ZY-MY-111
ZY-MY-111 is a selective interleukin-4-induced-1 (IL4I1) inhibitor (IC50 = 1.86 μM). ZY-MY-111 competitively occupies the catalytic pocket of IL4I1 and disrupts Trp-AHR signaling in cells. ZY-MY-111 promotes T cell proliferation, enhancing immune responses against the tumor cells. ZY-MY-111 can be used to study colon carcinoma and lymphoma.
For research use only. We do not sell to patients.
- Formula: C16H14ClFN2S
- Molecular Weight:320.81
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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IL4I1 1.86 μM (IC50) |
ZY-MY-111 (30 min) exhibits potent and selective inhibition against IL4I1 with an IC50 of 1.86 μM, while showing no inhibition of IDO1-mediated tryptophan metabolism even at 10 μM[1].
ZY-MY-111 (100 μM) shows stable binding to IL4I1, as demonstrated by a significant thermal shift (ΔTm = 4.5 °C) at 100 μM in thermal shift assay[1].
ZY-MY-111 (5.6 μM; 30 min) reversibly binds to IL4I1, as evidenced by time-dependent attenuation of its inhibitory activity in dialysis assays[1].
ZY-MY-111 (1.25-20 μM; 30 min) exhibits concentration-dependent effects on IL4I1-mediated oxidative deamination kinetics in substrate titration experiments[1].
ZY-MY-111 (1.25-20 μM; 30 min) shows mixed-type inhibition of IL4I1, with increasing Km and decreasing Vmax at higher concentrations, indicating dual binding to the catalytic site and an allosteric pocket[1].
ZY-MY-111 (24 h) dose-dependently suppresses basal AHR activation with an IC50 of 2.14 μM and compromises tryptophan-induced AHR signaling at 148 μM L-tryptophan co-treatment in HEK293T-XRE reporter cells[1].
ZY-MY-111 (1.25-10 μM; 36 h) suppresses CYP1A1 expression and this effect is attenuated in IL4I1-knockdown cells, confirming that its inhibition of AHR signaling is dependent on IL4I1 in HEK293T-XRE reporter cells[1].
ZY-MY-111 (1.25-5 μM; 36 h) suppresses key AHR pathway genes, and this effect is diminished when IL4I1 levels are reduced in HEK293T-XRE reporter cells[1].
ZY-MY-111 (10 μM; 24 h) significantly suppresses L-tryptophan (HY-N0623) (500 μM)-induced AHR nuclear accumulation and rescues the up-regulation of CYP1A1 expression in HT-29 cells[1].
ZY-MY-111 (2.5-20 μM; 72 h) dose-dependently restores CD8⁺ T cell proliferation in anti-CD3/CD28-activated hPBMCs at 1-20 μM, and this effect is completely abrogated by I3P and reversed by IL4I1-conditioned media blockade at 10 μM[1].
ZY-MY-111 (0.8-2.5 μM; 144 h) dose-dependently enhances the anti-tumor function of cytotoxic T cells, as revealed by quantification of tumor cell viability in GFP-expressing HT-29 cancer cells and anti-CD3/CD28-activated hPBMCs[1].
ZY-MY-111 (3 days) shows no significant direct inhibitory effect on the growth or viability of A20 or CT26 tumor cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
ZY-MY-111 (25 mg/kg; i.p.; twice a day) significantly suppresses CT26 tumor growth and remodels the immunosuppressive tumor microenvironment by blocking the IL4I1 signaling pathway, as evidenced by increased CD8⁺/CD4⁺ T cell ratio and effector memory T cell infiltration, along with reduced MDSCs and Treg frequencies in CT26 colon carcinoma-bearing mice[1].
ZY-MY-111 (50 mg/kg; i.p.; twice a day) shows no significant antitumor efficacy in immunodeficient NU/NU nude mice bearing CT26 tumors, suggesting that its tumor growth inhibition depends on T cell-mediated immune responses[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Female BALB/c mice (6–8 weeks old) were subcutaneously injected with 1 × 106 A20 B lymphoma cells in a 1:1 mixture of PBS and Matrigel in the right flank[1].
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Dosage:50 mg/kg
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Administration:i.p.; twice a day
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Result:Significantly suppressed tumor growth.
Increased the CD8⁺/CD4⁺ T cell ratio in tumor-infiltrating lymphocytes.
Induced a CD8⁺ T cell-mediated antitumor effect.
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Animal Model:Female BALB/c mice (6–8 weeks old) were subcutaneously injected with 1 × Female BALB/c mice (6–8 weeks old) were subcutaneously injected with 5 × 10⁵ CT26 colon carcinoma cells in the right flank[1].
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Dosage:25 mg/kg
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Administration:i.p.; twice a day
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Result:Significantly suppressed CT26 tumor growth.
Remodeled the immunosuppressive tumor microenvironment by blocking the IL4I1 signaling pathway.
Increased the CD8⁺/CD4⁺ T cell ratio in tumor-infiltrating lymphocytes.
Enhanced effector memory T cell infiltration.
Reduced MDSCs and Treg frequencies.
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Animal Model:Female NU/NU nude mice (6–8 weeks old) were subcutaneously injected with 5 × 10⁵ CT26 colon carcinoma cells in the right flank[1].
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Dosage:50 mg/kg
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Administration:i.p.; twice a day
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Result:Did not significantly inhibit tumor growth.
Showed no significant antitumor efficacy.
Failed to suppress tumor growth in the absence of T cells, suggesting that its antitumor effect depends on T cell-mediated immune responses.
Chemical Information
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Molecular Weight 320.81
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Formula C16H14ClFN2S
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SMILES
FC1=CC=C2NC(N(CC2=C1)CCC3=CC(Cl)=CC=C3)=S
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
ZY-MY-111 Related Classifications
HY-184554 Related Classifications
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