SN-38

Catalog No.S4908 Batch:S490802

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Technical Data

Formula

C22H20N2O5
Molecular Weight 392.4 CAS No. 86639-52-3
Solubility (25°C)* In vitro DMSO 40 mg/mL (101.93 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description SN-38 (NK012) is an active metabolite of CPT-11, inhibits DNA topoisomerase I, DNA synthesis and causes frequent DNA single-strand breaks. SN-38 induces autophagy.
Targets
Topo I [1]
(Cell-free assay)
In vitro

SN-38, a biological active metabolite of  CPT-11. SN-38 causes the strongest inhibition of DNA topoisomerase I, followed by CPT and then CPT-11. CPT-11 dose dependently shifts the position of relaxed DNA in the direction of nicked DNA, but SN-38 and CPT shows no effect on the position of relaxed DNA. SN-38 dose-dependently and time-dependently inhibit DNA synthesis. Respective IC50 values of SN-38, in DNA synthesis is 0.077 μM. The inhibitory effect of SN-38 on RNA synthesis is less than that on DNA synthesis and it does not inhibit protein synthesis. SN-38 caused frequent DNA single-strand breaks in P388 cells. [1]
In vivo

After oral dosing, peak SN-38 concentrations occurrs within 1 h, and the The percent unbound SN-38 lactone in murine plasma at 1000 ng/mL is 3.4 +/- 0.67%, whereas at 100 ng/mL the percent unbound is 1.18 +/- 0.14%. SN-38 lactone AUCs in micebearing human neuroblastoma xenografts are greater than in nontumor-bearing animals. [2]

Protocol (from reference)

Kinase Assay:

[1]
  • Topoisomerase I Assay

    One unit (the minimum amount for full relaxation of 0.5 μg SV40 DNA under the conditions of this study) of topoisomerase I, 0.5 μL of the test compounds, and 0.5μg SV40 DNA are added sequentially to the reaction buffer, which is composed of 25 mM Tris-HCl (pH 7.5), 50 mM KC1, 5 mM MgCl2, 0.25 mM EDTA disodium salt, 0.25 mM dithiothreitol, 15μg /mL bovine serum albumin, and 5% glycerol. Then, the reaction mixture (50 μL) is incubated for 10 min at 37 °C, and the reaction is terminated by treatment with 7.5 μL of a solution consisting of 1% sodium dodecyl sulfate, 20 mM EDTA disodium salt, and 0.5 mg/mL proteinase K for an additional 30 min at 37°C. The samples are mixed with 5 μL of the loading buffer containing 10 mM Na2HPO4, 31.3% sucrose, and 0.3% bromophenol blue. Relaxed (form Ir) DNA is separated from supercoiled (form I) and nicked (form II) DNA by electrophoresis on 0.8% agarose gel at 50 mA and 20 V for 17 h in the presence of 2 μg/mL CHQ, 10 mM EDTA, 30 mM NaH2PO4, and 36 Mm Tris-HCl (pH 7.8). After electrophoresis, the gel is stained with 0.05% ethidium bromide and photographed with UV light (302 nm). The amount of DNA is quantified using a densitometer.
Cell Assay:

[3]
  • Cell lines

    A-172, U-87, and LA-567

  • Concentrations

    0 -1000 nM

  • Incubation Time

    48 h

  • Method

    MTT assay
Animal Study:

[4]
  • Animal Models

    Male Sprague-Dawley rats

  • Dosages

    10 mg/kg

  • Administration

    i.v.

References

  • https://pubmed.ncbi.nlm.nih.gov/1651156/
  • http://www.ncbi.nlm.nih.gov/pubmed/ 9219511
  • https://pubmed.ncbi.nlm.nih.gov/12712458/
  • https://pubmed.ncbi.nlm.nih.gov/30587986/

Customer Product Validation

<p>HCT116 cells were pretreated with tested compounds for 1 hour and then cotreated with 1 μM SN-38 for 2 hours. Cell lysates were then subjected to Western blot analysis. Data shown are representative of three independent experiments. Con, concentration.</p>

Data from [ J Pharmacol Exp Ther , 2014 , 348(3), 432-41 ]

CRC lung metastasis was established after iv injection of HT-29 LuM3 cells (1.5×106 cells in 100 μl of PBS). The polymeric nanoparticles loaded with PX866 and SN-38 were administered iv 72h after HT-29 LuM3 cells injection every q24h for 4 days and continued every q72h for 26 days (10 μg/g dose in 300 μl of PBS). PX866+SN−38 combination treatment was administered iv 72h after HT-29 LuM3 cells injection every q24h for 4 days (10 μg/g PX866 + 10 μg/g SN-38 mixed in 300 μl of PBS). Control: Empty PNP. Green: GFP expressing HT-29 LuM3 cells.

