibits PD-L1 with an IC50 of 6.9 nM and abrogates immune suppression mediated by the PD-1/PD-L1 pathway. By inhibiting mTOR phosphorylation and downregulating the downstream target SREBP1, PD-1/PD-L1-IN-62 significantly reduces cholesterol and triglyceride levels to decrease lipid accumulation. PD-1/PD-L1-IN-62 promotes the infiltration of CD3+CD8+ T cells into tumor tissues, thereby effectively inhibiting tumor growth. PD-1/PD-L1-IN-62 can be used for the research of hepatocellular carcinoma[1].\n
体外研究
(In Vitro)

PD-1/PD-L1-IN-62 (ZQ8) (0.25-1 μM; 48 h) 对单独培养的 HepG2 细胞仅表现出极低的细胞毒性[1]。
PD-1/PD-L1-IN-62 (0.25-1 μM; 48 h) 可逆转 HepG2/Jurkat T 细胞共培养模型中 PD-1/PD-L1 介导的免疫抑制[1]。
PD-1/PD-L1-IN-62 (0.05-0.4 μM; 48 h) 可剂量依赖性地减少 PA/OA 诱导的脂肪变性 HepG2 细胞中的脂质蓄积，在 0.4 μM 浓度下可使胆固醇降低 41%、甘油三酯降低 19%[1]。
PD-1/PD-L1-IN-62 (0.05-0.4 μM; 48 h) 可在 PA/OA 诱导的脂肪变性 HepG2 细胞中呈剂量依赖性抑制 mTOR 磷酸化并下调 SREBP1 的表达[1]。
PD-1/PD-L1-IN-62 在 Palmitic acid (HY-N0830)/Oleic acid (HY-N1446) 诱导的脂肪变性 HepG2 细胞中的降脂作用与 PD-L1-mTOR-SREBP1 信号轴的调控相关[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

PD-1/PD-L1-IN-62 相关抗体:

Cell Cytotoxicity Assay[1]

Cell Line: HepG2/Jurkat T cell coculture
Concentration: 0.25-1 μM (coculture); 10 ng/mL IFN-γ (HepG2 pretreatment); PHA-P (HY-N7038A) (Jurkat pretreatment)
Incubation Time: 48 h (coculture); 24 h (HepG2 pretreatment); 48 h (Jurkat pretreatment)
Result: Reduced HepG2 cell viability in a concentration-dependent manner in the coculture model.
At 1 μM, reduced HepG2 viability to 65.4%, showing significantly enhanced potency compared to NP19 (73.3% viability) and BMS-202 (78.9% viability).

Western Blot Analysis[1]

Cell Line: PA/OA-induced steatotic HepG2 cells
Concentration: 0.05-0.4 μM (with PA/OA); 0.25 mM PA/0.5 mM OA
Incubation Time: 48 h
Result: Dose-dependently suppressed phosphorylation of mTOR, with a 40% reduction at 0.4 μM, while total mTOR levels remained unchanged.
Concomitantly, downregulated SREBP1 expression in a dose-dependent manner.
体内研究
(In Vivo)

PD-1/PD-L1-IN-62 (ZQ8) (10-20 mg/kg；腹腔注射；每日 1 次；连续 7 天) 可剂量依赖性地抑制荷 Hepa1-6 移植瘤的 C57BL/6 小鼠的肝细胞癌生长，同时还能增加肿瘤浸润细胞毒性 T 细胞数量并降低全身血脂水平[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 mice with Hepatocellular carcinoma[1]
Dosage: 10 mg/kg; 20 mg/kg
Administration: intraperitoneal; once daily; 7 days
Result: Achieved 75.1% tumor volume reduction and 64.7% tumor weight reduction, with no significant body weight fluctuations or overt toxicities observed.
Achieved 86.2% tumor volume reduction and 73.4% tumor weight reduction, with no significant body weight fluctuations or overt toxicities observed.
Increased the proportion of CD3+CD8+ cytotoxic T cells in tumor tissues to 5.5%.
Reduced serum triglyceride levels to 65.5% of the control group levels.
Reduced serum total cholesterol levels to 78.4% of the control group levels.
Induced a mild, non-statistically significant reduction in lipid accumulation within tumor tissues via Oil Red O staining.
分子量

560.73

Formula

C33H44N4O4
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

PD-1/PD-L1-IN-62 相关分类

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Keywords:

PD-1/PD-L1-IN-62PD-1/PD-L1mTORPD-1/Programmed death-ligand 1Mammalian target of Rapamycinhepatocellular carcinomaSREBP1PD-L1CD3+CD8+ T-cellC57BL/6 miceJurkat T cellPD-1/PD-L1 pathwayHepG2 cellsHepa1-6 xenograftsInhibitorinhibitorinhibit

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