NCTD-01
NCTD-01 is an orally active NF-κB inhibitor. NCTD-01 inhibits TNF-α-induced NF-κB activation by preventing IκBα phosphorylation/degradation and nuclear translocation of NF-κB subunits, and inhibits LPS/IFN-γ-induced nitric oxide production in macrophages. NCTD-01 inhibits the differentiation of naive T cells into regulatory T cells, downregulates transcripts of pro-inflammatory and immunosuppressive mediators in colorectal tumor tissues, reduces serum pro-inflammatory cytokines, and decreases Treg-related inhibitory proteins in colorectal tissues. NCTD-01 can be used for research on colorectal cancer.
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- No. CAS: 2768833-33-4
- Fòrmula: C12H12O5
- Peso molecular:236.22
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Actividad biológica
Descripciòn
NCTD-01 is an orally active NF-κB inhibitor. NCTD-01 inhibits TNF-α-induced NF-κB activation by preventing IκBα phosphorylation/degradation and nuclear translocation of NF-κB subunits, and inhibits LPS/IFN-γ-induced nitric oxide production in macrophages. NCTD-01 inhibits the differentiation of naive T cells into regulatory T cells, downregulates transcripts of pro-inflammatory and immunosuppressive mediators in colorectal tumor tissues, reduces serum pro-inflammatory cytokines, and decreases Treg-related inhibitory proteins in colorectal tissues. NCTD-01 can be used for research on colorectal cancer[1].
IC50 & Target
[1]|
NF-κB |
IκBα |
TNF-α |
Treg |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HeLa | IC50 |
35.68 μM
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Cytotoxicity against human HeLa cells assessed by SRB assay.
Cytotoxicity against human HeLa cells assessed by SRB assay.
|
42731188 |
| A549 | IC50 |
39.09 μM
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Cytotoxicity against human A549 cells assessed by SRB assay.
Cytotoxicity against human A549 cells assessed by SRB assay.
|
42731188 |
| MDA-MB-231 | IC50 |
37.91 μM
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Cytotoxicity against human MDA-MB-231 cells assessed by SRB assay.
Cytotoxicity against human MDA-MB-231 cells assessed by SRB assay.
|
42731188 |
| HCT-116 | IC50 |
28.76 μM
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Cytotoxicity against human HCT-116 cells assessed by SRB assay.
Cytotoxicity against human HCT-116 cells assessed by SRB assay.
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42731188 |
| HT-29 | IC50 |
26.84 μM
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Cytotoxicity against human HT-29 cells assessed by SRB assay.
Cytotoxicity against human HT-29 cells assessed by SRB assay.
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42731188 |
| DLD-1 | IC50 |
19.07 μM
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Cytotoxicity against human DLD-1 cells assessed by SRB assay.
Cytotoxicity against human DLD-1 cells assessed by SRB assay.
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42731188 |
| NCM460 | IC50 |
26.33 μM
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Cytotoxicity against human NCM460 normal colon cells assessed by SRB assay.
Cytotoxicity against human NCM460 normal colon cells assessed by SRB assay.
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42731188 |
In Vitro
Innate ImmunityCytokines & ChemokinesOxidative StressAnti-cancerAdaptive ImmunityImmune Tolerance & Immunosuppression
Innate Immunity
Cytokines & Chemokines
Oxidative Stress
NCTD-01 (50 μM) inhibits LPS/IFN-γ-induced NO production in Raw264.7 macrophages with an IC50 of 10.89 μM and a CC50 >50 μM[1].
Innate Immunity
Cytokines & Chemokines
NCTD-01 suppresses TNF-α-induced NF-κB activation in HEK293T cells with an IC50 of 17.84 μM[1].
NCTD-01 (25-50 μM) suppresses TNF-α-induced p65 nuclear translocation in DLD-1 cells at 50 and 25 μM[1].
NCTD-01 (12.5-50 μM; 4 h pre-incubation, 10 min TNF-α stimulation) blocks TNF-α-induced NF-κB activation in DLD-1 cells by restoring IκBα and reducing IκBα phosphorylation at 50 μM[1].
NCTD-01 (25-50 μM) suppresses TNF-α-induced p65 nuclear translocation in DLD-1 cells at 50 and 25 μM[1].
NCTD-01 (12.5-50 μM; 4 h pre-incubation, 10 min TNF-α stimulation) blocks TNF-α-induced NF-κB activation in DLD-1 cells by restoring IκBα and reducing IκBα phosphorylation at 50 μM[1].
Anti-cancer
NCTD-01 exhibits cytotoxic activity across HeLa, A549, MDA-MB-231, HCT-116, HT-29, DLD-1, and NCM460 cells, with greatest potency against DLD-1 colorectal cancer cells (IC50 19.07 μM)[1].
