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 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.

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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 Related Antibodies

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Description

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].

In Vitro

PD-1/PD-L1-IN-62 (ZQ8) (0.25-1 μM; 48 h) exhibits minimal cytotoxicity against monocultured HepG2 cells[1].
PD-1/PD-L1-IN-62 (0.25-1 μM; 48 h) reverses PD-1/PD-L1-mediated immunosuppression in a HepG2/Jurkat T cell coculture model[1].
PD-1/PD-L1-IN-62 (0.05-0.4 μM; 48 h) dose-dependently reduces lipid accumulation in PA/OA-induced steatotic HepG2 cells, decreasing cholesterol by 41% and triglycerides by 19% at 0.4 μM[1].
PD-1/PD-L1-IN-62 (0.05-0.4 μM; 48 h) dose-dependently inhibits mTOR phosphorylation and downregulates SREBP1 expression in PA/OA-induced steatotic HepG2 cells[1].
PD-1/PD-L1-IN-62's lipid-lowering effects in Palmitic acid (HY-N0830)/Oleic acid (HY-N1446)-induced steatotic HepG2 cells are associated with modulation of the PD-L1-mTOR-SREBP1 signaling axis[1].

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

PD-1/PD-L1-IN-62 Related Antibodies

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.
In Vivo

PD-1/PD-L1-IN-62 (ZQ8) (10-20 mg/kg; intraperitoneal; once daily; 7 days) dose-dependently inhibits hepatocellular carcinoma growth in C57BL/6 mice bearing Hepa1-6 xenografts, while also enhancing tumor-infiltrating cytotoxic T cells and reducing systemic lipid levels[1].

MedChemExpress (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.
Molecular Weight

560.73

Formula

C33H44N4O4
SMILES

OC(CC1)CN1CCCCCOC2=CC(C3=CC=CC(C4=NC(OC)=C(CNCCNC(C)=O)C=C4)=C3C)=CC=C2
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References
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PD-1/PD-L1-IN-62 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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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