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NL-26

NL-26 is a Topoisomerase I inhibitor. NL-26 stabilizes the covalent Topoisomerase I (Topo I)-DNA complex, prevents DNA religation and triggers the DNA damage response. NL-26 induces G₂/M cell cycle arrest and apoptosis in cancer cells. NL-26 can be used for the research of colorectal cancer.

Para uso exclusivo en investigación. No vendemos a pacientes.

Fòrmula: C₂₁H₁₉N₃O₄
Peso molecular:377.39

Almacenamiento:

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

NL-26 Chemical Structure

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Use of MCE Products

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

Actividad biológica
- Descripciòn
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Pureza y Documentación
Referencias
Calculators
Help & FAQs
Classifications
Bioz

Actividad biológica

Descripciòn

Ver todos los productos específicos de isoformas Topoisomerase :

Ver todos los productos específicos de isoformas DNA/RNA Synthesis :

In Vitro

NL-26 (48 h) potently inhibits the proliferation of HCT116 human colon cancer cells in vitro, with a GI₅₀ of 1.03 μM^[1].
NL-26 (48 h) inhibits proliferation of A549 human lung cancer cells (GI₅₀ = 4.35 μM) and 4T1 mouse breast cancer cells (GI₅₀ = 4.84 μM) in vitro, with minimal activity against HL-60, PC-3, HepG2, and normal H9C2 cells (GI₅₀ >10 μM)^[1].
NL-26 (0.6-2.4 μM; 7-10 days) potently and dose-dependently inhibits long-term colony formation of HCT116 human colon cancer cells in vitro, with near-complete suppression at 2.4 μM^[1].
NL-26 (0.6-2.4 μM; 12 h) dose-dependently induces G2/M phase cell cycle arrest in HCT116 human colon cancer cells in vitro, with a 37.4% G2/M population at 2.4 μM after 12 h of treatment^[1].
NL-26 (0.6-2.4 μM; 24 h) dose-dependently induces apoptosis in HCT116 human colon cancer cells in vitro, with a total apoptotic rate of 39.3% at 2.4 μM after 24 h of treatment^[1].
NL-26 (0.6-2.4 μM; 8 h) dose-dependently activates the DNA damage response in HCT116 human colon cancer cells in vitro, as evidenced by increased γH2AX and PARP-1 protein levels after 8 h of treatment^[1].
NL-26 (0.6-2.4 μM; 24 h) dose-dependently inhibits the migratory capacity of HCT116 human colon cancer cells in vitro, reducing wound closure to 20.53% at 2.4 μM after 24 h of treatment^[1].
NL-26 (0.6-2.4 μM; 24 h) dose-dependently inhibits the invasive capacity of HCT116 human colon cancer cells in vitro after 24 h of treatment^[1].
NL-26 (0.6-2.4 μM; 8 h) dose-dependently modulates apoptotic regulatory proteins in HCT116 human colon cancer cells in vitro, downregulating XIAP and Bcl-2 and upregulating Cleaved Caspase-3 after 8 h of treatment^[1].

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

Cell Proliferation Assay^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

7-10 days
Result:

Suppressed colony formation of HCT116 cells in a dose-dependent manner.
Almost completely eliminated colony growth at the highest concentration (2.4 μM).

Cell Cycle Analysis^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

12 h
Result:

Induced G2/M phase arrest in a dose-dependent manner.
Increased the G2/M phase cell population from 24.3% (control) to 37.4% at 2.4 μM.

Apoptosis Analysis^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

24 h
Result:

Induced apoptosis in a dose-dependent manner.
Increased the total apoptotic rate from 9.9% (control) to 39.3% at 2.4 μM.

Cell Migration Assay ^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

24 h
Result:

Significantly attenuated the wound closure rate of HCT116 cells in a dose-dependent manner.
Restricted the healing rate to 20.53% at the highest concentration (2.4 μM) at 24 h.

Cell Invasion Assay^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

24 h
Result:

Significantly reduced the number of invasive HCT116 cells in a dose-dependent manner compared to the control group.

Western Blot Analysis^[1]

Cell Line:

HCT116 human colon cancer cells
Concentration:

0.6, 1.2 and 2.4 μM
Incubation Time:

8 h
Result:

Induced a dose-dependent increase in γH2AX and PARP-1 protein levels, markers of DNA double-strand breaks and DNA damage response activation, respectively.\nInduced a dose-dependent downregulation of anti-apoptotic proteins XIAP and Bcl-2.
Induced a dose-dependent upregulation of pro-apoptotic Cleaved Caspase-3.

Parmacokinetics

Species	Dose	Route	C₀	T_max	T_1/2	AUC_0-t	AUC_0-∞	MRT_0-t	MRT_0-∞	CL	V_d
Mice^[1]	5 mg/kg	i.v.	746.4 ng/mL	0.03 h	3.7 h	1979.7 ng·h/mL	1986.5 ng·h/mL	3.641 h	3.673 h	2.52 L/h/kg	10.91 L/kg

In Vivo

NL-26 (20 mg/kg; i.v.; every other day; 14 days) achieves 55.1% tumor growth inhibition in HCT116 xenograft mice, with robust suppression of tumor cell proliferation and a favorable safety profile^[1].

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

Animal Model:

BALB/c-nu (female, SPF-grade, subcutaneous HCT116 xenograft model)^[1]
Dosage:

20 mg/kg
Administration:

i.v.; every other day; 14 days
Result:

Achieved a tumor growth inhibition (TGI) rate of 55.1%.
Markedly downregulated the proliferation marker Ki-67 in tumor tissues.
Showed no signs of systemic toxicity; maintained stable body weight comparable to control group, and showed no treatment-related lesions or tissue damage in major organs upon histopathological analysis.

Related Protocols :

Chemical Information

Peso molecular 377.39
Fòrmula C₂₁H₁₉N₃O₄
SMILES

O=C1COC2=CC=C3C(C=C(OC3=C2N1)C4=CC=C(C=C4)N5CCNCC5)=O
Envío

Room temperature in continental US; may vary elsewhere.
Almacenamiento

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

Pureza y Documentación

Instrucciones de manejo (2659 KB)

Referencias

[1]. Shi X, et al. Rational design and synthesis of flavonolactam derivatives as potent topo I inhibitors with antitumor activity. Eur J Med Chem. Published online March 28, 2026. [Content Brief]

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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100 mg

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