Art. -Nr.: HY-189698

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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CAS. Nr.: 2768833-33-4
Formel: C₁₂H₁₂O₅
Molecular Weight:236.22

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Please store the product under the recommended conditions in the Certificate of Analysis.

NCTD-01 Chemical Structure

CAS. Nr.: 2768833-33-4

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

NF-κB

IκBα

TNF-α

Treg

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Cellular Effect

Cell Line	Type	Value	Description	References
HeLa	IC50	35.68 μM	Cytotoxicity against human HeLa cells assessed by SRB assay. Cytotoxicity against human HeLa cells assessed by SRB assay.	42731188
A549	IC50	39.09 μM	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	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	Cytotoxicity against human HCT-116 cells assessed by SRB assay. Cytotoxicity against human HCT-116 cells assessed by SRB assay.	42731188
HT-29	IC50	26.84 μM	Cytotoxicity against human HT-29 cells assessed by SRB assay. Cytotoxicity against human HT-29 cells assessed by SRB assay.	42731188
DLD-1	IC50	19.07 μM	Cytotoxicity against human DLD-1 cells assessed by SRB assay. Cytotoxicity against human DLD-1 cells assessed by SRB assay.	42731188
NCM460	IC50	26.33 μM	Cytotoxicity against human NCM460 normal colon cells assessed by SRB assay. Cytotoxicity against human NCM460 normal colon cells assessed by SRB assay.	42731188

In Vitro

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].
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 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].
NCTD-01 (2.5-20 μM) reduces mouse primary lymphocyte viability to 40% at 20 μM, while Naïve CD4⁺ T cells retain 70-90% viability during Treg differentiation at 2.5-10 μM^[1].
NCTD-01 (2.5-10 μM) dose-dependently inhibits differentiation of Naïve CD4⁺ T cells into Tregs, reducing CD4⁺CD25^highFoxp3⁺ frequency to 1.13% at 10 μM^[1].

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

Western Blot Analysis^[1]

Cell Line:

DLD-1 cells
Concentration:

50, 25, 12.5 μM
Incubation Time:

4 h (pre-incubation); 10 min (TNF-α stimulation)
Result:

At 50 μM, NCTD-01 restored IκBα levels and reduced IκBα phosphorylation.

In Vivo

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].
NCTD-01 (200 mg/kg; intraperitoneal injection; daily; administered for 7 days during DSS induction) ameliorates DSS-induced colitis in mice by reducing body weight loss and colonic inflammation^[1].

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

Animal Model:

C57BL/6 (female, 5-6 weeks old)^[1]
Dosage:

200 mg/kg
Administration:

p.o.; daily; for 7 days during DSS induction
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.

Animal Model:

BALB/c (male, 5-6 weeks old)^[1]
Dosage:

50 mg/kg; 100 mg/kg; 200 mg/kg
Administration:

p.o.; daily; for 79 days
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 :

Chemical Information

CAS. Nr. 2768833-33-4
Molecular Weight 236.22
Formel C₁₂H₁₂O₅
SMILES

O=C(C1=C(C(OC)=O)C2C(C#C)CC1O2)OC
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Handling Instructions (2659 KB)

Verweise

[1]. Wang Y, et al. Cantharidin analogue NCTD-01 inhibits AOM/DSS-induced orthotopic colorectal carcinogenesis in mice by suppressing inflammation-driven tumorigenesis. Bioorganic chemistry. 2026 Sep 10;182:110507.

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

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NCTD-01

Alle NF-κB Isoform-spezifische Produkte anzeigen

Alle IKK Isoform-spezifische Produkte anzeigen

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