Adaptive Immunity
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
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Cell Line:DLD-1 cells
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Concentration:50, 25, 12.5 μM
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Incubation Time:4 h (pre-incubation); 10 min (TNF-α stimulation)
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Result:At 50 μM, NCTD-01 restored IκBα levels and reduced IκBα phosphorylation.
In Vivo
Anti-cancerCytokines & ChemokinesAdaptive ImmunityImmune Tolerance & ImmunosuppressionInnate ImmunityOthers
Anti-cancer
Cytokines & Chemokines
Adaptive Immunity
Immune Tolerance & Immunosuppression
Innate Immunity
NCTD-01 (50-200 mg/kg; intraperitoneal injection; daily; administered for 79 days) inhibits AOM (Azoxymethane) (HY-111375)/DSS-induced orthotopic colorectal carcinogenesis in mice, improves survival, maintains colon length, reduces proliferation and inflammation/immunosuppression markers, and modulates Treg-related proteins[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (female, 5-6 weeks old)[1]
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Dosage:200 mg/kg
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Administration:p.o.; daily; for 7 days during DSS induction
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Result:In the acute colitis model, mice receiving NCTD-01 exhibited reduced body weight loss, showing a protective trend comparable to that of the group receiving 5-Aminosalicylic acid (5-ASA) (HY-15027).
Notably, NCTD-01 improved survival rates relative to the model group.
Histopathological analysis via H&E staining further confirmed these findings.
The model group exhibited extensive mucosal ulceration, destruction of crypt architecture with abscess formation, marked inflammatory cell infiltration in the lamina propria, and near-complete loss of goblet cells.
In contrast, mice receiving NCTD-01 orally at 200 mg/kg showed reduced ulcerated areas in the colorectal mucosa, more regularly arranged crypts, increased goblet cell numbers, and substantially reduced inflammatory cell infiltration.
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Animal Model:BALB/c (male, 5-6 weeks old)[1]
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Dosage:50 mg/kg; 100 mg/kg; 200 mg/kg
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Administration:p.o.; daily; for 79 days
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Result:After 79 days, mice receiving NCTD-01 maintained higher body weights than the model group throughout the experiment.
By the final day, animals in the model group had lost approximately 15% of their initial body weight.
In contrast, NCTD-01 significantly mitigated this loss, compared with the model group, producing weight increases of 5%-15%.
Survival analysis at day 79 revealed clear differences between groups: the model group survival fell to 56%, and the low-dose NCTD-01 group (50 mg/kg) showed 85% survival.
The 5-ASA group had 92% survival.
No mortality occurred in the medium- and high-dose NCTD-01 groups (100 and 200 mg/kg), nor in the NCTD group.
Alleviated this shortening in a dose-dependent manner; the medium- and high-dose groups showed recovery of colorectal length to 8.92 cm (+14.5% vs model) and 9.42 cm (+20.9% vs model), respectively, compared to the model group.
Histopathological grading showed that the model group and the low-dose NCTD-01 group (50 mg/kg) predominantly developed moderately differentiated adenocarcinoma (G2).
In contrast, medium-dose (100 mg/kg) and high-dose (200 mg/kg) NCTD-01 significantly improved histological outcomes.
Notably, 50% of mice in the high-dose group presented with either normal mucosa or high-grade intraepithelial neoplasia, demonstrating significant suppression of malignant progression.
Dose-dependently suppressed this cellular proliferation, with the 200 mg/kg dose exhibiting the most pronounced inhibitory effect.
NCTD-01 significantly downregulated mRNA levels of IL-1β, COX-2, IL-6, and IL-10 in colorectal tissues, with reductions ranging from 40% to 80% compared to the model group.
TGF-β at 50 and 200 mg/kg showed a downward trend.
NCTD-01 induced dose-dependent decreases in serum IL-1β and TNF-α across the 50, 100, and 200 mg/kg groups, with the most pronounced inhibition at 200 mg/kg.
NCTD-01 significantly attenuated Foxp3 expression and reduced CD25 levels (P<0.05 at 50 mg/kg; P<0.001 at 100 and 200 mg/kg).
NCTD-01 downregulated PD-1 at 200 mg/kg.
NCTD-01 attenuated PD-L1 particularly at 50 and 200 mg/kg.
NCTD-01 markedly increased CD8 in the 200 mg/kg group.
Related Protocols :
- Kinase activity and phosphorylation assays
- Western Blot
- Cytoplasmic-Nuclear Fractionated Protein Extraction
- LPS-Induced Endotoxemia/Systemic Inflammation
- Naïve CD4+ T-cell subset differentiation/polarization
- Research Protocol for Inflammation-related Diseases
- Protocol for Kinase activity and phosphorylation assays
Chemical Information
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No. CAS 2768833-33-4
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Peso molecular 236.22
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Fòrmula C12H12O5
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SMILES
O=C(C1=C(C(OC)=O)C2C(C#C)CC1O2)OC
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
Calculators
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NCTD-01 Related Classifications
HY-189698 Related Classifications
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