Data from [ , , J Control Release, 2018, 275:85-91 ]

Antiproliferative effects of SN-38 in vitro on 8305C (C) and FB3 (D) cell lines. The antiproliferative effects of the drugs were studied after 72 h of exposure. The data are presented as percentage of vehicle-treated cells. The concentrations of drug that reduced cell proliferation by 50% (IC50) vs controls were calculated by a nonlinear regression fit of the mean values of the data obtained in triplicate experiments (i.e. at least 9 wells for each concentration). Columns and bars, mean values ± S.E., respectively. *, P < 0.001 vs. control.

Data from [ , , Cancer Lett, 2017, 411:35-43 ]

(B) HCT116 cells were treated with increasing doses of SN-38 and treated with 4 nM SN-38 for different time. Cell extracts were prepared and analyzed by Western blotting with indicated antibody. These experiments were repeated thrice. (C) HCT116 cells were transfected with 2 μg of EGFP-LC3 construct. At 8 h post-transfection, cells were treated with 4 nM of SN-38 for 48 h. And then cells were examined by confocal microscopy (magnification × 400). The percentage of cells showing accumulation of EGFP-LC3 in puncta (EGFP-LC3vac) was quantified. (D) LOVO and HCT116 cells were treated with 2 nM and 4 nM of SN-38 combined with 10 mM of 3-Methyladenine (3-MA) for 48 h respectively. Cell extracts were prepared and analyzed by Western blotting with indicated antibody. These experiments were repeated thrice. (E) Cells were treated with indicated concentrations of 3-MA and SN-38 for 48 h. Cell apoptosis was assessed by Annexin V-FITC/PI staining assay by flow cytometry. Columns, means of three determinations; bars, SD. (F) and (G) LOVO and HCT116 cells were transfected with 50 nM of NC siRNA, ATG5 siRNA respectively, and then were treated with increasing doses of SN-38 for 48 h, the knockdown effects on ATG5 were confirmed by Western blot analysis (upper panel). Cell viability was measured using CCK8 assay. Columns, means of three determinations; bars, SD.

Data from [ , , Free Radic Biol Med, 2017, 104:280-297 ]

Selleck's SN-38 has been cited by 104 publications

Activation of lysosomal iron triggers ferroptosis in cancer [ Nature, 2025, 10.1038/s41586-025-08974-4] PubMed: 40335696
Cisplatin and temozolomide combinatorial treatment triggers hypermutability and immune surveillance in experimental cancer models [ Cancer Cell, 2025, S1535-6108(25)00223-5] PubMed: 40513578
KEAP1 and STK11/LKB1 alterations enhance vulnerability to ATR inhibition in KRAS mutant non-small cell lung cancer [ Cancer Cell, 2025, 43(8):1530-1548.e9] PubMed: 40645185
The molecular and functional landscape of resistance to FOLFIRI chemotherapy in metastatic colorectal cancer [ Cancer Discov, 2025, 10.1158/2159-8290.CD-24-0556] PubMed: 40981426
A patient-derived T cell lymphoma biorepository uncovers pathogenetic mechanisms and host-related therapeutic vulnerabilities [ Cell Rep Med, 2025, S2666-3791(25)00102-8] PubMed: 40147445
AREG and EREG Are Predictive Biomarkers of Response to EGFR Inhibition in Gastroesophageal Cancer [ Cancer Res, 2025, 85(16):3111-3122] PubMed: 40637454
Synthesis of carbon dots from spent coffee grounds: transforming waste into potential biomedical tools [ Nanoscale, 2025, 17(16):9947-9962] PubMed: 40067158
Targeted Inhibition of CHD1L by OTI-611 Reprograms Chemotherapy and Targeted Therapy-Induced Cell Cycle Arrest and Suppresses Proliferation to Produce Synergistic Antitumor Effects in Breast and Colorectal Cancer [ Cells, 2025, 14(5)318] PubMed: 40072047
ATR Inhibition Synergizes With Alkylating PI Polyamide Targeting MYCN by Suppressing DNA Repair in MYCN-Amplified Neuroblastoma [ Cancer Sci, 2025, 10.1111/cas.70043] PubMed: 40052411
PD-L1-Targeting Nanoparticles for the Treatment of Triple-Negative Breast Cancer: A Preclinical Model [ Int J Mol Sci, 2025, 26(7)3295] PubMed: 40244130

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