2. Cell Cycle/DNA Damage Apoptosis
  3. Topoisomerase DNA/RNA Synthesis Apoptosis
  4. 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.

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NL-26

NL-26 Chemical Structure

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NL-26 Related Antibodies

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Description

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[1].

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.

NL-26 Related Antibodies

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 Tmax T1/2 AUC0-t AUC0-∞ MRT0-t MRT0-∞ CL Vd
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.
Molecular Weight

377.39

Formula

C21H19N3O4
SMILES

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

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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NL-26 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:

NL-26NL26NL 26TopoisomeraseDNA/RNA SynthesisApoptosisHCT116 human colon cancer cellsTopo I-DNA covalent complexapoptosisG2/M phase cell cycle arrestTopoisomerase IDNA damage response4T1 mouse breast cancer cellsA549 human lung cancer cellsHCT116 xenograft micecolorectal cancerInhibitorinhibitorinhibit

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